MCCQE 1 STUDY GUIDE WITH COMPLETE SOLUTIONS

HERPETIC WHITLOW Painful grouped vesicles on an erythematous base located on the distal finger Cause: Infection with HSV Treatment: Self-limiting disease Antiviral (e.g., acyclovir) may be beneficial ONYCHOCRYPTOSIS/ INGROWN NAILS Inflammation and soft tissue hypertrophy +/− secondary infection occurring when the lateral edge of the nail plate impinges on the nail fold ONYCHOCRYPTOSIS Cause: Onychomycosis Incorrect technique of nail cutting Repetitive trauma Poor foot hygiene; poorly fitting shoes Treatment Barrier placement between nail plate and nail fold Excision of the portion of nail plate pressing on the nail fold +/− Antibiotics Biphasic Anaphylaxis Recurrence of Sx 4 to 32 h (mean 10 h) after the initial episode. Occurs in up to 20% of patients and is due to the release of 2◦ mediators and the late-phase response. Protracted Anaphylaxis Refractory Resp distress or hypotension despite appropriate medical Rx. What Saves Lives? EPI, EPI, EPI Adults: 0.3 to 0.5 mg IM Children: 0.01 mg/kg IM I V EPI: 0.1 mg, dilute 0.1 mL 1:1,000 in 10 mL N/S Give 1 to 2 mL/min All patients presenting with signs or Sx of anaphylaxis get: • Measures to stop any continuing Ag exposure • Two large bore I Vs • Supplemental O2 • Cardiac and O2 sat monitoring • EPI IM or I V • Methylprednisolone 125 mg I V • Diphenhydramine 50 mg I V + ranitidine 50 mg I V MINOR BURNS • cleaning with soap and water or dilute antiseptic solution. Td immunization prn topical Abx: 1%silver sulfadiazine(Dermazine) , bacitracin (Baciguent), or bacitracin/neomycin/polymyxin B (Neosporin ointment). Occlusive, clean dressings should be applied regularly. Parkland Formula Fluid required (ml of RL) = 4 × kg body wt × TBSA • 1/2 given in first 8 h from time of injury, 1/2 given in next 16 h Anticholinergic Antihistamines, TCAs, phenothiazines, atropine Cholinergic Insecticides, nerve agents, nicotine, pilocarpine, urecholine Sympathomimetic Cocaine, amphetamines, MDMA (ecstasy), ephedrine, theophylline Opiate/sedative Heroin, morphine, benzodiazepines, barbiturates, meprobamate, EtOH Hallucinogens LSD, mescaline, phencyclidine, psilocybin CVS β-Blockers, CCBs Serotonin MAOI, SSRI, meperidine, TCA, L-tryptophan Cellular CO, H2S, cyanide TCAs Amitriptyline, doxepin Simple asphyxiants CO2, inert gases Drugs inducing metabolic acidosis (BP usually low) Ethanol, methanol, ethylene glycol, ASA, NSAID, tylenol Anticholinergic ''hot as a hare, dry as a bone, red as a beet, blind as a bat, and mad as a hatter'' • ↑ Temperature • Possible ↑ HR • Dry mucous membranes • Erythematous • Mydriasis • Disoriented, agitated • Reaching blindly for objects • Large ODs can lead to depressive state (sedation, coma) • ↓ bs and ↓ GI motility • Urinary retention Sympathomimetic ''fight or flight'' • ↑ HR • ↑ BP • ↑ Temperature • Wet mucous membranes • Diaphoretic • Erythematous • ↑ Psychomotor activity • Mydriasis • Agitated, ' reved up'' Serotonin ''wet dog shakes'' • ↑ Temperature • Whole body tremor • May be diaphoretic; shivering; fever; diarrhea • Altered or normal mental status • ↑ Reflexes • ↑ Tone Cholinergic ''secreting from every orifice''/ ''wet from head to toe'' • ↓ HR • May see ↓ BP • May see ↓ RR and Resp failure • Diaphoretic• Lacrimation• Salivation • Fasciculations • Miosis common, may see mydriasis • Altered or normal mental status • Nausea + vomiting • Defecation • Urination • Bronchorrhea Opiod or sedative/hyponotics ''depressed all over'' • ↓ RR• ↓ HR• ↓ BP • ↓ Temperature • Range from stuporous/drunk to coma • Miosis, possible nystagmus • ↓ LOC POISON labs: • Routine: CBC, Lytes, gluc., ASA + acetaminophen + EtOH levels, blood gas, serum Osm, ECG • Additional tests to consider: INR/PT, LFTs, RFTs, specific drug levels, β-HCG if fertile female, urine tox screen (often unhelpful from a Tx perspective, but can identify other drug exposures) Consider AXR indications = ''CHIPES'') ''CHIPES'' Calcium, Chloral hydrate, CCl4 Heavy metals Iron Potassium Enteric-coated Salicylates Elevated AG Acidosis ''MUDPILES'' Methanol Uremia Diabetic ketoacidosis/alcoholic ketoacidosis Paraldehyde Isoniazid, iron Lactate Ethylene glycol Salicylates Normal AG Acidosis ''HYPERCHLOREMIC'' Usually due to ++ saline administration because of high Cl content Narrow AG ''HARDUPS'' Hyperventilation Acetazolamide, acids, Addison disease Renal tubular acidosis Diarrhea Ureterosigmoidostomy Pancreatic fistula Saline Gastric Decontamination General principle: ↓ absorption or ↑ excretion of ingested poisons. Generally only effective if time since exposure ≤2 h or if delayed toxicity expected. There is limited data to support most methods of gastric decontamination. Activated Carchoal may have some benefit in specific instances Enhanced Elimination HemoDialysis or hemoperfusion as well as alkalinization of urine or diuresis are used to enhance elimination. Methanol • Delayed presentation common (can be 6-24 h) • OG, AG may be normal or elevated • ↓ LOC, ataxia, stupor, lethargy, coma • Visual complaints common: blurry vision, ↓ acuity, ''snowstorm'' perception • CNS effects: ↓ LOC, Parkinsonism in late stages Methanol Tx • EtOH has greater affinity for EtOH dehydrogenase and saturates it, preventing breakdown of methanol into its toxic metabolites • Fomepizole has even greater affinity and less S/Es than EtOH • NaHCO3 used for acidemia • Consider folate supplementation Methanol Metabolism to formic acid and elimination of folate stores leads to toxicity. Metabolism occurs by EtOH dehydrogenase in the liver Salicylates • Early: Resp alkalosis due to stimulation of CNS chemoreceptors • Late: metabolic acidosis • Severe toxic dose 300 mg/kg, toxic dose considered to be 150 mg/kg Salicylates • Symptom onset 3-8 h after ingestion • Dehydration common • Adults: mixed acid-base with Resp alkalosis and metabolic acidosis • Children: metabolic acidosis only; indistinguishable from Reye syndrome • Salicylate levels helpful to determine severity Salicylates • Whole Bowel Irrigation or Act