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HP Phone/Database/Note | 1994-04-03 | 252.6 KB | 7,792 lines

&Title &Note Cate&gory All Fields Category: ABG's / Acid-Base nmls: pH: 7.36-7.44 PaCO2: 35-45 PaO2:=109-0.43xage(years) HCO3 AG= Na - (Cl + HCO3) PCO2 Change of 10 = pH change of .08 pH change of 0.1 = [H+] change of 10 Acute vs Chronic Resp Acidosis= Change of [H+]/ Change of PCO2 <0.3=CHRONIC >0.8=ACUTE ACID BASE DISORDERS- 3 step approach 1. Determine acid or basic pH (nml=7.36-7.45) since body does not fully compensate for primary acid- base disorders 2. Calc Anion Gap: if eq or>20 there is a primary met acidosis regardless of pH or serum bicarb (body doesnt make lrg anion to comp for primary disorders) 3. Calc Excess Anion Gap: Total AG - nml AG {12} & add back to measured serum Bicarb conc. *If calc value >nml Bicarb (>30) then there is an underlying Met Alkalosis *If calc value <nml Bicarb (<23) then there is an underlying Met Acidosis OR: for every 1 point decr of HCO3 from nml PCO2 should decr from nml by 1.2 - if less than this then there is a compensating process OR: for every 10 point incr in PCO2 pH should drop by 0.8 DELTA:DELTA: ratio of dif Of AG from NML with dif of HCO3 from NML Ratio for: Lactate 1.6:1 Ketones 1:1 ANTIBIOTICS 1. Aerobic GNR: 1)Aminoglcosides 2)Cephalosporins 2-3rd gen 3)TMP/SMX 2. Anaerobes: 1)PCN, Amp,tetra,cephI-III, Clinda. 2)Cloramphenicol 3)Metronidizole (only Chlor/Flagyl cross BBB) 3. GPC/GPR: 1)PCN 2)PCN Resistant AbTx/ Extended Spectrum: a)IV: ox,naf,meth b)PO: clox, diclox 3)Meth Resistant Organisms: (S.Aureus, St.Epi, S.Fecalis) a)S.Epi: vanco +/- gent b)MRSA: Vanco 4)ENTEROCOCCUS: a)non SBE: AMP b)SBE: PCN/VANCO + AMINO 4. H FLU: (Assume Amp Resistance) 1)Chloramphenicol 2)TMP/SMX 3)3rd Gen Cepahalosporin 4)Amox + Clauvulanic Acid 5)Erythro + sulfa 5. Neisseria: 1) PCN, Chlor, Erythro, CephIII. 6. Pseudomonas: 1)Tobra, Amakacin, Gent 2)Ceftazidime 3)Imipenem-Cilastatin 4)Cipro . Cellulitis (usually due to grpA strep) 1. PCN VK 0.5-1gm PO QID 2. Erythro 500 mg po qid . Diabetic Cellulitis 1. Cefoxiten 1-2g IV q8 (good anaerobic coverage) . Meningitis: (most commonly S.Pneum or N.Mening) 1. For S. Pneumonia PCN 2million U IV q2 x 10-14d 2. For N. Meningitis: same as above 3. for H. Flu: Cefuroxime 3g IV q8 TMP/SMX 4. Gram - Rods= 3rd Gen Ceph w/ . UTI 1. Amp 500mg po qid 2. TMP/SMX DS one PO BID 3. cephalixin 500mg po qid C-DIF COLITIS: May suggest lactobaccili by yogurt ingestion caused partic by macrolides but any ABX TX: Flagyl, Vanco po, Bacitracin po antibiotics ACID-BASE 1) Metabolic Acidosis Anion Gap Na-(Cl+CO2) 10-14nl Ketoacidosis Lactic Acid Uremia Methanol Paraldehyde Ethylene Glycol Salicylates Simple Last 2 digits of pH=HCO3 Compensated pCO2 will 1-1.5x the HCO3 Non-Anion Gap Diarrhea, K sparing diuretics RTA, TPN, Hypoaldosteronism, Ureto-Ileal Diversions 2) Metabolic Alkalosis Dependent on drive to breathe pCO2 will 0.25-1.0X the in HCO3 3) Respiratory Acidosis Acute PCO2 HCO3, HCO3 1 for each 10 in pCO2 Chronic HCO3 4 for each 10 pCO2 4) Respiratory Alkalosis Acute pCO2 HCO3 1-3 for each 10 pCO2 Chronic HCO3 4-5 for each 10 pCO2 Only one that can compensate to normal pH acid base disorders ACIDOSIS METABOLIC ACIDOSIS A-MUD-PIE: for AG met acidosis A acetaldehyde M methanol U uremia-renal failure D DKA P Paraldehyde I infection/sepsis E ETOH/ethylene glycol S Salicylates AG ACIDOSIS: Ketoacids: DM, ETOH, Starvation, Lactate: circ or resp failure Rx & Toxins enzymes defects Poisons: 1)incr osm gap: methanol(TX w/ETOH) ethylene glycol(Tx w/ETOH) 2)nml osm gap: salicylates,manatol paraldehyde Renal Faiure -------------------------------------- Normal Gap: Hyperchloremic RTA, diarrhea, hypoaldo K+ sparing diuretics Carbonic Anhydrase Inhibitors Uterosigmoidoscopy OSMOLAL GAP: dif between calc & measured osmolality: clarifys whether AG is due extra osms such as Ethylene Glycol or Paraldehyde calc osmolality: 2Na+BUN/2.8+GLU/18 (nml osmolality=286) OR: for every 1 point decr of HCO3 from nml PCO2 should decr from nml by1.2 - if less than this then there is a compensating process OR: for every 10 point incr in PCO2 pH should drop by 0.8 DELTA:DELTA: ratio of dif Of AG from NML with dif of HCO3 from NML Ratio for: Lactate 1.6:1 Ketones 1:1 ABG's / Acid-Base nmls: pH: 7.36-7.44 PaCO2: 35-45 PaO2:=109-0.43xage(years) HCO3 AG= Na - (Cl + HCO3) PCO2 Change of 10 = pH change of .08 pH change of 0.1 = [H+] change of 10 Acute vs Chronic Resp Acidosis= Change of [H+]/ Change of PCO2 <0.3=CHRONIC >0.8=ACUTE types of acidosis aaa CODE PROCEEDUREs AIRWAY: position & obstruction BREATHING: ? intubation CARDIAC: ?pulse/BP, ? compression ? IV Access EKG RYTHEM: LABS: Lytes, CBCD, ABG, Mg, Ca Drugs(Dig, Theo, etc), ? X-ray ? PE, Pneumo, Tamponade ASYSTOLE Continue CPR, get IV access,intubate | EPI 0.5-1.0 mg IVP | ATROPINE 1mg IVP (repeat after 5min) (push fast) | consider bicarb/PACING BRADYCARDIA: sinus, junct, 2-3rd block + symtoms | ATROPINE 0.5-1.0mg | repeat atropine | ISOPROTERONOL 2-10 ug/min | External Pacer /Transvenous Pacer Continue CPR, get IV access,intubate | EPI 0.5-1.0 mg IVP | consider bicarb ? HYPOVOLEMIA ? TENSION PNEUMOTHORAX ? PE ? TAMPONADE ? ACIDEMIA ? HYPOXEMIA PVC's ? K+ level ? Bradycardia ? other RX | LIDO 1mg/kg (70-100mg) repeat 0.5mg/kg q2-10 min up to 3mg/kg (200-300mg) | PROCAINAMIDE 20mg/min up to 1000mg | BRETYLIUM 5-10 mg/kg over 8-10 min | ? Overdrive Pacing SVT: 1) Unstable: Synch Cardioversion 75-100 J | Synch Cardioversion 200 J | Synch Cardioversion 360 J | DRUGS w/intermittant cardioversion --------- SVT: 2) Stable Vagal Maneuver (CM, Valsalva) | Verapamil 5mg IVP (? Adenosine) | Verapamil 10 mg IVP after 15-20 min | ? Cardioversion, Dig, vs B-blockers ? pacing V-FIB/Pulseless V-TACH (check pulse: IF NO PULSE) IF WITNESSED: PRECORDIAL THUMP | CPR until Defib avail | DEFIB 200J (check pulse & rythem) | DEFIB 300J (check pulse & rythem) | DEFIB 360J (check pulse & rythem) | CPR if no pulse | EPI 0.5-1mg IVP | DEFIB 360J (check pulse & rythem) | LIDO 1mg/kg IVP | DEFIB 360J (check pulse & rythem) | Bretylium 5mg/kg IVP(300-400mg) | DEFIB 360J (check pulse & rythem) | ?? BICARB, more epi,lido,bret ______________________________________ V-Tach + Pulse: 1) UNSTABLE: ? sedation Cardiovert 50 J | Cardiovert 100 J | Cardiovert 200 J | Cardiovert 300 J | Cardiovert 360 J | if no conversion follow below with intermittant cardioversion ------------ V-Tac + Pulse 2) STABLE: LIDO 1mg/kg | LIDO 0.5mg/kg q8 min until resolved or up to 3 mg/kg | PROCAINAMIDE 20mg/min until resolved or up to 1000mg | Cardiovert starting @ 50 ACLS Code procedures ADDICTION: Physical Dependance: pharm property of opioids-- occurance of withdrawl syndrome after abrupt discontinuation of drug or admin of antagonist (may be produced by very little opiate exposure & may persist well beyond drug cessation) Addiction: implies psych state/behavior 1."behavioral pattern of drug use w/ compulsive use,securing of its supply and high tendency to relapse after withdrawl. -or-> 2."Compulsive use of substance resulting in physical,psychological, or social harm to user & continued use despite that harm (AMA task force) Drug Abuse: 1.use of agent outside social or medical norm as approved by a given culture 2.Rx use resulting in physical, psych, economic, legal, or social harm to the individual or others. Pseudoaddiction: in Cancer Pts w/addict behaviors due to iatrogenic underTx of pain Addiction in Chronic Pain Patient: a)intense desire for drug & concern over its continued availability b)evidence of compulsive drug use eg. unsanctioned dose increases & unapproved uses despite side FXTs c)1 or more of assoc behaviors including manipulation to acquire the drug Addiction irreg irreg @ 120-180 Assoc. w/MI Rheum Fever Pericarditis Hyperthyroidism HTN Co-Existing Conditions: increased A-V conduction: anxiety infection chf Aberrent Conduction: esp above rate 150 ASHMANS PHENOMENON: aberency after a long pause then aberrency after a short period (long-short) -Cardiovert Emergently if: angina, CHF, or Hypotension -Rate Control: digoxin 1-1.25 loading dose keeping <110 2nd line: Verapamil 5-10 IV Beta Blocker -Inderal 20-40 po q6 -Esmolol -Electrical Cardioversion: -unlikely to work if: chronic AF > 1yr LAE > 5cm -synch CV @ 50 joules in AFIB/Flutter Chemical Conversion -Quinidine 300mg q6 x 24 -procainamide Anticoagulation: -none if AF <3days -use coumadin 2 weeks before & 2 weeks after cardioversion Pacing: SSS, severe AV-node dissoc. Chronic Afib: dig to keep rate 80-100 ? life time antiocoag if paroxysmal Atrial Fibrillation A-a O2 Gradiant PAO2= FI02(PB-PH20)- PaCO2/R (760-47)FI02- PaC02/0.8 @ sea level on RA= 150 - (PaCO2/0.8) FOR A-a gradient:Subtract Value from PaO2 on ABG FIO2 NML Range: RA: 8-10mm 15%: <20 40%: <40 Note: Hypoventilation does not affect A-a gradient INCREAED A-aGradient: 1. diffusion defect 2. R -> L shunt 3. V/Q mismatch Age Correction: 2.5 + 0.25(age) TO r/o lt to Rt shunt: give 100% O2 & cal A-a gradient. - V/Q & diffusion defects correct - Shunts do not correct SHUNT: perfusion w/o vent (atelectasis) DEAD SPACE: Vent w/o perfusion (PE) ---------------------------------------- HYPOVENTILATION: PaO2 PaCO2 RA 100%O2 Alv hypovent down up NC NC high altitude down down NC NC regional V/Q mis down +/- up up/NC R-L Shunt down down up up diffusion defect down down up NC --------------------------------------- A-a O2 Gradient Alcoholism Anatabuse 250mg 2 qd in am for first two weeks, maintain 1-2 qam thereafter, chem 20 q 6 months Tranxene for outpatient alcoholic detoxification Heavy drinker/larger person 7.5mg 2 q6 x 4 doses 2 q8 x 3 doses 2 q12 x 2 doses 2 hs x 1 1 hs x 1 lighter drinker/smaller person 3.75mg 2 q6 x 4 doses 2 q8 x 3 doses 2 q12 x 2 doses 2 hs x 1 1 hs x 1 Alcoholism +W/D Bleed, doesnt want preg nl prl & tsh, has normal secondary sexual characteristics Warn to report: vision , headache. Yearly Prolactin, TSH Ammenorhea Anaphylaxis -Anaphylactic -- IgE-mediated -Anaphylactoid -- not IgE-mediated prob Complement mediated Presentation Airway wheezing stridor laryngeal edema Cardiac: incr vasc perm circulatory collapse hypotension GI:incr motility from histamine diarrhea urticaria flushing Treatment Airway -- intubate prn Breathing -- ventilate prn consider breathing treatments Circulation epinephrine 1:1000 1cc SQ or .3cc q5min 1:10,000 10cc IV .3-5cc antihistamines H1 blockers -- 50-100mg diphenhydramine H2 blockers -- cimetidine steroids 200 mg of solucortef 100 mg of solumedrol consider phenylephrine drip levo drip epinephrine drip DYE RXN: high prob of having another reaction Anaphylaxis MACROCYTIC ANEMIA: megaloblastic anemia: megalocytes lg oval RBCs & hyperseg polys Megaloblastic vs Macrocytic: BM Dx: megalo DNA grows @ > rate than cyto CAUSES 1. Accelerated Erythrocytosis: - due to increased RETICS 2. inc Membrane Surface Area: excessive plasma lipids absorbed into RBC MEMBRANE: most common w/liver Dz w/smear w/target cells (round macrocytes w/redundant membranes) 3. decr DNA Synthesis: RBC nuc maturation is arrested but cytoplasm maturtion continues lg RBCs - B12 deficiency: tapeworms vegi diet intestinal blind loops Lack of Intrinsic Factor (Pernicious Anemia) - Folic Acid deficiency: due to: dietary deficiency malabsorption - Rx Induced: ChemoTx/Dilantin SYMPTOMS of decr DNA SYNTHESIS: -low WBC & PLT prod (these need DNA too) -low LDH due to intramedullary hemolysis usually > 500units/dl -BM RBC/WBC w/open immature nuclei & mature cytoplasm. - Smear w/oval macrocytes & hypersegmented Polys - NEURO:low B12 assoc w/posterior column signs & atrophic glossitis PERNICIOUS ANEMIA: autoimmine absence of intrinsic factor Tx Immed since neuropathy is rapid give B12 1000 mics daily > 1 week then monthy due to enterohepatic circ -stool loss due to lack of IF reclaimation of B12 SCHILLING TEST: measuring B12 in Urine due to oversaturation of B12 in serum - give IM large doses not radioactive then give PO radioactive B12 if absorbed will show in Urine indicating pesenence of IF - If neg (no hot B12 in urine) may give IF to distinguish IF defic vs terminal ilium dz. Microcytosis ACD: due to chronic inflam Dz or CA: (unusual for Hgb < 7) -Reticuloendothelial blockade to Iron Use by BM: Iron stores are plentiful but have -usually w/slight microcytosis -BM stain reveals lots of Iron -Fe & TIBC are low w/nml or slightly elevated Ferritin -MCV/RBC > 13.5 CHRONIC BLEEDING THALASEMIA -MCV/RBC < 11.5 -MCV < 70 SPHEROCYTOSIS -MCHC>36 SIDEROBLASTIC Retic. count. CHRONIC HEMOLYSIS Normochromic Anemia: nml cell size & nml Hgb content Low Retic------------------------------ 1.Aplasia, hypoplasia, pancytopenia 2.BM infiltration: myeloma, carcinoma lekoerythroblastosis (blood smear w/immature white cells & nuc RBCs) EPO: Chronic Renal Failure Chrinic Infection BM Proliferation: HYPOTHROIDSM HYPOPITUITISM LIVER DISEASE EARLY High Retic----------------------------- 5. Sequestration Destruction HEMOLYSIS SICKLE CELL Norm or High Retic--------------------- 7. Loss ACUTE HEMORRAGE ====================================== FEUL ANEMIA low ferritin increased TIBC Low Fe SMEAR: microchromia MCV < 70 think Thallasemia TEAR DROP CELLS: MYELOFIBROSIS BM INFILTRATES NUCLEATED RBC: either early retics or HEMOLYSIS: VERY GREAT STIM OF RETICS often > 15% (bleeding gives~ 5%) on smear: spherocytes: flat w/o central pallor: Schiff cells: small amt of RNA w/blue tint DIRECT COOMBS: measure AB on pts RBC Pts RBC adding 2nd AB against Fc INDIRECT COOMBS: measure AB in pt serum pts serum add panel of sheep RBC IgG: WARM agglutinating IgM: COLD agglutinating Causes of Hemolysis G6PD(Oxidative failure SS/SC/ST Autoimmune warm cold *Most common cause of idiopathic AHA is undiagnosed LYMPHOMA Hereditary Spherocytosis Mechanical MAHA - vasculitis DIC Drugs - sulfonamide, moth balls Zieves Syndrome - Burr cells ZIEVES Syndrome -usu follows bout of heavy drinking -findings: fever, hepatomeegaly, jaundice, lipemia, brisk hemolysis, WITHOUT spleenomegaly Retic, 50% of Pt c spherocytosis -Liver BX fatty infil -Turbid plasma, with elevated lipids -RX: rest, good diet, & DC ETOH Anemias MACROCYTIC ANEMIA: megaloblastic anemia: megalocytes lg oval RBCs & hyperseg polys Megaloblastic vs Macrocytic: BM Dx: megalo DNA grows @ > rate than cyto CAUSES 1. Accelerated Erythrocytosis: - due to increased RETICS 2. inc Membrane Surface Area: excessive plasma lipids absorbed into RBC MEMBRANE: most common w/liver Dz w/smear w/target cells (round macrocytes w/redundant membranes) 3. decr DNA Synthesis: RBC nuc maturation is arrested but cytoplasm maturtion continues lg RBCs - B12 deficiency: tapeworms vegi diet intestinal blind loops Lack of Intrinsic Factor (Pernicious Anemia) - Folic Acid deficiency: due to: dietary deficiency malabsorption - Rx Induced: ChemoTx/Dilantin SYMPTOMS of decr DNA SYNTHESIS: -low WBC & PLT prod (these need DNA too) -low LDH due to intramedullary hemolysis usually > 500units/dl -BM RBC/WBC w/open immature nuclei & mature cytoplasm. - Smear w/oval macrocytes & hypersegmented Polys - NEURO:low B12 assoc w/posterior column signs & atrophic glossitis PERNISCIOUS ANEMIA: autoimmine absence of intrinsic factor Tx Immed since neuropathy is rapid give B12 1000 mics daily > 1 week then monthy due toenterohepatic circ -stool loss due to lack of IF reclaimation of B12 SCHILLING TEST: measuring B12 in Urine due to oversaturation of B12 in serum - give IM large doses not radioactive then give PO radioactive B12 if absorbed will show in Urine indicating pesenence of IF - If neg (no hot B12 in urine) may give IF to distinguish IF defic vs terminal ilium dz. ====================================== ACD: due to chronic inflam Dz or CA: (unusual for Hgb < 7) -Reticuloendothelial blockade to Iron Use by BM: Iron stores are plentiful but have -usually w/slight microcytosis -BM stain reveals lots of Iron -Fe & TIBC are low w/nml or slightly elevated Ferritin Normochromic Anemia: nml cell size & nml Hgb content 1.Aplasia, hypoplasia, pancytopenia 2.BM infiltration: myeloma, carcinoma lekoerythroblastosis (blood smear w/immature white cells & nuc RBCs) EPO: Chronic Renal Failure BM Proliferation: hypothroidsm hypopituitism liver disease ====================================== FEUL ANEMIA low ferritin increased TIBC Low Fe SMEAR: microchromia MCV < 70 think Thallasemia TEAR DROP CELLS: MYELOFIBROSIS BM INFILTRATES NUCLEATED RBC: either early retics or HEMOLYSIS: VERY GREAT STIM OF RETICS often > 15% (bleeding gives~ 5%) on smear: spherocytes: flat w/o central pallor: Schiff cells: small amt of RNA w/blue tint DIRECT COOMBS: measure AB on pts RBC Pts RBC adding 2nd AB against Fc INDIRECT COOMBS: measure AB in pt serum pts serum add panel of sheep RBC IgG: WARM agglutinating IgM: COLD agglutinating ACD: Inability to mobilize FE Mild hypochromic & microcytic Low Fe & TIBC w/high Ferritin anemias, more ISOPM Suction Pharm Monitor Stage 1: AMNESIA from start of induction to LOC -no decr in pain perception Stage 2: DELIRIUM uninhib excitation & rxn including vomitting, laryngospasm, HTN tachycardia & uncontrolled mvt -pupils dilated, divergent gaze irreg resp, breath holding Stage 3: SURGICAL ANESTHESIA central gaze, pupils constrict & resp are regular. Level reached when no somatic reflex to pain, or autonomic rxn such as Htn, tachycardia etc Stage 4: OVERDOSE Too deep: shallow or abscent resp dilated or nonreactive pupils or HypoTN -> Circ Collapse INDUCTION: BARBITURATES Ultra short acting barbiturates [thiopental(pentothal, thiamylal, methohexital] -produce rapid hypnosis w/o analgesia -low dose may incr airway reflexes and be hyperalgesic -decr metabolism and blood flow so useful in neuro/ICP cases -prod vasodil and cardiac depression Dose: IV induction: 2-7 mg/kg -low dose if otherCNS depressants or if hemodyn instability or spontaneous vent required -high dose for young & healthy pts or those tolerant to barbs such as alcoholics or for rapid sequence inductions w/o hypovolemia Side FXTs: -Allergy: anaphylaxis is rare-Tx w/EPI -Local urticaria, genl skin flushing -tachycardia -Skin infiltration: highly alk pH=11 -hiccups & myoclonus: mostly w/methohx --------------------------------------- Ketamine: phencyclidine- prod dissociative w/profound analgesia. <apnea -airway reflexes may decr-?aspiration -good for short proceddures -can be given IM: kids & uncoop pts -CVS:incr SNS :incr HR & BP -RESP: bronchodilation: good in asthmatics -DOSE: IV 1-3mg/kg / IM 5-10mg/kg onset 1min post IV or 5-8min post IM -eliminated by hepatic biotransformatio -SIDE FXTs: nightmares, halluc, delirium avoid in psych pts HTN & incr HR avoid in CVS Dz incr CBF so aviod in incr ICP stim oral secretions- pretx w/ antisialogue -atropine->dilirium --------------------------------------- Etomidate ======================================= ======================================= Neuromuscular Blockade Depolorizing Agents: ACh like actitions: -Succinylcholine (SCh): binds Ach recpt which is not cleared as quickly as ACh thus prod persistant end-plate depol & state of inexitability. FXT over when Sch degraded by PLASMA or PSEUDO Cholinesterase -musc fasicul followed by relaxation -no fade from tetany or To4 stim -no enhanced twitch after tetanic stim -Antagonized by nondepol agents SCh:Rapid Onset & Short Duration Side FX: -Fasiculations & Post-op musc pain: prevent w/sm doses of nondepol agent -Ganglionic Stim: incr HR & BP (decr HR in kid or adults after 2nd dose) preTx w/atropine will prevent bradycardia -Hyperkalemia: -Incr IOP -Incr Intragastric Pressure (modulate w/preTx w/nondepol agent -Prolonged block: in pt w/decr or inhib enzyme or genetically atypical enzyme Also seen at last trimester of preg, in liver Dz, Starvation, CA, Hypothyroid Burns, & Shock. -Malignant Hyperthermia: failure of masseter to relax or gen myotonia is a warning (also incr CO2 & HR) Nondepolarizing Agents: pure reversible competitive antagonism of the ACh receptor-Also may block other active structures such as ion channel etc -No fasiculations prior to block -Fade from tetanic or To4 stim -Post-tetanic potentiation -Antagonism by depol agents & ACHase -Potentiation w/ other NONdepol agents Steroidals: Vancuronim & Pancuronium Benzylisoquinolones: dTC, atricurium metocurine Side FX: -Spectrum of Cardiovasc FX SCH-rapid onset & short duration good if full stomach or short proc Atricurium: metab in plasma by pH ideal for pts w/renal or luver failure Pancuronium: vagolytic actions good in cases w/bradycardia or to counter fentanyl etc dTC: Sig Histamine release ca drop BP Since it is largely cleared in Bile it is good choice in renal failure REVERSAL OF NM Blockade: -usually spont but can be accelerated by anti-acetylcholinesterase agents that displace the blocking ligand ======================================= ======================================= Nicotinic: -NMJ: -Automnomic Ganglia Cells: SNS & PNS Muscarinic: -Pariph Post Ganglionic -Heart via Vagus -Sm Musc @ Bronchi & Bronchioles -GI: raises tone -GU: raises bladder tone/low shincter T -Secretory Glands: Stim Salivary, Lac, digestive, Tracheobronchial, & exocrine glands ======================================= ======================================= MONITORING MNB: 1.objective determination of degree of relaxation or recovery 2.adjust dose according to response 3.monitor for devel of stage II block 4.early sign of pt w/abnml plsma cholinesterase 5.to correlate resp status w/NM block --------- Single Twitch Monitor: usually on the ulnar for adductor pollocus response -place electrode on wrist over ulnar n. & deliver graded impulses -0.2msec/0.1Hz usually use -Establish control height of stim prior to admin of relaxant -then compare percent of control height when relaxant on board --------- TETANIC STIMULATION -detects whether response is sustained or fades during stimulus -freq ranges from 50-200Hz -peak tension reduced but sustained in depol block -peak height reduces & fades w/depol & phase II block -Tetanic fade is prejunctional event due to curare-like fxt on mobilization -of ACh during high frq stim --------- Train of Four T4 -4 supramaximal stim at freq of 2Hz repeated @ intervals no less than 10 sec apart -response is well separated but shows fade during partial curarization -In Nondepol block: elimination of 4th response = 75% depression of 1st response -disappearance of 3rd,2nd,&1st responses =80%,90%,&100% of 1st twich respectivly -Ratio of height of 4th twitch to 1st (T4 ratio) correlates to clin recovery -T4 ratio of .75 idicates single twich has returned to control level Anesthesiology Thromboangiitis Obliterans (Winiwarter Buerger Dz) (?hypersens rxn to tobacco) involves arts, veins & nerves typically in young males typically starts in sm art of hands & feet w/intense inflam rxn which chronically may turn to art or venous occlusion & fibrosis of neurovasc bundle Sx : superficial thrombophlebitis/ angiitis in young males who smoke or chew tobacco (older females also known) TX: Abstain from TOBACCO dubious pathology most w/Atherosclerotic Dz of carotids or cerebral arteries w/stasis thrombosis of more distal cerebral branches. Thromboangitis Obliterans ANKYLOSING SPONDYLITIS Assoc w/Inflammation of Axial Skeleton -clinically manifesting commonly as back pain & limited spinal ROM caused partic by Sarcoiliitis & ascending spinal inflammation ---------------------------------------- PREVELANCE: 1/100 white males < in blacks & asians Females as common as Men however females w/ less severe Dz process ----------------------------------------- DISEASE ONSET: ages 20-30 DISEASE COURSE: 1. begins w/gradual onset chronic low back pain assoc. w/morning stiffness improving w/exercise 2. Unremitting Low Back Pain for years w/severity ranging from mild->severe ---------------------------------------- SYMPTOMS: 1. Axial Skeletal Involvement a) SI Joints: typically symetrical b) Ascending Spinal Involvement: -due to enthesopathy @ annulus fibrosis attachment to Vertebrae c) Chest Pain: from inflamation at Chostovertebral, costosternal & intercostal tendons & Ligaments 2. Peripheral Joints: involved in more severe AnkSpondylitis. 3. Extraskelatal Sx: a) Eyes: Uveitis in 1/4 Pts w/AnkSpond Conjunctivitis +/- -usually self-limited w/o visual impairment b) CVS: Aortitis @ root-> Aortic Insuf - can extend to subaortic area-> heart block or mitral regurge c) Pulmonary: Fibrosis @ upper lobe resembles TB d) GU: common w/prostatitis (no symptomatic urethritis) COMPLICATIONS: 1. Fractures: spinal Fx's in pts w/ bamboo spine 2. Spondylodiskitis: disk lesions, can cause erosive changes @ adjoining Verts simulating disk space infection 3. Sinal Stenosis: Sx of leg Claudication due to encroachment on the Cauda Eq. ----------------------------------------- ======================================== Dx: BACKPAIN: differs from mechanical etiology by AnkSpond w/young onset and worse sx on wakening & relieved w/ exercise (Mechanical BP w/late onset worsening w/activity & relieved w/rest) Familial Association PHYSICAL EXAM: SI Tenderness Decresed Spine Mobility Decresed Chest Expansion XRAYS: 1. Pelvic A-P film: - Symetrical blurred irreg SI joint margins (early signs) - Periarticular sclerosis & bone erosion +/- joint space narrowing - indicates active spondylitis Spine Films: - Ascending spinal Involvement Late finding w/inflam @ attachment of annulus fibrosis - Periostitis: periosteal new bone formation @ enthesopathic sites -most commonly @ plantar fascia & achillies tendon TX: NSIADS are mainstay - Indomethacin: used @ minimal doses (typically 150mg total daily dose) - Phenylbutazone: used as last recourse - Steroids: local joint inj only no role for systemic steroids Ankylosing Spondylitis ANTIARRYTHMICS PROCAINAMIDE IV: Load 1gram @ 50mg/min then drip @ 2-6mg/min LIDOCAINE:load 50-100mg then 2-4mg drip BRETYLIUM: 5-10mg/kg IV bolus or 1-2 mg/min IVD ======================================= GROUP I: (NA channel blockers) -IA: quinidine (prod wide QRS/long QTc) Procainamide -IB: Lidocaine -IC: Flecainide encainide (depress conduction & prolong QRS & PR)1 GROUP II:(SNS Blockers) -Propraolol & Beta Blocker GROUP III:(Prolong Action Potential ? via blocking K+) -Bretylium Group IV:(Ca+ Channel Blockade) ======================================= LIDOCAINE: xylocaine Rx of choice for post-MI arrhythmias & V-tach DOSE:50-100mgIVB foll by 1-4mg/min (may give IM@ 300mgIM q2hours @Toxic levels:CNS FX-SZ's,slurred speech/drowsiness QUINIDINE: - used to suppress VT & PVC's - also used to CVT AFIB/FLUT to NSR CONTRA:2nd or 3rd block, incr Q-T -Discontinue if QRS widens -?CNS,Myocardial FX 2 PO forms: Quin Sulfate: 80% QUIN: 250-400mg q6 Quin Gluconate:60% QUIN:325-650mgq6-8 IV: gluconate given in emergency & very slowly:500mg in 50mgD5W inj@<60cc/min(??hypoTN & vasodil) PROCAINAMIDE: pronestyl tx PVC's,VT, or SVT SideFX:CNS,Myocardial, Rx-Lupus w/+ ANA/LE cell prep in 50-70%** 2 PO forms: -Procainamide:250-500mg PO q4 -Procain SR: 375-750mg PO q6 Antiarrythmia Drugs Heparin Warfarin(Coumadin) dosing General Instructions Keep vegetable diet constant Take at 5pm each night Normal Start D1-5mg, D2-5mg, D3-check am PT calc pm dose. Fast start D1-10mg, D2-check am PT calc pm dose D2 PT=1.1(INR) expected 1.5(INR) very high 1.8(INR) extremely high, will prob take 1mg daily dose. If INR=1.1, D2-10mg, expect D3 INR=1.4, 2.0 IS HIGH Target: INR PTr Thromboembolism 2-3 1.2-1.5 Overlap THERAPUTIC Warfarin & Heparin 48-72 Needed for program: ht wt billi(.8/.8) alb smoker? Cirrhosis CHF Prev ThEmb PREG Other Drugs Drug interactions on Warfarin Blood Level: by liver oxidase induction phenobarbital rifampin carbamazepine phenytoin glutethimide exposure to chlorinated insecticide chronic alcohol ingestion Warfarin Blood Level: by liver metabolism inhibition cimetidine ranitidine in doses >150mg erythromycin metronidazole phenylbutazone Warfarin Drug effects: by combined effect aspirn Anticoagulent Drugs ADULT RESPIRATORY DISTRESS SYNDROME 1. diffuse infiltrates on CXR 2. hypoxemia resistant to O2 Tx 3. stiff, poorly complient lungs - Pulm Edema may be seen @ PCW's 5-15 (lower than in CHF) 2 TYPES of ARDS: A) Primary Pulmonary ARDS: -acid aspiration -viral pneumonia -Pneumocystis pneumonia -------- B) Mult Organ System Failure as ARDS -sepsis -multiple trauma O2 toxicity: >24hours @ >60% FIO2 decrease pulm diffusing capacity High Alv Pressures: PEEP reqruits collapsed alveoli but may over- expand nml alveoli ADULT RESPIRATORY DISTRESS SYNDROME Resp fail in appropriate setting 1. Sepsis 2. Aspiration 3. Trauma 4. Mult transfusions 5. Pneumo 6. Pancreatitis 7. Liver cirrhosis 8. Toxins Mult risk factors increase risk Occurs within 48-72 hrs after initial insult Exclusion criteria: a) pulm edema b) underlying pulm disease Physiologic characterization: Hypoxia: Po2 less 60 Fio2 more than 50% Aao2 grad increased-> correct for age PATHOLOGY: Hyaline memb formation Fibrosis Pulm art thrombi Pulm vasc-remodeling vasc bed 1967-Ashbow & Petti termed ARDS HYPOXIA: 1)Decreased diffusion capaciy - reverses with 100% Fio2 2)Hypoventilation -nl AaO2 grad 3)Shunts -unaffected by 100% 4)Perfusion/Vent Mismatch -small correctin with 100% EXTRAVASCULAR WATER INCREASES LUNG VOLUMES: FRC reduced-loss of lung unit: surfactant, flooding Airways resistance increases Compliance reduced HETEROGENIOUS: dependent areas affected most Mortality: 60% of those with it in ICU Cause: Days 1-3: precipitant Sepsis before ARDS think GI Sepsis after ARDS- cause pneumo Known source/cause prog better MOF: Prdictive LAB Values Ph, HCO3-liver BUN/Cret=3.0-renal THERAPY: 1. Steroids-do not use/mort higher 2. PEEP-zero optimal,recruits alveoli splints(prevents derecruitment) reduces shunt -best PEEP increases compliance -increase ITP/ decreases CO -must do trials: pick level of PEEP that gives best hemodyn profile 3. High TV/PAW cause oxygen damage 4. Jet vent-not beneficial, rapid freq vol driving pressure freq/I/E ratio advantage in airway press,same mean AWP, less barotrauma 5. PCIRV=air-trapping, like PEEP 6. Extra-corporeal Co2 removal via memb ACUTE RENAL FAILURE 1)Prerenal, 2)Renal, & 3) Renal (UO inv. proportoinal to severity) ---------------------------------------- 1)PreRenal: inadequate perfusion - hemmorrhage, dehydration, low CO, vasc pooling, & renal art. obst. - NSAIDS if pts w/ CRF, CHF, elderly, nephrotic syndrome, diuretics ----------------------------- 2)Intrinsic Renal: Renovasc Dz, Glomerulonephritis, int Nephritis ----------------------------- 3)PostRenal: Obstruction: must be BILATERAL unless absent or impaired contralateral kidney ======================================= ATN: ischemic or toxic injury in renal vessels, glomerulus, & tubules causing decreased GFR & increased intratubular pressure A) Ischemic: may follow hypoperfusion or any pre-renal state (partic in elderly or w/nephrotoxins) B) Nephrotoxic: exogenous aminogly's, or contrast dye(w/i 48h).Endogenous myoglobinemia(coma/heat stroke) or hyoTN or sepsis related hemolysis DX of ATN: muddy brown casts & renal tubular cells in Urine Sed w/low Una=?contrast dye, GN, burns, or myoglobinuria w/heme+ dipsick & high CK: ? Rhabdo ATN Clin Course: starts w/decreased UO - BUN/Cr range 10-20 & 0.5-1.0 - If Oliguria persists>2weeks ? 2nd Dx - HyperKalemia: decreased excretion - Anion Gap Met Acid: Retained Acid (? role for lasix in ATN) -------------------------------------- NONIoNIC DYE:no advantage if nml renal fxn. Toxicity reduced sig if baseline renal failure. Risk is only partially reduced Acute Renal failure ARRHYTHMIA's ?underlying heart disease Vtac Vfib- ?acute ischemia Afib/flutter- lg atrium from thoracotomy ot MS Conduction disturbance: fibrotic or calcified AV tissue ? Hypoxia, hypercapnea, highT4 ? RX TOXICITY: (*renal/hepatic Dz) Dig, Theo, B2agonists, Quinidine Procainamide (quin&Pronestyl cause torsades de pointes which does not respond well to shock or chem conversion-must stop Rx) ?LYTES: high/low K+,high/lowCa++, low Mg++ SINUS TACH: NSR@100-170 ?infection,anxiety,pain,hypovolemia Rx(bronchodil's) TX:propranolol 1mgIVq5-10min/5mg max SINUS BRADY: NSR@<60:**no Tx if no Sx (Tx for CP,hypoTN,CHF) Causes;Rx's (Bblockers), lowT4 high ICP, 1) Atropine:0.6-1.0 IVB q5min/2mg MAX for malig brady resist to Atropine 2) Isoproteronol (increses MVO2) 3) ? temp vs perm pacemaker AFIB: tx to lower rate & Cvt to NSR 1)HEMODYN UNSTABLE: Synch Cardiovert strting @ 100 watts 2)STABLE RAPID RATE: Verapamil:.075mg/kg slow IVP (70kg=5.25mg)repeat after 30min w/ 0.15mg/kg (70kg=10.5.g) *(neg inotrope-carefulw/CHF or B-blockers)**(Contra in WPW) 3. STABLE w/RATE 90-140 give IV DIG .25mgIVP q3-4h til rate<80 4. No NSR: ? QUINIDINE(must lower DIG dose w/quinidine) 5. Cardiovert: must anticoagulate AFLUTTER: rate 280-350 w/var AV block ?highT4/COPD Carotid Massage may slow to det if Aflutter vs SVT Tx:same as AFIB except Cardioversion requires only 25-50watts also ? rapid atrial pacing SVT:from sustained re-entry if w/aberrant conduct like VTACH MANEUVERS: valsalva,gagging,**CSM** try CSM w/EKG before Rx's RX: 1)Verapamil 0.075mg/kg slow IVP (70kg=5.25mg)repeat after 30min w/ 0.15mg/kg (70kg=10.5.g) *(neg inotrope-carefulw/CHF or B-blockers)**(Contra in WPW) 2. Propranolol .5-1.0mgIVq5min to max of 5mg 3. Lidocaine: 50-100mgIVB (usually converts 25%) 4. CARDIOVERSION: if hemo comp start w/50 watts 5. ? rapid atrial pacing A-TACH w/BLOCK: rates=130 - 250 also common w/2-1 block ??Dig Toxicity TX: stop Dig & replace K+ PVC's: ?hypoxia,CHF,MI,MVP,Dig/Rx tox, lytes V-TACH: >3 wide QRS's @ 120-250 ?MI,CHF,RX Tox(dig/quinidine) Tx:1. STABLE: Lido 50-100mgIV foll by 50mgIV q2min x1 if no better:SHOCK always's follow re-est NSR w/ Lido LD: 50-100mg IV followed by Lido Drip:2-3mg/min for > 24hours Arrythmias Asthma Bronchospasm Peak Flow Rate(PEFR) at home Percent of personal Best Zones 80-100 Good 50-80 Add therapy <50 Contact Provider Inhaled steroids and chromolyn reduce bronchial hyperreactivity over time. Beta agonists do not. Steroids will work more often. Chromolyn works best for exercise incuced, allergic and younger patients. Asthma BACK PAIN: --------------------------------------- MAJOR CAUSES Tumors Trauma Congenital Degeneration Inflamation Infection Metabolic Mechanical Visceral ------------ 1. TUMORS A. Benign: neuinoma, ependimoma, meningioma, osteoid osteoma, hemangiomas, osteoblastoma B. Malignant: MM, osteosarcoma, METS 2. TRAUMA: lumbar strain vs Fx 3. CONGENITAL Dz: A. facet asymetry (Tropism) B. Spondylolysis & spondylolisthesis C. Transitional Vertebra 4. DEGENERATIVE Dz. a. OA b. Disk Herniation c. spinal stenosis d. nerve root entrapement 5. INFLAMATORY Dz a. Ankylosing Spondylitis b. Arachnoiditis c. RA 6. INFECTION a. TB, Zoster, b. meningitis, SI infection, abscess 7. METABOLIC: a. Osteoporosis b. Pagets Dz c. Diabetic neuropathy d. Gout 8. VISCERAL DZ a. Aortic Aneurysm b. Retroperitoneal Process c. PID ======================================== LOCAL vs REFERRED vs MUSCULAR Local: from irritation of nerve endings at site of pain causing stimuli (mets, lytic bone) usually assoc tenderness on local palpation or percussion - Disk herniation: neck or low back - METS & Osteoporosis: often get thoracic area(although colon & prostate CAcommonly get LS spine) - Pain from Musc strain of Disk hern usually subsides w/knee/hip flexion - Disk hern pain often worse w/sitting relieved w/ standing or walking - Pain of Spinal Stenosis occurs only on walking. - Pain of Vert Mets most prominant on lying flat - Pain of Spinal Cord Compression worsend w/ mvt- sleep seated. REFERRED PAIN: unknown mechanism felt @ distance from source not in dermatomal dist of nerve root. - Low back origin usually felt @ buttock or post thighs - rarely below knees. - Lumbar Spine referrs to flank, groin, or ant thighs - Visceral Pain may refer to spine (ex. panc CA) MUSCLE PAIN: injury or spinal lesion-> reflex paravertebral muscle spasm. -TRIGGER POINTS: areas of extreme sensitivity to Palpation w/pain felt locally & referred to distant sites. (may be source of myofacial pain synd) ---------------------------------------- DIRECT NEURAL PAIN SYNDROMES: RADICULAR PAIN: Sx of root compression - pain in overlying spine & local musc + pain in cutaneous dermatomes - pain is worse w/ positions that compress or stretch cord etc. - Increased pain from maneuvers that increase spinal pressure (sneezing, coughing, straining) - root is not directly pain sens but w/ chronic compression -> local edema, inflamation & demyelination DISK HERNIATION & ROOT COMPRESSION: Lumber Disks: root exit IV foramen above IV disk and below Vertebral body (L5-S1 disk herniation gets S1 root) -If herniation is very medial(uncommon) an L4-5 disk could compress S1 root instead of L5 since non-exiting roots traval medially down the cord Cervical Roots: exit above Vert Body (C5-6 disk herniation gets C6 root) FUNICULAR PAIN: compression of long tracts of spinal cord - dist more diffuse than ridicular Sx - usually increased w/mvts & maneuvers that increase spinal pressure (sneezing, coughing, straining) - often early c/o cord compression - < sharp than radicular pain often described as cold & unpleasant in EXT. SPINAL CORD COMPRESSION: - Earliest sign may be tenderness to percussion over vertebral body at site of compression. - Corticospinal Tract & Post Columns most vulnerable/ Spinothalamic & Back Pain BRAINDEATH: 1. Cortical: a. cerebral angiogram b. EEG (flat line) c. Radionuc flow Scan 2. Brainstem: a. carneal reflex b. dolls eyes c. impact convergence d. calorics w/nystagmus e. gag reflex **f. APNEA TEST 3. Irreversibility: r/o rev causes a. Shock, hypothermia Rx(barbs/musc relax) b. demonstrate no flow x 10 min 4. Other Criteria - pH < 7.5 & pCO2 > 60 on RA - no spont resp on vent X 15 min - no resp on RA X 3 min after 15 min 02 by ventilator - PCO2 > 60 after ventilation to good 02 sat (serial ABGs) NOTE: Once determined as Braindead: **** pt is ideal candidate for **** ORGAN DONATION Brain Death BRAIN TUMORS Gliomas: 45% Glioblastoma Multiforme 20% Astrocytoma 10% Ependymoma 6% Medulloblastoma 4% Oligodendricytoma 5% Meningioma 15% Pituitary Adenoma 7% MISC: 33% --------------------------------------- GLIOBLASTOMA: most common primary in adults Glioblastoma Multiforme(malignant glioma or astrocytoma grade 3 or 4) - age peak 45-55 m>f - most freq in frontal, temporal but can arise anywhere(rarely cerebellar,stem, or cord) Prognosis: uniormly poor for Glio M. Mets: rare outside CNS but widely invasive Survival: mean 9-12 months Tx: 1)Surg: resection is first choice however survival is not improved. but w/decompression prob improves quality of life 2)RT: not radio sens but since brain is highly tolerant of RT may give super high dose (5-6000 rads) -may prolong survival(17-38wks) 3)CHEMO: not rec for all cases since evidence shows only marginal fx with added morbidity -rec only for younger pts w/min neuro deficit -typically use BCNU/CCNU -? immunoTx,RT implants,BrachyTx --------------------------------------- ASTROCYTOMA: grade 1&2: much< common in adults than Glio Multi. -usually slow growing & sx usually pre-date the dx of tumor. -May start benign & transform to malignant state-> glio multiforme -thus bx may be misleading w/one part grade 1 & another grade 4 **thus prognosis is very uncertain TX: surgical resection - most extensive possible although complete resection usually is impossible -RT: postop is usually beneficial Prognosis: highly variable --------------------------------------- OLIGODENDROGLIOMAs: same as ASTROs 1&2 Brain Tumors CANCER PAIN -most commonly due to invasion of bone, or neural structures -also due to invasion of soft tissues, distortion/occlusion of blood vessels, or obstruction of a hallow viscus. -25% have pain from ChemTx or RadTx ----------------------------------------- Approach to Pts w/ Cancer Pain: 1. Identify underlying lesion 2. Clarify pathophysiology of pain (somatic, visceral, neuropathic etc) 3, Characterize the pain in relation to the patients other problems 4. Determine the contribution of pain to the overall impairment in quality of life ---------------------------------------- ORGANIC PAIN: 1. Nociceptive (Somatopathic): due to ongoing activation of periph nerves that are sensitive to pain 2. Neuropathic: due to aberrant process in PNS or CNS resulting from injury - some from deafferentiation ---------------------------------------- Rx for CANCER PAIN: NSAIDs, Opiates, & adjuvants "ANALGESIC LADDER" 1. Mild to moderate pain: NSAIDs +/- adjuvants 2. Moderate to severe pain: Weak opiates +/- NSAIDS or adjuvants 3. Severe pain: Strong opiate +/-NSAIDs or adjuvants ---------------------- NSAIDs: (including ASA & Tylenol) - analgesic mechanism prob unknown - ceiling dose beyond which no further analgesia is reached - usually require > dose than generally recomended (~1.5-2x) - offer additional analgesia when combined w/other non-NSAID analgesics - use w/caution in renal failure (least renal toxicity w/Sulindac) - use w/caution in blood diatheses/PUD (Tylenol, Salsalate, & choline magnesium salicylate) - All NSAIDs (except tylenol) worsen encephalopathy & OBS - pts on chronic & large NSAID doses need monitoring of stool guiac, UA, & BUN/Cr -------------------- OPIATES: 3 TYPES: agonist, agonist-antagonist & partial agonists WEAK OPIATES: same potency as strong opiates however toxicity at doses high enough to produce strong analgesia assoc w/ severe toxicity. (codeine, meperidine, propoxyphene) Toxicites: -Mixed Agonist-Antagonists: psychoto- mimetic reactions -Meperidine: causes CNS hyperactivity, myoclonus, tremulousness & seizures due to Normeperidine metabolite *(most prob w /renal insufficiency & prolonged use) -Propoxyphene: has toxic metabolite Norpropoxyphene w/ uncertain clin relevance at nml doses OPIATE 1/2 LIFE (T1/2): *(takes 4-5x T1/2 to reach steady state) Long T1/2: Levorphenol (12-15h) Methadone (15-57h) Propoxyphene (12h) ShortT1/2: Heroin (0.5) Moderate : All others (2-5h) DOSING: 1)start w/prn's to establish need & change to steady dose or 2)start low fixed dose w/rescues. Give rescues @ q2h ~5-15% toal daily opiate intake. Changing Opiates: switch to reduced equianalgesic dose (25% less than equivalent dose) ----------------------- ADJUNCT ANALGESICS: TCA's: effective for neuropathic pain (amitriptyline, imipramine & doxepin) Doxipin(sinequan) most sedating ANTICONVULSANTS: for Lancinating neuropathic pain including: phenytoin, carbamazepine, valproate, & clonazepam. BACLOFEN: GABA enhancement -???mech known to reduce pain of trigeminal neuralgia & possibly also general neuropathic pain LOCAL ANESTHETICS: for neuropathic pain of lancinating quality. These include mexilitine & tocainide & are choices of last resort METHOTRIMEPRAZINE: a phenothiazine w/ analgesia - used particularly in CA pts w/o good opiate response or sig N/V -highly sedating & hypotensive (other neuroleptics may be analgesic) CORTICOSTEROIDS: can improve analgesia, mood, & appetite. Particularly good in severe pain from bone mets or tumor infiltrating neural structures. DEXTROAMPHETAMINE & METHYLPHENIDATE: co-analgesic and helpful for opiate induced sedation. HYDROXYZINE: analgesic @ high parenteral doses w/benefit of anxiolsis & anti- emetic effects. --------------------------------------- CANCER PAIN SYNDROMES 1. Bony Involvement: most often painless when painful- NSAIDS work well suggesting role of PGs -BASE OF SKULL Syndrome: due to mets deposited at base of skull -ORBITAL SYNDROME: orbit lesion often presents w/retro/periorbital of frontal HAs +/- diplopia or visual changes. +/- Proptosis & extraopcular palsies. Lesions req CT for ID. -PARASELLAR SYNDROME: lesion invading cavernous sinus & spenoid bone pain&neuro sx similar to oribt synd -SPHENOID SINUS SYNDROME: may have uni- or bilateral HA-retro, periorbital, or frontal. Sensation of nasal fullness or stuffiness. Extension of lesion may compromise CNs- usually 1st w/ abducens palsy & diplopia. -MIDDLE CRANIAL FOSSA SYNDROME: lat to sella may involve one or more branches of Trigeminal Nerve or the gasseerian ganglion. Sx is ipsilateral facial pain - may be continuous or resemble trigeminal neuralgia. May have trigem sensory loss or lost corneal reflex. HEADACHE from traction, inflam or infiltration in dist of trigeminal, glossopharyngeal vagus or upper cervical nerves. Cranial Neuralgias: head/face pain w/o Glossopharyngeal Neuralgia: assoc w/ 1. syncope & hypoTN in mening mets 2. jugular foramen syndrdome 3. presenting sx of head/neck CA Trigeminal Neuralgia: assoc w/ 1. middle or post fossa tumors 2. lymphomatous meningitis (seen w/ atypical trigeminal neuralgia occurring w/ brief lancinating pain w/o trigger points) Cancer Pain --------------------------------------- CAUSES OF CHF: ============== Arrhythmia Excessive Dietary Na+ Excessive IV Fluids Drugs: -Dig noncompliance -Diuretic noncompliance -Blockers -Cardiotoxins: daunorubicin -NSAIDS -Narcan: opiate withdrawl Pregnancy High Output: fever, anemia, A-V fistula & hyperthroidism Myocarditis: rheumatic & otherwise ======================================== Reversible Causes: ------------------ anemia Hyperthyroidism Arrhythmia Thiamine Deficiency EtOH abuse Surgically repairable valve dz Atria Myxoma CHF CLASSIFICATION FORRISTER class: based on swan data class I: nml PCWP nml CO class II: low PCWP & low CI class III: nml CI/high PCWP ClassIV: high PCWP/low CI KILLIP: based on phy signs NY HEART ASSOC.: class 1: sx only w/> than nml activity class 2: sx during ordinary activity class 3: sx only w/min activity class 4: sx at rest #1: REDUCE overall cardiovasc risk. inappropriate diet, high glucose/DM hypothyroidism, Rx that incr Chol HTN, smoking, obesity (CV risks: male,HTN,cigs,DM,Obesity FHX, low HDL) (High RISK= CV dz + 2 or > of above) #2: Rx THERAPY: pts resistant to change of diet or habits & w/isch heart dz - if LDL > 160 after reasonable trial @ reduction then Rx is appropriate. GOAL: reduce HDL to < 130 LDL= total chol - (tag/5 + HDL) --------------------------------------- GEMFIBROZIL(lopid)- decr TAG incr HDL ***only modestly decr LDL particularly if pt has nml TAGs. LOVASTATIN(mevacor)- potent decr LDL ***only modestly decr TAG & incr HDL NIACIN: decr LDL & incr HDL ***give w/ASA to avoid flushing -liver toxicity- raises -makes DM worse -increases uric acid -? PUD --------------------------------------- Lovastatin & Gemfibrizol in combination has incr risk of myopathy. Cholesterol CONVERSIONS TEMP: 40C=104F/39=102.2/38=100.4/37=98.6 C=(F-32) x 5/9 F=(C x 1.8) + 32 1inch=2.54cm 1cm=0.3973 1lb=0.454kg 1kg=0.45kg 1L=1.06qt=33.81oz Conversion Formulas CRANIAL NERVES: (LR6SO4)3 I. OLFACTORY II. OPTIC III. OCULOMOTOR -3rd Nerve Palsy: ?DM, neoplasm, aneurysm @ circle of willis, *-in compressive 3rd nerve Dz: pupil usually dilated *-in ischemic 3rd nerve Dz: pupil is spared (not dilated) IV. TROCHLEAR: CN3,4,6 Disorders: Tolosa-Hunt Syndrome: painful combined unilateral palsies due to parasellar granuloma Pituitary Apoplexy: acute onset of uni- or bilat ophthalmoplegia & visual field defect w/HA &/or drowsiness Migranous Ophthalmoplegia: attacks of occular palsy assoc. w/ classic migraines V. TRIGEMINAL: feel masseter &temporalis muscles. Test jaw opening & sens all over face. Test Corneal reflex -Trigeminal Neuralgia: freq paroxysms of severe pain in lips, gums, checks, or chin lasting seconds to minutes (rarely in ophthalmic div of CN5) Typically starts in middle to old age Pain is often stmulated @ trigger pts *No sensory deficit. Tx w/ carbamazepine (1-1.5mg daily in divided doses) effective in 75%. If fails, surgical gagliolysis or suboccipital decompression . -Trigeminal Neuropathy: presents w/SENS loss or jaw muscle weakness. Caused by tumors @ middle cranial fossa, trigeminal nerve, or mets. VII. Facial: lesions of CN7 or its nuc prod hemifacial weakness including muscles of forehead & orbic. occuli - Lesion @ middle ear: loss of taste over ant 2/3 of tongue - Lesion @ int aud meatus: involvement of auditory & vestibular nerves - Lesion @ PONS: usually affects CN6 as well as Corticospinal Tract Bells Palsy: facial paralysis found in 23/100,000 annually. weakness evolves over 12-48h- sometimes w/retroaural pain. 80% recover in w/i weeks- months. Tx=protecting eyes during sleep. Prednisone 60-80mg qdx5d then tapered over another 5d(not firmly established therapy) Ramsey Hunt Syndrome: due to Herpes Zoster infection geniculate ganglion. different from bells palsy by vessicular eruptions in pharynx, ext aud canal, & other areas Acustic Neuromas: often compress CN7 Pontine Tumors/Infarcts: lower motor neuron facial weakness VIII: VESTIBULOCOLCLEAR vertigo: lesion in vest div. conduction loss: due to structural dz of ext aud canal or middle ear due to tumor, infection, or trauma sensorineural loss: due to damage to hair cells of Organ of Corti from excessive noise, viral inf, ototoxic drugs, temporal bone fractures, meningitis, Menieres dz or tumors IX: GLOSSOPHARYYYNGEAL Glossopharyngeal Neuralgia: intense pain in tonsilar fossa of throat- may be precipitated by swallowing. NO sens or motor deficit. Tx: w/tegratol or dilantin may help. May need surgical div of CN9 from medulla X: VAGUS XI: ACCESORY XII: HYPGLOSSAL: supplies ipsilat tongue Cranial Nerves COPD EMPHYSEMA: "Pink Puffer" -Prominant Dyspnea w/scant sputum prod -widened A-P diameter w/hyperresonance -increased E:I ratio w/diminished gas exchange & low->nml PaO2 & PaCO2 -PFTs w/reduced flow rates & dif cap & evidence for gas trapping -Hypercapnea & Cor Pulm occur Late -CXR w/hyperinflation, bullae, Sm Heart -Resp Failure w/serious sequelae BRONCHITIS: "Blue Bloater" -chronic cough & mucus -minimal dyspnea -Pts ofter overwgt & cyanotic -Coarse Rhonchi & Wheezing -ABG w/low PaO2 & high PaCO2 (50:50) -CXR w/Vasc Cong Marks @ base,Lg heart -PFTs w/reduced flow, elevated RV & low-nml DC -episodes of Resp Failure common & respond well to Tx. ======================================== EMPHYSEMIC BROCHITIC Age @ Dx 60 50 Dyspnea Severe Mild Cough Mild Chronic Chronic PaCO2 35-40 50-60 Chronic PaO2 65-75 46-60 HCT 35-45 50-55 PULM HTN @ Rest none->mild mod->severe w/Exercse moderate severe CorPulmonale rare common Elasticity Poor nml Resistance nml->mild inc high Diffusing reduced nml->low Capacity ======================================== RENAL FUNCTION ======================================== CREATININE CLEARANCE:(cockroft-gault eq) (140-Age) (wgt in Kg) ---------------------(X 0.85 if Female) (72) (Serum Cr) ======================================== Endogenous Creatinine: primarily excreted by glomerular filtration Affected by: age, sex, dietary protein exercise, drugs & Dz DRUGS requiring dose change w/renal fxn - H2 BLOCKERS: accumulates w/renal dz & may interfere w/Cr excretion thus increasing serum levels - AMINOGLCOSIDES: - Some Beta LACTAM Antibiotics: - Some Beta BLOCKERS: Renal FXN & the Elderly: Cr Clearance may decrease w/age from nml renal aging & GFR may decline @ 10cc/min for each decade over 40 REF: Friedman: Corr of Est Renal Fxn JAMA 37:145-149,1989 Creatinine Clearance CSF ANALYSIS PRESSURE: 75-150mmH2O in lat decub pos PROTIEN: 15-45 mg/dl LD: 1/10 of serum GLUCOSE: 45-85 (60-70% of blood) COLOR: if yellow (xanthochromic) may indicate subarach bleed(previos bleed) or dark yellow indicating subarach block. -abnml color seen w/prot >100 CELLS: total cell CT: 0-5/cu. mm 2-10=borderline pleocytosis 25-50=elevated pleocytosis >50=severe pleocytosis (>500 usually purulent menigitis w/ predominant granulacytes) (300-500 w/predom lymph or monos -viral, syphilis,TB,lyme,partially tx'd bact inf, MS in 50%, sarcoid) (>40% MONOs c/w subarachnoid bleed) HEART PRESSURES PA systolic1 15-30 diastolic 4-12 Mean 9-16 RV Peak Systolic 15-30 EDRV 0-8 RA Mean 0-8 PCW 2-10 CARDIAC INDEX(l/min/m2):2.8-4.2 CVS Pressure Values CYSTIC FIBROSIS -autosomal recessive -50% pts live > 20 years old -Pulm. infections usually related to pseudomonas aeroginosa and S.Areus -Pancreatic insufficiency in all by age adulthood Cystic fibrosis delerium: acute change in MS that fluctuates during day "sun downing" usually very treatable -?Rx -?Infection -?CHF/Hypoxia -?Metabolic: gluc, Na, Ca+, -?CNS/CVA/Subdural Dementia: chronic > 2 weeks less fluctating usually resistant to Tx check TFT B12 lyme titer vdrl DELERIUM Incidence: 25-60% Hosp Mortality: 10-65% DX: 3 of 4 [1,2 and (3 or 4)] 1. Acute onset or Fluctuating course 2. Inattention 3. Disordered Thinking/speech 4. Altered Level of Consciousness -Alert (nml) -Vigilant (hyperalert) -Lethargy (drowsey-easily aroused) -Stupor (difficult to arouse) -Coma (unarousable) DELERIUM DEMENTIA ONSET: abrupt insidius DURATION: brief mo-yrs ATTENTION impaired nml unless severe SPEECH disorganized ordered ETIOLOGY: D-E-L-E-R-I-U-M Dementia Lytes, lungs, heart, kidney,Brain, Injury,Pain Stress Unfamiliar Environment Metabolic MEDS: Seditives: benzo, barbs, sleepers Narcotics, Anticholinergics, Antihistamines, TCAs, AntiPD Antiarrhythmics(Quin,Norpace) Dig, Lido, Beta-BlKs,Aldomet H2 blockers, Steroids, lithium metoclopramide, NSAIDS, AntiSz Risks: visual impairement severe illness cognitive impairement dehydration TX:-stabilize sleep: avoid sleep interupting procedures or Rx interv -activties: avoid restraints or bedrest orders, encourage ambulation -ENV: glasses, hearing aids, dentures rooms w/clocks & calander home possessions family visits -COMMUNICATION: verbal schedules pt inv in decision making Delerium Rotavirus EPIDEMIOLOGY 3 serological types, type 2 produces most serious disease. Most common cause of diarrhea in infants and young children in developed countries. Incubation period is 24 - 72 With parvoviruses(Norwalk) account for 80% of pediatric diarrhea. TREATMENT Nonspecific Prompt fluid and electrolyte replacement Prolonged disaccharidase deficiency possible with Rotavirus Keep fluid intake above 150ml/kg/day in young infants. Feedings should be LESS frequent and of larger amounts than usual. Dehydration Replace total deficit over 24-48 hrs Sever Dehydration(10%) initial lab: Na,K,CO2 HCO3 H pH Pco2 K below 3-4mEq/kg per 24 Repair mmaint D1 total(ml/kg) 100ml/kg(65ml/kg 1st 24 135ml/kg 200 Pediatric Diarrhea DIASTOLIC HEART FAILURE (DHF) 40% all CHF w/nml systolic Fxn - w/ diastolic dysfxn w/better prog than w/systolic dysfunction (Systolic dysfxn is often complicated by sig diastolic component) INCREASED DIASTOLIC FILLING PRESSURE FROM NON-COMPLIANT VENTRICLE: 1. enlarged heart reaches limits of pericardial expansion 2. hypertrophic myocardium stretches less than nml myocardium 3. Interstitial or regional fibrosis causes restricted diastolic filling Seen in Pts w/ -mild-moderate HTN or ischemic HeartDz Dx of Diastolic Dysfunction:NO GOLD STD (Dx of Exclusion) 1. Maintain high index of suspicion 2. Consider complete CHF Dif-Dx 3. r/o systolic dysfxn: nml EF & size 4. ECHO: LVEF & heart size 5. Assessment of rate of diastolic filling & rate of filling in both rapid phase & atrial contraction phase: w/worsening diastolic fxn, amt of filling from atrial contrac increases & ratio of filling from atrial contraction/rapid phase is > 1. (complicated by chages in preload, afterload, age, MR CAUSES OF CHF: 1. Restrictive diastolic filling: pericarditis & mitral stenosis 2. Myocardial Overload: MR & AS 3. Myocardial Dysfxn: MI, myocarditis or idiopathic cardiomyopathy - No Dig: - No Afterload Reduction: assumes poorly fxning heart & won't improve CO *Cautious Diuresis: overdiuresis may lead to low output state from increased filling pressures for nml CO. -Ca+ blockers & -blockers may improve fxn (particularly in IHSS) -Ca+ blockers may improve active relaxation & passive filling -blockers slow rate for increased filling time Systolic Dz: -Dig: Inotropy -Nitrates & diuretics: reduce Preload -ACEI's: reduce afterload Diastolic Heart Failure DIGITALIS TOXICITY - no arryhthmia unique to dig toxicity - any sudden cardiac rhythem change is suspicious in digitilized pt - Suspect in pts on dig & QUINIDINE must decrease dig by 1/2 when pt on quinidine SX: anorexia, fatigue, visual disturbance confusion(in elderly) EKG SIGNS: 1. bradycardia in pt w/previously nml or fast HR 2. tachycardia in pt w/previously nml or slow HR 3. any reg-irreg rythem in previously nml pt 4. Unexpected regularity in previously irreg pt DIG LEVEL: toxicity may occur @ levels < 1.0 Digitalis Toxicity DISSECTION: Aortic Dissection: tear of intima -almost always related to HTN and/or medial necrosis - most commnly bleed in pericardium on L - Acute <2wks 67-75% die in this period TYPES I. extends from ascending to arch or even down decending aorta II. ascending aorta only III. descending aorta (usually distal to L subclavian) -dissecting hematoma can propogate in retrograde direction CAUSES: -HTN most commom cause -Marfans -Pregnancy (?hormonal etiology) -Aortic Stenosis - Particlarly Bicuspid -Coarctation (rare) -Syphilis -Trauma -Ehlers-Danlos synd -relapsing polychondritis PRESENTATION: -CP: sharp, most intense @ onset, -radiation of pain to back -syncope from CAD or carotid flow compromise -travals from one area to another -CVA like Sx from obstruction of carotid -periph neuropathy due to diminished blood supply to a limb -or spinal pain or paralysis from clipping off spinal arteries -Horners synd: from compression of superior cervicle ganglion -vocal cord paralysis from pressure on the recurrent laryngeal nerve -SVC Syndrome -hemmorhagic pl. effusion -MI -Mesenteric Infarcts -------------------------------------- PE: BP: pseudoHTN: diff BP R-L due to insufficient blood flow to one brachiocephalic art but nml in the other -Bruit or murmer of AI -? pericard effusion or tamponade ---------------------------------------- DIAGNOSIS: AORTOGRAPHY: gold standard CT SCAN: need "dynamic study" w/ quick bolus of dye U/S: transthoracic= 70-80% sens transesophageal>98% sens MRI: take long time/cant monitor CXR: widened mediastinum -if their is 1cm between calcium layers in aortic knob -NGTube displaced by aneurysm to R TX: prevent extension & rupture - decrease pressure (lower BP) & shearing force (lower HR) --Nipride(Tachy fxts) & beta blocker --Labetalol: alpha and beta effects --Trimethiphan: not first line but gang blocker w/side fxs on bladder. Who Gets Surgery: PROXIMAL: all w/surg due to high mort DISTAL: may mng medically unless hemodynamicaly unstable compromise an organ etc PROGNOSIS: unTX: poor 20% die in 24hours 60% die in 2weeks 90% die in 3months TX'd: Type I & II need surgery w/20% mortality rate -Type II aneurysms which are distal can be managed w/RX -Surg req if growing III dissection bleeding, or Pain Dissecting Aneurism DIABETIC KETOACIDOSIS & NON KETOTIC HYPEROSMOLAR COMA -Give insulin, glucose (keep @250), K+ and fluids SX: Anorexia, N/V, increased UO -- Abd pain, alt MS, & Kussmaul breathing or coma may ensue -- frank pancreatitis can occurr -Watch lytes, q4-6hours fingerstick glucose q1-2hours I&O's for fluid balance - May also follow AG but watch rate of change as much as total value LABS: hypergly, prerenal azotemia, Met acidosis from BHBA & AAA K+/Phos may be nml or elevalted Low Mg, high amylase check plasma ketone(once only) 1. ID precipitating condition - ?infection: - ?insulin pump-?malfunction -------------------------------------- 2. Control hyperglycemia - Adequate insulin dose (5U/hr)IVD (or .15U/Kg) or IM - with adequate fluids & hydration: glucose will decrease by 100mg/dl/h - Continue Insulin while adding glucose to keep glucose @ 250 since hyperglycemia usually resolves prior to ketosis - Follow fingersticks q1-2 hours - Late Cerebral Edema avoided by keeping glucose from dropping below 250. -------------------------------------- 3. Control ketosis - Serum HCO3 reflect response of acidosis to tx. - After initial serum ketone are + further levels may be misleading since BHBacid to AAA. - Continue Tx until Urine Ketones are negitive (& perhaps also AG). - Don't stop Insulin Tx abruptly convert drip to NPH(20 U sq) & reg **give reg & NPH while IV insulin still running then stop IVD after approx 1h - Type 4 RTA- may persist several days after resolved DKA- serum bicarb may not become completely nml -------------------------------------- 4. Replace Electrolytes & Fluids - Hypokalemia: may be masked by met acidosis & occasional hyporeninemic hypoaldo - Hypophospatemia: seen after recovery from DKA ** Don't need to replace replacement may be dangerous *however: if drops below 1.0 may cause rhabdomyalysis or CHF or impair DPG or ATP metabolism - Watch I&O's to keep up w/ renal & GI fluid loss ======================================== NON KETOTIC HYPEROSMOLAR COMA ----------------------------- 50% Mortality Rate:FROM -Osmotic diuresis w/Pt unableto keep up intake w/urine fluid loss-volm depletion leads to prerenal azotemia - ALSO: high Protien Tube feeds peritoneal dialysis, high carbo intake, & osmotic agents such as mannitol or urea REASON FOR HOC:Infection, MI, drugs(thiazide,pentami), trauma/injury Labs: glucose ussually +/-1000 . mild met acidosis Lactic acidosis if HCO3<10 & nml plasma ketones fluids (usually 10L deficit) - 2-3L NS over 1-2hour - as gluc approaches nml, give D5 Insulin: drip or sq to control gluc Diabetic Ketoacidosis Drug interactions on Warfarin Blood Level: by liver oxidase induction phenobarbital rifampin carbamazepine phenytoin glutethimide exposure to chlorinated insecticide chronic alcohol ingestion Warfarin Blood Level: by liver metabolism inhibition cimetidine ranitidine in doses >150mg erythromycin metronidazole phenylbutazone Warfarin Drug effects: by combined effect aspirn Drug interactions by mechanism liver oxidase induction ---Causing Drug --- --- Blood Level --- phenobarbital warfarin rifampin digitoxin carbamazepine quinidine phenytoin mexiletine glutethimide ketoconazole exposure to cyclosporine chlorinated dexamethasone insecticide prednisolone chronic alcohol oral contraceptiv ingestion metabolism ---Causing Drug --- --- Blood Level --- cimetidine warfarin ranitidine >150mg nifedipine quinidine lidocaine theophylline phenytoin --------------------------------------- erythromycin cyclosporine warfarin carbamazepine triazolam theophylline --------------------------------------- alcohol warfarin --------------------------------------- isoniazid phenytoin --------------------------------------- ketoconazole cyclosporine --------------------------------------- metronidazole warfarin --------------------------------------- phylbutazone warfarin phenytoin tolbutamide --------------------------------------- allopurinol azathioprine 6-mercaptopurine --------------------------------------- cyclosporine lovestatin prednisolone Renal elimination ---Causing Drug --- --- Blood Level --- phenylbutazone methotrexate probenecid penecillin salicylat ---Causing Drug --- --- Blood Level --- cimetidine procainamide & NAP Multiple mechanisms ---Causing Drug --- --- Blood Level --- quinidine digoxin&digitoxin ---Causing Drug --- --- Blood Level --- amiodarone digoxin cyclosporine verapamil pharmacodynamic interactions ---Causing Drug --- --- Drug effect --- indomethacin adrenergic block piroxicam anti-HTN other NSAIDS diuretics (except ASA & sulindac) Drug Interactions, common ones ---Dysfunctional Uterine Bleeding --- Treatment Ovral-21, 3 pills D1, then i po bid 9D, Bleeding stops in 24hrs Dysfuntional Uterine Bleeding Fishman's quick reference ECG Rate:?escape rate (for bradycardia (must use 6 sec cycle x 10) Rythem: ?regular (? NSR) ?p waves (unifocal vs multifocal) ?p:qrs (PAC's, noncaptures) ?p-r intervals (AV block) ?qrs intervals (Vent rythem, BBB) Axis: vector I with AVF Atrial Escape Rythem: 60 - 80/min Junctional Escape Rythem: 40 - 60/min Ventricular Esacpe Rythem:20 - 40/min Nml p-r:0.12-0.20 (3 - 5 small boxes) 1 small box = 1mm = 0.04 sec 1 large box = 5mm = 0.20 sec Nml qrs:0.06-0.10(1.5-2.5 sm boxes) Sinus Arrythmia: rythem varies with resp - all p's identical Wandering Pacemaker: irreg p's with changing atrial ectopic foci(nml rate) MAT: same as wandering pacemaker with atrial tach (rate > 100) PAT: Atrial focus at 150-250/min with unifocal p's (if p's are visible) PJT: Junctional focus at 150-250/min (qrs may be slightly widened) PAC: Atrial ectopic focus discharging prematurely (? uni vs multifocal) PVC: Vent ectopic focus discharging prematurely (? uni vs multifocal) 1o AV block: p-r>.2sec (one lg sq) 2o AV block: Wenkebach: p-r increases with each qrs/ last one too long to capture Mobitz II: some p's don't capture (occasional missed qrs's)2:1,3:1 etc 3o AV block: p's don't capture any qrs's/ if qrs is narrow than junct. if qrs is wide than vent pacing BBB: Prolonged QRS (can't determine vent hypertrophy) RBBB: rsr' in V1or2 LBBB: rsr' in V5or6(can't determine infarction) HEMIBLOCK: L-ant: LAD>-30 or predominant S>Rwave in II,III & F Q Waves: = infarction (can't use AVR) sig when: >1mm/.04sec (1 sm box) or >1/3 size of qrs complex ST elevation: = acute injury (with q-wave=acute infarct; ? tmural infarct) ST depression = injury (may reflect subendo infarct) NON Q WAVE Infarct: either sig ST elevation or depression T inversion: = Ischemia (normal T wave is usually up if qrs is up) Anterior Infarct: q's in V1-4 (LAD) Posterior Infarct: ST depression in V1&2 with large r wave (RCA) (r wave = inverted q wave in V1&2 since it is a posterior reflection) Inferior Infarct: q's in II,III,& F Lateral Infarct: q's in V5-6,I,& L (circumflex) LVH: increased voltage in I, III or V1,5,or6 (s in V1 + r in V5or6 > 35mm) (r in V5or6 > 26mm) (r in L > 11mm) RVH: large R/small T wave in V1 and RAD (r in V1>7mm/s in V1<2mm) LAH: tall p's in II,III, & F (>2.5mm) RAH: notched/biphasic long p's in I & sinusoid p's in V1 Q-T Interval: should be < 1/2 R-R int (for rates >65) -?congenital vs acquired -?rheumatic fever, myocarditis, CVA ?low Ca+,Mg++ ?quinidine,procan,phenothiaziazides ?hypothermia, excessive dieting -delays repolarization may lead to V-arrhythmias, syncope, Torsades WPW: SA node conducts aberrent pathway with pre-excitation of vent (?accesory bundle) with delta wave as sloping upstroke of QRS PE(Pulm Embolism): flipped T in III -pattern may look like IMI -R vent Strain (flipped T's V1-6) -Transient RBBB -Tall peaked p's in II,III,&F PERICARDIAL EFFUSION/TAMPONADE 1) low voltage 2) S-Twave eevations 3) electrical alternans NOTE: alternation of p's & QRS is sig for malignant effusion P-Mitrale: c/w MS -> wide notched p in in I & II w/flat,diphasic, or inverted p in III. HYPOKALEMIA: 1)gradual ST depression 2)small T waves 3)prominant U waves (hump off of T) 4)prolonged PR 5)large wide P-waves advanced: 6)wide QRS,ST-dep,Tinv HYPERKALEMIA: 1)Tall thin T-waves 2)Prolonged PR (later) 3)STdep & QRS widen 4)Finally, P's disappear HYPOCALCEMIA: Prolonged QT HYPERCALCEMIA: Short QT HYPOMAGNESEMIA: Prolonged QT LOW VOLTAGE: 1. Diffuse Ischemic Dz 2. CHF Txd w/ DIG 3. Myxedema 4. Cardiomyopathy 5. Constrictive Pericarditis ST DEPRESSION: 1. Dig Effect 2. Diffuse Ischemia 3. LV Strain 4. Ant & Inf MI 5. SEMI 6. Hypokalemia EKG Quick Reference Electrolyte content PO Liquids Na+ K+ HCO3 -------------------------- Coke 0.4 13 13.4 7-up 7.0 0.5 0 Ginger ale 3.5 0.1 3.6 Gatorade 22. 2.6 - Apple juic 1.3 30 - Grape juic 0.4 31 32 Grapefruit 2.0 20 22 Orange jui 0.4 38 38.4 Pineapple <1 35 35 Tomatoe ju 120 70 10 Jello 1box 144 54 - Pedialyte 30 20 14 Na-K-Glucos 26 27 Lytren 25 25 18 Electrolytes in PO fluids THYROID STORM CNS, Fever, transient neuro deficit usually due to some stressor: -MI, infection, Hyperthyroid Heart: Dig resistant Verapamil: Rx of choice PREOP: ? beta blocker ?iodine halt thy horm prod MYXEDEMA Coma temp, low BP, coma, bradycardia nonpitting edema, minimal eyebrows allopecia ? scar on neck low reflexes High CK (from muscle inv of edema) Diluted total body fluid Fluid overloaded EKG w/low voltage ABG: hypovent, CO2 retaining r/o secondary hypothy (pit) TX: careful w/fluids - give steroids to protect against adrenal insufficiency DONT give synthroid:could induce collapse due to inc metab ----------------------------------- ADRENAL INSUFFICIENCY tan, low bp, seizure, low Na/high K, fever ALSO: hypoglycemia, hypercalcemia (steroids block Ca+ uptake in gut by Vit D - so with no steroids leads to hyperCa+) Endocrine Emergencies EYE SIGNS IN NEURO EXAMINATION Frontal Eye Feilds: in each lobe nmlly: Rt side moves eyes to Lt Lt side moves eyes to Rt Lesion: eyes deviate toward area of lesion. Dolls Eyes: Occulocephalic Reflex (valid only if pt unconscious) Nmlly: eyes move opp of head mvt Lesion: front eye fields: can't move eyes away on head mvt on side of lesion brainstem: can't move bilat PUPILS: Asymetrical: idiopathic or Trauma Pinpoint: Pontine lesion Oval (other one=pinpoint): midbrain --occulomotor N. damage Argyle-Robinson: No light Reflex w/ intact accomodation Optokinetic Reflex: move stripped tape to Lt - nml eyes w/nystagmus to right Calorics: Cold water: nystagmus away Warm water: nystagmus same side Cold in both ears: nystagmus up Warm in both ears: nystagmus down In COMA: cold H2O: slow deviation to side of stim- may fixate ICP: papiledema no venous pulsations check for increased blind spot MLF: (from ?MS vs DM) opposite eye stops @ midline on lateral gaze / converges normally Eye Signs in Neuro Exam FLUIDS -------------------------------------- Pleural Fluid: TRANSUDATE EXUDATE LDH <200 >200 LDH pl/serum <0.6 >0.6 total Protein <3.0 >3.0 (gm/100cc) Pl fl protein/serum tot protein <0.5 >0.5 appearance clear ++ +/- white/milky(chylothorax) ++ purulent(empyema) ++ foul smell(abaerobes) ++ hemorrhagic(mesothelioma) ++ anchovy paste(amebiasis) ++ Sp Gravity <1.016 >1.016 pH 7.4 <7.3 ?TB >7.3 ?CA <7.2 ?CTube Cells WBC <1000/mm3 >1000/mm3 RBC <10,000/mm3 >10,000/mm3 -------------------------------------- CEREBROSPINAL FLUID Fluid specimin values Hematopoietic Growth Factors: ---------------------------------------- hematopoeisis directly regulated by BM microenvironment & growth factors (-interferon & TNF also implicated) Myeloid & Lymphoid cells from one common pluripotent stem cell STROMAL CELLS: fibroblasts & adipose cells -produce & deliver growth factors -bind growth factors w/high affinity ALL HEME GROWTH FACTORS: -all are glycoprotiens -bioactivity at picomolar levels -many have actions on more than one cell line. -some stim mature cells may stim mature cells to enhance survival & possibly trigger further released factor(s) CHROMOSOMAL BASIS: CHROMOSOME 5: Many human CSF's are clustered on the long arm of CHROM5 w/GM-CSF closely linked w/IL3 w/M-CSF, its receptor,& IL5 @ distance CHROMOSOME 17: G-CSF CHROMOSOME 7: ERYTHROPOIETIN LATE ACTING FACTORS: G-CSF,M-CSF, & EPO - liniage restricted/stim terminal division & differentiation of their specific cell lines INTERMEDIATE FACTORS: multi CSF's: GM-CSF & IL3- stim several cell lines @ intermediate stage of differentiation - ERYTHROID cells require "BURST" activity provided by GM-CSF & IL3 - GM-CSF acts @ later stages of gran & mono pathways EARLY ACTING FACTORS: IL6 & IL1 (hemopoietin or endogenous pyrogen) - affect primitive heme cells -may render most primitive stem cells sensitive to multi-CSF's & later acting factors (via stim division or up regulating receptors) -NO INHERENT GROWTH STIM FXTs -prob synergistic factors: combined w/other factors permits sig growth -IL1 also has mult other actions on hepatocytes, lymphocytes & induction of fever Hematopoietic Growth Factors: - specific protiens classified by cell type they regulate 1. Interleukins: prod by lymphocytes & reg their activity & production 2. Erythropopetin: prod by kidney to stim RBC production 3. CSFs: act on mylocytic cell lines - GCSF: stim prod of granulocytes - GMCSF:stim prod of gran & macros - MCSF: stim macrophage production - Multi-CSF or IL3: stim grans ,macros, eos, masts, rbcs, & multipotent blast colonies. (act synergisticall & poss in cascade) ---------------------------------------- ERYTHROPOIETIN: (discovered 40yrs ago & purified 1977) -hydrophobic glycoprotein -acts on erythroid progenitor cells (works exclusively on RBCs -Normally tightly linked to unknown mech of tissue oxygenation & likely under feedback regulation -Made on demand de-novo not from preformed stores -Some made in Liver (accounting for basal levels seen in anephric pts) ---------------------------------------- GM-CSF:(recombinant) (made by some malig cells: hairy cell T-cell leukemia) - glycosylated polypeptide (127 aa's) - degree of glycosylation inversely proportional to activity - high & low affinity receptors on nml granulocytes,monos, eos, & precursors(none on lymphoid or RBC) - Some Tumor cells w/GMCSF receptors that are functional (? malignant control vs. antagonist Rx) - ACTIVITY: stims formation of BM colonies of grans,mono/macros,& eos -activity is potentiated in combo w/ M-CSF or G-CSF & IL3 -May promote growth of megakaryo's -may counter AIDS Assoc. neutropenia -partly corrects the AZT effect of myeloid hypoplasia -may enhance neutrophil fxn in AIDS -may stim growth of myeloid leukemia -enhance MONO's ability to kill tumor cells (cell cytotox/phago) -w/Endotoxin + GM-CSF leads to increased TNF production -lowers serum cholesterol -IN Aplastic Anemia: may be benificial -IN Myelodysplastic Synd: clearly increases periph leuks & increased BM cellularity W/?? of induction & prolif of leukemic clones (thus tx of MD is limited) -IN Post ChemoTx: either prevent or restore chemotx induced myelotoxicity (<neutropenia & thrombocytopenia) -IN BM Transplant: increased rate of BM (neutros & plts) proliferation ---------------------------------------- G-CSF: found in bladder ca squamous ca hepatoma (glycosylated peptide) - stims granulocyte & macro colonies - Synergistic w/IL3 to stim megakaryo's & blast colonies - Synergistic w/GM-CSF to stim grans & macro colonies - may stim prolif of leuk cells - differentiation factor for myeloid leukemia ---------------------------------------- M-CS (Fisrt from urine then panc CA) now recombinant from yeast -dimer of 2 polypeptides -weak stimulator of macro-mono colonies -synergism w/GM-CSF, G-CSF, & IL3 -activity in-vivo yet unproven ---------------------------------------- INTERLEUKIN 3: recombinant from -glycoprotien -low density of receptors on nml hematopoietic cells -only released by activated T-Cell -induces colony formation of myeloid, eryroid, & megakaryocyte progenitors -probobly works on early hematopoietic progenitors (may work in Aplsastic Anemia) -synergistic w/G-CSF, GM-CSF -synergistic w/IL6 for early blast cell colony formation -no human in-vivo trials yet Hematopoetic Growth Factors Goodpastures Syndrome: -Glomerulonephritis (usually cresentic) -Pulmonary Hemorrhage -**Anti-glomerular basement membrane Ab SX: fever & myalgias may be primary sx -rapidly progressive renal failure with nephrtic synd mild severe (urine sediment w/RBCs & RBC casts) -Pulm infiltrates, hemoptysis, cough & dyspnea. -Lung dz comes before renal dz by days weeks -Fe def anemia in cases of long standing pulm bleeding DX: circ IgG anti-BM Ab in > 90% cases Bx: renal tissue w/cresentic prolif glomerulonephritis. Cresents > 80-100% of glomeruli TX: short/pulse course high dose steroids -alkylating agents of ? help -plasmaphores & chemoTx of ? help -nephrectomy for extreme intractible cases Goodpasture's Syndrome GOUT: only 5% of hyperuricemic's get gout 1. hyperuricemia 2. recurrent arthritic attacks 3. urate crystals in synovial fluid with Leukocytess 4. Tophi: aggregates of mono Na+ urate 5. Uric acid nephrolithiasis 6. Renal Dz involving interstitium & vessels Primary Gout: unknown met defect -lasts ~7-10 days Secondary Gout: a)Reduced urate excretion: -renal dz -diuretics q -volm depletion -competition: DKA, Lactic Acidosis, ketosis b)Other -Increased purine synthesis -Type I glycogen storage dz -Myeloproliferative Dz -Lymphoproliferative Dz -Hemolytic & Pernicious Anemia -Thalassemia -Inf Mono -some Carcinoma's -Drugs: Contravitals Gout Arthritis: from monosodium urate crystals in joints->phagocytosis by leukocytes & recruitment of more leuks joint space->increasing inflam rxn. 1. monosodium urate crystals in joint fluid under polorized microscopy (neg birefringent) 2. serum uric acid & urine crystals 3. Joint X-rays 4. If ? of overproduction, may measure erythrocyte HGPRT & PRPP levels Clinical Sx: 1. usually monoarthritis but may be poly arthritis. 2. Podagra; attack of lg toe eventually seen in 90% 3. attack subsides spontaneously after days->weeks 4. W/chronic unTx'd Gout->nodular urate deposits develop, commonly of helix & antihelix of ears, ulnar surface of forearms, & achilles tendon. 5. Nephropathy: may be due to deposit of urate crystals in renal interstitium or obstruction of collecting system & ureter by crystals Tx: duration of SX proportional to duration of therapy (no TX unless pt is symptomatic or has urate renal stones or excretes > 1100 mg uric acid/day) 1. Colchicine or NSAIDS (indocin) (may give IV Colchicne) 2. prophylax w/chronic cholchicine or indocin (good for chronic internittant Sx) 3. Uricisuric Tx: probenecid, sulfinpyrazone (use w/presence of tofi) 4. Allopurinol: inhib XANTHINE OXIDASE & decrease uric acid synthesis (never use during acute attack) 5. Avoid all precipitants & keep low purine rich diet CARDIAC PHYSICAL EXAM SIGNS PULSES: Paradoxes: fall in BP >10 w/inspiration -seen in Tamponade & Obstructive Lung Dz Pulsus Parvus: weak upstroke due to decreased stroke volm(hypovolemia, LV-failure, AS, MS Pulsus Tardus: delayed upstroke (AS) APICAL IMPULSES: -Lat & Downward: LV dilitation -Prominant Presystolic Impulse: HTN, AS, Hypertrophic Cardiomyopathy -Double Systolic Apical Impulse: Hypertrophic cardiomyopathy HEART SOUNDS: S1: shutting of mitral valve Very Loud: MS Very Soft: CHF, MR, COPD S2: Closing of the Aortic Valve Wide Split: MR, Pulm Stenosis Fixed Split: ASD Narrow Split: Pulm HTN Paradoxical Split: narrowsw/inp: AS Loud A2: systemic HTN Soft A2: AS Loud P2: Pulm Art Htn Soft P2: Pulm Stenosis S3: Rapid Ventricular Filling heard best w/bell @ apex nml in kids. In Adults indicated Volm Overload S4: Atrial Contraction w/reduced vent contraction heard best w/bell @ apex reflects noncompliant ventrical heard in AS, HTN, ischemic & HTN cardiomyopathy Opening Snap: Mitral Valve Opening follows S2 heard @ LLSB (in MS) (apex in MS): MURMERS SEM: related to blood flow across semi- lunar valves: "midsystolic" + spaces between S1 & S2 PANSYSTOLIC: no space between S2: occurring w/regurgitant flow across AV valves. EARLY DIASTOLIC: typically w/regurg flow across incompitant semilunar valves AS: Loud Creshendo/Dechreshendo (SEM) - heard best @ base & rad to neck - increase w/ squating - decrease w/ valsalva, standing - Late slow rising carotid upstroke w/ decreased intensity - strong apical impulse - narrow pulse pressure(in severe AS) MR: Holosystolic w/radiation to axilla - increase w/ squating - decrease w/ valsalva, standing - no correlation between intensity of murmer & severity of MR ** LOUD S1 AI: Low Pitched Early Diastolic murmer immed after S2 - early SEM - high pitched - widened pulse pressure(sig > SBP) - Bounding pulses - Water Hammer pulse @ wrist w/ rapid rise & sudden collapse - Cappilary pulsation @ nail bed base ** absent or diminshed S1 PI: same as AI MS: Mid-to-Late Diastolic: low pitched -increase w/Llat position or cough -diastolic rumble & opening snap - accentuated S1 ---------------------------------------- Cardiac Exam HEMATURIA usually looks worse than the drop in HCT DIF DX OF HEMATURIA Kidney Stone Pyelonephritis (less bloody) Cystitis: hemmorhagic Infection: TB, Shistosamiasis Tumor: renal (all pts except teens) renal cell & transitional cell Trauma Glomerulonephritis has to have proteinuria unlikely cause Drugs\toxins\nsaids AVM - unlikely Polycystic kidney dz - autosomal dom Sickle trait - Thrombotic\ infarct Coagulopathy- TESTS:1. UA,CBC,CA+,Uric,ESR,KUB 2. U/S, CT, IVP(??) 3. Hematuria HEMOCHROMATOSIS ??Autosomal Ressecive Dz. DZ based on inc absorption of Fe w/Fe deposition in the Liver, Heart, Pancreas, & other organs Males affected > than Females SX: Hepatomegaly, inc pigmentation, inc Fe, Cardiac Conduction Abnormalities, Cirrhosis, & Diabetes LAB Dx: inc serum transaminases, inc Fe in serum, inc Ferritin -Liver Bx w/Fe in Kupfer cells & hepatocytes (Fe in kupfer cells alone relect hemosiderosis) TX: repeated phlebotomy (unTx pts carry risk of HEPATOMA) Hemochromatosis Pediatric Hematology HCT-2sd -2 / 2SD 1-3d 2w 1m 2m 6m 6m-2y 2-6y 12- m 18y f Pediatric Hematology Hgb-2sd MCV-2 WBC/ 2SD PLT 108/98 18.1/9-30 290 1-3d 18 108/95 18.9/9 -34 192 2w 16 105/88 11.4/5-20 252 1m 14/10.7 101/91 10.8/5-19 2m 11.2/9.4 95/84 " 6m 12.6/11.1 76/68 11.9/6-17 6m-2y 12.0/10.5 78/70 10.6/6-17 150-350 2-6y 12.5/11.5 81/75 8 /5-15 12- m 14 /13 88/78 7.8/4 18y f 14/12 90/78 " " Adult m 15 90/80 7.4/4 -11 150-350 f 14/12 " " " Under 1m, capillary Hgb exceeds venous: 1hr=3.6g; 5d=2.2g; 3w=1.1g diff Pediatric Heme Values HEMOPTYSIS -Bronchiectasis in 20-30% -in cases w/chronic scarring from old TB lesions, usually due to post-TB Bronchiectasis Hemoptysis HEPARIN PROTOCOL 1. Bolus 5,000 - 10,000U 2. Drip 12,500 U in D5W 250cc= 50U/cc -run @ 15 to 25 U/Kg/hr (typically start @ 1000U/hr) ****=20cc/hr***** 3. Start drip 90 min after Bolus 4. PTT 6 hours after Bolus dose & after each change in drip 5. Adjust drip by PTT (2-2.5 nml) PTT Adjustment(cc/hour) --------------------------------- 30-37 up by 3 38-45 up by 2 46-75 no change 76-90 down by 2 >90 down by 3 CHECK UA QOD & Guiac all Stool Heparin Protocol Hirsutism Serum Testosterone - nl: suggests idiopathic hirsutism and excludes major ovarian disorders but not mild ovarian hyperthecosis or decreased sex binding hormone, these are not treated differently Androstenedione, dHEAsulfate - 80-200ng/dl: ovarian hyperthecosis or polycystic ovaries(Stein-Leventhal) FSH/LH normal ovarian hyperthecosis observe ^LH,Vor low nl FSH: PCO - >200 suggest ovarian neoplasm Hirsutism HISTIOCYTOSIS X non neoplastic histiocyte rxn of unknown etiology Classic Triad: 1. punched out lesions on skull XRay 2. Exothalmos: due to histiocyte retro-orbital infiltr. 3. Diabetes Insipidus Histiocytosis X HIV PNEUMONIA MALIGNANCY:lymphoma CVD AdenoCA SARCOID PROTAZOA: PCP VIRAL: Influenza RSV,Adenovirus EBV, Hsv, VSV FUNGAL:Crypto Histo Blasto Aspergillis BACTERIA: Mycoplasma Legionella HFlu, Pneomcoccus, TWAR & other Chlamydia Psitticosis MAI/TB PARASITES: strongaloidies DX: cults, cold agglut, legionella, CMV/viral studies, CD4 (majority of PCP w/CD4<200) Broch Specimen: for silver stain AFB, Viral, Fungal TX For PCP: sulfa better than pentamidine since faster acting than pentamidine & less expensive. HIV Pneumonias HIV AZT for tcell <500, pentam till 200 in asymptomatics. In symptomatic AIDS 1200/day for one onth, then reduce to 600/day. 500/day in asymptomatic. Septra DS thrice a week 30 to 40 % rash Dapsone 100 twice a week with pyramethine 25 twice a week . check g6pd before. rash granulocytopenia. Leukovorin may treat gran with 5 mg a day. Initial lab for new HIV asymptomatic tcell, p24, B2microglob, toxo igg, cmv igg, hsv igg, hep b status, rx - hepatovax, pnuemovax, flu shot no live virus vaccines B2microglob and p24 to decide in azt in marginal counts at 300 tcell see q6m tcell at 200 see q3 pcp proph after 6m on pentam monthly chest xray for breakthrough pcp in upper lobe infiltrate. if on oral EPO erythropoetin 10,000u 3/wk sq for hct <30 and epo<500. I initiate dose at 100u/kg/dose, may need to increase to 150-200u/kg/dose after 1-2 months. Produces euphoria. Pentamadine treatment General Notes Patient must be taught to stop the air flow BEFORE taking the nebulizer from the mouth. He/she should practice turning off the regulator a few times before you connect the nebulizer to the tank regulator. The patient should never remove the nebulizer without first stopping the air flow. The exhaust system of the room where the treatment are done pumps the room's air directly to the outside. Anything released into that room will not enter the rest of the office or building. To date there is no evidence of harm to staff giving pentamadine treatments from the pentamadine. Staff in HIV clinics have converted there TB tests. Pretreatment Patients should take bronchodilator if they smoke are asthmatic have had coughing with previous pentamidine treatments. Pretreatment will be two puffs of Maxair five minutes apart, fifteen minutes before the pentamidine treatment should start. Treatment Notes Check nebulizer for leaks prior to starting treatment. Instruct patient to observe for leaks during treatment. After treatment Offer patients mint or candy to eliminate after-taste Ordering Information 1800-766-4321 Recording answers, indicate ordering desired. State Company is Lyphomed and order Nebupent one vial a time Terms are net 30. Delivery is about one week usually. Reimbursement notes Medical requires that the 300mg dose be billed as two separate 150mg doses each treatment. They do not pay for administration but pay approximately 134 for the medication and 9 for the nebulizer. Check MediCal bulletin 174, 8/89. Dental care for HIV very important. sources California Dental Association 443-0504 734-5429 971-9800 HIV General Notes HYPERTENSION ======================================== HTN CRISIS: severe htn w/DBP>140=life threat from CVA, retinal hemorrhage, & renal damage DX: DBP>140 FUNDI: papilledema NEURO/MENTAL STATUS CHANGE ABNORMAL RENAL SEDIMENT TX: 1. NIPRIDE (Na Nitroprusside) titrated to desired BP 2. HYDRALAZINE: direct vasodil no decrease in renal blood flow -can usein aotemia. -causes reflex tachycardia careful in MI pts due to increased MVO2 3. Diazoxide: direct art-dilator causes severe reflex tach & long 1/2 life makes for prolonged hypotention 4. NTG: short 1/2 life avoid in IHSS, AS or increased ICP. 5. LABETALOL: alpha & beta blocker alpha & B1 & B2 beta effect 8x more potent than alpha -if paradox HTN think PHEO -reserpine: depletes catachols post gang -aldomet: central anti sympath and highly sedating -trimethiphan: gangionic bocker does not cause reflex tach -- USE IN DISSECTING ANEURYSM -phentolamine- alpha blocker used in pheo, clonidine withdrawl -incr gastric secretion, reflex -may want to add beta blocker -clonidine- central alpha blockade very long action -ACEI: ======================================= HYPERTENSION (BP=COxTPR) BP > 140/90 in men over 45 160/95 in women over 45 130/90 in any adult < 45 RISKS: CVAs, CAD, CHF PRIMARY HTN: "Essential" or Idiopathic = 90 % of all cases SECONDARY HTN: a) Renal: -Renovascular HTN: -due to renal art atherosclerosis in elderly pts or fibromusc involvment in young women both leading to <RBF & stim of renin-angiotenson system +/- abd bruit - glom or tubular dz -renal art stenosis - renin producing tumors - high Na retension states b)Endocrine: - hyperthroidism - adrenal cortex dz - cushings - hyperaldosteronism - congen adrenal hyperplasia: all due to partial mineralo-corticoid activity-> Na & H2O retension - adrenal medulla dz - pheochromocytoma 50% w/episodic htn 50% w/constant htn Sx= flushing,diaphoresis,wgt loss, diarrhea urine Metanephrine & vanillylmandelic - hypercalcemia - Exogenous Estrogen (BCPs) due to stim of renin-angioten - Corticosteroids - acromegaly c) Coartation of the Aorta: - mechanism d) HTN of Pregnancy e) Neurogenic HTN: -increased HTP -dysautonomia -encephalitis -brain tumor f) Hypervolemia g) Systolic HTN: in cases of high CO (aortic insuf, pagets, AV fistula) ---------------------------------------- Accelerated HTN: evidence of mild-moderate target organ damage(brain, heart, kidney, or retina) Malignant HTN: rapidly progressive HTN almost always assoc w/damage to: -retina (hemorrhage or papilledema) -heart (MI or CHF) -Kidney (hematuria, proteinuria, RISK FACTORS: obesity, high Na diet, cigs, inactivity, BCPs, hyperlipids Medical TX: step 1. diuretic or B-blocker step 2. add a B-blocker, methyldopa, or clonidine step 3. add hydralazine or prazocin step 4. add ACE inhibitor or minoxidil NOTE: only b-blocker & ACE reduce cardio- hypertrophy Hypertension Hyponatremia SX: Nausea, HA, Malaise, SZ or Coma DX:-Plasma OSMs= real vs. pseudo (2x plasma[Na]+ gluc/18 + BUN/2.8) -Urine OSMS -Una+ CAUSES 1. Effective Volm Depletion: - fluid loss from GI, renal or skin - Diuretics Admin: thiazides - CHF - Hepatic Cirrhosis 2. SIADH: - Neuro or Psych Event(CVA,psychosis) - ADH prod Tumors: Oat cell - RX: Chlorpropamide & Carbamazepine, Cyclophosphomide - PULM Dz: Pneumonia, Sarcoid - Post-Op States - Prolonged Nausea 3. Adrenal Insufficiency 4. Hypothyroidism 5. Renal Failure 6. Primary Polydipsea 7. Reset Osmostat 8. Pseudo Hyponatremia (Posm nml or -Hyperglycemia: of gluc by 62 = Na+ by 1mEq/L -marked hyperlipidemia -marked hyperprotienemia Hyponatremia PANHYPOPITUITISM Initial decreases:GH>LH>FSH>TSH>ACTH Head CT: get sella study Head MRI: best test unless very acute check Prl,GH,T4,TSH,Cort/ACTH (E2,FSH,LH) Insulin hypoglycemia .1 unit/kg measure cortisol & GH q15min (must get BS<40 w/sx) Myterypone block cortisol synth TRH Stim test: test not that good -ETIOLOGY: adenoma pit apoplexy: bleed lymphocytic hypophyeal infil Hypopituitism DATE: NAME: AGE: SEX: Onset & progression character & severity precipitating, aggravating & relieving site and radiation PMH: illness, operations,hospital admissions DH: current meds, allergies, adverse rxn.s SH: job, hobbies, smoking, drinking, travel abroad, domestic problems, pets, heating type, smokers in family. GEN: No pain. No tiredness. No recent weight loss or gain. No sleep disturbances CV: No chest pain. No dyspnoea No orthopnoea. No palpitations RS: No cough. No sputum, No wheezing. No haemoptysis. GI: Good appetite. No dysphagia. No polydipsia. No heartburn. No flatulence. No recent change in bowel habits. No diarrhoea. No constipation GU: Waterworks OK? No frequency. No urgency. No haematuria. NS: No dizziness. No blackouts. No loss of balance. No muscle weakness, No parasthesias. No difficulty with vision. No hearing problems. Memory good. GEN: height,weight,hydration, consciousness, attitude, mood. No pallor, jaundice, or cyanosis. No finger clubbing. No lymphadenopathy. HEENT: Eyes Ears Nose throat & mouth thyroid trachea CHEST & LUNGS: breathing posture (kyphosis, scoliosis, lordosis) A-P diameter not increased symmetrical thoracic expansion. No wheezes or crackles audible. No decreased vocal fremitus. resonant to percussion in all lung zones. CVS: BP: Pulse: No Leg Oedema. No varicosities. JVP WNL. PMI not displaced. S1 & S2 heard w/o extrasystolic sounds or murmurs. Abdomen: No distention. Soft, nontender to palpation. Bowel sounds present. Liver nontender w/ edge palpable, soft, smooth about 2 cm below rt costal margin. kidneys, and spleen nonpalable. No masses palpable. Genitourinary: PR: no fissures. no skin tags, stool soft, Prostate palpable? Bladder nontender , not distended. NS: CN: #1:OK,#2:OK,#3:OK,#4:OK,#5:OK,#6:OK, #7:OK,#8:OK,#9:OK,#10:OK,#11:OK,#12:OK Gait: Speech: No tremors or dyskinesias. Muscle strength symmetrical, grade 5. Tendon & plantar reflexes intact and symmetrical. Impression: Plan: H&P form IGA Nephropathy most common cause of hematuria from glomerular cause Most common in young males serum IgA 50% cases w/nml serum Compl Bx of skin over volar surface of forearm often w/caps w/IgA, C3 & fibrin deposits (henoch schonlien purp) -renal Bx w/focal & seg prolif GN *** diffuse mesangial IgA deposits often w/C3 & properdin (fibrin reactive antigens also commonly seen) Prognosis: variable & usually slowly progrssive (50% will reach end stage renal dz w/i 25years of DX) -HTN, Nephrotic synd or Azotemia @ time of Dx assoc w/poor prognosis IgA Nephropathy INFERIOR WALL MI: 40-50% of all MI's --------------------------------------- - generally have <prob than AWMI - 50% will have complications or features assoc w/increased risk: 1. Heart Block 2. Precordial ST depresion 3. RV Infarction -Caused by occlusion of dom artery in >70%(AV nodal art off of DOM Art) THROMBOLYTIC Tx: option for IMI w/ anterior ST depression 1. Heart Block: 19% incidence 2nd-3rd degree block w/IMI- -Assoc w/>20% mortality rate **-Marker of increased MI size -1/2 have gradual progressive block w/remainder abruptly attain highest degree of block they wii reach -Heart Block seen w/i 3 days -Usually responds to Atropine BEZOLD-JARISCH REFLEX: increased vagal tone from ischemic stimulation of afferents adjacent to AV node leading to PNS/Vagus output w/ sinus bradycardia, hypoTN, and possibly heart block ETIOLOGY: 1. blocked blood flow to AV node 2. high vagal tone from the Bezold-Jarisch reaction 3. ischemia released K+/adenosine leading to transient heart block 4. assoc of LAD stenosis which provide colaterals to the AV node via the septal perforators -- still w/ conflicting evidence ________________________________________ Aminophylline blocks ADENOSINE RECEPTORS reverses AV FX & may Tx atropine resistant heart block ---------------------------------------- PRECORDIAL ST-SEGMENT DEPRESSION -seen in approx 1/2 pts w/IMI -Predicts larger IMI by CK's -also predicts > severity of wall motion abnormality & <LVEF ETIOLOGY: of >infarct size & >complic's -- prob NOT due to reciprocal reflection of internal current or injury 1. Ant ischemia from concomitant LAD Dz 2. Inferoposterior infarct w/posterior ST elevation reflected as ST depress ---------------------------------------- RV INFARCTION ------------- -Seen in 1/3 of pts w/IMI (1/10 w/AMI) 1/2 of these w/hemodyn compromise -IMI w/RV usually proximal RCA lesion -RV Infarct most reliably predicted by right-side ECG w/ST elevations of >1mm in right precordial leads partiularly in V4r when assoc w/ II,III,&AVF. 90% sens & specificity w/80% predictive value ** Since Right Side ST-elevation resolves early in IMI - MUST DO RIGHT EKG EARLY IN IMI Tx of RV INFARCT: 1. fluids: increase filling of RV to maintain preload 2. Avoid Rx that Venodilate & reduce RV filing 3. Hypotension after SL NTG w/IMI -should ?? RV involvement 4. Dobutamine & Dopamine in failing CO, hypotention or shock MI -Inferior Wall type Immunization Schedule Catch up <7y First visit DTP/OPV/TB/(MMR if<15m) 1mo intrvl Hib if 18-60m 2mo intrvl DTP/OPV 4mo intrvl DTP/(OPV in endemic area) 10-16mo int DTP/OPV 11-12yo MMR 14-16YO tD >7Y First visit Td/OPV/TB/MMR 2mo intrvl Td/OPV 8-14mo int Td/OPV 11-12yo MMR 14-16yo Td HIV IMMUNIZATION 2mo age DTP/IPV 4mo age DTP/IPV 6mo age DTP/IPV 12mo age TB 15mo age MMR 18mo age Hib 24mo age Pneumovax over 6mo age Flu yearly 11-12y age MMR (REF RCID 1988;p45) DPT L leg TET L arm MMR R deltoid Hib R deltoid Hep L Deltoid Flu L arm PEDS Immunization Sched. (all inhale agents good bronchodil) Halothane most neg chronotropic sweet smeet-good induction most potent MAC .77 limit EPI 2mic/kg(sens cat rec) Enflurane (ethrane) most neg inotropic bad smeell- poor inductant MAC 1.68 limit EPI 11 mic/kg Isoflurane (forane) least metabolized & somewhat neg inotropic may cause tachycardia bad smell-poor inductant MAC 1.34 limit EPI 7mics/kg N2O: MAC >100% & decr mac of other Rx and decr toxicity -mild amnestc mild analgesic -N2O will burn in combo w/ incr FIO2 and high temp (laser)-keep fio2 < 40 or 30% (pull ET tube if fire) Anesth. Inhalation Agents E*** SPLIT MIXED INSULIN REGIMEN **** 1)Calculate Total Dose = 0.7 U/Kg AM Dose: 2/3 total dose; give 2/3 as NPH and 1/3 as Regular. PM Dose: 1/3 Total Dose: give 1/2 to 2/3 as NPH and 1/3 to 1/2 as regular insulin. Note: 2/3= 0.6667 , 1/3= 0.3333 Insulin should be given 30 min. before breakfast and dinner. 2)Interpreting blood glucose levels. 7 AM Value is 2 to PM NPH dose 12 PM value is 2 to AM regular dose 5 PM value is 2 to AM NPH dose. 9 PM value is 2 to PM regular dose. So, if glucose is too high, increase the insulin dose and if glucose is too low, decrease the insulin dose. ADJUST DOSES IN 2-5 UNIT INCREMENTS; then evaluate the results after a period of time. 3) Three syndromes of early AM glucose abnormalities in this regime: 10PM 3AM 7AM ------------------ 1)Somogyi: 90 40 200 2)Dawn: 110 110 150 3)Waning: 110 160 220 1)Somogyi: decrease NPH dose at dinner and give a portion at bedtime or give more food at bedtime. 2)Dawn Phenomenon: (2 to GH release @5-8 AM) divide the NPH dose between dinner and bedtime. 3)Waning: Increase NPH at dinner, or give at bedtime. 08-AUG-93 8:47:11 Insulin Regime Split/mixed INTUBATION NeuroMusc Block Agents: must 1st estab ability to mask vent!! -should reach deep anesthesia prior to intub since light state w/incr airway reflexes 1. elevate occiput w/chin up 2. extend neck: sniffing position 3. open mouth widely 4. insert blade along R side of tongue then turn & advance to midline sweeping tongue to L until epiglottis comes into veiw Blades: Miller(strait) Mac(curved) if cant see V-Cords: press on thyroid EXTUBATION: Anesth. Intubation INTERSTITIAL LUNG DISEASE Dz progresses from acute pneumonitis to diffuse pulmonary fibrosis from inflam (gallium lung scan usually positive) INTERSTITIAL PULMONARY FIBROSIS:~50% of all interstitial lung Dz is idiopathic IDIOPATHIC PF: usually progressive usuallty fatal w/i 5 years of onset a. Diffuse interstitial pneumonitis b. Bronchiolitis obliterans c. interstitial pneumonits -------------------- IPF w/Known Cause: 1. Environmental: silica, asbestos, cadmium, mercury, pneumoconiosis organic dust, gases, fumes 2. Granuloma: Sarcoid, hypersensitivity pneumonitis 3. Infectious: viral, bacterial, fungal pneumocystis carinii & mycoplasma pneumonias/pneumonitis 4. Rx induced: nitrofurantoin, PCN amiodorone, tocainide, bleomycin, busulfan, methotrexate, chlorambucil cyclophosphamide, BCNU, gold salt 5. Connective Tissue VDz: a) RA: 50% pts w/RA w/abnml lung fxn **rarely causes symptoms b) SLE: uncommon complication, seen with acute, patchy inflamation c) Dermatopolymyositis 6. Progressive Systemic Sclerosis: fibrosis w/little inflamation 7. Histiocytosis X: disorder of MONO/ macrophage system (related to Litterer Siwe & Han Shuller Christian Dz-->EOSINOPHIL GRANULOMA -seen between ages 20-40 -90% are present or former smokers -complicated w/freq pneumothorax's -no tx 8. Chronic Eosinophilic Pneumonia; F>M pts often w/hx of asthma w Sx of wgt loss, fever, chills, fatigue, dyspnea, -CXR w/"photo-negative" pulm edema pattern w/central sparing -very responsive to corticosteroids 9. Goodpastures Syndrome: relapsing pulm hemhorrhage, anemia & renal failure. -due to circ anti-basement membrane antibodies 10. Radiation Pneumonitis 11. Lymphangic Carcinomatosis 12. Chronic Uremia 13. Chronic gastric aspiration ======================================== Dx: ? Hx of cough, dyspnea, ? signs of velcro rales, cyanosis clubbing, rt heart failure (late) CXR: nml in ~10% -reticulonodular apearance(LATE) ground glass appearence(EARLY) PFTs: c/w restriction (low VC,TLC,DC) BRONCOSCOPY: possibly 2 dif findings: 1) Lymphocytes: sarcoid, berylliosis, silicosos, hypersens pneumonitis 2) Neutrophils: asbestosis, CVD, IPF ---------------------------------------- 1. remove offending agent 2. antibiotics as appropriate 3. O2 in pts w/hypoxemia 4. Steroids: variable response 5. Immunosupressive Tx: cyclophos for wegners granulomatosis Lung Disease, Interstitial Infectious disease Observation Incubation Isolation --------------------------- ---------- Chickenpox Varicella 10-21d 7-21d p exposr Until vesicles crusted Infectious frm 2d a rash Diphtheria 2-6d 7d fr last contact or until - cx Until 2 - nose & throat cx 24hrs apart (4wks if no rx) Hepatitis A 2-6w 6wks p exp Enteric & Bld prec 3wk p jaundice Hepatitis B 6w-6m 6m p exp Entrc & Bld prec while HbSAg+ Meningococcal Meningitis 1-7d 7d frm lst exp 1st 24hrs p starting ab Mononucleosis 2-8w Observe only Saliva contact for 3m Mumps 2-3w 2-3w frm 1st exp 7d bef to 9d p swelling Pertussis 5-21d 2w frm lst exp, quar if <6y & unvac'd 5-10d(4w if unrxd) Poliomyelitis 5-35d 5d for prodrml minor illnes secretions 1w, stool 6w Rubella 2-3w 12-20d p exp Duration of catarrh & rash (commun p 5th d incub period Rubeola 10-12d 14d fr exp Until 5d p rash Strep throat & Scarlet fever 1-7d 7d p exp 24h p ab start Infectious Dz. Isolation periods IV FLUIDS Replacement: WEIGHT PER DAY PER HOUR First 10 Kg 100cc/Kg 4cc/Kg/h Second 10 Kg 50cc/Kg 2cc/Kg/h > 20 Kg 20cc/Kg 1cc/Kg/h Bolus Volumes: 10cc/Kg for low U.O. 20cc/Kg for Electrolyte Replacement: Na 1-2 mEq/Kg/day Cl 1-2 mEq/Kg/day K 1-2 mEq/Kg/day Ca 0.2-0.3 mEq/Kg/day Mg 0.35-0.45 mEq/Kg/day PO4 10 mmol Fluid Replacement: Gastric 0.45NS w/ 20mEq KCl/L Biliary (Nl: 1L/day) LR w/ 1 amp HCO3/L Pancreatic (Nl: 1L/day) LR w/ 2 amps HCO3/L Small Bowel (Nl: 5L/day) LR IV Fluid calculations Neonatal Jaundice Physiologic Peak billi: 6mg/dl @ D2-4 & 10-12mg/dl @ D5-7 Breast-milk: Incidence: 1/200, 3/4 offspring of mom Peak billi:15-25mg/dl @ W2-3 Lasts 4w-4m Other causes: Sepsis Hematoma, caput Gilbert Syndrome Intestinal Obstruction Maternal-fetal transfusion Pyloric Stenosis(8% at vomiting onset) Blood group incompat Crigler-Najjar Management Guides Billi Birth mg/dl wt <24h 24-48h 49-72h >72h <5 All 5-9 All ****** 10-14 >2500g IIIIIII I billi>12mg <2500g 15-19 >2500g <2500g 20&+ =PhotoRx *=PhotoRx if Hemolysis =Exchange =Exchange if Hemolysis =Exchange considered Investigate if PhotoRx or Exchange Treat as in next billi category if: Perinatal asphyxia Respiratory distress Metabolic acidosis(pH 7.25 or below) Hypothermia (temp < 35 Low serum protein (5g/100ml or less) Birth weight <1500Gm Sx of clinical or CNS deterioration Peds Neonatal Jaundice NEPHROLITHIASIS 1. Calcium Phosphate Stones: - hyperparathyroidism - idiopathic hypercalcuria - medullary sponge kindney 2. Calcium Oxalate Stones: - hypercalcemia - idiopathic hypercalcuria - excessive oxalate ingestion - Vit C abuse - Sm Bowel resection - primary hyperoxaluria 3. Uric Acid Stones: NOT RADIOPAQUE - persistantly concentrated urine - acidic urine - hyperuricosuria - hyperuricemia (gout) - excess dietary purine/ ChemoTx 4. Cystine Stones: cystinuria NOT ON XR 5. Struvite Stones: (either triple phos or Mg-ammonium-Calcium-Phos) -UTI: by urease producing organisms -proteus, providencia, klebs, pseudomonas, serratia, enterobact. High pH: favors calcium phos & oxalate & struvate Low pH: favors uric acid & cystine stones Low Volm: favors uric acid stone 24hour Urine Collection: for volm, pH, calcium phos, uric acid, oxalate, cystine Na, Cr, K+, Uric Acid Stones: oral Bicarb to alkalinize urine (>7.0) -restrict dietary purines or give allopurinol if indicated Cystine Stones: oral bicarb to keep urine pH7.5 -Acetazolamide @ bedtime to maintain nocturnal urine alkalinity -If severe or non-complient pt-may use Penicillamine Calcium Phos Stones: tx hyperPTH by surg -distal tubular acidosis ? w/u -idiopathic hypercalcuria: tx w/diuretic or oral neutral potassium phosphate Calcium Oxalate Stones: restrict oxalate rich food -restrict Vit C < 500mg/day -give diuretics or K+phosphate Struvite Stones: Antibiotics Kidney Stones Latex Allergy Allergy to protein from sap. Latex is nonspecific term for sap from over 2000 species of trees. Vulcanization discovered in 1839. Polyisopropene polymerizes to form the rubber Brazilian rubber trees have highest percentage of polymer(40%) Numerous Type IV hypersensitivity inducing chemicals are added to the rubber during curing process. Glove latex often contians up to 3% protein which is high by typical standards. First case reports of anaphylaxis to latex in 1980's. Usually in children with spina-bifida. France has better data than US. Onset of anaphylaxis to gloves later than when reaction to anesthetic agent - 30-90min. Reaction from contact of surgeon's gloves with moist peritoneum. RAST test is not very sensitive Tryptase remains elevated for several hours. pts may not have hives or wheezing, may look like vasovagal. Tryptase level will not elevate in sepsis, hypotension, vasovagal Is Powder the culprit? Cheaper way of making gloves! Some health workers get asthma, conjunctivitis, coryza, and/or facial edema from being in room with glove powder. Some cross reactivity with banana and tropical fruit allergy and latex allergy. Also chestnut, walnut cross reactivity. Glove brand variability Gloves vary widely in antigenicity Other articles to watch for: balloons(itchy lips after blowing up) rubber balls condoms wheel chair tires tournequits crepe rubber shoe soles endotracheal tubes some catheter IV port seals! Some multidose seals Distinguish type of reaction eczema vs contact hives vs generalized hives, coryza, conjunctivitis. No standard means of screening for allergy available. 10% of nurse test postive to latex (France?) Good screening question as part of drug history: "Do you get itchy lips from blowing up balloons?" latex allergy LEUKEMIA: Bone Marrow hypercellular & infiltrated w/monomorphic blasts (nml BM elements are reduced). - Characterized by immature blasts in BM and Smear ALL: common in Kids/ 85% occur in Kids. 90% of all Leuk in kids is ALL AML: common in adults w/incidence increasing w/age: M1->M5 ---------------------------------- ALL vs AML: ALL: leuk-lymphoblasts typ smaller than AML & have round/convoluted nuclei with minimal cytoplasm. -90% w/terminal deoxynucleotidal transferase (TdT)-rare in AML -60% ALL w/cells expressing the COMMON ALL ANTIGEN (CALLA) but neg for surface Ig or T-cell markers -20% ALL cases of T-cell type w/expres of T-cell markers -5 % ALL cases of B-cell type: Burketts Lymphoma (L3 in the FAB) -15 % of Null cell type --------------------------------------- AML: Larger Blasts than in ALL w/lower nuc/cytoplasm ratio -Cytoplasm of AML blast may stain for enz mrkers (peroxidase or esterase) -AML Blasts may contain AUER BODIES -Pts w/Acute Promyelocytic Leukemia (M3) may present as DIC PROMYELOCYTIC LEUK: abnml promyelocytes w/giant granules- often assoc w/DIC MONOCYTIC or MYLOMONOCYTIC LEUK: cerebriform monoblast components. Commonly w/skin or gum infiltration Survival is shorter than other AMLs. ERYTHROLEKEMIA: Abnml Nucleated RBCs typically poorly responsive to Tx. ---------------------------------------- THERAPY: for both AML & ALL - carry 20% early mortaity 1.CHEMO: initially w/ablation of the leukemic cell line. In AML it is usually nec to ablate all nml BM which is called INDUCTION TX. ALL: usually easier to select ALL blasts sparing nml cell AML: INDUCTION Tx usually produces hypoplastic phase prior to recovery of nml BM. This phase is assoc w/ high mortality/morbidity 2.RT: used in ALL to sterilize sanctuary sites of late relapse (CNS/Testes) 3.BM TRANSPLANTATION: definitive Tx for acute leukemia- usuall requires pt in remission. 4. SUPPORTIVE Tx: a)Heme: watch Hgb, Plts, & maintain Lytes and Uric acid -use allopurinol if nec b)Infections: -good hand washing -long term catheters instead of peripheral indwelling lines -strict rectal care -rigorus ctrl of any infection signs w/broad ABTx coverage -temps on ABTx require Antifungals -if temps despite ABTx & Ampho can consider granulocyte transf although benefitis contraversial PROGNOSIS: AML: poor for adults. w/best care 75% w/remission & 25% die W/remission: duration typically 12-18 months (some claim 20% cure rate) ALL: in kids >95% complete remision w/>50% likely cured ---------------------------------------- CLL: an adult >50 w/mature lymphocytosis Dx: -Peripheral smear w/mature lymphocytosis -BM w/infilt by mature lymphoctes -enlarged SPLEEN -Lymphadenopathy Tx: Conservitive since survival is not increased w/any known Tx -early CLL (stages 1-2) no Tx -late CLL: tx w/alkylating agents (Chloambucil) +/- steroids & might consider total body RT. ---------------------------------------- CML: suspected in pts w/high WBC & splenomegaly Dx: Smear: ranging from mature polys to immature blasts Philadelphia Chromasome: in BM precursor cells Very Low Leuk Alk Pho Levels Prognosis: median survival 3-4 years most pts die during blast crisis when dz converts to AML Leukemia Lithium. Start one qd on full stomach x 2d, then 1 bid x2d then tid. check level after 900/d dose for 3 days. target .7-.8 best .6-1.1 range ok. Caution not to change diet esp salt intake. OD effect physical depression, sedation lethargy progressing to coma. If still depressed ad anafranil in low dose, synergistic. LITHIUM TOXICITY abnormal neuro findings w/o antichol sx CV: myocarditis w/arrhythmias prolonged QT int & ST-T changes Renal Lithium LIVER DISEASE Hepatitis: see file "Hepatiti.txt" ---------------------------------------- ETOH Hepatitis: acute syndrome seen w/ heavy EtOH consumption Features: Fever, jaundice, hepatomegaly, w/progression->signs of chronic liver Dz ascites, variceal bleeds etc Labs: leukocytosis, high SGOT(AST)<350 low albumin high total Bili modest rise in Alk Phos & dir Bili SGPT(ALT) almost always < SGOT(AST) Low Plts: in 10% cases Bx w/fatty liver, lots of Polys alcoholic hyaline (mallory bodies) hepatocyte necrosis & occasionally sclerosis of central veins TX: supportive suppl B vits (especially thiamine & folate w/2500-3000cals / day Steroids: controversial role ----------------------------------------- Fatty Liver: from EtOH interference w/ hepatic lipid metabolism - asymptomatic hepatomegaly - elevated GGPT, & SGOT/PT & alk phos --Prognosis is excellent if complete abstanence from EtOH ----------------------------------------- EtOH Cirrhosis (Laennec's Cirrhosis) -probobly squelea of EtOH Hepatitis -prob reflects reduced blood flow from fibrotic obstruction -> portal HTN & diminished hepatocyte metab fxn Complications: Ascites due to increased hydrostatic pressure(portal HTN) & reduced oncotic pressure (low albumin). Also, increased aldosterone (from altered liver metab) -> Na+ & H2O retention. Tx ascites w/Na+ restriction(500mg/d) Varices: due to development of collateral vessels partic in esoph & hemorrhoidal plexi. Encepalopathy: ? prod of false neurotrans & mercaptans & fatty acids. ?ammonia,azotemia,hypokalemia Tx w/lactlose to trap ammonia or PO neomycin to inhib GI flora that convert protein to ammonia & restrict dietary protein to<40g/d Hepatorenal: mortality 90-100% -nml kidneys w/afferent art constriction -decreased GFR & RBF Tx: usually unsuccessful ??LeVeen Shunt/Portocaval shunts & liver transplant ???? Coagulopathy: due to hepatic synth dysfxn ------------------------------------------ NON-ETOH CIRRHOSIS: similar to EtOH type ------------------------------------------ Hepatic Vein Thrombosis(Budd-Chiari) -due to hypercoagulability, Abd trauma pancreatitis, or use of BCPs. -Presents w/ascites -Bx w/centrolobular congestion -attempt to catheterize vein are unsucc -portocaval shunt may prolong survival -Mortality is 50-90% Splenic Vein Thrombosis: -From abd trauma, pancreatitis, tumor ---------------------------------------------- Liver Diseases-non hepatitis -BUTTERFLY RASH: erythema over malar eminance: spares nosolabial folds -DISCOID RASH: raised erythema patches w/edematous plaques & adherent scales -SYMETRCAL ERYTHEMA @ shoulders, chest, neck, arms -ALOPECIA -Raynauds Phenomenon -Photosensitivity (partic lg ulcers) -Nasal or Oropharyngeal ulcers -Livedo Reticuclaris -SEROSTIS: pleuritis/pericarditis -ARTHRITIS:tender, swollen, effusions -RENAL: proteinuria, active sediment renal insufficiency, cellular casts -HEME: anemia (ACD/Hemolysis) leukopenia thrombosis due to lupus anticoag ITP -CARDIAC: pericarditis verrucous edocarditis myocarditis coronary vasulitis conductcion abnormalities -NEURO: Seizures, psychoses, depression transverse myelitis aseptic meningitis -PULM: Pl Effusions, Pleuritis pulm infil, vasculitis -GI: oral ulcers, Abd Pain,vomitting -EYES: conjunctivitis, sicca synd ======================================== LABS: ANA: anti dsDNA & Smith(antiSM) LE Cell: -false+ STS known pos for >6mo confirmed by TPI of FTA test (anti-dsDNA w/ tendency to renal Dz) ===================================== DRUG INDUCED LUPUS: -caused by procainamide, hydralazine, isoniazid, hydantoins, quinidine, Trimethaione -NO anti-dsDNA or anti-SM (Rx induced w/ssDNA & antiHistone AB) -Higher freq of anti-HISTONE -50% w/serositis: pleural/pericardial involvement -ANA is + in ~ 100% (it takes 4-6 wks to gen measurable AB) (Pts need to be on Rx at least 6mo to acquire Rx induced Lupus) -PROGNOSIS: much better than SLE w/reversal after d/c offending agent ---------------------------------------- JOINTS: NSAIDs SKIN: topical steroids anti malerials(chlorequine=plaquenil) sunscreens RENAL: steroids azathioprine(Imuran):immunosup Cytoxan(Cyclophos):alkylators (IV cytoxan + low dose predn. may preserve renal fxn best) Plasmaphoresis (+Imuran) for life threatening vasculitis CNS: Steroids, Anticonvulsants, neuroleptics HEMOLYTIC ANEMIA: Coombs+:high dose steroids ITP: Steroids, Danazol, splenectomy SLE -Lupus LYME DISEASE Definition: systemic, tick bourne dz w/manifestations including derm, rheum neuro, & cardiac. The best clin marker is the ECM rash seen in 60-80% of pts ORGANISM: Borrelia Borgdorferi (a spirochete) 1.ECM: skin lesion typically begining as red macule or papule & expanding over days-weeks to a large round lesion often w/partial central clearing. - to be ECM lesion must be =/> 5cm - 2ndary lesions can occur - Annular erythematous lesions devel w/i several hours of a tick bite & are hypersens rxn not ECM - ECM that is expanding is usually accompanied by acute/intermittant Sx: -fatigue, HA, fever, arthralgia, stiff neck or myalgias 2.LATE MANIFESTATIONS: a) Musculoskelatal: recurrent attacks over weeks-months, of swollen joints sometimes assoc w/chronic arthritis in one or few joints. -arthralgia, myalgia & fibromyalgia syndrome are not enough to base dx of LYME DZ. b) CNS: Lymphocytic meningitis, cranial neuritis, partic Facial Palsey (may be bilat) ridiculopathy, & rarely encephalomyelitis. -HA, fatigue, parasthesias, or stiff neck are not enough to base dx of Lyme Dz. *aseptic meningitis c)Cardiac: Acute onset high grade (2nd-3rd block) A-V conduction defect that resolve in days-weeks & sometimes assoc w/myocarditis -palpitations, bradycardia, BBB, or myocarditis are not sufficient to base dx of LYME DZ. 3.EXPOSURE: defined as having been in wooded, brushy, or grassy area in an endemic county not > 30 days before the onset of ECM. A HX OF TICK BITE is not required. 4.LAB CONFIRMATION: a)isolates spirochete from body fluid b)detects dx levels of IgM or IgG to the spirochete in serum or CSF c)detects an important change in Ab levels in paired acute & convalesant serum samples. d)EXCLUDE FALSE +'s: SYPHILIS etc ---------------------------------------- ANTIBOTIC TX 1.Early Lyme Dz: doxycycline 100mg po bid x 10-21d amoxacillin 500mg po tid x 10-21d erythromycin 250mg po qid x 14-21d (**< effective than doxy or amox) 2.Lyme CARDITIS: ceftriaxone 2g iv qd x 14d pen G 20mil Units iv x 14d doxycycline 100mg po bid x 14-21d amoxacillin 500mg po tid x 14-21d (PO route reserved for mild cases) 3.Lyme MENINGITIS: ceftriaxone 2g iv qd x 14-21d pen G 20mil Units iv x 10-21d (divided doses) 4.Lyme FACIAL NERVE Sx: same as PO doses for early dz x21d 5.Lyme ARTHRITIS: doxycycline 100mg po bid x 30d amox & probenicid 500mg po qid x 30d ceftriaxone 2g iv qd x 14-21d pen G 20mil Units iv x 14-21d ---------------------------------------- Lyme Disease MARFANS SYNDROME CT dz including several heterogeneous groups w/ dif biochem abnormalities FEATURES: -Dolichostenomelia: inapprop long limbs compared to trunk) -Arachnodactaly: -Pectus excavatum -Joint laxity -Scoliosis -Inguinal Hernia -Aortic Aneurysm -Ectopia Lentis: lens displaced upward Marfans Syndrome MEA1: (3Ps) pancreas, pit, parathyroid 1. hypercalcemia w/high PTH due adenoma single lobe of parathyroid 2. Pancreatic adenoma w/hyperglycemia) 3. Pituitary adenoma of ant pit - high PRL - testicle become soft - MEA2: pheo, carcinoid, PTH MEA syndromes METABOLIC ACIDOSIS A-MUD-PIE A acetaldehyde M methanol U uremia-renal failure D DKA P Paraldehyde I infection/sepsis E ETOH/ethylene glycol S Salicylates AG ACIDOSIS: Ketoacids: DM, ETOH, Starvation, Lactate: circ or resp failure Rx & Toxins enzymes defects Poisons: 1)incr osm gap: methanol(TX w/ETOH) ethylene glycol(Tx w/ETOH) 2)nml osm gap: salicylates,manatol paraldehyde Renal Faiure -------------------------------------- Normal Gap: Hyperchloremic RTA, diarrhea, hypoaldo K+ sparing diuretics Carbonic Anhydrase Inhibitors Uterosigmoidoscopy Acidosis, Metabolic MANAGEMENT OF ACUTE MYOCARDIAL INFARCT 1)Oxygen 2)Nitroglycerin oral to IV except w/inferior wall decr. BP or Rt. Ventricular MI & BP<90 3)Morphine for analgesia 4)Countershock for V. Tach. 5)Atropine w/: -Sinus Bradycardia w/Hypotension -Type I 2nd degree AV block -Inferior MI -Asystole -To counteract Hypotension & Bradycardia after Nitro 6)Monitor w/ EKG 7)Swan-Ganz Catheter w/: -CHF, severe & Progressive -Cardiogenic Shock -Acute MI w/ Papillary Muscle rupture or V. Septal Defect 8)Lidocaine for: -Acute MI, ischemia w/ PVC -V. Tach or V. Fibrillation 9)Pacemakers w/: -Asystole -Complete Heart Block -Right Bundle Branch Block -Left Bundle Branch Block -Type II 2nd Degree AV Block -Type I 2nd Degree Block not responding to Atropine. -Bradycardia not responding to Atropine 10)Investigations: -AST, LDH, CK-MB -Echocardiography -Infarct Scitigraphy (Technetium 99 Pyrophosphate) 11)Beta Blockers in: -Reflex Tachycardia -Hypertension without CHF -Tachyarrthmias -Post Infarction Angina -Atrial Fibrillation -NOT IF: HR <60 Systolic BP <100 L. Ventricular Failure Peripheral Hypotension Type I or II AV Block Complete heart block COPD 12)Calcium Channel Blockers for: -Post infarct Angina -Non Q Wave Infarct Angina -Post Angioplasty to decr. spasm 13)Thrombolytic Agents : (Streptokinase, rTPA,Urokinase) -Follow treatment with: -IV Heparin for 3-4 days -160 mg Aspirin daily -IV or Topical Nitro for 24-48 Hours Post 14)Baloon Angioplasty: -if within 6 hours p onset of pain -if thrombolytic agents fail. 15) the end. MI Management, acute MENTAL STATUS CHANGE/ CONFUSION: labs:Gluc,lytes,H/H,drug levels ? CNS,drugs,Infection,Metabolic,endocrine psych. CNS:dementia;Alzh,multi-infarct,PD,NPH Malignancy;CNS,Mets,Paraneo synd Head Trauma:sub/epi dural Post ictal, CVA, HTN, Thiamine,B12 RX:EtOH-DT's, narcotic/sedatives NSAIDs,AntiHTN's(B-blockers),TCA's BNZ's,steroids,cimetidine,antihist anticholinergics METABOLIC:high or low glucose,Na,Ca hypoxemia,^CO2,fat emboli uremia,hepatic encephalop CHF, ENDOCRINE:high or low T4 or adrenals INFECTION:Lyme,Sepsis,vasculitis,men encephalitis, brain abscess PSYCH:psychoses,mania,depression Physical Exam:nuchal rigidity,papilled dil pupil=DT's,withdrawl pin pupil=narcotic use Mental Status changes/confusion MYCOSIS FUNGOIDES LYMPHOMA Lymhoma of Skin: either primary or 2ndy manifestation of various lymphomas -myc fungoides is most common w/skin lesion- rarely w/visceral involvement until late stges of skin lesions Lesion: may be confused w/excema, psoriassis, or dermatitis & Bx may not be diagnostic -late lesions have are typically patchy w/central clear or polycystic areas Bx may be Dx in late lesions Thymus Dependant Lymps: same cells as found in skin, viscera & Blood Blood Smears: lg lymphs w/scant cytoplasm & folded nuclei PROGNOSIS: early stage: several decades Once Histo Dx made: median surv=5 yrs Pts w/skin tumors,ulcers or lymphatic involvement have median survival=30mo TX: Topical mechlorehamine PhotoTx w/psoralens & Uv Whole Skin electron beam Tx -- early systemic chemo of no avantage Mycosis Fungoides Lymphoma BEAU'S LINES Transverse grooves in nail plate, usu most prominent in thumb. Indicate temporary cessation of nail growth followed by regrowth Become apparent several weeks after noxious event: severe febrile illness rx with cytotoxic drugs Stevens-Johnson synd newborns 1-2 mo after delivery localized trauma to nail bed Onychomadesis complete shedding of nail plate, more severe form of Beau's Lines Onycholysis Distal separation of nail plate from nail bed Causes: psoriasis trauma certain medications(tetracyclines) candida tinea(usu with subungual debris) thumb sucking chronic wet exposures treatment Trim back nail avoid water contact topical antifungal Koilonychia(Spoon nail) Causes Autosomal dominant Iron deficiency Hypothyroidism Hemochromatosis Lichen planus Nail pitting Reflects abnormlity of proximal nail matrix growth Psoriasis Alopecia areata Occasional pit may be normal variant Longitudinal groves From any process causing inflammation in nail matrix: Trauma Lichen planus Psoriasis alopcia areata Darier's disease histiocytosis X Graft-vs-host Wide longitudinal grooves Growths pressing on nail matrix periungual warts digital mucous cysts periungual fibromas of tuberous sclerosis Transverse ridging Inflammation of proximal nail fold candidal paronychia atopic dermatitis Median nail dystrophy Longitudinal groove or split in center of nail plate, usu thumb. Secondary splits can radiate out from central groove resembling a fir tree. familial habitual pick, pull or bite cuticle 20 nail dystrophy of childhood Beginning at few months to years of age nails show increased ridging, eventually all nails become dull with rough sandpaperlike quality. psoriasis lichen planus alopecia areata pachyonychia congenita Psoriasis Can produce: Pitting onycholysis(with or without subungual debris) nail thickening with distortion or loss of upper surface of nail leukonychia partial or complete nail shedding Lichen planus Can produce: Longitudinal striation depressed ridges nail thinning and scarrng Pterygium formation-proximal nail fold and cuticle fuse with nail plte (characteristic in lichen planus, but rare) Clubbing Most commom pediatric causes congenital cyanotic heart disease cystic fibrosis Other cause thyroid disease chronic active hepatitis Hereditary Familial Pacydermoperiostosis(associated with scalp redundancy and thickening of hands and feet, onset at puberty Racket nails Short ad broad nails, but in contrast to clubbing, angle formed by the proximal nail fold and nail plate is not altered. Confused with clubbing autosomal dominant or associated with cartilage-hair hypoplasia and other skeletal dysplasias. Fingernail Signs NEPHROTIC SYNDROME **Loss of protein(Particularly albumin) via urine & generalized edema NOTE: since steroids increase GFR they will increase prot loss **Nephrotic Edema: due to Na+ retention from increased sympathetic effect (**not from low oncotic pressure) EFFECTS OF NEPHROSIS: 1. Edema: as above 2. Hyperlipidemia: from liver stim 3. Hypercoagulopathy:from liver stim & loss of antithrombin III 4. Susceptibility to Infection: from low Ig's & compliment Dz causing Nephropathy: MEMBRANOUS GN MEMBRANOPROLIFERATIVE GN NIL DZ: in kids AMYLOID KIDNEY nephrotic Syndrome NEURAL BLOCKADE OF PAIN ---------------------------------------- Phenol: last 3-6mo (may last as briefly as mintues to many months) - less profound block than EtOH - has both direct anesthetic & lytic FX - used in concentration of 4-10% disolved in 10-100% glycerol or in water - large doses cause seizures & CVS FX - Hyperbaric & mixing in glycerine allows using gravity EtOH: used as 50% & 100% concentrations depending on inj site - burns on injection - hypobaric thus inj below nerve so EtOH rises to site Glycerol: used for trigeminal ganglia ---------------------------------------- Indications: 1. pain localized enough to be blocked 2. absence od cagulopathy -particularly if epidural block 3. CVS stability to tolerate any possible change in BP ---------------------------------------- Neuolytic Blockade: - effective against nococeptive pain - ineffective against neuropathic pain Celiac plexus block: ideal for pain from pancreatic CA retroperitoneal metasteses peritoneal carcinomatosis colon or stomach CA liver/sleen capsule distension (needle placed ant to V-bodies @ T12-L1-> delivering 40-50cc 50% EtOH) - success = 57-95% under flouro or CT - may be done visually during laparotomy when inoperable panc CA is found Subarachnoid Block: restricted to pts w\advanced dz, unilat pain limited to a few spinal segments. - Caution if pain is bilat or widespread or due to lesion of unknown etiology Complication of Subarachnoid Blocks: 1. spinal HA mechanical nerve damage infection/arachnoiditis 2. Extra Nerve Block Effects: motor paresis shincter function loss impairment in sensation dysesthesias ----------------------- Subdural Blockade REF: Ferrer-Brechner T: "Anes Tech for Mgt of CA Pain" CANCER 63:2343-7 1989 Anesth. Nerve Blocks SPINAL CORD/ROOT COMPRESSION ________________________________________ NERVE ROOT INJURY: sensory supply ----------------- Angle of Jaw & Back of Scalp:------>C2 Neck area Front & Back to Scapula-->C3 Over SCAPULA & Top of Chest/Back--->C4 Lat Upper Border of Arm / Deltoid:->C5 Lat Forearm + thumb:--------------->C6 Over Tricepts, Mid Palmer Forearm to between first two fingers:---->C7 Medial Forearm + Little Finger----->C8 Axilla down to Olecranon----------->T1 Nipples---------------------------->T4 Umbilicus-------------------------->T10 Upper Lat Thigh Front & Back------->L2 Lower Med Thigh to Ant/Med Knee:--->L3 Below Med Knee to Medial Malleolus->L4 Below Lat Knee to Mid Shin Across to Top of Medial Foot to Arch-- -->L5 Mid Lat leg to lat Malleolus to Lat Foot -across toes & most Lat Sole->S1 Behind Knee------------------------>S2 ======================================== PERIPHERAL NERVE ASSOCIATED AREAS Ant Chin/Jaw up to Front of Ear & Midline of Ant Neck--->Mandibular N. Angle of Jaw to Ear: Gt.->Auricular N. Forehead----------------->Ophthalmic N. Above nipples to Neck---->Supraclav. N. Lat upper Arm------------>Axillary N. Med upper Arm->Medial Brachial Cutan N. Tricepts------>Post Brachial Cutaneous N. Lat Forearm-->Lat Antebrachial Cutan. N. Med Forearm-->Med Antebrachial Cutan. N. Middle of Back of Forearm-->Post AntiB N. Mid 3rd Finger to Thumb on Back of Hand \------------------> Radial Nerve Mid 3rd Finger to Pinky on Front & Back \------------------> Ulnar Nerve Palmer thumb to mid 3rd Finger->Median N Lat Upper Leg----->Lat Fem Cutaneous N. Ant Thigh--------->Ant Fem Cutaneous N. Medial top 1/2 of thigh--->Obturator N. Back Upper Leg--->Post Fem Cutaneous N. Lat Lower Leg---->Lat Sural Cutan N. Med Lower Leg---->Saphenous N Mid-Back of Calf->Sural N. Top of Foot--->Superf. & Deep Peroneal N Sole of Foot->Plantar branch of Tibial N. ======================================== PATTERNS OF VISCERAL PAIN REFERRAL: Viscera Roots Pain Referred TO ======= ===== ================ Heart t1-5 chest & arms Stomach t5-9 xyphoid region Duodenum t6-10 xyphoid->umbilicus pancreas t7-9 upper abd & back Gallbladder t6-10 rt upper abd appendix t11-12 RLQ Kidney t9-L2 CVA & penis prostate S2-4 glans & Lumbar area ======================================== Sympathetic Afferents to Dermatomes: (SYMP COL= C8->L2) ---------------------------------------- C8-----------------> C2-C4 T1-T3--------------> Trigeminal Area & C2-C4 T4-----------------> C5-C6 T5-T7--------------> C5-T9 T8-----------------> T5-T11 T9-----------------> T6-L1 T10----------------> T7-L5 T11----------------> T9-S5 T12----------------> T10-S5 L1-----------------> T11-S5 L2-----------------> T12-S5 ======================================== Spinal Nerve root sensory levels NEURO EMERGENCIES 1500 gm = avg brain wgt 1900 cc = avg csf space 3.5 cc O2/100g brain tissue/min DETERMINANTS OF CEREBRAL o2 -temp: change of +/- 10 degree can change o2 by 50% -neuro activity: prop to O2 use o2 decr by 50% w/flat line ------------------------------------ CBF = 50cc/min (MAP-ICP) -O2 demand -PaO2: CBF inc w/ decr PaO2 -PaCO2: CBF inc w/ decr PaCO2 -CPP:cerebral perfusion pressure CPP=MAP - ICP constant from 60-180 *curve shifts w/chronic HTN & thus dont drop press suddenly on pts w/chronic htn ICP: child <8 adult <10 closed head trauma <20 temporal lobe lesion <15 MONRO-KELLIE DOCTRINE: fixed skull 80% IC Volm = brain 10%= blood 10%= CSF (w/incr icp comp blood/csf 1st) MONITORING ICP: 1. Ventriculostomy: cath into lat vent via hole in skull (Gold Stnd) - if mass fxt or coagulopathy may be problem. Prone to infection - Popoff valve can allow drain of csf above set ICP 2. Subdural Bolt: subdural space peripheral measurement - edema makes inaccuate - can let CSF out but not in 3. Infra Red Cath: strictly measures pressure - closed in subdural space -------------------------------------- Mannitol: .25-1gm/kg mannitol rebound: mannitol gets into brain stimulating edema avoid bolus doses -use lasix & diamox after 1st mannitol GOAL: serum Osm 310-320 low maintainance fluid 1cc/kg/h incr nutrition requirements - high cal low volm Sedation: -narcotics are OK if PO2/PCO2 are nml Neuro Emergencies NITROGLYCERINE -Good acute reduction of BP -Tolerance w/prolonged use=>3 MECHS 1. Depletion of sulfhydral cofactors required for vasodil action 2. Activation of endogenous vasoconst mechanism 3. Expansion of intravasc volm w/loss of hemodynamic efficacy **1 study showed NTG SLx1 can dilate nml & stenotic portions of coronary arteries **Other studies show NTG better than CaBlockers @ stenotic vasodilation ------------------------------------- To be active: NTG metabolically converted to NITRIC OXIDE requiring Cysteine(Sulfhydryl Cofactors). NTG exerts vasodil FX by stim Guanylate Cyclase in Sm. Musc Cells=> increased GMP. TOLERANCE: despite less FXT's on BP: -Assoc w/ less angina -reduced mortality (25-30%)@12,24,36mo -unclear if Venous, Arterior, or arteriolar FXT -Some PTs w/&others w/o tolerance highly individually based responses -Rx delivery not an issue except transmucossal(too rapid claerance) -The higher the dose->more likely the tolerance and longer nitrate free period to recover -------------------------------------- PREVENTING or REVERSING NTG TOLERANCE: **Cannot overcome w/increasing Dose. SULFHYDRYL DONORS: Methionine, n-acetylcysteine, or Captopril -based on nitric oxide as neccessary metabolite of nitrites w/sulfhydral cofactors converting this Rxn **NITROPRUSSIDE does not require intermediate nitric oxide & does not have tolerance. INTERMITTANT THERAPY: allows recovery to nml meyabolism by repletion of sulfhydryl cofactors. -Optimal duration of Nitrate Free Period is unclear(10-12hr most commonly used) -use lowest possible # of effective doses w/nitrate free period (improving exercise performance) Nitroglycerine guidelines Routine Orders -Aspiration Prevention El HOB 30deg On side of worse lung Suction PRN Sputum C&S Bronchodilators -Seizure Precautions Dedrest Pad siderails Suction at DS Intub Try at BS IV Line Neurochecks -NG tube removal Clamp 4h DC if Nausea free or vol mas 1200-1500 Repl-1/2NS+20megK -Off Service ADm DX Current Prob Course by prob Things to do -DC Note Adm date DC date Prim DX Sec DX Procedures Consults Course 2lines/Inf/Transf Dispo Instructions Condition -PreOp NOte Indication Procedure Consent Premed Allergies Blood HCT/UA/Lytes Pt/Ptt Cbc/Diff PE affected area Postop Planning Post op note PreOp DX PostOp Dx Proc Desc Anesth Fluids I/O Blood I/O Tubes Location Condition PostOp Hct Findings -PostOP Orders To floor when stable Procedure VS Q15x4, Q30x2, Q1hx2, Q2hx2,, Q4hx4, Q8h Allergies Diet Adv as Tol IV Adult-D5.5Ns+20meqK/l maint Infant D5.5Ns=20meqK/l Pain Med VitC 500mg Po BID FeSO4 300mg PoTID Anticoag? Stool Soft Antibiotic? LABS: CBC-DF,Lyte,Bun,Cr,Glu, in RR; then Qdx3 XRAY? Drains to suction Incentive Spirometer Q2h Call in No: void... Replace NG Suction: 1/2NS+20meqK/L Ambulate w assist q5h then TID Situp TID Strict I/O Routine Orders ORTHOSTATIC HYPOTENSION SX: transient lightheadedness- syncope w/ visual changes, neck or head pain, dyspnea, profound weakness DIF DX: DRUGS: antiHTN, diureics, TCAs,ETOH, Nitrates, BNZs, THC, DIET PILLs VOLM DEPLETION: hemorrhage,diuresis, GI loss etc. ARRYTHYMIA: HTN: renovasc HTN, Pheo REFLEX VASODIL: Vasovagal syncope carotid sinus syncope, ADRENAL HYPOFXN: primary adrenal insuff hypoaldosteronism PREGNANCY FEVER NECK SURGERY(disruption of baroceptors) PRIMARY AUTONOMIC FAILURE -mult Sys atrophy (shy drager) -ideopathic orthostatic hypotension -selective NE failure -familial dysautonomia -baroreceptor deafferentiation SECONDARY AUTONOMIC FAILURE -DM,AMYLOID,Paraneoplastic(lung), CNS TUMOR,GuikkionBarre,TabesDorsalis B12,B1 defic,heavy metal poison SX of AUTONOMIC DYSFXN: -constipation,anal sphincter incomp w/ -fecal incontinance, decreased sweating, night blidness from inability to dilate pupil, nasal stuffiness from loss of alpha vasoconstriction, impaired erection and ejaculation. SUPINE HTN: often accompanied OH HEART RATE:autonomic failure underlys fall in BP on standing not accompanied by rise in HR Orthostatic Hypotension OTITIS MEDIA WITH EFFUSION (OME) USE OF STEROIDS First try antibiotic alone as 10-30% will respond. For persistent chronic effusion use 1 mg/kg/day prednisone, tapered over 7-14d with TMP/SMZ as first chioce. STOP or taper steroid if exposed to CHICKENPOX and give acyclovir at onset of rash. Prophylax Responders that are either otitis prone or high risk: OM 3/last 6m or 4/last year Down syndrom cleft palate craniofacial abn immunoglobulin deficiencies age <2y age first Om <6m group day care attendance Prophylaxis: amoxicillin 20mg/kg/d sulfisoxazole 50mg/kg/d Tmp/smz 10-20mg/kg/d Warn to stop antibiotic if rash other than chickenpox appears USE OF TUBES No benefit in children who had surgery for CLEFT PALATE: 70 children, 54% had tubes. No difference in speech developement between those rx'd with tubes for OME and those not. Audiological thresholds worse in tube group, more abnormal otological findings (Robson AK et al. J Laryngol Otol 106:788-792,Sept92) Otitis Media Oxygen therapy Home Oxygen requirements for Medicare PO2 < 56, O2 Sat < 89%. L/m %O2 -------------- 1 24 2 28 check ABG for COPD >2.5L 3 31 4 36 5 40 6 45 Face mask 50% 60% 75% 100% Adjusted by tech. Monitor sat >90 <92 COPD, 92-94 CAD ---Oxyhemaglobin dissociatioc curve Shouler usu at PaO of 60mmHg means that PaO2 above don't sig increase O2 content While decreasing PaO2 below causes large decr in O2 content. -Shifts to right with ^temp DPG H+ pH 7.62 7.44 7.2fs ------ ------ ------ ------ 90%Sat 45mmHg 60mmHg 70mmHg <-Shoulder 80%Sat 35mmHg 45mmHg 50mmHg ------------- ------ ------ Oxygen Therapy PAGETS DISEASE Chronic Dz of Bone w/incr rates of bone resorption, formation, & BM fibrosis -affects primarily adults >40yrs & of West Europe descent -Dx made through Xrays & rarely bone Bx & supported by incr Alk Phos or urinary hydroxyproline levels ETIOLOGY: unknown CLIN FEATURES: 80-90% aSX or w/few Sx -Dx often found by incidental high Alk Phos or by XRAY appearance -Sx are non-specific such as pain often confused w/OA or aging -Bone Pain is Most common Sx rarely in hands, feet or ribs. -Feafness either by 8th nerve compress or bony changes in middle ear -High Output Failure if >35% skelatan involved due to lg volm of blood shunted through highly vasc bone -also may be assoc. w/calc AS -HA: from cranial bone changes -Osteogenic Sarcoma: late complication DX: extremely higer serum Alk Phos (must r/o osteomalacia, rickets, incr PTH, fibrous dysplasia, mets) -serum Ca+, PTH, Phos are usually nml due to re-use after bone change serum Ca+ can rise if pt immobile -hydroxyproline: AminoAcid from Collegen released without being reused in 24h urine levels > 1-2grams TX: Dz typically benign course unless w/neuro sx, pain, CHF, of hyperCa+ -Calcitonin: inhibs bone resorption can reduce pain in weeks -Biphosphonates: Etidronate binds hydroxyapitite & inhib bone resorption & reduce pain & Alk Phos -may induce osteomalacia & incr Fxs due to reduced miniralization Paget's Disease -1/3 of Americans may be treated for chronic pain (CP) -50 million people partially or totally disabled by CP -700 million work days lost/year to CP -80 billion dollers/year expense for CP --------------------------------------- -~25% of CP pts are Rx dependant -~15% of CP pts considered Rx abusers (most commonly codiene & oxycodone) ------------------------------------- SOMATIC/VISCERAL PAIN: -typically due to infiltartion of tissue w/activation of nociceptors NERVES FIBERS: Mechanoceptors: A-Delta Afferents Polymodal Nociceptors: C Afferents A)Myelinated Fibers: 10% are nociceptic -"UNIMODAL" respond almost exclusively to noxious mechanical stimuli -conduct impulses @ 5-50m/sec in range of A-delta & rarely A-beta -Activation of a single fiber can produce sharp, stinging pain -5-100X higher threshold for activation than other mechanoreceptors B)Unmyelinated Fibers: 90% nociceptic -typically "POLYMODAL" responding to mechanical, thermal, & Chem stimuli -conduct impulse @ velocity of 0.6-2.0 m/sec (in C range) -assoc w/dull, burning, aching pain C) SENSITIZATION: 1. lowered threshold for activation following injury 2. increased intensity of response to noxious stimuli 3. onset may be w/spontaneous activity 4. may occur minutes after injury & last for hours. 5. may be mediated by K+,adenosine, triphosphate, bradykinin & PGs(E2) D) SOMATIC PAIN: 1. typically well localized 2. usually constant 3. freq described as aching or gnawing 4. most common type in Cancer Pts E) VISCERAL PAIN: 1. typically poorly localized 2. often refferd to cutaneous points 3. often described as deep,squeezing and pressure +/- N/V/diaphoresis (example: angina) F) REFERRED PAIN: 1. ? dual innervation of somatic and visceral structures by common afferents 2. Possibly visceral nociception afferents converge w/somatic input into common spinothalamic tract in dorsal horn cells & the brain misinterprets visceral input as input from cutaneous source. ---------------------------------------- DEAFFERENTIATION PAIN: from injury to the PNS &/or CNS 1. typically described as constant, dull, squeezing & aching w/ paroxysms of burning &/or shock/electric sensations 2. Paroxysms due to spontaneous & ectopic firing of damaged periph nerves 3. Epileptiform activity from periph nerve damage due to activity in the medial thalamus 4. Poorly reponsive to opiates or procedures (such as cordotomy) ---------------------------------------- BACK PAIN: 1. Backache: acute/chronic pain not associated w/movement 2. Lumbago: acute/chronic pain assoc w/movement with pain-free intervals(eg.pain on turning in bed/ rising from a seat) 3. Sciatica: referral of pain from back across the pelvis & down the leg-into the foot. Usually from lumbar disk dz inv sciatic nerve roots. 4. DJD 5. Tumor pain ------------- PAIN PERCEPTION: related to: -magnitude of stimuli -physiology of involved tissue -ethnic,psychosocial & emotional factors -economic impact and ramifications ---------------------------------- PAIN MECHANISMS: - nocioceptors-> periph sens nerves-> ->spinal cord->thalamus->cortex ------------------------------- **ACUTE->CHRONIC Pain Reflex Cycle** 1.cycle due to reflex contraction of muscles involved w/ spinal dermatome 2.-> pain-spasm-pain cycle w/inflam rxn -> more pain 3.-> reflex sympathetic vasoconstriction 4.->decreased blood supply to muscles 5.->more pain & renewed cycle ----------------------------- TRANSITION FROM ACUTE->CHRONVIC PAIN: -character of pain is disimilar from original injury or pain Sx -pain looses its Dx value ------------------------- Sx of Chronic Pain: - saddness, hostility, anxiety, frustration & depression - excessive preoccupation w/pain - unrealistic plans for the future - increased bed rest - decreased recreational & vocational activities ------------ TX of CHRONIC PAIN Pain, Chronic Panic Disorder Xanax or Clonipin for panic attacks. Clonipin probably cheaper. Serax and Restoril better for prn outpatient sleepers or second line for generalized anxiety. First line for generalized anxiety should be Buspar or similar agent. For Chronic sleeper try Trazedon 25-50 hs esp in older patient. At this dose should not produce priapism in men. For short term sleeper in controlled setting such as hospital use Chloral Hydrate 500 as it has no effects on sleep architecture. It does pose more danger in overdose that benzodiazepams. Panic Disorder Pap Smears Cytobrush ok for squamous lesion, misses adenocarcinaoma Abnormal Pap Smear Any of below on report: Adenomatous Atypia Koilicytosis Parakeratosis Dysplasia colpo&bopsy Inflammation ONLY asses risk for chlamydia/std (any 2 of below): under 25 new partner within 6 months partner with dysuria or discharge cervical friability spotting heavier period high risk then bring back for chlamydia check STD Positive Rx as indicated Negative repeat pap in three months or consisder colposcopy and biopsy if persistent inlfammation Low risk repeat pap/wet mount 3mo or consider colposcopy & biopsy if persistent inflammation Provera effects: allow 2 months from course before Endometrial or Endocervical biopsy For repeat pap smear allow at least 3 months for pap related trauma to heal. Reid's Colposcopic Index 0-2 3-5 6-8 HPV or CIN I CIN I/II CIN II/III MARGIN 0 POINTS Condylomatous or micropapillary contour Indistinct borders Flocculated or feathered margins. Jagged, angular lesions. Satellite lesns, AWE extends beyond TZ 1 POINTS Reg lesns w smooth straight outlines Sharp periph margins 2 POINTS Rolled, peeling edges Internal borders between areas of dif appearance COLOR 0 POINTS Shiney snow white Indistinct AWE, semi-transparent vs opague 1 POINTS Shiny, off-white Intermediate white 2 POINTS Dull oyster gray VESSELS 0 POINTS Uniform fine caliber Randmly arranged w poorly formed pattrn Nondilated capillary loops Ill-defined areas of fine punctation or mosaic 1 POINTS Absence of surface vessels p AA soak 2 POINTS Definite punct or mosaicism Individual vessels dilated, arranged in sharply demarcated, well defined patterns IODINE STAINING 0 POINTS Uptake with mahogany brown color No uptake by a low grade lesion(<2/6) 1 POINTS Partial uptake Variegated, tortoise-shell appearance 2 POINTS No uptake of high grade lesion(>3/6) MusMustard yellow CRYOCONE CERVIX Ice ball to 5-10 mm beyond lesion D/c 3-6wk, no sex, tampon, douche FU: Pap, pelvic, colposcopy Q 4m x 3, then Q6m x 1 yr Enla gel 5% (Astra): apply x 20min, wipe off. Intravaginal 5FU(Effudex): topical 2d/wk x 8-12wk motrin 800 1hr before pea sized amt to vulva avoid clit, urethra, scrotum protect w/vaseline Domboro's soak, Aveno for irritation Pap Smears PERICARDITIS Idiopathic (postviral\ infecious (viral, bact,TB,fungal, amebic, toxo CVD: SLE,RA,Scleroderm Drug-Lupus: procain/hydralazine Acute MI Trauma POST MI/Dresslers Post Pericardiotomy Post Mediastinal RT Uremia Sarcoidosis Neoplasia Leakage of Aorta into pericard sac Familial Med Fever pericarditis PULMONARY EMBOLI: Origin of Emboli: -(80-90%) large lower extremity & pelvic veins -Rt Atrium (CHF, A-Fib, indwell cath) -Hepatic & Renal Veins -Tricuspid Endocarditis or upper extremity thrombi in IV drug abusers Predisposing Pathology: 1) Stasis, 2) Endothelial Damage 3) Hypercoagagulable State Predisposing factors: immobility OCP's pregnancy, stroke, neoplasm,obesity SLE, nephrotic synd, polycythemia, IBD, shock, CHF -HIP & Knee surgery/any surgery -Any pt in Hosp approx 30% will have DVT PROPHYLAXIS: low dose heparin: decr risk fro 30-5 Adj Dose Heparin: PTT in high nml range -effective 24h prior to surg Coumadin 2mg/d 1-2d prior to surg -followed by full Tx post-op Pressure compression device: cause sys -anticoagulation Venous Thrombi(Red): Fibrin & RBC's Art Thrombi (white): Plt dense Etiologic Factors: 1. Lack of Endogenous Anticoag Factors a) antithrombin III b) protien C c) protein S 2. TPA - impaired synth & release 3. Plasminogen - abnml fxn or quantity 4. Antiphospholipid Atibodies - in SLE cause of Art & Venous thrombi 5. Exogenous Estrogen: dose related hypercoagulable state (risk unrelated to duration of use) Presentation: -uncomplicated embolus w/dyspnea -pulm infarct syndrome(pleuritc CP +/- hemotysis -circulatory collapse (<10%) RISK: compounded w/age, obesity, CHF presence of CA, acute MI, prior DVT or PE & immobilization 1. Low: age<40 w/uncomplicated surg age>40 w/minor surg 2. Moderate: age >40 w/gen surg>30min 3. High: major orthoSurg on low limbs or age>40 w/extensive abd/ pelvic surg for malignant dz (fatal PE in 1-5%) 1.Common: Most common Tachypnea (>50%): Dyspnea, tachypnea, tachycardia, cough, rales, pleuritic CP, angina 2. Less Common(10-40%): hemoptysis, low fever, JVD, DVT signs syncopre, altered MS 3. Rare(<10%) weezing, DIC, abd pain EKG Signs: S1 Q3 T3 (40% w/nonspec T wave changes) S-T wave abnormalities PACs, PVCs, atrial tach Rt atrial strain, RBBB, RAD(or LAD) Atelectasis elevation of hemidiaphragm (lost volm) pleural effusion "knuckle sign" PA tapers abruptly pulm infarction: pre-existing CV dz LAB Signs: -98% of all PE Pts w/abnml A-a grad or w/ PaCO2 <36 (sens not specific) V/Q scan: inj radiolabeled albumin & - inhaled inert hot xenon ** (Pos: 50% false + rate) ** 1. Nml: reliably excludes PE 2. Low Prob: 20-40% are pos (same for intermit & matched result) 3. Int Scan: abnml perf + infl on CXR 4. Matched defect: due to broncho- constriction 5. High Prob: 86% accuracy if large perfusion defect or segmental -only 37% if sub segmental (confirmed by pulm angio) PAgram:Pulm Arteriogram: definitive Dx - Morbidity: 4-6%- increased in Pts w/ RV-EDP > 20mmHg - must do prior to thrombolysis, embolectomy, or anticoag in Pt w/ bleeding risk FX of PE on Right Ventricle: - Massive PE leads to increased RV afterload- enlarged RV, shifts vent septum to Lt & decreased LV preload - leading to decreased CO - leads to RV dilation & ischemia from reduced coronary flow in systol ------------------------------------ TREATMENTS: Heparin: indicated in PE, suspected PE & DVT - 1/2 life=60-90 min - Bolus dose: give prior to definitive *** Dx to prevent early mediator- induced pulm vasoconstriction & bronchoconstriction by thrombin activation & PLT aggregation - Acts by binding Antithrombin III which inactivates Thrombin & inhibits coagulation - Duration of TX: gen continued 7-10d - Early Ambulation is Discouragedsince fresh thrombi may embolize prior to adherence to vein wall (7-10 days) - Maintainance Drip or Sq post bolus - IV 12,000 - 18,000 IU/hour - SQ 12,000 - 14,000 IU q12 hour (test PTT midway between sq inj) -------------------------------- Coumadin: for long term maintainance - antagonist of Vit K - depleates clot factors II, VII, IX, X - Effectivenes depends on depletion of clotting factors - FacII(Prothrombin) 1/2 life =60 hours- no use in rushing - Give 10mg PO x 3d, get PT on 1st & 3rd day - To prevent recurrent PE: 6mo of TX unless definitive studies show cleared DVT & PE (IPG & Lung Scan) ---------------------------- THROMBOLYTIC TX: 1. hemodynamically unstable Pts 2. rTPA within 3 days of surgery Streptokinase, Urokinase, & TPA - act to facilitate fibrinolysis by converting plasminogen to PLASMIN which hydrolyses fibrin,fibrinogen & blood coag factors - TRIALS show thrombolytic Tx superior to heparin in improving PAgrams, hemodynamic indices, & perf scans ***-particularly in massive PE's - F/U TRIALS: thrombolysis w/<longTerm residual pulm clots & pulmonary diffusion capacity than w/Heparin (seen @ 2weeks, 1yr, & 7yrs) - NO dif w/TPA by IV or intrapulm Cath - UROKINASE: direct act of plasminogen (isolated from human urine) - STREPTOKINASE: must bind plasminogen & then become plasmin activator (isolated from grpC B-hem Strep) - rTPA: "CLOT SPECIFIC" thrombolysis Activates Plasminogen-plasmin only significantly inpresence of fibrin which facilitates conversion of plasminogen, **** thus producing localized FCTs - 100mg infusion x 7 hours may be superior to 50 mgX 2hrs ---------------------------- CONTRAINDICATIONS to THROMBOLYSIS: Absolute Contraindications: -active internal bleeding -recent surgery -? aortic aneurysm -recent head trauma/CNS TUMOR/CVA -Ophthal bleed--?DM -BP> 200/120 -------------------- Relative Contraindications -recent minor trauma -Hx: chronic severe HTN -active PUD /bact endocarditis -Bleeding diathesis/Anticoag Tx -sig Liver/ kidney Dysfxn -age > 75 -prior streptokinase (particularly -within initial 6-9mo period) Complication of thrombolysis: - bleeding (1% intracraneal) - antibody formation (w/SK) - allergic Rxn (w/SK) - fever (w/SK) - resistance to thrombolysis ISOPROTERONOL: beta agonist: bronchodil, pulm/syst vasodilator, & +inotrope - in Pt w/ MILD PE & cardiac failure - lowers pulm HTN & increases CO TX FOR UNSTABLE PT w/PE 1. Thrombolysis 2. Embolectomy(only for central emboli) 3. Tranvenous Catheter Embolectomy 4. IVC Filter Recurrent PE: may lead to pulm HTN and Cor Pulmonale REF: Biebuyck JF: PulmThromboembolism: Dz Recog. & Pt Mgt.Anesthesiology 73:146-64,1990 Pulmonary Emboli PANCREATITIS 1. ETOH 2. Biliary Tract Dz (gallstones) 3. Postop abd/Post ERCP 4. Trauma 5. Metabolic: High TGA, PTA, Calcium Renal Failure Fatty Liver of Preg 6. Infection: Mumps, Viral Hep, Mycopl 7. Connective Tissue/Vasculitis: -SLE,Necrot Angitis, TTP,HSP 8. Rx: Azathioprine Sulfa, Thiazides, Lasix, Estrog, Tetracycline, Valproate, Chlothalidone, Procainamide, methyl dopa ?STEROIDS 9. Ulc Colitis/Duodenal Divertic 10. Duodenal Ulcer-Penarating RANSON CRITERIA: (Risk Factors on Hosp Admission) increasing age hypotension tachycardia abnml pulm findings abdominal mass fever 1st attack of pancreatitis (Risk Factors after 48 hours) HCT > 10% w/hydration &/or HCT<30% Requirement of massive fluids/colloid hypocalcemia hypoxia w/or w/o ARDS albumin Azotemia Charcots Triad: pain, jaundice, fever Reynolds Pentad: + hypotenson & confusion TREATMENT Demerol, NPO, NGT only if N/V, Aggressive Volm Repletion (3rd spacing) Monitor serum Ca, Mg, Glucose, HCT Pancreatitis HEPATITIS: viral: A, B, C, & D General: malaise, anorexia, fatique, Immune Complex: arthralgia, urticaria (partic in HBV) Flu Sx (partic in HAV) Jaundice: 50% in HAV, 33% HBV Tender Hepatomegaly Splenomegaly: ~20% ---------------------------------------- HAV: RNA virus trans by fecal-oral rt. incubation=2-6 wks Onset: Abrupt Severity: usually mild Jaundice: only ~50% are icteric Chronic Sequelea:NO chronic Hepatitis Recovery: 99% Mortality: 0.1% Infectivity: 1-2 wks after jaundice TX: supportive Prophylaxis: ISG Dx: HA-Ag(IGM) in serum 4X rise in serum antiHA-Ag(IgM&G) draw 2 weeks apart ---------------------------------------- HBV: DNA virus trans by parenteral rt. Pts at Risk: IV abusers, gay men, & pts recieving bloodprods Incubation=4-24 wks Onset: Insidious Severity: often severe Jaundice: only ~33% are icteric Chronic Sequelea: 5-10% go on to Chronic Hepatitis Recovery: 85-90% Mortality: 1-3% Infectivity: During HBsAG is + TX: supportive Prophylaxis: HBIG, HB vaccine Dx: HBs-Ag or Anti-HBc(IgM) = acute inf Anti-HBc(IgG) = acute inf only if 4x risein titer ---------------------------------------- HCV (NANB): No Virus ID Transmission by parenteral rt Incubation=2-25 wks Onset: Insidious Severity: often mild Jaundice: only ~20% are icteric **Chronic Hepatitis: 20-40% w/fulminant or chronic active Recovery: variable Mortality: 1-2% TX: supportive Prophylaxis: ??ISG Dx: by exclusion: no dx tests --------------------------------------- HDV: sm defective RNA virus infectious only w/HBV inf relying in HBV protiens for its replication Transmission: Parenteral rt. incubation=4-8 wks Onset: often Abrupt Severity: often severe Jaundice: unknown Chronic Sequelea: unknown Recovery: unknown Mortality: unknown TX: supportive Prophylaxis: unknown Dx:Delta-Ag or Anti-Delta-Ag in serum --------------------------------------- Hep E Virus: water born found in ASIA ======================================= ? Chemicals: ABX(ketoconizole) Anesthetics, Tamoxifen Mevocor (lovastatin) ETOH(ast>alt) --------------------------------------- Pthology: all viral types are the same: -mononucular cell infiltration -cellular ballooning & necrosis -condensed cytoplasm w/pyknoticnuclei (acidophilic bodies) --------------------------------------- Immune Serum Globulin: effective after exposure to HAV ??HBV/HCV Hep B Immune Globbulin: HBV antisera gives passive immunity after HBV inf Hep B Vaccine: surface Ag ======================================= Fulminant Hepatitis: 1-2% w/HBV or HCV (rare w/HAV). Partic common w/HDV!! -Presents w/progressive jaundice & hepatic encephalopathy w/ascites. -Hepatorenal syndrome is common -High PT is early sign -Early high transaminase levels fall & hepatomegaly reduces from necrosis -mortality varies w/age; approaches 90-100% w/age > 55yrs ---------------------------------------- Chronic Persistant Hepatitis: follows HBV & HCV infections -mildly elevated transaminases for>6 mo -Bx w/periportal lymphocytic infiltrate & no extension beyond portal triads & no fibrosis -Usually asymptomatic w/benign course --------------------------------------- Chronic Active Hepatitis: HBV & HCV -elevated transaminases for>6 mo -Bx w/ necrosis, inflamation & fibrosis bridging portal areas & central veins -may progress to CIRRHOSIS w/signs of chronic liver dz(spiders,caputmedusae) -Tx:?? alpha-interferon --------------------------------------- Chronic Carrier State: 0.2% w/HBV - prob also w/HCV --------------------------------------- HEPATOMA: assoc w/ HBV 2-4x more common in males androgens,estrogen, antitrypsin III, viral cirrhosis, alpha toxin from peanuts (seen in africa & asia) --------------------------------------- Cholestatic Hepatitis: Alk Phoselevated out of proportion to LFTs- must r/o biliary obstruction Pancreatitis: noted in 10-40% of cases ---------------------------------------- Rx Induced Hepatitis: assoc w/any Rx presenting w/variable findings Acetominophen:Tx w/ N-acetylcyctiene which binds toxic metabolite &provides cysteine for glutathione synthesis Bili Metab dysfxn: partic w/estrogens & androgens Interference w/Protein Metab: tetracycline causes microvesiclar fat in hepatocytes Immune Rx Rxn: Isoniazide Halothane Chlopromazine Methyldopa ketoconizole ------------------------ ETOH Hepatitis: acute syndrome seen w/ heavy EtOH consumption Features: Fever, jaundice, hepatomegaly, w/progression->signs of chronic liver Dz ascites, variceal bleeds etc Labs: leukocytosis, high SGOT(AST)<350 low albumin high total Bili modest rise in Alk Phos & dir Bili SGPT(ALT) almost always < SGOT(AST) Low Plts: in 10% cases Bx w/fatty liver, lots of Polys alcoholic hyaline (mallory bodies) hepatocyte necrosis & occasionally sclerosis of central veins TX: supportive suppl B vits (especially thiamine & folate w/2500-3000cals / day Steroids: controversial role ----------------------------------------- Fatty Liver: from EtOH interference w/ hepatic lipid metabolism - asymptomatic hepatomegaly - elevated GGPT, & SGOT/PT & alk phos --Prognosis is excellent if complete abstanence from EtOH ----------------------------------------- Charcots Triad: pain, jaundice, fever Reynolds Pentad: + hypotenson & confusion Hepatitis POLYMYOSITIS & DERMATOMYOSITIS idiopathic inflam muscle Dz assoc w/proximal muscle weakness Sx: prox musc weakness cpk elevations inflammatory infiltrates Skin Rash more common in children CLASSIFICATION: 1. Adult Polymyositis 2. Adult Dermatomyosistis 3. Poly or Derm assoc w/malignancy 4. Juvenile Derm or Polymyositis 5. OVERLAPP: Assoc w/other Rheum Dz (SLE, RA, Sys Sclerosis, & Sjogrens) --------------------------------------- ETIOLOGY: ??viral autoimmunity impairment cellular dysfxn ? pts produce lymphotoxin that is toxic to muscle CLIN FEATURES: RASH: erythematous patches over face, neck, upper chest, & extensor surfaces -typically scaling & atrophic -heliotropic eyelids: violet swelling of eyelids -Grotons Sign: erythematous patches over metacarpophalangeal & PIP joints LUNG: chronic interst Dz partic w/jo-1 antibody JOINT: mild symetrical inflam arthritis occurs rarely Muscle: skelatal, pharyngeal, resp, & cardiac (heart not common) DX: Polymositis & Dermatomyositis PRESSORS: DOBUTAMINE:alpha:+/-, B1:+++, B2:+,DA:0 SVR:-, CO:+, PCW:- DOPAMINE: alpha:+++, B1:++,B2:0,DA:+++ SVR:+/-, CO:+, PCW:+/- EPI: alpha:4+, B1:+++,B2:++,DA:0 SVR:-, CO:+, PCW:- NE: alpha:4+, B1:++, B2:0, DA:0 SVR:+, CO:+/-, PCW:+ PHENYLEPH: alpha:5+, B1:0, B2:0,DA:0 SVR:+, CO:-, PCW:+ ISOPROT: alpha:0, B1:4+, B2:4+,DA:0 SVR:-, CO:+, PCW:- Pressor Drugs-Autonomic Receptors PROTEINURIA NML Levels: <150mg urine prot /day major component is albumin CAUSES: 1. PRERENAL: w/struct intact nephron a) Too Much Protein -Rhabdo: myoglobin -Hemolysis: Hbg -Plasma Cell Dyscrasia: light chain -DIC: fibrin split products -Pancreatitis: amylase b) Hemodynamic Change: fxt glom caps favoring increased perm to protein -CHF -Pericarditis -Strenuous Exercise -High Fevers 2. RENAL PARENCHYMAL DISEASE: a)GN: partic Focal GN(membranous & nil) -usually major component=albumin -nephrotic sx=edema,low serum alb) b)Tubulointerstitial Nephritis: may be idiopthic or from systemic dz or drug rxn -< selective prot loss: <albumin loss -may lose TAMM-HORSFALL Protein & B2 microglobulin 3. ORTHOSTATIC PROTEINURIA: -some pts w/urine prot only on standing -24hour urine prot usually constant @ .5-2.5g/day Proteinuria-causes RANSON'S CRITERIA INITIAL Age>55yrs WBC>16000 Blood glucose>200mg% Serum LDH>350 IU/L Serum AST>250 SFU/dL INITIAL 48 HOURS HCT fall>10% BUN rise>5mg/cL Serum Ca<8mg/cL HCO3 deficit>4mEq/L PaO2<60mm Hg Fluid sequestration>6L Ranson's Criteria Key: P-Palm ER-Erythema T-Trunk S-Sole M-Macules/ar PAP-Papular PU-Pustular MM-MucusMembranes UL-Ulcer UR-Urticaria VS-Vesicles/ular PG-Pigmented EX-Extremity Diseases begin MACULO-PAPULAR RUBEOLA(Red Measles) DDX: Exanthem Subitum, Rubella, Echo, Coxsackie, Adeno, EBV, Toxo, MENING, ScarletFever, Rickettsial, Serum Sickness, DRUGS -Koplick spots after 2-3D of conjunctivitis & coryza -Must have cough (3C's) -Conjunctivitis (3C') -Photophobia -Fever rises in STEPs -Fever with ONSET of rash vs roseola (Exanthem Subitum) rash starts as T -Involves the FACE vs Rickettsial (spares face) -May ITCH RUBELLA(German Measles) DDX: EBV(CBC), Enterovirus (No sub-occipital LN) Prophylaxis: Text Preg Fem HI, Vacc RA 27/3 -In non-neonates a milder disease -Conjenital infant infective up to 12-18mo! -Prodrom: Retro-auricular LN, p-cervical LN, sub-occipital LN; tender LN 1D PRIOR to rash -Enanthem: Rose spots on soft palate, extend to fuces -NO PHOTOPHOBIA -3D rash, last day pinpoint, similar to goose flesh of scarlet fever -May see arthralgia esp in F -Fever usu<101(38.4) -Rash, Fever slight +/- coryza & conj ROSEOLA DDX: Meningitis, FUO, Kawasaki -Rash appears when Fever of 3-4D STOPS -High fever(103-106), but child looks better than should -Epi: Spring/Fall -No typical enanthem -WBC to 16-20k 1st 1-2D of fever, then to 3-5k ERYTHEMA INFECTIOSUM(5th's Disease) DDX: rubella, enterovirus, SLE, atyp measles, DRUG -No prodrom -Rash in 3 stages: 1 & 2 may alt 1 slapped cheek 2 eryth M-pap on T & EX 3 Fades to lacey, retic pattern, then recurrs up to 39D! -Often ITCHY -Rash lasts 2-39?D -Rare complications -May go to school -Inc 7-28D -NO rx CHICKENPOX -Rash: sm er M > vs > scab -Abrupt onset of rash & fever -Give ZIG to babies of infected mom within 4D of L&D SCARLET FEVER -Rash, fever, sore throat together -Rash: goose bumps on sunburn -Confluent on face with Circumoral sparing -Strawberry tongue, then coated tongue SCALDED SKIN SYNDROM -First day like Scarlet Fever HIVES(Urticara) -RAISED er patches that come and go over hours SYSTEMIC ONSET JRA -Cyclic fever to 103, very sick with fever -Looks well (usu in AM), in between fever spikes -small red pink M w central pallor, ^ in febrile periods Other M-PAP Viral Arbo: also scarlatinaform Coxackie: also VS, PU EBV amp rash AMPICILLIN RASH Most common nonimmunologic drug reaction in children. May occur in up to 18% of children given oral ampicillin. Median time to onset=9D, range 1-14D Fine eryth mac and pap begin on trunk then spread peripherally. NOT URTICARIAL nor TARGET OF EM or TEN FIXED DRUG ERUPTION Discrete plaques of DUSKY erythema, usually few in number. Develope hours to days agter drug exposure Central blistering often present Mucous membr of lips or penis common typically resolve leaving ashy gray hyperpigmentation Readminisration of offending drug will produce lesions in same precise anatomical location. Common causes: ASA barbiturates phenolphthalein tetracyclines Bacterial M-PAP Psittacosis Chlamydia: P & S Erysipelothrix: Red M Hands & Fingers Leptospirosis: all body, P & S Listeria: M w central necrosis Mycobac. Leparae: PG changes Salmonella: rose spots on T Strep. Pyogenes: Scarlet Fever, Erythema marginatum(T EX) Strep. Moniliform P & S Staph.: Scalded skin Spirilium Minus: rat bite, red purple T P S Treponemum(Syphilis Trep. Carateum(Pinta): ER M, DE-PG Ricketsial Typhus: rsh T > EX Tsutsugamushi Rocky Mtn Spt: 1st lesion VS Fungal Tinea Parasitic Malaria-urticarial Toxo: spares P S Ancylostoma Duodenale & Necato amerianus(hookworms): ITCHY PAP > VS Ancylostoma braziliensis: creeping eruptions: linear, itchy Wuchereria filaria Onchocerc Volvulus: erysipeloid, +/- itching Schistosomiasis: ER M > Itching > VS Trichinella spiralis: ER Multiform +/- UR Scabies: Itchy, ^ skin folds Pediculosis(lice); Itchy M Flea bites: Itchy grouped M Collagen Disease JRA: small red pin M, central pallor, ^ in febrile periods SLE: ER, or scaly Dermatomyositis: scaly ER, ^ extensor Joints Unclassified Anaphylaxis: Itchy, buttocks, legs Erythema Multiforme: ER M & PAP, VS on MM or skin Kawasaki(MucoCut Lymphnode Synd) -High prolonged fever 2-3D > Rash, Conj, Straw tonge, P & S ER, cracked lips Ulcerative Candida: superficial skin & MM on ER bases Chancroid: Painful, shallow UL, purulent Diptheria(Cutan) shallow UL w firm body Leishmaniasis: M PAP > UL Lymphogranuloma Venereum: UL of genital, MM Sporotrichosus: ND at site of thorn puncture > UL Syphilis: UL w indurated border at primary site, painless, heals spont 2-3wks TB & Atyp: PAP or ND of skin > UL Tularemia: UL at organism entry site Yaws: UL granulomatous skin lesion NODULAR Erythema Nodosum: E ND of Extensor surgaces of body Causes: strep, N. Men, Mycobac, Tularensis, Cocci, Histo, Blassto, Leishmania, EBV, Cat Scratch, Collagen Vascular, IBD(UC), Granulomatous colitis Leishmaniasis: Purple PAP or ND > UL > crust Leprosy: ND of face, ears, elbows, knees, buttock; DE-PG, anesthetic TB(Lupus vulgaris): PAP ^ > ND > PU Syphilis Scaling Eczema: E-M-PAP > VS - scaling > oozing Psoriasis: thick silver scales SLE: ER, or scaly Vesiculo-Bullous VIRAL Coxackie: Hand, foot mouth (MM) Herpes Simplex: skin, lips mouth pharynx Smallpox: MPap > VS > scabs, one crop Varicella(chicken pox) MPAP > VS > scabs, succesive crops Bacteria Strep Pyog: ER > weeping VS > crust Impetigo - staph - mon scabbing Ricketsia Rickettsial pox: urban rat bite Fungal: ID reaction Parasitic: Scabies Non Infectious: Insect bite, DRUG, dermatitis herpetiformis, incontinentia pigmenti, epidermolysis bullosum, pemphigus, pemphigoid, Dermatitis, exzema, Petechial purpuric Bacterial: Anthrax: PAP central hemorrhagic necrosis Nisseria Mening: Petechial + purpuric Pseudomonas aeromonas: Red ER > purplish > ND w +/- central necrosis Spider Biit Ricketsial Typhus: endothelial cell damage Rocky Mtn Spotted Fever Viral:Arbo(dengue, hemorrhagic, diffuse petechial & purpuric EBV, CMV, Hep from vasculitis Noninfectious: Leukocytoclastic vasculitis Erythematous Macules Tinea corporis: Itchy raised ring, central clearing w Normal sensation Subacute contact dermatitis Erysipelas Nummular eczema: M Pap Tuberculoid leprosy: anesthetic central clearing, DE-Pg, Loss of flare response & sweating LUPUS SARCOID Mycosis Fungoides Skin Rashes ACUTE RENAL FAILURE ARTIFACTUAL: Ketones (AAA) DRUGS: tagamet/sulfa (block secret cr) PRERENAL: decreased GFR -hemorrhage -CHF -Renal Artery Stenosis POSTRENAL: RENAL; -ATN:60%post-op,38% medical,2%pregnancy -ischemia from hypotension -Nephrotoxins:aminoglycosides, contrast dye, chemoTX, Hgb & MYOgb. -INTRINSIC RENAL DZ: -GN -Tubulointerstitial nephritis -Radiation Nephritis -Renal Vasculitis / SLE -Crystal or ParaProtien Dz --------------------------------------- CLIN FEATURES OF ARF: ANURIA: either obstruction or bilat cortical necrosis 1.AZOTEMIA: -BUN can be high from STEROIDS & tetracycline (catabolic Rx's) -Cr elevated by CIMETADINE & TMP (block Cr Secretion) & musc breakdown -Cr artificially high w/ketones (AAA) 2.URINE VOLM DYSFXN -Anuria: <100cc/day -Oliguria: <400cc/day -Polyuria: >3L/day 3.URINALYSIS: -Hyaline Casts:suggest pre-renal -Brown Pigmented Casts: +/- renal tubular cells seen in 75% of ATN cases. If no RBCs & +dipstick must be hgb or myoglobin -RBCs: suggest calculi, trauma, inf or tumor -Leuks: suggest infection vs immune mediated inflam or allergy -Eosinophils: seen in 95% of allegic interstitial nephritis 4. URINE CHEMISTRIES: FeNA: Frac Na Excretion: [(Una/Pna)/(Ucr/Pcr) x 100] values <1% suggests prerenal dz >1% suggest renal parench dz Renal Failure Index: [Una/(Ucr/Pcr) x 100] values <1% suggests prerenal dz >1% suggest renal parench dz BUN/Cr ratio: >20 usually = prerenal --------------------------------------- Acute Renal Failure Respiratory Distress Child -------------Croup Score--------------- SIGN 0 1 2 3 Stridor none only w mild w severe agitatn rest at rest Retraction none mild mod severe at rest Air entry nl mild mod marked Color nl nl nl cyanotic Level of nl restls restls lethargc conscious when when disturb undistrb --------- CROUP-SCORE CLINL-SEV MANAGEMENT <=4 mild Outpt mist 5-6 mild-mod Outpt if: child imp in ER p mist & >6 mo & parent reliable 7-8 mod Admit racem epi >=9 severe Admit ICU, race epi, intub? -------- Differential of Stridor------- Viral Epiglo- Bac Tra- Retroph Croup otitis cheitis Abscess HX:---- ------ ------- -------- ------- Age 2m-4y 3-6y & 2-4y Chld - adult adult Prodrom or URI Pharyn- URI gitis/ trauma Onset Grad Fulmint Variable Slow Dysphg +++ +++ ---------Differential of Stridor------- (cont) Viral Epiglo- Bac Tra- Retroph Croup otitis cheitis Abscess SIGN:-- ------ ------- -------- ------- Fever Low High, High, Variabl grade toxic toxic Stridor +++ ++ +++ + Droolng -(?) +++ +++ Posture lying sitting variable variabl ---------Differential of Stridor------- (cont) Viral Epiglo- Bac Tra- Retroph Croup otitis cheitis Abscess TESTS:- ------ ------- -------- ------- WBC <10000 >10000 >10000 >10000 X-ray Sub- Swollen Subglott Widened glotic supra- irregu- retro- narrow glottis larity pharynx CXs Parain H. flu S Aureua Staph, RSV Strep Strep, Anaerob PEDS Respiratory Distress ACUTE RESPIRATORY FAILURE low O2<50, high CO2>45, or Exhaustion 1. Apnea 2. PaO2 <50 despite increased FIO2 3. PCO2 >50 w/pH<7.25 4. Ventilation is inefficient or exhausting. RR>30 Special Cases: 1. COPD: accustomed to PaO2<50 2. Drug Overdose: resp depression can be rapid Type1:NONHYPERCAPNEIC:low O2 w/nml CO2 usually from V/Q mismatch ?pneumonia,infection,aspiration PE,Fat Emboli,ARDS ** Can give O2 safely w/good CO2 blowoff. Type2:HYPERCAPNEIC: low O2 w/high CO2 from decresed alveolar ventilation & v/Q mismatch ?low resp drive, decreased musc fxn-MG/GB/polio/Trauma CO2 RETAINERS:use low flat O2 levels PCO2: inv. proportional to alv vent PCO2: prop to vent & V/Q - changes in V/Q fxt PaO2 not PaCO2 -------------------------------------- Respiratory Failure -------------- RSV -------------------- SX: Wheezing Respiratory distress Grunting SN: Hyperinflation Perihilar densities Lymphocytosis WU: Nasal smear IFA for RSV Para/Influenza Adeno Chlamydia Blood/Urine CX CXR Sequelae; Infants <3 mo, risk of apnea, especially as degree of respiratory distress Prematurity, Infant's apneic risk until age is 12 months from CONCEPTION! RX: Hospitalize if question of APNEIC epsiode for 2-3 days, longer if severe respiratory distress. Consider antibiotic Cefuroxime 50mg/kg Q8. Aluterol neb Q3h Fluids D5 NS & 20meq KCl/L PEDS RSV Renal Tubular Acidosis Distal [Type 1]: inability to lower urine pH despite acidosis - may be due to: - autosomal dominant trait - autoimmune disease - obstruction - amphotericin assoc w/ hypokalemia, hypercalciuria, & ostemalcia Proximal [type II]: defect in HCO3 reabsorption, assoc w/ -glucosuria -aminoaciduria -phosphaturia -May be due to: -myeloma -drugs -renal transplant -tx requires lg amounts of bicarb which aggrevates hypokalemia 3. Type IV: Assoc w/: - hyperkalemia & - Low Renin/Aldo levels - DM - advanced age - chronic interstitial nephritis - nephrosclerosis Renal Tubular Acidosis SARCOIDOSIS Systemic Disease: Noncaseating Granulomas:in lungs & other organs. -usually presents as mediastinal or hilar lymphadenopathy w/pulm infiltrates & cutaneous & ocular lesions. -Less Common Features: - peripheral adenopathy - erythema nodosum - arthritis - hepatosplenomegaly - hypercalcemia - diffuse & local CNS involvement - Cardiomyopathy - depressed delayed-type hypersensitivity ------------------------------------------ Incidence: AGE: most common @ ages 30-50 RACE: American Blacks 10-18X>incidence ----------------------------------------- CLINICAL FEATURES: 1. Pulmonary: involved in 90% of cases a) Sx:fatigue cough- non-productive dyspnea- on exertion hemoptysis, CP, pleurisy: rare b) PFT's: may be nml but most often w/ - impaired diffuse capacity - lung restriction - reduced VC c) CXR: enlarged nodes w/+/- - faint interstitial infiltrate - diffuse nodular infiltrates - variable degrees of lung fibrosis including honeycombing d) STAGING: Stage 1. Bilat hilar adenopathy w/ nml lung parenchyma Stage 2. bilat hilar nodes + interstitial infiltrate Stage 3. Interstitial infilt's alone Stage 4. Fibrosis 2. SYSTEMIC INVOLVEMENT: a) Uveitis: common->may lead to blindness b) Skin: in 1/3 all pts- -Erythema Nodosum occurs early & indicates a good prognosis -All other skin lesions indicate chronic progressive course c) Bone/Joint: transient polyarthritis assoc w/erythema nodosum. Also may have cystic bone destructive d) CNS: may present as Bell's Palsy & other Cranial Neuropathy's, peripheral neuropathies, & poss granulomatous meningitis. e) Cardiac: arrhthymias & conduction disturbance (?sudden death) f) Calcium: hypercalcemia, renal stones, & hypercalcuria. (~25%) -due to hypersens to Vit D w/increased intestinal absorption of Calcium ------------------------------------------ 1. ? in all pts w/ - pulm/mediastinal adenopathy - interstitial pulmonary fibrosis - erythema nodosum - uveitis - hypercalcemia/ calcium renal stones 2. ACE Level: not diagnostic but may indicate dz & marks Tx progress 3. Tissue Biopsy: transbronchial Bx associated w/high yeild 4. Gallium 67 lung scan - nonspecific ----------------------------------------- TX: STEROIDS=> used in clin sig dz ----------------------------------------- PROGNOSIS: variable course 1. In most: resolution ocurs in <2yrs & does not recur 2. 25% w/progressive dz w/serious disability- commonly w/multi-sys involvement 3. 5% die from respiratory failure ---------------------------------------- sarcoidosis SEIZURES Initial Questions: 1) How long? 2) What is the pt. doing? 3) Protection? Initial Action: ABC's IV access Send CBC, 6/60, Ca, Mg, PO4 Continuous cardiac and BP monitoring Establish reason for seizure: Electrolytes Infection Structural Abnormality Therapy: Ativan 1mg IVP followed by 1-2mg q 5min up to 8mg total. Dilantin Load 10-20 mg/kg Do NOT push faster than 50 mg/min if seizure lasts longer than 5 min or recurs without regaining consciousness, then INTUBATE -- Status Epilepticus Connect EEG If seizure does not stop with Dilantin load, then try another 5 mg/Kg. If seizure is not stopped after additional Dilantin, then Pentobarbital coma. Seizures -management SEIZURES: dimwit D=drugs: theo,neuroleptic,EtOH,Demerol BNZ's,PCN od,LIDO, Amphetamine cocaine, I=ID:meningitis/encephalitis: Coxackie virus, HSV,Mycoplasma I=Ischemia M=metabolic: 4H's hypo:gly,nat,cal,mag (low gluc,Na,Ca+,Mg+) Uremia,hypoxemia,hypercap HTN W=withdrwal:ETOH I=idiopathic: Epilepsy vs CNS vasculitis T=trauma: CNS bleed,CVA, TUMOR T=TUMOR LABS: lytes,Ca,Mg,Alb,Rxlevel,BUN,Cr, glucose,CBCD,AcuCheck,ABG,ToxSc -- also serum Prl & CPK useful TREATMENT:**(Tx trauma Sz w/Dilantin alone to avoid CNS depres) 1. if low glucose: thiamine 100mg IV follwed by D50W 50cc slowIVP 2. IV access always w/NS(noD5)!! 3. Diazepam:2mg/min IVP upto 20mg start dilantin after 10mg 4. Get 2nd IV (val&dilantin dont mix) 5. Dilantin:18mg/kg(1250mg/70kg) @<25-50mg/min (watch for arrythmia's & hypoTN) 6.STATUS:Sz>30min:get ICU a)?intubation b)Phenobarb:8-20mg/kgIV@30-60mg/min c)Diazepam Inf:100mg in .5L D5W @ 40cc/hr=(8mg/cc) Seizures -causes SHOCK Cardiac hypovolemic sepsis obstructive Cardiac: MI, valve, arrythmia valve dz: v-wave on PCWP tracing and lo CO Hypovolemic: lo CO and lo PCWP Obstruction: PE and Tamponade Tamponade: equalization of pressures Sepsis: Distributive Shock, high CO low svr etc PRESSORS: DOBUTAMINE:alpha:+/-, B1:+++, B2:+,DA:0 SVR:-, CO:+, PCW:- DOPAMINE: alpha:+++, B1:++,B2:0,DA:+++ SVR:+/-, CO:+, PCW:+/- EPI: alpha:4+, B1:+++,B2:++,DA:0 SVR:-, CO:+, PCW:- NE: alpha:4+, B1:++, B2:0, DA:0 SVR:+, CO:+/-, PCW:+ PHENYLEPH: alpha:5+, B1:0, B2:0,DA:0 SVR:+, CO:-, PCW:+ ISOPROT: alpha:0, B1:4+, B2:4+,DA:0 SVR:-, CO:+, PCW:- Shock -types SIADH Etiology: 1. NEOPLASM: lung, duodenum, pancreas, brain, thymus, bladder, prostate 2. PULM: pneumonia, TB, bronchiectasis, emphysema, status asthmaticus 3. INTRACRANIAL: trauma, infection, hemorrhage, hydrocephalus 4. POSTOP: surg-stress, PEEP vent, anesthetics 5. RX: Chlorpropamide, thiazides, AVP, oxytocin, chemoTX, tegratol,MAOI's TCA's 6. OTHER: Gullain Barre, LABS: hyponatremia urine osm>serum osm Una>30mEq/L nml BUN,Cr, nml TFTs,adrenal & cardiac fxn 1. Fluid restriction to .5-1L/day 2. Demeclocycline 300-600mg PO bid -use for chronic SIADH (caution in pts w/hepatic dz. may cause nephro DI & photosensitivity. 3. If Severe (seizures): tx w/hypertonic saline & lasix sIADH Solitary Pulmonary Nodule: 20% of chest film nodular densities are nipple, bone pleural or artifact. Calcification Patterns Benign Central Popcorn Concentric Diffuse Malignant Stippled Eccentric Biopsy Route after CT Bronchoscopy Central loc 2cm or larger Involves brochus Percut needle Peripheral Smaller than 2cm Not involving bronchus Chest Xray observation intervals if 2y films not avail: 1 3 6 12 18 24 months Non-calcified nodule Low risk of malignancy Mod-high risk but wish avoid surg and reliable. Sol Nodule CXR: confirm w nipple markers, obliques or fluoro Obvious Calc Not Calc Get old films No Growth 2y No films; new; growing CT Scan Benign, calc, <2.5cm, smooth edges Suspicious: noncalc, >2.5cm, ill- defined or irreg edge Asses Risk Low risk CXR: 1 3 6 12 18 24 months No growth Growing Biop or thoracotomy Medium/High Risk Biop or thoracotomy Solitary Pulmonary Nodule SPONDYLARTHROPATHIES Group of Inflamatory Arthritides -distinct from rheumatoid disease CLINICAL FEATURES 1. prom involvement of AXIAL skelaton -particularly @ SI joint 2. Extremity involvement is usually oligoarticular & asymetrical 3. Enthesopathy: prom inflam of tendons & ligs (plantar fasciitis, achilies tendonitis, & chostochondritis) 4. Organ Involvement: Conjunctivitis, Uviitis, urethritis & <commonly Aortitis & Prostatitis. ----------------------------------------- LABS: No good tests ESR not reliable RF neg rarely w/anemia or high Plts (as common in other inflam Dz) X-RAY: 1. Changes c/w periosteal new bone formation @ enthesopathic lesion 2. Less common w/erosive changes typically occuring in hips, SI joint & shoulders GENETICS: Assoc. w/ HLA-B27 alloantigen ======================================= ======================================= ANKYLOSING SPONDYLITIS Assoc w/Inflammation of Axial Skeleton -clinically manifesting commonly as back pain & limited spinal ROM caused partic by Sarcoiliitis & ascending spinal inflammation ---------------------------------------- PREVELANCE: 1/100 white males < in blacks & asians Females as common as Men however females w/ less severe Dz process ----------------------------------------- DISEASE ONSET: ages 20-30 DISEASE COURSE: 1. begins w/gradual onset chronic low back pain assoc. w/morning stiffness improving w/exercise 2. Unremitting Low Back Pain for years w/severity ranging from mild->severe ---------------------------------------- SYMPTOMS: 1. Axial Skeletal Involvement a) SI Joints: typically symetrical b) Ascending Spinal Involvement: -due to enthesopathy @ annulus fibrosis attachment to Vertebrae c) Chest Pain: from inflamation at Chostovertebral, costosternal & intercostal tendons & Ligaments 2. Peripheral Joints: involved in more severe AnkSpondylitis. 3. Extraskelatal Sx: a) Eyes: Uveitis in 1/4 Pts w/AnkSpond Conjunctivitis +/- -usually self-limited w/o visual impairment b) CVS: Aortitis @ root-> Aortic Insuf - can extend to subaortic area-> heart block or mitral regurge c) Pulmonary: Fibrosis @ upper lobe resembles TB d) GU: common w/prostatitis (no symptomatic urethritis) COMPLICATIONS: 1. Fractures: spinal Fx's in pts w/ bamboo spine 2. Spondylodiskitis: disk lesions can cause erosive changes @ adjoining Verts simulating disk space infection 3. Spinal Stenosis: Sx of leg Claudication due to encroachment on the Cauda Eq. ----------------------------------------================= ====== ================= Dx: BACKPAIN: differs from mechanical etiology by AnkSpond w/young onset and worse sx on wakening & relieved w/ exercise (Mechanical BP w/late onset worsening w/activity & relieved w/rest) Familial Association PHYSICAL EXAM: SI Tenderness Decresed Spine Mobility Decresed Chest Expansion XRAYS: 1. Pelvic A-P film: - Symetrical blurred irreg SI joint margins (early signs) - Periarticular sclerosis & bone erosion +/- joint space narrowing - indicates active spondylitis Spine Films: - Ascending spinal Involvement Late finding w/inflam @ attachment of annulus fibrosis - Periostitis: periosteal new bone formation @ enthesopathic sites -most commonly @ plantar fascia & achillies tendon TX: NSIADS are mainstay - Indomethacin: used @ minimal doses (typically 150mg total daily dose) - Phenylbutazone: used as last recourse - Steroids: local joint inj only no role for systemic steroids ======================================= ======================================= REITERS SYNDROME: (Seronegative reactive arthritis) - strongly assoc w/ HLA B27 MHAntigen. -predominantly lower extremety oligo arthritis triggered by urethritis, cervicitis, or dysentary infection. **TRIGGERED BY INFECTIONS** -variably presents w/mucocutaneous lesions, inflam eye Sx, or sacroilitis --------------------------------------- Etiology:-clamydia or myoplasma urethritis -Diarrhea; Shigella, Salmon, Yersinia campylobacter CLINICAL FEATURES: -often starts @ young age -often seen 1-3wks after urethritis or dysentary -Sx occur serially not simultaneously SYMPTOMS: Arthritis: usually LE & chronic and relapsing Enthesopathy: inflam of tendons & ligs Achillies Tendonitis & Plantar Fasciitis most common Dactylitis (sausage toes) is inflam inflam of both joint & tendon common Sacroilitis: Asymetrical ivolvement of SI joit in approx 20% w/reiters. GU: urethritisis common. Also common w/ prostatitis Occular: conjuncivitis & ant uveitis is common. Conjunct is usually acute and self limited. Uveitis is often chronic Mucoctaneous: oral ulcers are typical KERATODERMA BLENNORRHAGIC: scaling plaque like lesion anywhere on body -resembles psoriasis CIRCINATE BALANITIS: painless erosion that is erythematous on glan penis CV: transient pericardial rubs, 1st degree Heart Block, & in severe cases valve insufficiency or HB. 1. cliical as above 2. HLA B27 MH antigen 3. synovial fluid mildly inflam w/neutro predominance 4. XR's w/asym oligoarticular erosions joint narrowing, & periarticular osteopenia -also periosteal bone formation -assymetric sacroiliitis DIFFERENTIAL DX: Gonococcal arthritis Gout/Pseudogout (crystal) arthritis rheumatic fever related arthritis THERAPY: 1. control pain & reduce inflamation 2. EXERCISE to preserve joints & prevent contractions 3. NSAIDs 4. Steroids 5. Azathioprine & MTX 6. **ABX do not alter course*** ======================================= Spondyloarthritis Sensitivity: probability a test is + when Dz is present (true positive) Specificity: probobility a test is neg when Dz is not present (true negative) Sens not specific: false negatives Specific not sens: false positives +Predictive Value: prob that Dz is present when test is + -Predictive Value: prob that Dz is present when test is - BioStatistics Superior Vena Cava SYNDROME (not necessarily an emergency) SMALL CELL, histo, TB, distended neck veins plethoric face swollen r arm sleep changes lightheaded cough ? Central line placement ? XR, doppler, mri, venogram -Bronch or mediastinography if possible -if small cell give chemo -if non-sm cell give RT Superior Vena Cava Stndrome SYNCOPE vasovagal vs orthostatic hypoTN vs cardiac vs CVA/TIA vs seizure ========================================= VASOVAGAL -visceral reflux -psychophysiologic -carotid sinus -glossopharyngeal neuralgia ORTHOSTASIS -hypovolmia -hypotensive drugs -neurogenic:idiopathic -pheochromocytoma -systemic mastocytosis CARDIAC -reduced CO: AS, PE, MI w/pump failure, tamponade -dysrhythmia or asystole -vertebrobasilar TIA, spasm -subclavian steal -basilar migraine SEIZURE OTHER: hypoxia, hypoglycemia, anemia hyperventilation ----------------------------------------- LABS CBC, lytes, mg, ca+, EEG, EKG, CXR, ABG 24h Holter V/Q if suspected PE Syncope Tanner - Breast Preadolescent, papilla elevation only Breast bud stage, breast & papilla elevated as sm mound, areola dia. Breast & papilla size, no separation of contours Areola & papilla form secondary mound above breast contour Mature, only papilla projects, with areola recessed to general breast contour Tanner Pubic Pubic hair no diff from abd hair. Sparse,long,slightly pig downy hair, straight or s curled, cheifly at penis base or along labia. Hair is darker,coarser, & more curled; spread sparsely over junction of pubes. Adult type hair, covered area adult Adult type hair, adult coverage. Male Genital Prepubertal. Scrotum and testes slightly enlarged; skin of scrotum reddens and changes in texture. Penis lengthens; testes and scrotum enlarge further. Penile growth continues in length and width; glans developes. Adult appearance. Mean Ages of Tanner ( 1 s.d.) Female Male Breast T2 11.2 Genital T2 11.9 Pubic Hair T2 11.9 1.5 12.3 Genital T3 13.2 Axillary Hair 13.1 0.8 14.0 Breast T3 12.4 Menarche 13.3 Pubic Hair T3 12.7 0.5 13.9 Genital T4 14.3 Regular Menses 13.9 Pubic Hair T4 13.4 1.2 14.7 Breast T4 13.1 Facial Hair 14.9 Breast T5 14.5 Genital T5 15.1 Pubic Hair T5 14.6 1.1 15.3 Ref Lee, PA: J. Adol Hlth Care 1:26,1980 PEDS Tanner's Stages TB mycobacterium tuberculosis SOURCE: human transmission - especially pulm TB pt =pts w/tubercle bacilli in sputum are most infectious) =pt in whom are TB+ by sputum cult alone are much < infectious =transmitted by aerosol drops & penetrate bronchi & lungs ---------------------------------------- Pathophysiology..................... PRIMARY INFECTION: usually latent but sometimes w/clin signs: either skin, fever, nodes, or x-ray focus SKIN RESPONSE/PPD: + after few weeks of exposure to tuberculin EARLY POST PRIMARY RESPONSE: miliary TB, meningitis or pleuricy LATE POST PRIMARY TB: lesions in lymph nodes, joints, bones or abd REAACTIVATION OF PRIMARY TB FOCUS: usually following wakening of immune fxn or exogenous reinfection --> leads to caseous focus in lung that liquifys & proliferates microbes. -once drained via bronchi-> the focus remains as a TB pulm cavity ---------------------------------------- DIAGNOSIS: SITE: Most often lungs but 30% extrapulm **Pulmonary TB**: AGE: all ages >>in 20-35 year old males Sx: persistant cough +/- fever, anorexia hemoptysis. TUBERCULIN TEST: neg result r/o dz unless pt is moribund/cachectic, has measles/pertussis virus, on steroids or in 3rd trimester of pregnancy **POSITIVE RESULT:Little Dx value since could mean either past BCG vac or old primary inf w/o active dz. SPUTUM: Imperitive to get 2 sputum smpls 2cc/each for micro smear exam **Extrapulmonary TB** Tuberculosis THROMBOLYTIC TX -------------------- May Have > 20% reocclusion rate Absolute Contraindications: -active internal bleeding -? aortic aneurysm -trauma from CPR -recent head trauma/CNS TUMOR/CVA -Ophthal bleed--?DM -BP> 200/120 -------------------- Relative Contraindications -recent trauma or surg -Hx: chronic severe HTN -active PUD -Bleeding diathesis/Anticoag Tx -sig Liver Dysfxn -prior streptokinase (particularly -within initial 6-9mo period) --------------------------- INDICATIONS: Group I: -< 70yo w/CP c/w acute MI & -ST elevation @ 2contiguos leads -Tx < 6 hours from onset ---------- Group IIa: -70 - 75 yo w/all same as Class I -all pts w/acute MI> 6h after event but w/persisting CP -pts w/re-infarct after thrombolytic therapy ---------- Group IIb: -event w/i 6-24 hours -age>75 w/same as group I -Pts w/CP & < severe EKG changes who can be Tx'd in < 24h --------- Class III -CP w/ 1)>24 hours post event 2)CP of unknown onset & now gone 3)unclear cause of CP _____________________________________ F/U after THROMBOLYSIS CLASS I: 1. Heparin Drip: start w/or after thrombolysis 2. ASA 160mg PO qD immediately 3. IV NTG or NTP for 24 - 48 hours 4. IF Pt w/HTN, reflex tachycardia or rapid A-fib : early IV B-blocker followed by PO B-blocker 5. Early CATH if evidence of Ischemia 6. B-blockers after Thrombolytic Tx from:: reduce incidence of reinfarct TIMI :: and ischemia (best if w/i 2h) IIb :: -no FXT on mortality or LVEF _____________________________________ THROMBOLYTIC TX: 1. hemodynamically unstable PE 2. rTPA within 3 days of surgery Streptokinase, Urokinase, & TPA - act to facilitate fibrinolysis by converting plasminogen to PLASMIN which hydrolyses fibrin,fibrinogen & blood coag factors - TRIALS show thrombolytic Tx superior to heparin in improving - F/U TRIALS: thrombolysis w/<longTerm residual pulm clots & pulmonary diffusion capacity than w/Heparin (seen @ 2weeks, 1yr, & 7yrs) - NO dif w/TPA by IV or intrapulm Cath - UROKINASE: direct act of plasminogen (isolated from human urine) - STREPTOKINASE: must bind plasminogen & then become plasmin activator (isolated from grpC B-hem Strep) - rTPA: "CLOT SPECIFIC" thrombolysis Activates Plasminogen-plasmin only significantly inpresence of fibrin which facilitates conversion of plasminogen, **** thus producing localized FCTs - 100mg infusion x 7 hours may be superior to 50 mgX 2hrs ---------------------------- Thrombolytic Therapy THYROID CA: very common (5%) -mortality is low ---------------------------------------- 4 Types: Papillary,follicular,Medullary, & Anaplastic all Carcinoma's 1. Papillary: 60 of all Thyroid CA -1/2 all pts <age 50 -grows slowly & spreads by lymphatics -few recurrances w/tx 2. Follicular: 25% of al Thyroid CA -more malignant than papilary CA -mets to bone, lungs & liver -50% 10yr survivalrate 3. Medullary: 5% of all Thyroid CA -from C-cells (parafollicular cells) =>calcitonin prod cells & more malig variety may secrete high calcitonin -20% are famillial 4. Anaplastic CA: 10% of all throid CA -affects older pts -highly invasive, mets widely -usually w/death w/i months of Dx ------------------------------------------- Surgery : either lobectomy or total thyroidectomy Suppression Tx: many thyroid tumors are dependant on TSH stim-> TSH is suppressed w/L-thyroxine (no effect of throidomegaly) Radioactive Iodine: follicular CA often accumlate iodine (papillary CA also) Papillary, Follicular, & Medullary tx'd w/surgery, radioactive iodine & thyroid hormone suppression Thyroid CA Thyroid Storm SX: HTN, Palpitations, febrile, Tachy High suspicion if pt is FEBRILE other SX: n/v/ :due to stress infection Lugol's Soln: K+Iodide: prevents iodine metab of thy hormones propothiouricil: ?Steroids: usually must give in myxedema coma due to immune syndrome(schmitds) from co-antibody against thyroid & adrenals (so must give steriod w/synthroid since synthroid will stim adrenals) Thyroid Storm Tia: 1/3 will have stroke in future. If tia reported within 10 days of onset patient should be urgently evaluated with probable hospitalization and either asa or heparin and ct scan, carotid ultrasound etc. Consider CEA if >50% stenosis or a compound ulcerated plaque. Most common cause of death in TIA patient is MI-about 6%/year.(STROKE 20,340 1989; Stroke 21;848, 1990;Current Therapy in Newurologic Disease-3;) CEA may be done in patients in 1 - 2 weeks if they have stable deficits and a normal ctscan. Patients whose ctscan show recent infarct should wait 6 weeks. Carotid artery stenosis of about 50% has 90% chance of progression in 6 months if accompanied by 1) Coronary Artery disease 2)LDL > 120 3) Fibrinogen level >400. Torsades stop 1a antiarrythmics may use overdrive pacer or iv magnesium due to low mg, quinidine follow corrected q-t int: corrected for rate: q-t/square root of r-r IF UNSTABLE cardiovert lidocaine ISOPROTERONOL Torsades management TRAUMA: leading cause of death in ages 1-38 ABCDE's: airway, breathing, circulation disability, evaluation Check for: Tension pneumothorax/ hemothorax, flail chest,external hemorrhage Airway: -? Shock, respiratory compromise, maxillofacial Fx -? MSchange & ? need for Cervical collar -? Intubation: resp faiure - if cervical injury->nasotracheal intubation (avoid NT intubation if facial or basalar skull Fx) SHOCK: 1.Hemorrhage: most common cause of shock -Massive external or expanding ABD must send to emergant OR -Extremity/Pelvic Fx: associated hematoma's can contain lots of blood -FLAIL CHEST: 4or more rib Fx's in 2 places on hemothorax-> discordinate chest wall movement. Tx= ETT+PEEP -TENSION PNEUMOTHORAX: diminished BS hyperresonance to percussion, & deviation of trechea contralaterally TX: place 16-18 angiocath into pleural space @ MCL/2nd intercostal space. Later place chest tube -Tension pneumothorax/hemothorax, flail chest, Pericardial Tamponade Trauma PRESENTATION: (very simillar to hemolytic uremic anemia) 5 Major Features: hemolytic anemia (nonimmune/microvasc) thrombocytopenia (purpura) fever neuro sx renal failure -------------- fever microangiopathic hemolytic anemia thrombocytopenia fluctuating neuro sx purpura renal failure +/-mucosal bleeding +/-jaundice ------------------- COURSE: fulminant w/>50% dead w/i 6weeks of Dx 1. Anemia: w/struct damaged RBCs 2. Low PLTS (<20,000) 3. Elevated RETICS 4. Elevated FSPs 5. Elevated WBC 6. Elevated serum LDH 7. Elevated indirect BILI 8. Bone Marrow w/ erythroid hyperplasia w/adequate or increased megakaryocytes 9. Azotemia 10.Urine w/ RBCs,Bact,Hgb,& gran casts PATHOPHYSIOLOGY: ?? loss of endotheial antiPLT aggregation factor (prostacycline). Leads to thrombosis plt consumption. -give plasma to replace prostacycline -give prostacycline -give steroids +/- -give gamma globulin +/- TUMOR MARKERS AFP HBsAg+, hepatoma, testicular CA, gestational CA bHCG testicular CA, gestational CA LDH testicular CA CEA colon CA PAP (acid phos)- prostate PSA prostate CA125 ovarian CA15-3 Breast CA CA19-9 Pancreatic CA possible markers MCA (mucinous carc assoc ag) MAM-6 (epithelial membrane ag) MSA (mamary serum ag) TAG 75.4 (tumor assoc glycoprot) CA50 ( Tumor Markers UREMIA signs & sx assoc w/prog inability to perform renal excretory, secretory, & regulatory fxns. SX: anorexia, N/V, lassitude, pruitis, twitching, anemia, bleeding CAUSE: unknown - suspects are: (phenols, org acids, urea, guanidine & middle molecules w/mw 500-200) -Protien Restriction (0.6g/kg/d) may acutely BUN & retard progression of RF (controversial) Uremia Dx./Tx. VASCULITIS: BY VESSEL SIZE: --------------- Small Vessel: Hypersensitivity Vasc Wegeners Granulomatosis Allergic Angiitis (churg-strauss) Sm/Med Vessel:PAN Med/Lg Vessel:Giant Cell Arteritis Large Vessel: Takayasu's Arteritis --------------------------------------- ARCH: giant cell & Takyasus(pulseless) Takyasu:arm claudication/pulseless acutely systemic sx:aches etc SYSTEMIC VASC: All w/ANCA (PAN,Wegeners,churgSt) MEDIUM VESSEL PAN:deep,organ inv5skin etc WEG:renal & pulm findings c-ANCA spec. for wegeners p-ANCA spec. for PAN SKIN INVOLVEMENT: primary -known inciting -unknown causes (HSP) BY PATHOLOGIC CLASSIFICATION: ----------------------------- 1. Systemic Necrotizing Vaculitis: a)PAN b)Allergic Angiitis(churg-strauss) c)Polyangitis Overlapp Syndrome 2. Wegeners Granulomatoses 3. Giant Cell 4. Hypersensitivity Vasculitis a)Serum Sickness b)Henoch-Schonlein Purpura c)Drug-induced Vasculitis d)Vasculitis of Infection e)Vasculitis of Neoplasm f)Vasculitis of Coll Vasc Dz --------------------------------------- ======================================= VASCULITIS ----------------> --------------------------------------------------------- ------ ------------------------------ CLIN SYND FEATURES VESSEL SIZE CELLULAR INFILTRATE DX TX ========================================================= ====== ============================== HYPERSENS predom skin SMALL(caps Leukocytoclastic Skin Bx support VASCULITIS involvent (& venules) Vasculitis visceral involvment minimal & self-limited --------------------------------------------------------- ------ ------------------------------ CLIN SYND FEATURES VESSEL SIZE CELLULAR INFILTRATE DX TX ========================================================= ====== ============================== POLYARTERITIS multi-system SMALL & MED Necrotizing Organ Bx 1)Steroids NODOSUM major arterial ARTERIES Arteritis @ or Visceral 2)Cytotoxic ischemic lesion sparing Vessel Branch Angiography toxic Rx lungs & spleen Points Rx's & nodose skin lesions are uncommon ========================================================= ====== ============================== ALLERGIC 1.Often Hx of VARIABLE Granulomas Lung Bx 1)Steroids ANGIITIS & Allergies & Asthma VESSEL SZ w/eosinophils 2)Cytotoxic (Churg- 2.+ Lung Involvement caps, venules Rx Straus Dz) 3.+ Blood Eosinophilia & arterioles ========================================================= ====== ============================== WEGENERS 1. Resp Tract Invol. SMALL Necrotizing Lung Bx 1.Cyclo- GRANULOMA- 2. +/- Prominant arteries Granulomas in Phosphamide TOSIS Renal Impairment veins up & low airways, 2.Stroids lungs & kidneys ========================================================= ====== ============================== GIANT CELL Assoc w/PMR LARGE Giant Cell & Temporal Steroids ARTERITIS usually elderly especially Mononuclear Art Bx (temporal high ESR temporal infiltrates arteritis) Sx often relate artery to cranial arts ========================================================= ====== ============================== TAKAYASU's occurs in young LARGE Giant Cell & Aortography ARTERITIS females(often asian) Aortic Mononuclear 1.Steroids Sx= Large Vessel Arch infiltrates 2.Vasc claudication Surgery ========================================================= ====== ============================== RHEUMATIC Overlapp w/RA, SLE SMALL& Variable Bx of 1.Steroids VASCULITIS & others MEDIUM involved 2.Cytotoxins ========================================================= ====== =============================== organs Vasculitis types,causes Risk factors Surgery Orthopedic, thoracic, abdominal, and GU procedures Neoplasms Pancreas, lung, ovary, testes, urinary tract, breast & stomach Trauma Fractures of spine, pelvis, femur, tibia Immobilzation Acute MI, CHF, CVA, postop convalescence Pregnancy Estrogen use Hypercoagulable states Deficienciesof antithrombin III, protein C, or protein S; circulating lupus anticoagulant; myeloprolifer- ative disease; dysfibrinogenemia; DIC Venulitis Thromboangiitis obliterans, Beh ets's disease, homocystenuria Previous DVT Diagnosis Bedside difficult, Unilateral extremity swelling IPG(impedence plethysmography) Predictive value for PROXIMAL thrombi ~90%, much leS for calf Duplex doppler U/S Predictive value for PROXIMAL DVT approaches 95% I125-fibrinogen scan detects >90% of CALF vein thrumbosis, less sensitive for proximal thrombi, takes 48-72 to become positive Differential DX Muscular trauma or hemorrhage Ruptured popliteal cyst lymphedema postphlebitic syndrome nerve compression arthritis tendinitis fractures arterial occlusive disorders treatment PROXIMAL DVT Prevention of pulmonary embolism is major goal Nursing Bedrest with extremity elevated until edema and tenderness subside Heparin Target aPTT 2 May cause thrombocytopenia(5%) lead to arterial thrombosis & ischemia Warfarin Target 4-7s beyond control or INR 2-3 Overlap therautic level with Heparin 48-72 Treat 3-12m FIRST episode if malignancy and hypercoagulable state ruled out, indefinite RECURRENT DVT and if malignancy and hypercoagulable state NOT ruled out ISOLATED CALF VEIN DVT treatment is controversial as incidence of PE is low. Risk of propagation to proximal DVT is 20%. Choice Anticoagulate for 6WEEKs or follow with serial noninvasive tests PROPHYLAXIS When: Venous Thrombosis VERTIGO ??TIA ??Acoustic Neuroma Nystagmus to side of lesion Menieres Dz: hydrops of endolymph or too much endolymph volm Labyrythitis: most comonly viral & <common in the elderly --can be from vasculitis or neuritis ??Aminoglycoside Ototoxicity ??Lacunar Infarct: deep internal capsule w/infarct not reaching cortex -usually from thrombi not emboli -usually assoc w/HTN Vertigo causes Vital Signs Pediatric AGE Mean Pulse Resp Blood-Press Premature 125/75-175 30-60 35-56 syst Newborn 140/90-190 30-60 75/50 1-6 mo 130/85-175 30-40 80/46 6-12 mo 115/75-155 24-30 96/65 12-24 mo 110/70-150 20-30 99/65 2-6 yr 105/70-140 20-25 100/60 6-12 yr 95/65-125 16-20 110/60 >12 yr 82/57-107 12-16 120/60 PEDS vital signs WIDE COMPLEX TACHYCARDIA (VT&SVT) SVT w/wide Complex: 1. BBB (like VT @ fast rates) may unmask w/vagal maneuvers 2. WPW: accesory pathwayst 1. Fusion or capture beats 2. V-Tach/SupraV-Tach. POST INFARCT VENTRICULAR ARRYTHMIAS --------------------------------------- VFIB ~85% of all arrythmias in acute MI -VT, PVC or SVT only 10%, -bradycardia's= 5-6% AIVR: most common after thrombolysis -due to ventricular automaticity -70 to 100 beats/min -unclear why prolonged AIVR can lead to VFIB or VT VT: monomorphic- usually from reentry VFIB: highest risk w/i 4hours of MI - nonlethal VFIB "in the acute seting" <48h post MI, doesn't influence post discharge cardiac mortality or rate of sudden death PROPHYLACTIC LIDOCAINE: studies show: 1. 1/3 decreased rate of postMI VFIB 2. increased early mortality 3. no reduction in overall risk from ** arrythmic event (also increased tendency to cause CNS & cardiac side FXTs in elderly or pts w/ LV dz) -Tx should last no longer than 24hour WARNING PVCs: no evidence that Tx prevents VFIB B-BLOCKERS: increase threshold for VFIB in "acutely ischemic" myocardium - arrythmia mortality is not influenced by early b-blockade in acute MI LATE VENTRICULAR ARRYTHMIAs >48-72h rated as benign,potentially lethal, or lethal 1. Benign: pts w/o sig HDz & nml LV function who have minimally or asymptomatic PVCs or nonsustained VT(<30sec). -Pts @ very low risk for sudden death & Tx is only for Sx 2. Potentially Lethal: in pts w/organic HDz who have minimally or asymptomatic PVCs or nonsustained VT(<30sec). -24h Holter 7-14d post MI w/PVCs (>10/hour) or nonsustained VT predicts increased 1&2 year cardiac & sudden death mortality TX: B-blockers, quinadine, procainamide & disopyramide. -none w/proven risk/benefit 3. LETHAL: VFIB or Sustained VT(>30sec) w/hemodynamic compromise & requiring cardioversion -typically seen in pts w/HDz w/LV dz -Most post MI sudden death is heralded by sustained VT -VT or VFIB >2d postMI-> high risk for recurrance or sudden death. -empiric antiarrythmic Tx associated w/ 80% one year mortality -holter monitoring < accurate than EPS for guiding Tx -EPS guided ablative surgery may remove reentrant substrate -implantable defibrillator; most effective TX - require thoracotomy once stable implantation - survival= 98% @ 1yr & 95% @ 5yrs Signal Averaging EKG: detects & quantifys late potentials from arrythmogenic myocardium in ST segs (areas w/high potential for reentry). **late potentials rarely seen in nmls & usually seen in pts w/VT -high negative predictive value!! -mediocre pos predictive value MI, typical V. arrythmias after WEGENERs GRANULOMATOSIS system necrotizing vasculitis w/ -necrotizing granulomas of lung as well as nose, throat, & bronchi -focal necrotizing glomerulonephritis -multisystem small vessel vasculitis Etiology: thought to be hypersens rxn to unknown inhaled antigen. ?HLA B8 ag -pulm lesion in 95% cases. -Lung lesions usually multinodular, bilateral (+/- granulomas). ->50% w/elevated circ immune complex RF and IgG,IgA is common -PMNs w/antineutrophil antibody (ANCA) -34% w/radiographic + & biopsy + pulm lesions w/ no symptoms CLINICAL Sx: -TRIAD: upper & low pulm infil & glomerulonephritis -unlike GOODPASTURES usually without DIFFUSE pulm infiltrates DX: by Bx of lung or kidney. - ANCA: may be from blood or broch washings TX: very sensitive to cyclophosphomide +/- steroids -unTx'd disease is often fatal within months t years -Dz relapse in 50% pts Wengers Granulomatosis WILSONS DISEASE Autosomal Ressesive Dz w/copper deposits which can progress to fulminant hepatic failure. Other visceral damage may occur in the brain, kidneys and Cornea (Kayser-Fleischer rings). Adult Dz often w/CNS Involvement DX: made by serum Ceruloplasmin Also w/ Hepatic Copper on Bx TX: W/ D-Penicillamine Wilsons Disease SPINAL CORD/ROOT COMPRESSION ________________________________________ NERVE ROOT INJURY: sensory supply ----------------- Angle of Jaw & Back of Scalp:------>C2 Neck area Front & Back to Scapula-->C3 Over SCAPULA & Top of Chest/Back--->C4 Lat Upper Border of Arm / Deltoid:->C5 Lat Forearm + thumb:--------------->C6 Over Tricepts, Mid Palmer Forearm to between first two fingers:---->C7 Medial Forearm + Little Finger----->C8 Axilla down to Olecranon----------->T1 Nipples---------------------------->T4 Umbilicus-------------------------->T10 Upper Lat Thigh Front & Back------->L2 Lower Med Thigh to Ant/Med Knee:--->L3 Below Med Knee to Medial Malleolus->L4 Below Lat Knee to Mid Shin Across to Top of Medial Foot to Arch-- -->L5 Mid Lat leg to lat Malleolus to Lat Foot -across toes & most Lat Sole->S1 Behind Knee------------------------>S2 ======================================== PERIPHERAL NERVE ASSOCIATED AREAS Ant Chin/Jaw up to Front of Ear & Midline of Ant Neck--->Mandibular N. Angle of Jaw to Ear: Gt.->Auricular N. Forehead----------------->Ophthalmic N. Above nipples to Neck---->Supraclav. N. Lat upper Arm------------>Axillary N. Med upper Arm->Medial Brachial Cutan N. Tricepts------>Post Brachial Cutaneous N. Lat Forearm-->Lat Antebrachial Cutan. N. Med Forearm-->Med Antebrachial Cutan. N. Middle of Back of Forearm-->Post AntiB N. Mid 3rd Finger to Thumb on Back of Hand \------------------> Radial Nerve Mid 3rd Finger to Pinky on Front & Back \------------------> Ulnar Nerve Palmer thumb to mid 3rd Finger->Median N Lat Upper Leg----->Lat Fem Cutaneous N. Ant Thigh--------->Ant Fem Cutaneous N. Medial top 1/2 of thigh--->Obturator N. Back Upper Leg--->Post Fem Cutaneous N. Lat Lower Leg---->Lat Sural Cutan N. Med Lower Leg---->Saphenous N Mid-Back of Calf->Sural N. Top of Foot--->Superf. & Deep Peroneal N Sole of Foot->Plantar branch of Tibial N. ======================================== PATTERNS OF VISCERAL PAIN REFERRAL: Viscera Roots Pain Referred TO ======= ===== ================ Heart t1-5 chest & arms Stomach t5-9 xyphoid region Duodenum t6-10 xyphoid->umbilicus pancreas t7-9 upper abd & back Gallbladder t6-10 rt upper abd appendix t11-12 RLQ Kidney t9-L2 CVA & penis prostate S2-4 glans & Lumbar area ======================================== Sympathetic Afferents to Dermatomes: (SYMP COL= C8->L2) ---------------------------------------- C8-----------------> C2-C4 T1-T3--------------> Trigeminal Area & C2-C4 T4-----------------> C5-C6 T5-T7--------------> C5-T9 T8-----------------> T5-T11 T9-----------------> T6-L1 T10----------------> T7-L5 T11----------------> T9-S5 T12----------------> T10-S5 L1-----------------> T11-S5 L2-----------------> T12-S5 ======================================== Nerves Spinal levels Unsuccessful Emergency Medical Resuscitation. NEJM 325:1393 1993 Outcome of Cardiac Arrests attempted outside of Hospital arriving without vital signs and requiring further resuscitaion. 185 cases were reviewed to assess efficacy & cost effectiveness of continued ACLS beyond unsuccessful resuscitation. Study cases from between 10/85 & 6/87 Inclusion Criteria are: - arrival to ER by ambulance - no pulse or respirations - initial resuscitation outside hosp - continuation of ACLS on arrival - All pts included regarless of primary cause of arrest (cardiac,resp,OD) Exclusions: - Arrest due to trauma or drowning - pt age under 16 years Witnessed arresets & Bystander initiation of CPR could not be accounted for with accuracy Resuscitation included either BLS or ACLS, Costs were collected & adjusted to 1991 stanedards. Fees for professional services were excluded OUTCOMES: - 9% successful resuscitations (no sig dif in age,race,arrest cause) - 16/185 survived resusitation - 0/16 survivers lived to be discharged - 1/16 survivors regained consciousness - all survivors had primary cardiac events prior to resuscitation except one which had a subarachnoid bleed - In Survivors F>M (no dif w/age/cause) - Improved survival if Hx of CHF - Survival not improved whether quicker response or use of ACLS - No resuscitation was sucssessful if EMS response was > 10min - Survival declined if EMS traval time to scene of arrest was > 8min (not sig) - Survial was improved when < 15min passed before pt presented to ER - Avg time from EMS call to ER was >35 min - Of the 16 pts resusitated: - mean hosp course 12.6 days (1-132) (1 comatose pt lived 4 months) - Total cost for hospitalization of the 16 survivors was $180,908.00 ($11,307/pt) - Costs for the unsuccessful resuscitation attempts were estimated at between 100,000 & 150,000. ===================================== TAKEHOME: We need to increase our resourses for fast effective response to cardiac arrest in the field and use these data to back off of treatment in the face of futility when adequate resuitation in the field has failed. ===================================== DISCUSSION CPR is 30 yrs old, initially intended as a maneuver for acute "REVERSIBLE" arrest, now ACLS is used more widely. In Hospital resuscitation is limited, especially in the elderly or anyone with severe underlying disease (Renal Failure, Pneumonia, Cancer, Sepsis) Most often, Arrests w/VF & CAD Improved Outcome: Witnesses CPR started by a bystander Initial rytmem of VF or VT early defibrillation In Seatle (w/quick response time & extensive lay education) survival of pts w/ VF arrests occurring outside hosp is 30% who live to discharge. 350,00 cardiac arrests annually in US > 2/3 occurr outside of Hospital eq>It is known that cardiac arrest that lasts > 15min is an independant predictor of death Predominant rhythems in field were VT/VF & were EMD & Asystole in ER -prob reflects EMD & Asystole as terminal rhythems with poor prognoses. The only predictor of positive outcome from cardiac resuscitation is total resuscitation time of < 15 min Kellerman et al (1988) found 1.4% of 281 pts survived to Discharge after arrest in feild. "There is no ethical imperitive requiring physicians to perform procedures in the absence of at least a modicum of medical benifit."(NEJM 315:1347-51, 1986) CPR invented in 1960: first trial showed 70% success rate.(JAMA 173:1064-7 1960) NEVER REPRODUCED Most studies show survival rates < 15% (unless Pts w/CA,chronic illness or repeated arrests are excluded) - Initial Success rate = 16 - 45 % Suurvival to Discharge = 5-23% - while many studies show successful resuscitation in > 30-40% of all arrests, survival to hospital Discharge is always < 15% with sig proportions leaving without full mental or physical function. - Pts w/metastatic CA, Acute CVA, sepsis or pneumonia do particularly poorly. Patients & families are often in the position of choosing between A CHANCE OF LIFE OR CERTAIN DEATH. These people do not know the details of an ICU or the limitations and ramifications of resuscitation. PT Autonomy calls for patitients to have the option of refusing any TX. - They do not have the right to demand a nonbeneficial or harmful procedure. Too often CPR is offered on te basis of compassion for patients who cannot reject resuscitation when it requires accepting the futility of any further medical intervention in bringing a cure. "There are better ways to deal with the distress of death than to offer CPR as a high tech placebo." "The issue of patient autonomy is irrelevant when CPR has no potential benefit. The physicians duty to provide responsible medical care precludes CPR, either as a routine process in the absense of a desicion by a patient or as a response to a patients misguided request for such treatment in the absense of adequate information. In such cases, it is not the physicians responsibility to offer CPR. Both physicians and patients must come to terms with the inability of medicine to postpone death indefinitely. CPR - success Vs Failure RISK: Needlestick 0.3% infected male to female < 50% STAGING: majority pt ASx Absolute CD4(helper) # (nml=350-1200) PERSISTANCE STAGE: low viral product w/seroconnversion CD4 to 200 range plateau for to several years CD4 > 500 low risk for opp infection CD4 <50: High risk for opp inf (follow trend since labs vary by 20-30%) B2 microglobulin level -sm mw prot synth & secreted by cell involved w/ HLA I maj histocomp Ag's (by interferon and infections) -HIV+ & +B2MG = inc risk of AIDS (>5mg/dL) HIV p24 level: Eliza for p24 Ag (not fed licensed) In late Dz pt may make more P24Ag HIV Ag & P24 may be detected prior to seroconversion Plasma HIV co-culture ======================================= LABS: ELIZA & Western Blot ELIZA: Tests for HIV Ab: (tests against HIV Ag) False +'s occur partic if +ANA,RF,cryoglobs,or PREGNANT False -'s in early HIV <12mo due to lack of Ab production High + pred value in high incidence population inexpensive & widely available (high index of suspicion makes +result not repeated due to impr ELIZA) (if low seroprevelance group :+ is likely false lab error) WB: IMMUNOBLOT: viral Ag 4% false pos (ususally screened out by eliza) High + pred value in high incidence population More Expensive Than ELIZA variable reproducibility indeterminant either: -early disease or crossRx AB re check at 3months PT EVAL: ? VD hepatitis, toxoplasma, ? where do they live, ?pets 1st tests: PPD, toxo serology, Hep screen, VDRL CD4 T4 helper cell count if >500 check q6months if 200-500 begin AZT & check q6mo if close to 200 check q3months if <200 begin PCP prophylaxis & re-check q3-6 months (infection risk @ CD4 < 200) TX: TX for CD4 < 500 AZT: well tol if used early DATA: improves survival decreases opp infections increases CD4 transiently Decreaes prgression to AIDS Dose:500mg qd in 100mg po q4 TOXICITY: incr MCV in everyone anemia, leukopenia DDI:didanosine VIDEX -raises CD4 count -survival studies not in yet -thus only for those who cant take AZT TOXICITY:-pancreatitis (9%) can be fatal -priph neuropathy (34%) DOSE: must chew tabs >75kg 300bid <50kg 125bid 50-74kg 200bid PCP DZ TX: -bactrim: 15-20mg/kg/d x 3wks -pentamidine: 3-4mg/kg/d x 3wks For mild to mod DZ: -Dapsone/TMP: 100mg qd & 20/mg/kg/d Experimetal tx: clinda/primiquine trimetrexate/leucovorine STEROIDS: for po2<75 on RA PCP PROPHYLAXIS:(for all w/CD4<200 or if pt has had PCP) BACTRIM: 1 ds poqd PENTAMIDINE AERO: 300mg q month CRYPTOCOCCAL MENINGITIS: Ampho B:in initial episode FLUCONOZOLE: for chronic suppression (200mg qd) TB: if HIV+ - 10% chance of reactivation each year -if PPD+ >5mm INH prophylaxis TOXOPLASMA: 95% is recrudesence 80% relapse if not tx Typically: focal brain lesion (50-70% are toxo - others are: lymphoma, PML, herpes, TB,Kaposes -lesion typically by basal ganglia .5-11.6cm vs 30cm for lymphoma) TOXO TX: - Sulfadiazine/PYM/folinic Acid - Clinda/PYM - Azithromycin/clarithromycin/???? HIV PNEUMONIA MALIGNANCY:lymphoma CVD AdenoCA SARCOID PROTAZOA: PCP VIRAL: Influenza RSV,Adenovirus EBV, Hsv, VSV, FUNGAL:Crypto Histo Blasto Aspergillis BACTERIA: Mycoplasma Legionella HFlu, Pneomcoccus, TWAR & other Chlamydia Psitticosis MAI/TB PARASITES: strongaloidies DX: cults, cold agglut, legionella, CMV/viral studies, CD4 (majority of PCP w/CD4<200) Broch Specimen: for silver stain AFB, Viral, Fungal TX For PCP: sulfa better than pentamidine since faster acting than pentamidine & less expensive. --------------------------------------- DIARRHEA bacteria: salmonella, shigella, camplyo, yersinia, C-dif, listeria, MTB/MAI protozoa: entamebae histolytica cryptosporidium, microsporidiosis isospora(tx w/bactrim), giardia, strongoloides virus: CMV, Adenovirus malignancy: lymphoma (sm bowel), KS drugs: ddi, megase, fungal: candida, histo(if from midwest) --------------------------------------- \ HgB /Segs/bands/lymphs/monos/Basos/Eos \ / CBC: WBC ----- MCV-MCH-MCHC / \ / HCT \Platelets / BUN Electrolytes: Na+ | Cl- / (and SMA6) ------------------Creatinine K+ | Bicarb \ \ Glucose Lab Value Shorthand All Notes MEDICAL.NDB DOCUMENTATION NOTE ====================================================== this file contains brief notes on about 150 different medical subjects. They are the combined work of three different physicians who have contributed their own personal notes on various topics. I will not attempt to differentiate the authors in the notes themselves. Rather, I will simply credit each equally. They are: Scott Fishman, MD Alan Galitz, MD Robert S. Williams, MD These notes are copyrighted freeware. The users are free to use and modify this file to suite their own personal information needs. This file and its contents may not be sold for profit. This file may be transferred to others in either its original form or in modified form as long as this note is included. The authors make no claim whatsoever about the suitability of this software for any purpose. The authors take no responsibility for any medical decisions made, or the outcomes of any medical decisions made, based on the data contained in this file. Every effort has been made to ensure that the information is of good quality, but it is the users' responsibility to verify the data before using it. If you wish to contribute your own work to this Notetaker File: Please send the notes in .NDB format for inclusion in the collection. They will be merged into this file and included in the next version uploaded. Additionally, you will be added to the list of authors. You may submit contributions by either Binary Email or by mailing me the file on a 3.5" MSDOS diskette. Robert S. Williams, MD 612 W. Franklin St. #7D1 Richmond, VA 23220 Tel: (804) 788-0746 CIS UID: 76167,2773 Internet: 76167.2773@compuserve.com Copyright 1994 Robert S. Williams, MD. All Rights Reserved. aaa READ ME FIRST