Card 1Coronary Territories
Which leads show ST elevation in a SEPTAL infarct, and which artery?
V1 to V2. Left anterior descending (proximal septal branches).
How to use this page. The guide sections cover everything the practice form tested, with pearls, traps, and the session's misses called out. Below them, the full flashcard deck: in Quiz mode the backs hide until you click a card. The Qbank holds all 217 cards reauthored as board-style questions.
1. How This Form Tests
- "Most appropriate NEXT STEP" is the dominant verb. It rewards the immediate threat-to-life action, not the definitive one. "Definitive management" flips the same facts to the other answer (needle decompression vs chest tube).
- Diseases repeat across competency domains. This form asked pneumothorax five times, hypothyroidism four times, GERD three times, CDH twice, scoliosis twice, rotator cuff twice, TOS twice. Expect one entity drilled from diagnosis, management, and OMM angles.
- Read the stem before the exhibit. Several image questions (CDH, STEMI angiogram) were fully answerable from the text. The film usually confirms what the vignette already said.
- OMM stems carry decoy findings. Four or five structural findings are listed; usually one matters. Autonomics questions embed the answer's level and pad the rest.
- Stated negatives are answers. "No inflammation of the vaginal walls," "no desquamation," "trachea midline," "denies scotomas": the writers put negatives in to kill specific options. Read what each test was negative FOR.
2. OMM
2.1 The autonomics master table (7 questions on this form)
Every autonomics question ran the same two filters: which organ, then which division. Each wrong option got exactly one filter right.
| Region / Organ | Sympathetic level | Parasympathetic source (treat at) |
|---|---|---|
| Head and neck, upper airway | T1-T4 | Vagus (OA, AA, C2); sphenopalatine ganglion for nasal mucosa |
| Heart | T1-T5 (left-sided predominance) | Vagus (OA, AA, C2) |
| Lungs | T2-T7 | Vagus (OA, AA, C2) |
| Esophagus | T2-T8 (distal / GE junction T5-T6) | Vagus |
| Stomach, liver, gallbladder | T5-T9 (stomach left, liver/GB right) | Vagus |
| Small intestine | T9-T11 | Vagus |
| Appendix / cecum / ascending colon | T10-T11 | Vagus (to splenic flexure) |
| Kidney and upper ureter | T10-L1 | VAGUS (the one people misfile as sacral) |
| Descending / sigmoid colon, rectum | T12-L2 | Pelvic splanchnics S2-S4 (sacral rocking) |
| Bladder, lower ureter, pelvic organs | T11-L2 | Pelvic splanchnics S2-S4 |
| Uterus / ovaries | T10-L2 | Pelvic splanchnics S2-S4 |
| Upper extremity | T2-T8 | NONE. Extremities are sympathetic only |
| Lower extremity | T11-L2 | NONE |
The two engineered traps: (1) the sympathetic level of the right organ offered when the question asks parasympathetic, and (2) sacral techniques offered for the kidney or stomach. Vagus reaches the kidney; the sacrum does not.
2.2 Direct vs indirect: the technique direction table (4 questions)
| Technique | Position into | Activating force |
|---|---|---|
| Muscle energy (direct) | Restrictive barrier, all 3 planes | Patient contracts TOWARD the freedom/ease, physician resists (postisometric relaxation), then engage new barrier |
| HVLA (direct) | Restrictive barrier | Physician thrust |
| FPR (indirect) | EASE, after flattening the AP curve | Compression or torsion, hold 3-5 s |
| Counterstrain (indirect) | Position of comfort, SHORTEN the muscle | Hold 90 s (120 for ribs), SLOW passive return |
| Still (combined) | Starts INDIRECT at the ease, adds compression, then carries THROUGH the barrier to finish direct | Compression/traction + arc of motion |
| BLT (indirect) | Balance point of ligamentous tension | Respiratory cooperation |
For an ESlRl segment: ME positions into flexion, right SB, right rotation (barrier) and the patient pushes toward extension-left-left. FPR and Still both START at extension, left SB, left rotation (ease). The form asked this three ways and the FPR and Still answers were identical.
2.3 Viscerosomatic three-axis check
Session miss (gallbladder). A viscerosomatic answer must match on all three axes: LEVEL (gallbladder T5-T9, so T7, not T4-T6), TYPE (viscerosomatic reflexes are TYPE II: single segment, rotation and sidebending SAME side; a type I neutral group curve is postural, not visceral), and SIDE (rotation toward the involved organ: gallbladder right, stomach/esophagus left). Right neighborhood on level alone still loses.
2.4 Chapman points tested
| Organ | Anterior point |
|---|---|
| Esophagus | ICS 2, near sternum |
| Upper lung / lower lung | ICS 3 / ICS 4 |
| Stomach hyperacidity | ICS 5, LEFT (GERD question) |
| Liver / gallbladder | ICS 5-6, RIGHT (the mirror trap) |
| Stomach peristalsis | ICS 6, left |
| Pancreas / spleen | ICS 7 right / ICS 7 left |
| Duodenum | ICS 8, RIGHT, costochondral (duodenal ulcer question) |
| Colon | Iliotibial band (NOT the chest wall) |
2.5 Acute vs chronic tissue texture (2 questions)
| Acute | Chronic | |
|---|---|---|
| Texture | Boggy, edematous (bronchiolitis stem: "warm, boggy T1-T4") | Fibrotic, ropy, stringy (allergic rhinitis stem) |
| Temp / moisture | Warm, moist | Cool, dry |
| Red reflex | Persists | Fades quickly |
2.6 Other OMM answers on this form
- Somatic dysfunction is named for the direction of EASE. Radial head gliding freely anteriorly = anterior radial head dysfunction. Anterior radial head pairs with supination free; posterior with pronation (nursemaid's elbow).
- Counterstrain positions shorten the muscle. Plantaris (origin above the knee, inserts via Achilles): plantar flex the foot AND flex the knee.
- Collateral ganglia (IBS question): celiac below xiphoid, superior mesenteric between xiphoid and umbilicus, inferior mesenteric between umbilicus and pubis. Midline tension there = sympathetic hypertonicity to the gut.
- Sacral rocking normalizes pelvic splanchnic (S2-S4) parasympathetics for the distal colon (ulcerative colitis stem).
- Elevated first rib (inhalation dysfunction) is the structural finding of thoracic outlet syndrome; scalene hypertonicity narrows the interscalene triangle.
- Sacral apex tenderness + pain sitting + dyspareunia + painful defecation after macrosomic delivery = sacrococcygeal strain with pelvic floor dysfunction (levator ani attaches to the coccyx).
- Back labor (occiput posterior): sacral counterpressure.
3. Pulmonary
3.1 Pneumothorax: the complete set (FIVE questions)
| Presentation | Type | Key findings | Answer |
|---|---|---|---|
| Tall thin young smoker, sudden pleuritic pain | Primary spontaneous | Decreased breath sounds, HYPERRESONANCE | Small: observe + O2. Large/symptomatic: chest tube |
| On pneumonia/COPD, stable, CXR shown | Secondary spontaneous | Same exam, poor reserve | Tube thoracostomy, nearly all admitted |
| Trauma, JVD, hypotension, NO film in stem | Tension | Clinical diagnosis, never wait for imaging | Needle decompression (5th ICS ant. axillary per ATLS), THEN chest tube |
| Stable pneumothorax, film obtained | Simple | Trachea midline, BP normal | Chest tube (no needle needed) |
Session miss (MVC, JVD + hypotension + midline trachea). Tracheal deviation is a LATE, INSENSITIVE sign; its absence does not exclude tension. Tamponade and tension pneumothorax share obstructive shock (JVD + hypotension), so those findings can never discriminate. Only the respiratory exam can: hyperresonance + absent unilateral breath sounds = tension pneumothorax; clear equal lungs + muffled heart sounds = tamponade. Also: decompress BEFORE intubating; positive pressure converts simple to tension.
Verb rule: "next step" in tension = needle. "Definitive management" = chest tube, always, even in tension.
3.2 Pneumonia empiric therapy: the four-question ladder
- Q1. CAP, HAP/VAP, or aspiration? HAP (>48 h after admission) and VAP (>48 h after intubation) exit immediately to antipseudomonal beta-lactam (pip-tazo, cefepime, meropenem) PLUS vancomycin or linezolid. Aspiration requires a RISK FACTOR in the stem (altered consciousness, alcohol, stroke, dysphagia, seizure, tube feeds, poor dentition); the RLL alone proves nothing since it is the most common site for ALL pneumonia. Aspiration gets ampicillin-sulbactam.
- Q2. Where treated? Ward: ceftriaxone + azithromycin, OR respiratory FQ alone. ICU: beta-lactam + macrolide or beta-lactam + FQ; NEVER FQ monotherapy in the ICU.
- Q3. Outpatient: comorbid or allergic? Healthy: amoxicillin 1 g TID (or doxycycline). PCN allergy: macrolide or doxycycline. Comorbid (heart/lung/liver/renal disease, DM, EtOH, malignancy, asplenia) or recent abx: beta-lactam + macrolide, or FQ.
- Q4. MRSA / Pseudomonas risk? MRSA triggers: prior MRSA isolate, IV abx within 90 d, severe CAP, post-influenza necrotizing/cavitary. Give vancomycin or linezolid. Pseudomonas triggers: prior isolate, IV abx 90 d, bronchiectasis/CF, chronic steroids. Give pip-tazo, cefepime, meropenem, or LEVOFLOXACIN.
The facts that decide these: HCAP was retired in 2016 and nursing home residence alone justifies nothing. Macrolides DO cover pneumococcus (typical AND atypical), which is why one drug works empirically; amoxicillin covers typicals only, so an allergy moves you BROADER. Moxifloxacin has no Pseudomonas activity (levo and cipro do) but DOES cover anaerobes (levo does not). Daptomycin never treats pneumonia (surfactant inactivates it). De-escalate on culture. CAP 5 days minimum + afebrile 48-72 h; HAP/VAP 7 days.
3.3 Organism patterns tested
| Clue | Organism / answer |
|---|---|
| Young adult, gradual onset, URI prodrome, myalgia | Mycoplasma: macrolide or doxy (no cell wall, beta-lactams useless). Cold agglutinins, bullous myringitis |
| Diarrhea + confusion + hyponatremia | Legionella: urinary antigen, macrolide or FQ |
| Currant jelly sputum, alcoholic, bulging fissure | Klebsiella: ceftriaxone if susceptible; ESBL needs carbapenem; no anaerobic coverage from ceftriaxone |
| Post-influenza necrotizing/cavitary | Staph aureus incl. MRSA: add vancomycin or linezolid |
| "Opacity" on a report | Non-committal word: covers consolidation, atelectasis, effusion, mass. Do NOT infer lobar consolidation from it |
3.4 Lung cancer workup (two questions, opposite answers)
Uncharacterized nodule on CXR → CT chest first. Characterized CENTRAL/hilar mass → bronchoscopy (+EBUS). Peripheral → CT-guided needle. Then histology forks it: small cell almost never operated. Staging = PET-CT PLUS brain MRI (PET cannot read the brain). PET-positive nodes need tissue confirmation. PFTs gate resection. Sputum cytology is low sensitivity; PET is never the diagnostic step.
3.5 The rest
- PE: post-op/immobility + dyspnea + tachycardia + NORMAL CXR. Stable: heparin (LMWH). Massive (SBP <90): add thrombolysis to anticoagulation. Recent surgery is a lytic contraindication. Warfarin never starts alone (protein C/S dip); antiplatelets never treat venous clot. Heparin "allergy" = think HIT: use argatroban, fondaparinux, or a DOAC.
- CDH: scaphoid abdomen + bowel in chest + mediastinal shift. Confirm with CXR; definitive = surgical repair after stabilization. Never bag-mask; chest tube would hit bowel.
- Bronchiolitis: <2 y, URI prodrome then wheeze/tachypnea. Clinical diagnosis, supportive care only. No steroids, no bronchodilators, no CXR, no viral panel. First wheeze in an infant is NOT asthma.
- Foreign body aspiration: SUDDEN onset mid-play in a 1-3 y old beats everything. Epiglottitis has fever + toxicity + tripod; croup has barking cough + prodrome. Keep the child calm, rigid bronchoscopy. Expiratory film: unilateral hyperinflation.
4. Cardiology
4.1 Coronary territories
| ST elevation in | Territory | Vessel |
|---|---|---|
| V1-V2 / V3-V4 / V1-V4 | Septal / anterior / anteroseptal | LAD |
| V5-V6, I, aVL | Lateral | LCx (the "electrically silent" vessel) |
| II, III, aVF | Inferior | RCA 80% (AV node 90%, so blocks), LCx 20% |
| Tall R + ST depression V1-V3 | Posterior | RCA/LCx via PDA; confirm V7-V9 |
| V4R | RV | Proximal RCA: preload dependent, NO nitrates, give fluids |
| aVR + diffuse depression | Left main / 3-vessel | Not a territory; often shock |
Every inferior STEMI gets a right-sided ECG. Wellens (biphasic/deep T inversion V2-V3, pain free) = critical proximal LAD, no stress test, straight to cath.
4.2 Murmurs and maneuvers
| Finding | Lesion |
|---|---|
| Midsystolic click + late systolic murmur | MVP (myxomatous leaflet, chordae snap) |
| Holosystolic, apex, radiates to axilla | MR |
| Holosystolic, LLSB, LOUDER with inspiration | TR (Carvallo; RIGHT = InspIRation) |
| Crescendo-decrescendo, carotid radiation, parvus et tardus | AS (SAD: syncope 3 y, angina 5 y, dyspnea 2 y) |
| Blowing diastolic decrescendo, wide pulse pressure | AR |
| Opening snap + diastolic rumble | MS: loads the LEFT ATRIUM (P mitrale, AFib); LV is protected |
| Continuous machinery | PDA |
| Harsh systolic, LOUDER standing/Valsalva | HCM |
The two murmurs that get LOUDER with decreased preload (standing, Valsalva): HCM and MVP. Everything else softens. Handgrip (afterload up): MR/AR/VSD louder, AS/HCM softer. Squatting reverses MVP: click later, murmur shorter.
4.3 Heart failure hemodynamics
- Congestion (orthopnea, rales, edema, S3) = elevated LV filling pressure. Symptom relief = decrease preload (loop diuretic, nitrates). Mortality = the four pillars: ARNI/ACEi, beta blocker, MRA, SGLT2i.
- New HFrEF, no valve disease → find the etiology: ischemia first (nuclear stress or cath). Diabetes silences angina; "denies chest pain" excludes nothing.
- S3 = dilated volume-overloaded ventricle (normal in youth/pregnancy). S4 = stiff ventricle; impossible in AFib.
4.4 Arrest and arrhythmia
- Torsades, pulseless: defibrillate. Magnesium is the torsades answer only WITH a pulse. Amiodarone prolongs QT, wrong in torsades. Hypokalemia + hypomagnesemia (alcohol withdrawal) is the substrate; you cannot replete K until Mg is fixed.
- Wide-complex rules: pulseless = defib; unstable with pulse = synchronized cardioversion; stable monomorphic = amiodarone.
- Vasovagal syncope: trigger + prodrome (warmth, diaphoresis, nausea) + brief LOC + instant full recovery. Prodrome is SYMPATHETIC (cholinergic sweat glands); the faint is the vagal Bezold-Jarisch phase. Cardiac syncope: exertional, supine, no prodrome, family history of sudden death.
- Syncope + inappropriate bradycardia = rate-limiting drug (beta blocker, non-DHP CCB, digoxin, clonidine). Atenolol is renally cleared, accumulates in elderly. Volume depletion gives tachycardia instead.
4.5 AAA (three questions)
| Scenario | Answer |
|---|---|
| Screening | One-time US, men 65-75 who EVER smoked (Grade B) |
| Large AAA + severe COPD | EVAR (avoids laparotomy/cross-clamp). Open repair when: hostile anatomy (short/angled neck, poor iliac access), young patient needing durability, no surveillance compliance, connective tissue disease, mycotic, failed EVAR. EVAR needs lifelong endoleak surveillance |
| Pain + hypotension + anemia + pulsatile mass | Ruptured AAA (retroperitoneal if no peritonitis): straight to OR, permissive hypotension, no CT. Pathogenesis = degeneration of the tunica MEDIA |
5. Endocrine
5.1 Hypothyroidism (FOUR questions)
| Presentation | Tested point |
|---|---|
| Comatose, hypothermic, bradycardic, delayed DTRs, periorbital edema | Myxedema coma: confirm free T4; treat EMPIRICALLY, hydrocortisone BEFORE levothyroxine (adrenal crisis), passive rewarming |
| Goiter + delayed reflexes + LDL 180 + TSH 10 | Levothyroxine BEFORE any statin: thyroid hormone upregulates LDL receptors; statin in myxedema = myopathy risk. Screen secondary causes of dyslipidemia first |
| Fatigue + WEIGHT GAIN + menometrorrhagia + infraorbital edema + pallor | Hypothyroidism, not anemia: pallor is DOWNSTREAM (low EPO + iron loss from menorrhagia) |
| Hypothermia + bradycardia + memory loss + dry skin on HCTZ | TSH. Hyponatremia is a CONSEQUENCE of hypothyroidism; sodium is the runner-up, not the answer |
Session miss. Chose pernicious anemia off pallor. B12 deficiency causes weight LOSS and demands NEUROLOGIC findings (subacute combined degeneration). Weight gain + myxedema + menstrual havoc = thyroid. Recurring signature list: hypothermia, bradycardia, weight gain, dry skin, delayed reflex RELAXATION, cognitive slowing, hyponatremia, high LDL.
5.2 B12 done right (the contrast question)
Crohn/terminal ileum + falls + LOST PROPRIOCEPTION/VIBRATION + weakness + neuropsychiatric change = B12 (subacute combined degeneration: dorsal columns + corticospinal tracts). Folate deficiency looks identical hematologically but NEVER causes neuro disease; treating with folate alone masks the anemia while cord damage progresses. MMA + homocysteine both up in B12; only homocysteine in folate.
5.3 CAH (session miss)
2-week-old, vomiting, dehydration, ambiguous genitalia = 21-hydroxylase deficiency. No aldosterone: LOSE sodium, RETAIN potassium: HYPOnatremia + HYPERkalemia + acidosis. The vomiting-pattern answer (hyperNa/hypoK) belongs to 11-beta and 17-alpha deficiencies, but both cause HYPERTENSION, impossible in a dehydrated shocked infant. Crisis at 1-3 weeks (maternal steroids cover birth). Confirm 17-OHP; treat saline + dextrose + hydrocortisone, then fludrocortisone. Reason from the finding that names the disease (genitalia), not the loudest symptom (vomiting).
5.4 Other endocrine answers
- Whipple triad + recurrent hypoglycemia: supervised 72-hour fast with simultaneous insulin, C-peptide, proinsulin, sulfonylurea screen. C-peptide high = insulinoma; suppressed = exogenous insulin.
- Prerenal azotemia: BUN/Cr > 20, FENa < 1%, urine osm > 500, bland sediment. Treatment and test in one: IV crystalloid. Hold metformin, ACEi, NSAIDs. ATN: 10-15:1, FENa > 2%, muddy brown casts.
- Anorexia nervosa endocrine panel: LOW FSH/LH (hypothalamic, hypogonadotropic), HIGH cortisol and GH with low IGF-1, low T3 (euthyroid sick), normal prolactin. Refeeding syndrome = hypophosphatemia. BMI <15 or syncope admits.
- Presbyopia: mid-40s reading difficulty, all negatives clean = loss of accommodation (parasympathetic, CN III, ciliary muscle). Anticholinergics mimic it.
6. GI
6.1 GERD three ways
Chapman: ICS 5 LEFT. Viscerosomatic: T5-T9 sympathetic, distal esophagus T5-T6, type II, rotated LEFT (esophagus/stomach are left-sided). Management: PPI-refractory + hiatal hernia + complication (bleeding, stricture, Barrett) = fundoplication. Supine positioning worsens reflux; H2 blockers are inadequate; sucralfate is an adjunct.
6.2 Upper GI bleeding
- Cirrhotic + hematemesis: octreotide (splanchnic vasoconstriction) now. Bundle: airway if obtunded, restrictive transfusion (Hgb 7), CEFTRIAXONE prophylaxis (mortality benefit), EGD banding within 12 h, TIPS if refractory. Propranolol is PROPHYLAXIS only, contraindicated during the acute bleed.
- NSAID ulcer + brisk bleed: hematochezia can be UPPER GI if transit is fast (posterior duodenal ulcer, gastroduodenal artery). Duodenal ulcer is the most common cause of UGIB. Duodenum Chapman: right ICS 8.
- Sudden epigastric pain + free air + peritonitis: perforated ulcer: surgery NOW, resuscitate concurrently. CT wastes time when the plain film already shows it. Endoscopy is CONTRAINDICATED in perforation. Upright CXR detects 1-2 mL free air.
6.3 The rest
- Appendicitis: anorexia + constant RLQ pain worse with walking + guarding; appendicolith on CT predicts failure of antibiotics-only, so OR. US first in children/pregnancy. Ovarian torsion is the female distractor: sudden colicky pain + adnexal mass + Doppler US.
- Pyloric stenosis: 3-6 wk firstborn male, NONBILIOUS projectile vomiting, hungry, hypochloremic hypokalemic (classically alkalotic; severe dehydration can mask with acidosis). US: muscle >3-4 mm, channel >15-17 mm. FLUIDS AND ELECTROLYTES BEFORE PYLOROMYOTOMY, never an emergency. Bilious vomiting = malrotation = UGI series instead.
- Hepatitis A: daycare clusters, fecal-oral ("vowels hit the bowels"), prodrome then jaundice + dark urine + clay stool. Never chronic. Reportable. PEP = vaccine within 14 d. Hepatitis B: same two-phase picture, blood/sexual routes; IgM anti-HBc = acute; adults clear >95%.
- Giardia: daycare/backpacker, >7 days foul watery stools + flatulence, NEGATIVE routine cultures (they only find bacteria). Stool antigen/PCR. Tinidazole. No blood, no fever (no invasion).
- IBS: pain relieved by defecation + stress-worsened + normal exam. Supporting OMM finding: midline collateral ganglion tension.
7. OB/GYN
7.1 Fetal monitoring
VEAL CHOP. Late decels (nadir after contraction peak) = uteroplacental insufficiency: intrauterine resuscitation (position, fluids, O2, stop oxytocin); if refractory = DELIVER. Forceps require COMPLETE dilation (9 cm kills the option), +2 station, ruptured membranes, known position. Variables = cord: reposition, amnioinfusion. Sinusoidal = fetal anemia. Tachysystole (>5/10 min) = stop oxytocin, terbutaline. Cord prolapse = elevate presenting part, immediate cesarean.
7.2 Early pregnancy and infection
- Threatened abortion: bleeding + CLOSED os + appropriately doubling hCG (>53%/48 h) + sac in uterus = repeat US in 1 week. No bed rest (harmful myth), no progesterone, no D&C. Rh-negative bleeders get anti-D. The os drives the whole classification table.
- ASB in pregnancy: the one setting you treat asymptomatic bacteriuria (20-30% progress to pyelo). Screen at first visit. Nitrofurantoin (not ≥38 wk), cephalexin, amoxicillin, fosfomycin. NEVER FQs or tetracyclines; TMP-SMX avoided 1st trimester and near term. Pyelo in pregnancy = admit + IV ceftriaxone, then suppression.
- PID with peritoneal signs = inpatient cefoxitin/cefotetan + doxycycline. Admission: pregnancy, TOA, failed orals, severe illness, cannot exclude appendicitis. FQs no longer cover gonorrhea.
- BV in pregnancy: clue cells + pH >4.5 + thin fishy discharge = PRETERM LABOR risk. Metronidazole safe. BV does not cause ectopics (that is PID/chlamydia tubal scarring).
7.3 Cervix vs vagina (session miss)
Mucopurulent cervicitis + friable cervix + leukocytes but NO organisms on Gram stain or wet mount = CHLAMYDIA (obligate intracellular, invisible on stain; the leukorrhea IS the clue). Trichomonas is a VAGINITIS (the stem said "no vaginal wall inflammation") and is diagnosed BY the wet mount (motile flagellates), so a clean wet mount excludes it. A wet mount reports two things: leukocytes (host) and organisms (pathogen). Only organisms name a diagnosis. Pregnant chlamydia: azithromycin, never doxycycline; test of cure.
7.4 The rest
- Incontinence: exclude UTI first (positive nitrite = culture BEFORE anticholinergics: they worsen retention). PVR separates overflow. Kegels are first-line for stress AND urge AND mixed; stress ladder adds pessary, bulking, midurethral sling. Urge: bladder training then antimuscarinic or mirabegron (elderly). DIAPPERS for reversible causes.
- Cystitis vs pyelo: uncomplicated cystitis = nitrofurantoin x5 d, TMP-SMX x3 d, or fosfomycin x1. Nitrofurantoin and fosfomycin NEVER treat pyelo (no tissue levels). Pyelo = cipro/levo outpatient (ceftriaxone dose first if FQ resistance >10%), ceftriaxone inpatient. No doxycycline in pyelo, that is the PID regimen. Age alone is not "complicated." Postmenopausal recurrence: vaginal estrogen.
- Ovarian cancer risk: family history/BRCA/Lynch is the big one; OCPs are PROTECTIVE 30-50% (incessant ovulation hypothesis). Risk = more ovulation (nulliparity, early menarche); protection = less (multiparity, breastfeeding, OCP, tubal ligation).
- Pap intervals: none <21; 21-29 cytology q3y; 30-65 cytology q3y or HPV/co-test q5y; stop >65 with adequate negatives. Continue after hysterectomy only if done FOR CIN 2+.
- Pregnancy dermatoses: vesicles at margins + periumbilical + flu prodrome + systemic sx = PEMPHIGOID GESTATIONIS (anti-BP180, fetal SGA/prematurity risk). PUPPP: striae, SPARES umbilicus, no vesicles, no systemic sx, primigravida. ICP: itch without rash, bile acids. Pustular psoriasis: flexural sterile pustules, hypocalcemia.
- DMPA: most likely side effect = IRREGULAR BLEEDING (then amenorrhea 50-70% at 1 y). Weight gain, reversible BMD loss (black box), delayed fertility ~10 mo. NOT VTE (no estrogen); ideal when estrogen contraindicated.
- Primary dysmenorrhea: normal exam + onset near menarche = NSAIDs first (block prostaglandins at the source, start before menses), then OCPs; imaging/laparoscopy only for secondary features or treatment failure.
- HSDD: desire absent, arousal and orgasm intact, distress present, everything else excluded (regular cycles kill perimenopause; anhedonia denial kills depression).
8. Pediatrics
8.1 Exanthems and palms/soles
CARS involves palms and soles: Coxsackie, RMSF (wrists/ankles spreading IN, doxycycline at ANY age, treat empirically), secondary Syphilis (diffuse, non-pruritic). Plus Kawasaki (desquamation wk 2) and scarlet fever (desquamation in recovery). The numbered diseases mostly SPARE palms/soles and are identified by SEQUENCE: measles (3 Cs + Koplik, cephalocaudal, confluent, sick child, vitamin A + airborne isolation + report); rubella (posterior auricular/occipital nodes, well child); fifth (slapped cheek AFTER contagion ends; aplastic crisis, hydrops); roseola (fever breaks THEN rash); varicella (crops in different stages; contagious 1-2 d pre-rash until ALL crusted; PEP vaccine ≤3-5 d).
8.2 Neonatal and infant calls tested
| Stem | Answer |
|---|---|
| Blood in stool, well breastfed neonate, home birth | APT TEST first: alkali denaturation separates fetal from swallowed MATERNAL blood (cracked nipples). Well infant = maternal until proven otherwise. Home birth flags missing vitamin K (PT if fetal) |
| 3-6 wk firstborn male, projectile nonbilious vomiting | Pyloric stenosis: US; fluids/K before pyloromyotomy |
| Scaphoid abdomen + respiratory distress | CDH: CXR confirms, surgery after stabilization |
| Vomiting + ambiguous genitalia at 2 wk | Salt-wasting CAH: hypoNa/hyperK (see Endocrine) |
| <2 y URI prodrome then first wheeze | Bronchiolitis: supportive only |
| Echolalia, no response to name, object over people at 18 mo | EARLY INTERVENTION referral on suspicion, do not wait for formal diagnosis (M-CHAT at 18/24 mo). Echolalia itself proves hearing |
8.3 Heme and syndromes
Session miss (Fanconi). Short stature + supernumerary thumbs + PETECHIAE + cafe au lait + hepatosplenomegaly = Fanconi anemia (DNA repair, marrow failure at ~7-8 y, chromosomal breakage test, AML risk). VACTERL shares limb + vertebral findings but has NO hematologic or cutaneous component. Discriminate on the findings only one diagnosis explains, never on the overlap.
- ITP vs TTP: ITP = ISOLATED thrombocytopenia, post-viral young woman, observe >30k, steroids/IVIG. TTP = pentad (fever, plt, MAHA with schistocytes, renal, neuro), ADAMTS13, Coombs NEGATIVE (mechanical shear, not antibody on RBC), PLASMA EXCHANGE, platelets contraindicated. Precipitants: idiopathic mostly; ticlopidine/clopidogrel, quinine, pregnancy, HIV.
- Sickle cell vaccines: functional asplenia = encapsulated organisms: MCV4 starting at age 2 (a decade early), PPSV23 at 2, penicillin prophylaxis to 5. Live vaccines still fine.
- SJS vs SSSS: drug exposure + TWO mucosal sites (hemorrhagic lip crusting + conjunctivitis) = SJS; stop the drug, burn unit, ophthalmology. SSSS SPARES mucosa (toxin cleaves desmoglein-1, superficial), Nikolsky positive, desquamates.
- BECTS (rolandic epilepsy): nocturnal facial/guttural seizures, family history, outgrown: interictal EXAM IS NORMAL (spikes only on EEG). Tics disappear in sleep, the opposite.
- Axillary mass with central papule at puberty = polymastia (accessory breast tissue on the milk line). Polythelia = nipple only.
- GCS: E4V5M6. Confused speech = V4; eyes to voice = E3; obeys = M6 (that stem = 13). Minimum 3. ≤8 intubate. Intoxication never explains a low GCS without imaging.
9. Neuro / MSK
9.1 Localization tables
| Stroke territory | Signature |
|---|---|
| ACA | LEG > arm weakness, frontal release signs, abulia, gait apraxia, urinary incontinence |
| MCA | Face/arm > leg, aphasia (L) or neglect (R), gaze toward lesion |
| PCA | Homonymous hemianopia with macular sparing |
| Wernicke (inferior L MCA) | Fluent nonsense + no comprehension + R field cut; misread as delirium; MRI w/ DWI |
| Root | Reflex | Motor | Sensory |
|---|---|---|---|
| C5 | Biceps | Shoulder abduction | Lateral humerus |
| C6 | Brachioradialis (support forearm, strike distal radius) | Wrist EXTENSION, elbow flexion | Thumb, index, lateral forearm |
| C7 | Triceps | Elbow extension, wrist FLEXION, finger extension | Middle finger |
| C8/T1 | none | Finger flexion / intrinsics | 4th-5th digits / medial forearm |
9.2 Bleeds and pressure
- Epidural: temporal blow, middle meningeal artery, BICONVEX, does not cross sutures, ipsilateral blown pupil (uncal herniation, CN III) + contralateral posturing, craniotomy now. Subdural: bridging veins, crescent, crosses sutures, elderly/alcoholic/anticoagulated.
- SAH with negative CT: CT sensitivity falls after 6 h; xanthochromia (2-12 h old blood) on LP confirms. Constant RBCs tubes 1-4 vs falling in traumatic tap. Then CTA, coil/clip, nimodipine x21 d.
- NPH: wet-wobbly-wacky, gait FIRST; ventriculomegaly out of proportion to atrophy; tap test then VP shunt; gait improves most. Alzheimer = hippocampal atrophy, memory first, normal gait.
- MS: BILATERAL INO is pathognomonic in a young woman (MLF plaques; a stroke cannot do it bilaterally). Dissemination in space and time, MRI + oligoclonal bands, IV steroids for relapse.
9.3 MSK diagnosis set
| Stem | Diagnosis + key |
|---|---|
| Positive drop arm, weak abduction, intact rotation | Supraspinatus tear (isolated). Global tear would weaken ER/IR too. Cuff map: supraspinatus/empty-can, infraspinatus/ER, teres minor/Hornblower, subscapularis/lift-off. Supraspinatus initiates 0-15 then depresses the humeral head, which is why drop arm fails at 90 |
| DIP droops, full passive, no active extension | Mallet finger: STACK SPLINT in continuous extension 6-8 wk; one flexion resets the clock. ORIF only if >1/3 articular surface or subluxation. Untreated leads to swan neck. Boutonniere = central slip, PIP flexed/DIP extended. Both deformities occur in RA; RA hits MCP/PIP and SPARES DIP (OA and psoriatic hit DIP) |
| Kanavel signs after puncture | Flexor tenosynovitis: IV abx + hand surgery OR, never bedside I&D |
| Anterior knee pain, stairs + sitting, weak VMO, tight lateral structures | PFPS: myofascial release of the tight lateral chain + VMO/hip strengthening. NEVER immobilize |
| Extension-provoked LBP, 60s, stiffness gel phenomenon | Degenerative spondylosis (facets). Flexion-provoked = discogenic. Add neurogenic claudication (relief sitting/leaning, shopping cart sign, variable distance) = stenosis: MRI, because the diagnosis is neural compression and plain films cannot show neural elements. Vascular claudication: fixed distance, rest relief, skin/hair changes, ABI |
| Athlete, hyperextension sport, midline lumbosacral pain | Spondylolysis (pars, L5, Scotty dog collar) / spondylolisthesis (slip). MRI if films negative |
| Rib hump that RESOLVES with sidebending | Functional curve (handedness, short leg): evaluate reversibility FIRST, then standing postural films, then lift. Persistent hump = structural: full-spine standing films, Cobb (observe <25, brace 25-45 immature, surgery >45-50) |
| Diffuse non-dermatomal arm paresthesia + scalene tension or hand swelling | Thoracic outlet syndrome; structural finding = elevated (inhalation) first rib. Adson/Wright/Roos. "No proximal root compression" is the stem's way of excluding radiculopathy |
10. ID / Derm / Eye
| Stem | Answer + discriminator |
|---|---|
| White oral plaques that SCRAPE OFF leaving bleeding base | Candidiasis (+ heartburn = esophageal = AIDS-defining; fluconazole). Bleeding after scraping PROVES it came off. Leukoplakia and oral hairy leukoplakia do NOT scrape. Hemophilia + old transfusion = HIV vector |
| HIV, white retinal patches + hemorrhage ("pizza pie"), CD4 <50 | CMV retinitis: valganciclovir + ART. Toxo = "headlight in fog" WITH vitritis; ARN = painful, rapid; Candida = string of pearls |
| V1 vesicles + nose tip (Hutchinson sign) | Herpes zoster ophthalmicus: urgent ophtho slit lamp + high-dose oral antiviral ≤72 h. No topical steroids without ophtho |
| Painless sudden monocular loss, cherry-red spot, pale retina, RAPD | CRAO: stroke equivalent, carotid workup, check ESR/CRP for GCA in >50 |
| Gram-negative intracellular diplococci in urethral discharge | Gonorrhea: ceftriaxone 500 IM + doxy unless chlamydia excluded. The mirror of the cervicitis miss: stain positive names gonorrhea, stain negative with inflammation points at chlamydia |
| Painful ulcers + uveitis + arthritis, young man | Behcet: ocular involvement = systemic steroids first; azathioprine is the steroid-sparer. Reactive arthritis has PAINLESS ulcers |
| Fever/arthralgia/pleuritis on procainamide | Drug-induced lupus: ANTIHISTONE (+), anti-dsDNA (-), renal/CNS spared, resolves off drug. Culprits: procainamide, hydralazine, isoniazid, minocycline, TNF inhibitors. Stark contrast: idiopathic SLE = dsDNA/Smith |
| Vanc infusion: flushing, normal vitals | Vancomycin flushing reaction (MRGPRX2 mast cell, not IgE): SLOW to ≥60 min + antihistamine, do NOT label allergy. Anaphylaxis = hypotension/airway/2+ systems: IM epi 0.3-0.5 mg 1:1000 anterolateral thigh, no waiting. MRSA pneumonia alternative if true allergy: linezolid, never daptomycin |
| Tongue/lip swelling on ACEi, 5 years in | Bradykinin angioedema: stop PERMANENTLY (class effect), airway first; NOT dose- or time-dependent; antihistamines/epi work poorly; ARB cautiously later |
| Nightly cough, fall trigger, prior episodes | Persistent asthma in a child: daily inhaled corticosteroid, not scheduled albuterol |
| Psoriasis clue set | Nail pitting + "dry patches" + DIP arthritis = psoriatic arthritis; seronegative, HLA-B27 family, dactylitis, pencil-in-cup |
11. Biostatistics (11 questions, ~8% of the form)
11.1 Confidence intervals (4 questions, one rule)
Ratio measures (RR, OR, HR): significant iff the 95% CI excludes 1. Difference measures: excludes 0. The point estimate is the effect size; the interval bound is not ("RR 1.5, CI 1.05-2.00" is a 1.5-fold increase, not 2-fold). A big point estimate with a wide interval crossing 1 means NOTHING (few events). Smallest-but-significant beats biggest-but-crossing (OR 1.04, CI 1.01-1.07 was "the best predictor"). Statistical significance = distinguishable from null; clinical significance = magnitude. Observational designs support association, so say "probably increases," never "reducing X will reduce Y."
11.2 Study design selection (4 questions)
| Cue in stem | Design |
|---|---|
| Rare disease, limited time/money | Case-control (sample on outcome; odds ratio; recall bias) |
| Rare exposure; incidence or RR needed | Cohort. Prospective = follow forward; retrospective = existing records |
| Prevalence, burden, service planning | Cross-sectional (fails for rare disease; no temporality; healthy worker effect) |
| Strongest evidence an intervention works, assignable | RCT (randomization = INTERNAL validity, balances unknown confounders; external validity = who was enrolled) |
| Assigned exposure + follow-up in the options but no "RCT" | Prospective cohort (the architecture answer) |
11.3 The rest
- Test selection: 2 groups continuous = t-test; 3+ continuous = ANOVA (pairwise t-tests inflate type I; post-hoc Tukey finds which pair); categorical = chi-square (Fisher if cells <5); non-normal = Mann-Whitney / Kruskal-Wallis.
- NNT = 1/ARR (|EER - CER|). Shape-recognition: 1/difference = NNT; ratio of rates = RR; cross-product = OR; difference over CER = RRR.
- Empirical rule: 68/95/99.7 at 1/2/3 SD (exact 95% = 1.96). SD spreads individuals; SEM = SD/√n spreads the mean.
- p = 0.049: probability of data this extreme IF null true, loosely "~5% chance due to chance." Never a probability the point estimate is correct.
- Bias sorting: who got in = selection (referral/Berkson, healthy worker); how measured = information (recall: case-control; observer). Lead-time and length-time haunt screening.
- Power = 1 - beta (≥80%); type I = false positive (alpha), type II = false negative.
12. Ethics / Medicolegal (9 questions)
12.1 The 4 Ds, tested three times
| Stem | Element at issue | Verdict |
|---|---|---|
| Injection then stroke, causation unproven | Proximate cause missing | Case fails ("prevailing factor" language) |
| On-call physician refuses HIV patient, patient dies | All four present; act of OMISSION | Liable (on-call = duty; no right to refuse for HIV; ADA + EMTALA exposure) |
| Contraindicated bupropion, no seizure occurred | DAMAGES missing | No merit (breach without harm is not actionable) |
12.2 Autonomy: the three-way split
Session miss (breast mass). The axis is whether the refusal is INFORMED. "After extensive counseling" + settled preference = respect autonomy (tongue lesion). "AFRAID" + no counseling described + less invasive options unoffered (core needle, FNA) = CONFERENCE, keep talking. Comatose + no directive + care cannot change outcome = FUTILITY. Double effect = intended good with foreseen unintended harm (morphine for terminal dyspnea): needs an actual harm being caused, not care withheld.
12.3 Statutes and reporting
- EMTALA (part of COBRA 1986, tested twice): screening exam owed BEFORE any insurance question; insurer preference never delays it. Stabilize, then transfer appropriately. Personal physician penalties, not malpractice-insurable.
- Anti-Kickback Statute (Social Security Amendments of 1972): CRIMINAL, intent required, rent tied to referral volume. Stark: CIVIL, strict liability, physician self-referral, mandatory exceptions. The word "criminal" picks AKS.
- Reporting: suspected child abuse (anogenital warts >3 y) = CPS; elder abuse = APS (never ask permission, never confront the abuser, never route through household members, assess safety before discharge). Reportable STIs = syphilis, gonorrhea, chlamydia, HIV, chancroid (HPV/HSV are not): report AND health department does confidential partner notification; if both CPS-type and health-dept duties exist they run in parallel. EPT legal for GC/CT, never syphilis.
- Interrupted firearm suicide attempt = admit (voluntary here); insurance denial is irrelevant; "feels better now" is not safety; no sedative scripts; police only for means removal.
- Mass casualty triage: greatest good for the greatest number; expectant category exists; triage is dynamic; chemical event = decontaminate before entry.
- Baby-Friendly: rooming-in, feed on demand within 1 h of birth, no formula marketing, no glucose water. Vaccine shortage priority = highest complication risk PLUS protectors of the unvaccinatable (infant in a household with a neonate beat the 65-year-old with post-illness GBS; isolated hypertension is not a qualifying comorbidity).
13. The Miss Playbook
Eight misses in ~165 questions. Six shared one failure mode. These are the rules, in the order they were paid for.
1. Family history is uninterpretable without age of onset (prostate). Ask when before asking what syndrome. A remembered association applied at the wrong point in the disease course is still wrong (germline testing criteria are written for men who HAVE cancer).
2. Viscerosomatic answers must match level AND type AND side (gallbladder). Type II, toward the organ, dead-center level.
3. Localize cervix vs vagina before naming an organism (chlamydia). Read negatives as inclusion criteria: "no organisms on stain" points AT the unstainable organism.
4. Discriminate on what only one diagnosis explains, never the overlap (Fanconi vs VACTERL). Petechiae had no VACTERL explanation.
5. The loudest finding is often downstream (hypothyroid vs pernicious anemia; CAH). Pallor and vomiting were consequences; weight gain, myxedema, and ambiguous genitalia named the disease.
6. Match the imaging to the structure that defines the diagnosis (stenosis needs MRI, plain film cannot show neural elements).
7. An informed refusal is respected; an unexplored one is explored (breast mass). Scan for whether counseling already happened.
8. Never let an insensitive sign rule OUT (midline trachea in tension pneumothorax). Same family: absent Murphy sign, no palpable olive, no splenomegaly in mono. When two diagnoses share a physiology, only the system findings that differ can decide.
The single habit that catches all of these: after choosing an answer, name the stem finding your choice CANNOT explain. If one exists and it is specific, change your answer.
Flashcards: Coronary Territories24 cards
Card 2Coronary Territories
Which leads show ST elevation in an ANTERIOR infarct, and which artery?
V3 to V4. Left anterior descending.
Card 3Coronary Territories
ST elevation in V1 to V4. Territory and culprit vessel?
Anteroseptal. Left anterior descending (LAD).
Card 4Coronary Territories
ST elevation in V5, V6, I, and aVL. Territory and culprit vessel?
Lateral wall. Left circumflex (or a diagonal branch of the LAD).
Card 5Coronary Territories
ST elevation in I and aVL only. Territory and vessel?
High lateral. Left circumflex or first diagonal.
Card 6Coronary Territories
ST elevation in II, III, and aVF. Territory and culprit vessel?
Inferior wall. Right coronary artery in ~80 percent, left circumflex in ~20 percent.
Card 7Coronary Territories
ST elevation across V1 to V6 plus I and aVL. Territory and vessel?
Extensive anterior. Proximal LAD (or left main).
Card 8Coronary Territories
Which leads localize a POSTERIOR infarct, and which vessel?
V7 to V9 (posterior leads). Right coronary artery or left circumflex, via the posterior descending artery.
Card 9Coronary Territories
How does a posterior MI appear on a STANDARD 12-lead ECG?
Indirect mirror-image signs in V1 to V3: ST DEPRESSION, tall broad R waves, and upright T waves. Confirm with posterior leads V7 to V9.
Card 10Coronary Territories
Which lead shows ST elevation in a RIGHT VENTRICULAR infarct, and which vessel?
V4R (right-sided ECG). Proximal right coronary artery, before the RV marginal branch.
Card 11Coronary Territories
ST elevation in aVR with diffuse ST depression in 6+ leads. What does it mean?
Left main coronary artery or severe triple-vessel disease. Often cardiogenic shock. Not a standard STEMI territory.
Card 12Coronary Territories
What does the posterior descending artery (PDA) supply, and where does it arise?
Inferior wall and posterior third of the interventricular septum. Arises from the RCA in ~85 percent (right dominant), from the LCx in ~8 percent (left dominant), both in the rest (codominant).
Card 13Coronary Territories
What does the LAD supply?
Anterior wall of the left ventricle, anterior two-thirds of the interventricular septum, and the apex.
Card 14Coronary Territories
What does the left circumflex supply?
Lateral and posterolateral wall of the left ventricle. Gives the PDA in left-dominant circulation.
Card 15Coronary Territories
What does the right coronary artery supply?
Right atrium, right ventricle, SA node (~60 percent), AV node (~90 percent), and the inferior wall via the PDA.
Card 16Coronary Territories
Which artery supplies the SA node? The AV node?
SA node: RCA in ~60 percent, LCx in ~40 percent. AV node: RCA in ~90 percent.
Card 17Coronary Territories
An inferior STEMI is on the monitor. What is the immediate next ECG step and why?
Obtain a RIGHT-SIDED ECG (V4R) to look for RV infarct, because RV infarction is preload dependent.
Card 18Coronary Territories
Why are nitrates dangerous in a right ventricular infarct?
The failing RV is preload dependent. Nitroglycerin drops preload and can cause profound hypotension. Treat with IV fluids instead.
Card 19Coronary Territories
Inferior MI with bradycardia or AV block. Which artery, and why?
Right coronary artery. It supplies the AV node in ~90 percent of people, and inferior MI also triggers a Bezold-Jarisch vagal reflex.
Card 20Coronary Territories
What reciprocal changes accompany an INFERIOR STEMI?
ST depression in I and aVL (the high lateral leads).
Card 21Coronary Territories
What reciprocal changes accompany an ANTERIOR or high lateral STEMI?
ST depression in II, III, and aVF (the inferior leads).
Card 22Coronary Territories
Deep symmetric T-wave inversions or biphasic T waves in V2 to V3 in a pain-free patient. Name and meaning.
Wellens syndrome. Critical PROXIMAL LAD stenosis. Do not stress test. Send to catheterization.
Card 23Coronary Territories
Upsloping ST depression with tall symmetric T waves in the precordial leads. Name and meaning.
De Winter T waves. A STEMI equivalent indicating acute proximal LAD occlusion. Activate the cath lab.
Card 24Coronary Territories
Which infarct territory is most often "electrically silent" on a 12-lead ECG?
Posterior and lateral, supplied by the left circumflex. It produces no direct ST elevation on standard leads.
Flashcards: Murmurs20 cards
Card 25Murmurs
Midsystolic CLICK followed by a late systolic murmur. Diagnosis and mechanism?
Mitral valve prolapse. The redundant myxomatous leaflet billows into the left atrium until the chordae snap taut (the click), after which regurgitation begins (the late murmur).
Card 26Murmurs
HOLOSYSTOLIC murmur at the apex radiating to the AXILLA. Diagnosis?
Mitral regurgitation. Blowing quality, loudest at the apex, radiates to the left axilla. Louder with handgrip (increased afterload).
Card 27Murmurs
HOLOSYSTOLIC murmur at the left lower sternal border that increases with INSPIRATION. Diagnosis?
Tricuspid regurgitation. Inspiration increases right-sided venous return, so all RIGHT-sided murmurs get louder (Carvallo sign).
Card 28Murmurs
CRESCENDO-DECRESCENDO systolic murmur at the right upper sternal border radiating to the CAROTIDS. Diagnosis?
Aortic stenosis. Associated with pulsus parvus et tardus (weak, delayed carotid upstroke), a soft or absent S2, and an S4.
Card 29Murmurs
Triad of symptoms in aortic stenosis, and what each predicts.
SAD: Syncope (average survival 3 years), Angina (5 years), Dyspnea/heart failure (2 years). Symptom onset is the indication for valve replacement.
Card 30Murmurs
BLOWING DECRESCENDO DIASTOLIC murmur at the left sternal border, best heard leaning forward. Diagnosis?
Aortic regurgitation. Wide pulse pressure with numerous eponymous signs: water-hammer (Corrigan) pulse, head bobbing (de Musset), nail bed pulsation (Quincke), femoral bruit (Duroziez).
Card 31Murmurs
Opening SNAP followed by a low-pitched DIASTOLIC RUMBLE at the apex. Diagnosis?
Mitral stenosis, almost always rheumatic. A shorter S2-to-opening-snap interval means MORE severe stenosis. Leads to left atrial enlargement, atrial fibrillation, and stroke.
Card 32Murmurs
CONTINUOUS "machinery" murmur heard in both systole and diastole. Diagnosis?
Patent ductus arteriosus. Loudest at the left infraclavicular area. Treat with indomethacin to close; prostaglandin E1 keeps it open when a ductal-dependent lesion requires it.
Card 33Murmurs
HARSH systolic murmur at the left sternal border that gets LOUDER with Valsalva and standing. Diagnosis?
Hypertrophic cardiomyopathy. Dynamic left ventricular outflow tract obstruction. Decreasing preload shrinks the LV cavity and worsens obstruction.
Card 34Murmurs
Which TWO murmurs get LOUDER with decreased preload (standing, Valsalva)?
Hypertrophic cardiomyopathy and mitral valve prolapse. Every other murmur gets SOFTER when preload falls. This is the highest-yield maneuver distinction in cardiology.
Card 35Murmurs
What happens to the MVP click and murmur with STANDING or VALSALVA?
Less preload means the leaflet prolapses sooner: the click moves EARLIER (toward S1) and the murmur becomes LONGER.
Card 36Murmurs
What happens to the MVP click and murmur with SQUATTING or leg raise?
More preload delays prolapse: the click moves LATER (toward S2) and the murmur becomes SHORTER.
Card 37Murmurs
How do you use INSPIRATION to localize a murmur?
Inspiration increases right-sided venous return, so RIGHT-sided murmurs get LOUDER (tricuspid and pulmonic). Expiration favors LEFT-sided murmurs. Mnemonic: RIGHT = InspIRation.
Card 38Murmurs
How does HANDGRIP change murmurs, and why?
Handgrip raises afterload (systemic vascular resistance). It makes mitral regurgitation, aortic regurgitation, and VSD LOUDER, and makes aortic stenosis and hypertrophic cardiomyopathy SOFTER.
Card 39Murmurs
Distinguish aortic stenosis from hypertrophic cardiomyopathy on maneuvers.
Both are harsh systolic murmurs. AS gets SOFTER with Valsalva/standing and radiates to the carotids. HCM gets LOUDER with Valsalva/standing and does NOT radiate to the carotids. AS has a delayed weak carotid upstroke; HCM has a brisk bifid one.
Card 40Murmurs
Which chamber bears the load in MITRAL STENOSIS, and what ECG finding follows?
The LEFT ATRIUM. The left ventricle is protected (underfilled). ECG shows left atrial enlargement: P mitrale, a broad notched P wave in lead II and a deep terminal negative deflection in V1.
Card 41Murmurs
Match each valve lesion to the chamber that bears the load.
Mitral stenosis: left atrium (LV protected). Mitral regurgitation: left atrium AND left ventricle (volume overload). Aortic stenosis: left ventricle (pressure overload, concentric LVH). Aortic regurgitation: left ventricle (volume overload, eccentric dilation).
Card 42Murmurs
An S3 gallop means what, and when is it normal?
Rapid early diastolic filling of a dilated, volume-overloaded ventricle. Pathologic in heart failure, mitral regurgitation, and dilated cardiomyopathy. NORMAL in children, young adults, and pregnancy.
Card 43Murmurs
An S4 gallop means what, and when is it never normal?
Atrial contraction against a STIFF, non-compliant ventricle. Seen in left ventricular hypertrophy, aortic stenosis, hypertension, and ischemia. Never normal in the presence of atrial fibrillation, because it requires organized atrial contraction.
Card 44Murmurs
Is antibiotic prophylaxis indicated for mitral valve prolapse?
NO. Current guidelines restrict endocarditis prophylaxis to prosthetic valves, prior infective endocarditis, unrepaired cyanotic congenital heart disease, and cardiac transplant with valvulopathy.
Flashcards: Pneumothorax11 cards
Card 45Pneumothorax
Is tension pneumothorax a clinical or a radiographic diagnosis?
CLINICAL. Never delay decompression to obtain a chest radiograph. If a stem hands you a CXR, the patient was stable enough to image, which argues AGAINST tension.
Card 46Pneumothorax
List the signs of a TENSION pneumothorax.
Hypotension (the cardinal sign), tachycardia, distended neck veins, tracheal deviation AWAY from the affected side, absent breath sounds, hyperresonance, severe hypoxia, altered mental status.
Card 47Pneumothorax
Tension pneumothorax: what is the immediate intervention, and what follows it?
Immediate NEEDLE DECOMPRESSION, then tube thoracostomy. The needle is only a temporizing bridge, never definitive.
Card 48Pneumothorax
Where do you place the needle for decompression in an adult?
5th intercostal space at the anterior axillary line (current ATLS preference). The older 2nd ICS midclavicular site fails in roughly a third of adults because the catheter is too short for the chest wall.
Card 49Pneumothorax
Large or symptomatic pneumothorax, patient hemodynamically STABLE, CXR obtained. Management?
Tube thoracostomy (chest tube). No needle needed, because there is no tension physiology.
Card 50Pneumothorax
What is the DEFINITIVE management of a tension pneumothorax?
Tube thoracostomy. Needle decompression only converts a tension pneumothorax into a simple one.
Card 51Pneumothorax
Why must you decompress a pneumothorax BEFORE intubating?
Positive pressure ventilation forces more air into the pleural space and converts a simple pneumothorax into a tension pneumothorax with cardiovascular collapse.
Card 52Pneumothorax
Small primary spontaneous pneumothorax, minimally symptomatic. Management?
Observation with supplemental oxygen (oxygen speeds pleural air reabsorption). Generally for a rim under about 2 cm or under 15 to 20 percent.
Card 53Pneumothorax
Who gets a primary spontaneous pneumothorax?
Tall, thin, young men who smoke. Caused by rupture of an apical subpleural bleb. Marfan syndrome is a classic association.
Card 54Pneumothorax
What is a SECONDARY spontaneous pneumothorax, and why does it need a chest tube?
Pneumothorax on top of existing lung disease (COPD, pneumonia, cystic fibrosis, malignancy). Reserve is already poor, so nearly all get a chest tube and admission regardless of size.
Card 55Pneumothorax
Test-taking: how does the verb of the question change the pneumothorax answer?
"Most appropriate NEXT STEP" rewards the immediate action (needle decompression if tension). "DEFINITIVE management" rewards the chest tube. Same clinical facts, different answer.
Flashcards: Pneumonia Empiric Rx28 cards
Card 56Pneumonia Empiric Rx
Define community-acquired pneumonia (CAP) by timing.
Onset in the community, or within 48 hours of hospital admission.
Card 57Pneumonia Empiric Rx
Define hospital-acquired pneumonia (HAP) by timing.
Onset MORE than 48 hours after admission, in a patient who was not intubated at the time of admission.
Card 58Pneumonia Empiric Rx
Define ventilator-associated pneumonia (VAP) by timing.
Onset MORE than 48 hours after endotracheal intubation.
Card 59Pneumonia Empiric Rx
What happened to the category "healthcare-associated pneumonia" (HCAP)?
RETIRED by the 2016 IDSA/ATS guidelines. It over-predicted resistant organisms and drove unnecessary broad-spectrum use. Escalation is now driven by individual risk factors, not by residence or healthcare contact.
Card 60Pneumonia Empiric Rx
Does living in a nursing home, by itself, justify empiric vancomycin?
No. Since HCAP was retired, nursing home residence, dialysis, recent hospitalization, and wound care are NOT independent indications for MRSA or Pseudomonas coverage.
Card 61Pneumonia Empiric Rx
What are the components of CURB-65?
Confusion (new), Urea (BUN over 19 mg/dL), Respiratory rate 30 or more, Blood pressure under 90 systolic or 60 diastolic, and age 65 or older. One point each.
Card 62Pneumonia Empiric Rx
How does the CURB-65 score determine disposition?
0 to 1: outpatient. 2: inpatient ward. 3 or more: consider ICU.
Card 63Pneumonia Empiric Rx
What defines SEVERE community-acquired pneumonia (IDSA criteria)?
1 major OR 3 minor. Major: septic shock requiring vasopressors, or mechanical ventilation. Minor: RR 30 or more, PaO2/FiO2 250 or less, multilobar infiltrates, confusion, uremia, leukopenia, thrombocytopenia, hypothermia, hypotension needing aggressive fluids.
Card 64Pneumonia Empiric Rx
Empiric therapy for OUTPATIENT CAP in a previously healthy patient?
Amoxicillin 1 g three times daily, OR doxycycline, OR a macrolide (only where local pneumococcal macrolide resistance is under 25 percent).
Card 65Pneumonia Empiric Rx
Empiric therapy for OUTPATIENT CAP with comorbidities?
Beta-lactam (amoxicillin-clavulanate or cefpodoxime) PLUS a macrolide or doxycycline, OR respiratory fluoroquinolone monotherapy.
Card 66Pneumonia Empiric Rx
Which comorbidities upgrade an outpatient CAP regimen?
Chronic heart, lung, liver, or renal disease; diabetes; alcohol use disorder; malignancy; and asplenia.
Card 67Pneumonia Empiric Rx
Empiric therapy for INPATIENT non-ICU (ward) CAP?
Beta-lactam (ceftriaxone, cefotaxime, or ampicillin-sulbactam) PLUS a macrolide, OR respiratory fluoroquinolone monotherapy.
Card 68Pneumonia Empiric Rx
Empiric therapy for ICU / SEVERE CAP?
Beta-lactam PLUS a macrolide, OR beta-lactam PLUS a fluoroquinolone. Fluoroquinolone MONOTHERAPY is never adequate in the ICU.
Card 69Pneumonia Empiric Rx
In which CAP settings is fluoroquinolone monotherapy acceptable, and where is it not?
Acceptable: outpatient with comorbidities, and inpatient ward. NOT acceptable: ICU or severe CAP, which always needs a beta-lactam in the regimen.
Card 70Pneumonia Empiric Rx
What does a respiratory fluoroquinolone (levofloxacin, moxifloxacin) cover?
Strep pneumoniae including penicillin-resistant strains, Haemophilus influenzae, Moraxella, the ATYPICALS (Legionella, Mycoplasma, Chlamydophila), enteric gram negatives, and anaerobes. That breadth is why it substitutes for a beta-lactam plus macrolide.
Card 71Pneumonia Empiric Rx
List the risk factors that trigger empiric MRSA coverage in CAP.
Prior MRSA respiratory isolate (strongest predictor), IV antibiotics within 90 days, severe CAP requiring ICU or ventilation, locally validated high MRSA prevalence, and post-influenza necrotizing, cavitary, or empyematous disease.
Card 72Pneumonia Empiric Rx
Which drugs provide MRSA coverage in pneumonia?
Vancomycin or linezolid. Linezolid has superior lung penetration. NEVER daptomycin.
Card 73Pneumonia Empiric Rx
List the risk factors that trigger empiric Pseudomonas coverage in CAP.
Prior Pseudomonas isolate, IV antibiotics within 90 days, structural lung disease (bronchiectasis or cystic fibrosis), and chronic corticosteroids or immunosuppression.
Card 74Pneumonia Empiric Rx
Which drugs provide antipseudomonal coverage?
Piperacillin-tazobactam, cefepime, meropenem, or LEVOFLOXACIN (also ciprofloxacin, aztreonam, ceftazidime).
Card 75Pneumonia Empiric Rx
Which respiratory fluoroquinolone does NOT cover Pseudomonas?
MOXIFLOXACIN. Levofloxacin and ciprofloxacin do cover it. If a stem builds a Pseudomonas risk profile, moxifloxacin is the wrong fluoroquinolone.
Card 76Pneumonia Empiric Rx
Empiric therapy for HAP or VAP?
Antipseudomonal beta-lactam (piperacillin-tazobactam, cefepime, or meropenem) PLUS vancomycin or linezolid for MRSA. Both are covered empirically in every case.
Card 77Pneumonia Empiric Rx
When do you add a SECOND antipseudomonal agent in HAP/VAP?
Septic shock, structural lung disease, or a unit with high local resistance. Add an aminoglycoside or an antipseudomonal fluoroquinolone.
Card 78Pneumonia Empiric Rx
Empiric therapy for aspiration pneumonia?
Ampicillin-sulbactam, OR a respiratory fluoroquinolone plus metronidazole. Routine anaerobic coverage is now DISCOURAGED unless there is lung abscess or empyema, since most aspiration pneumonia is caused by ordinary CAP organisms.
Card 79Pneumonia Empiric Rx
What is the minimum treatment duration for CAP, and what are the stop criteria?
Minimum 5 days, AND the patient must be afebrile 48 to 72 hours and clinically stable before stopping.
Card 80Pneumonia Empiric Rx
What is the treatment duration for HAP and VAP?
7 days. Extend only for lung abscess, empyema, Pseudomonas, or other resistant organisms.
Card 81Pneumonia Empiric Rx
Why can daptomycin never be used for pneumonia?
It is inactivated by pulmonary surfactant. Daptomycin is correct for MRSA bacteremia, endocarditis, and skin infection, but always wrong for lung infection.
Card 82Pneumonia Empiric Rx
What role does procalcitonin play in pneumonia management?
It does NOT decide whether to START antibiotics. A low value never justifies withholding empiric therapy in a sick patient. It may help decide when to STOP.
Card 83Pneumonia Empiric Rx
Sputum culture returns a single organism with sensitivities. What is the next management step?
DE-ESCALATE to the narrowest effective agent and stop the redundant empiric drugs. Continuing double coverage after the organism is known is the wrong answer.
Flashcards: Pneumonia Drill22 cards
Card 84Pneumonia Drill
DRILL. Healthy 30-year-old outpatient, CAP, no allergies, no comorbidities. Prescribe.
AMOXICILLIN 1 g three times daily. Narrowest spectrum with the best pneumococcal coverage. (Doxycycline is an equally acceptable alternative.)
Card 85Pneumonia Drill
DRILL. Healthy 30-year-old outpatient, CAP, PENICILLIN ALLERGY, no comorbidities. Prescribe.
MACROLIDE (azithromycin) or DOXYCYCLINE. Both cover typical AND atypical organisms. Doxycycline is often preferred where pneumococcal macrolide resistance exceeds 25 percent.
Card 86Pneumonia Drill
DRILL. Outpatient CAP in a patient with COPD, diabetes, CHF, CKD, cirrhosis, alcohol use disorder, malignancy, or asplenia. Prescribe.
Beta-lactam (amoxicillin-clavulanate or cefpodoxime) PLUS a macrolide or doxycycline. OR respiratory fluoroquinolone monotherapy.
Card 87Pneumonia Drill
DRILL. Outpatient CAP in a patient who received antibiotics within the past 90 days. What changes?
Escalate to the comorbid-outpatient regimen (beta-lactam plus macrolide, or a respiratory fluoroquinolone) AND choose a DIFFERENT class than the one recently used. Recent antibiotics also raise MRSA and Pseudomonas risk.
Card 88Pneumonia Drill
DRILL. Admitted to the medical WARD with CAP, not ICU. Prescribe.
Ceftriaxone (or cefotaxime or ampicillin-sulbactam) PLUS azithromycin. OR respiratory fluoroquinolone monotherapy, which IS acceptable on the ward.
Card 89Pneumonia Drill
DRILL. Admitted to the ICU with severe CAP. Prescribe.
Beta-lactam PLUS macrolide, OR beta-lactam PLUS fluoroquinolone. NEVER fluoroquinolone monotherapy in the ICU.
Card 90Pneumonia Drill
DRILL. ICU CAP patient who also had a prior MRSA respiratory isolate. Prescribe.
Beta-lactam plus macrolide, PLUS vancomycin or linezolid. Severe CAP alone is already an MRSA trigger; a prior isolate makes it certain.
Card 91Pneumonia Drill
DRILL. CAP in a patient with bronchiectasis or cystic fibrosis. What must you add?
ANTIPSEUDOMONAL coverage: piperacillin-tazobactam, cefepime, meropenem, or levofloxacin. Structural lung disease is a Pseudomonas risk factor.
Card 92Pneumonia Drill
DRILL. Pneumonia developing on hospital day 5 in a non-intubated patient. Classify and prescribe.
HAP. Antipseudomonal beta-lactam (pip-tazo, cefepime, or meropenem) PLUS vancomycin or linezolid. Both MRSA and Pseudomonas are covered empirically in every case.
Card 93Pneumonia Drill
DRILL. Pneumonia developing 3 days after intubation. Classify and prescribe.
VAP. Same as HAP: antipseudomonal beta-lactam PLUS vancomycin or linezolid.
Card 94Pneumonia Drill
DRILL. Aspiration pneumonia in an alcoholic with poor dentition. Prescribe.
AMPICILLIN-SULBACTAM. One drug covering oral anaerobes, streptococci, and most gram negatives including Klebsiella.
Card 95Pneumonia Drill
DRILL. Aspiration pneumonia in a patient with a PENICILLIN ALLERGY. Prescribe.
MOXIFLOXACIN monotherapy (it has anaerobic activity), OR levofloxacin plus metronidazole, OR clindamycin.
Card 96Pneumonia Drill
DRILL. Necrotizing or cavitary pneumonia following influenza. What must you add?
MRSA coverage: vancomycin or linezolid. Post-influenza necrotizing pneumonia is a defined MRSA trigger.
Card 97Pneumonia Drill
DRILL. Alcoholic with currant jelly sputum and an upper lobe cavity with a bulging fissure. Organism and drug?
Klebsiella pneumoniae. Ceftriaxone for susceptible strains. If ESBL is suspected (prior antibiotics, healthcare exposure, prior ESBL), use a CARBAPENEM.
Card 98Pneumonia Drill
DRILL. Pneumonia with diarrhea, confusion, and sodium of 128. Test and drug?
Legionella. Urinary antigen test. Treat with a macrolide (azithromycin) or a respiratory fluoroquinolone (levofloxacin).
Card 99Pneumonia Drill
DRILL. PREGNANT patient with outpatient CAP. Prescribe, and what must you avoid?
AZITHROMYCIN. Avoid DOXYCYCLINE (fetal tooth staining, bone) and FLUOROQUINOLONES (cartilage). Amoxicillin is also safe in pregnancy.
Card 100Pneumonia Drill
DRILL. 4-year-old with uncomplicated CAP. Prescribe.
HIGH-DOSE AMOXICILLIN (90 mg/kg/day divided BID). First-line for pediatric CAP because Streptococcus pneumoniae is the dominant pathogen.
Card 101Pneumonia Drill
DRILL. School-age child or adolescent with gradual-onset pneumonia and prominent malaise. What changes?
Consider Mycoplasma and add or substitute a MACROLIDE. Atypicals become much more common after age 5.
Card 102Pneumonia Drill
DRILL. Patient with a history of penicillin ANAPHYLAXIS needs inpatient CAP therapy. Prescribe.
Respiratory FLUOROQUINOLONE (levofloxacin or moxifloxacin) monotherapy on the ward. Avoid all beta-lactams including cephalosporins after true anaphylaxis. For ICU-level disease, pair the fluoroquinolone with aztreonam plus vancomycin.
Card 103Pneumonia Drill
DRILL. Sputum culture returns pan-sensitive Streptococcus pneumoniae on day 2. What do you do?
DE-ESCALATE to the narrowest effective agent, usually amoxicillin or penicillin G, and stop the redundant coverage. Continuing broad empiric therapy after the organism is known is the wrong answer.
Card 104Pneumonia Drill
DRILL. When can you stop antibiotics in CAP?
Minimum 5 days AND afebrile 48 to 72 hours AND clinically stable. HAP and VAP get 7 days. Extend only for abscess, empyema, or resistant organisms.
Card 105Pneumonia Drill
DRILL. Which single fact makes MACROLIDE monotherapy possible for outpatient CAP?
Macrolides cover BOTH typical organisms (including Streptococcus pneumoniae) AND atypicals. Amoxicillin covers typicals only. That asymmetry is why a penicillin allergy moves you to a broader-spectrum drug, not a narrower one.
Flashcards: Pneumonia Organisms23 cards
Card 106Pneumonia Organisms
Contrast the CLASSIC radiographic pattern of typical vs atypical pneumonia, and state its real-world reliability.
Classic teaching: typical (pneumococcus, Klebsiella, H. flu) gives focal LOBAR CONSOLIDATION with air bronchograms; atypical (Mycoplasma, Chlamydophila, viral) gives DIFFUSE PATCHY interstitial infiltrates with findings worse than the patient looks. IMPORTANT: this correlation is UNRELIABLE in practice. Mycoplasma can consolidate and pneumococcus can look patchy. Guidelines do NOT use radiographic pattern to select therapy.
Card 107Pneumonia Organisms
Which pneumonia drugs cover TYPICAL organisms, ATYPICAL organisms, or both?
Amoxicillin: typical ONLY (best pneumococcal activity, narrowest spectrum). Macrolide, doxycycline, and respiratory fluoroquinolone: BOTH typical and atypical. This is why a single agent can be used empirically without identifying the organism.
Card 108Pneumonia Organisms
Do macrolides cover Streptococcus pneumoniae?
YES. That is why macrolide monotherapy is first-line for healthy outpatients. The limitation is RESISTANCE: pneumococcal macrolide resistance runs 25 to 30 percent in much of the US, so guidelines restrict monotherapy to areas under 25 percent. Many clinicians now prefer doxycycline for this reason.
Card 109Pneumonia Organisms
A healthy outpatient with CAP and NO drug allergy. What is first-line and why?
Amoxicillin 1 g three times daily. It has the best pneumococcal coverage and the narrowest spectrum. A penicillin allergy is what removes it and moves you to a macrolide or doxycycline, which happen to also cover atypicals.
Card 110Pneumonia Organisms
On a radiology report, does "opacity" mean the same thing as "consolidation"?
No. "Opacity" is a deliberately non-committal descriptor covering consolidation, atelectasis, effusion, or mass. "Consolidation" specifically means alveolar filling. Do not infer a lobar alveolar process from the word opacity alone.
Card 111Pneumonia Organisms
Why is the RIGHT LOWER LOBE the most common site for pneumonia of ANY cause?
The right mainstem bronchus is wider, shorter, and more vertical than the left, so aspirated or inhaled material preferentially enters it, and gravity carries it to the base. RLL location alone therefore does NOT distinguish aspiration from ordinary CAP.
Card 112Pneumonia Organisms
Which lung segments are involved in aspiration, and how does position change it?
SUPINE: superior segment of the right lower lobe, or posterior segment of the right upper lobe. UPRIGHT: basal segments of the right lower lobe.
Card 113Pneumonia Organisms
List the risk factors that make aspiration pneumonia the diagnosis.
Altered consciousness, alcohol use disorder, stroke, dysphagia, seizure, dementia, recent intubation or extubation, tube feeds, poor dentition, and GERD. An aspiration stem ALWAYS supplies one. Absent any risk factor, do not diagnose aspiration from the lobe alone.
Card 114Pneumonia Organisms
Which pneumonia organism causes "currant jelly" sputum, and who gets it?
Klebsiella pneumoniae. Classic in alcohol use disorder, diabetes, and aspiration. Causes UPPER lobe cavitation and a BULGING FISSURE from the inflammatory exudate's volume.
Card 115Pneumonia Organisms
Do third-generation cephalosporins cover Klebsiella? What are the two caveats?
Yes, ceftriaxone covers susceptible Klebsiella. Caveat 1: NO anaerobic coverage, so add metronidazole or use ampicillin-sulbactam for aspiration. Caveat 2: ESBL-producing strains hydrolyze third-generation cephalosporins and require a CARBAPENEM.
Card 116Pneumonia Organisms
Which third-generation cephalosporin covers Pseudomonas?
Ceftazidime. Ceftriaxone and cefotaxime have NO antipseudomonal activity.
Card 117Pneumonia Organisms
Which antibiotics provide reliable ANAEROBIC coverage?
Ampicillin-sulbactam, piperacillin-tazobactam, amoxicillin-clavulanate, metronidazole, clindamycin, carbapenems, and MOXIFLOXACIN. Macrolides, ceftriaxone, and levofloxacin do NOT.
Card 118Pneumonia Organisms
Young adult, gradual onset, prodromal URI, prominent myalgia, patchy bilateral infiltrates. Organism and treatment?
Mycoplasma pneumoniae (walking pneumonia). Treat with a macrolide or doxycycline. Beta-lactams FAIL because Mycoplasma has no cell wall.
Card 119Pneumonia Organisms
Name two classic extrapulmonary findings of Mycoplasma pneumoniae.
Cold agglutinin autoimmune hemolytic anemia (IgM), and bullous myringitis. Also erythema multiforme and Stevens-Johnson syndrome.
Card 120Pneumonia Organisms
Pneumonia with high fever, diarrhea, confusion, and HYPONATREMIA. Organism, test, and treatment?
Legionella pneumophila. Diagnose with a URINARY ANTIGEN test. Treat with a macrolide or respiratory fluoroquinolone. Also causes elevated LFTs. Associated with water systems, air conditioning, and cruise ships.
Card 121Pneumonia Organisms
Which pneumonia organism produces "rusty" sputum and is the most common cause of CAP?
Streptococcus pneumoniae. Lobar consolidation, abrupt onset, rigors, high fever.
Card 122Pneumonia Organisms
Post-influenza pneumonia that is necrotizing or cavitary. Which organism?
Staphylococcus aureus, including MRSA. This is one of the risk factors that triggers empiric MRSA coverage in CAP.
Card 123Pneumonia Organisms
A healthy young outpatient with CAP has a PENICILLIN ALLERGY and no comorbidities. What do you prescribe?
A macrolide or doxycycline. Reserve fluoroquinolones for patients with comorbidities, recent antibiotic exposure, or high local macrolide resistance, because of tendon rupture, QT prolongation, C. difficile, and aortic aneurysm risk.
Card 124Pneumonia Organisms
How much cross-reactivity exists between penicillins and cephalosporins?
Low and side-chain dependent, not ring dependent. Roughly 1 to 3 percent for third-generation cephalosporins, higher for first-generation agents whose R1 side chain resembles penicillin. A history of ANAPHYLAXIS to penicillin still warrants avoiding beta-lactams entirely.
Card 125Pneumonia Organisms
Why is oseltamivir wrong for a patient 3 weeks into a respiratory illness?
Neuraminidase inhibitors must be started within 48 HOURS of symptom onset to alter the course of influenza. A focal lobar opacity also indicates bacterial infection, not influenza.
Card 126Pneumonia Organisms
Why are aminoglycosides never used for outpatient community-acquired pneumonia?
They cover aerobic gram negatives only, penetrate lung tissue poorly, require parenteral administration and serum level monitoring, and carry nephrotoxicity and ototoxicity.
Card 127Pneumonia Organisms
Which viscerosomatic tender points correspond to the lungs, and which autonomic division?
T2 to T7, SYMPATHETIC. Parasympathetic supply to the lungs is the vagus, addressed at the OA, AA, and C2 region.
Card 128Pneumonia Organisms
Pneumonia in a patient with COPD or a smoker. Which two organisms rise in likelihood?
Haemophilus influenzae and Moraxella catarrhalis. Both are beta-lactamase producers, so amoxicillin-CLAVULANATE is preferred over plain amoxicillin.
Flashcards: Fetal Monitoring16 cards
Card 129Fetal Monitoring
What does the VEAL CHOP mnemonic stand for?
Variable = Cord compression. Early = Head compression. Accelerations = OK. Late = Placental insufficiency.
Card 130Fetal Monitoring
Describe an EARLY deceleration: timing, mechanism, and management.
Gradual fall that MIRRORS the contraction (nadir at the peak). Caused by fetal head compression triggering a vagal response. Benign. No intervention.
Card 131Fetal Monitoring
Describe a LATE deceleration: timing, mechanism, and management.
Gradual, symmetric fall BEGINNING AFTER the peak, returning to baseline only after the contraction ends. Caused by uteroplacental insufficiency. Start intrauterine resuscitation. If recurrent and refractory, DELIVER.
Card 132Fetal Monitoring
Describe a VARIABLE deceleration: timing, mechanism, and management.
ABRUPT fall (onset to nadir under 30 seconds), variable in shape and timing relative to contractions. Caused by umbilical cord compression. Reposition the mother, consider amnioinfusion.
Card 133Fetal Monitoring
What are the components of intrauterine resuscitation?
Reposition to left lateral decubitus, IV fluid bolus, supplemental oxygen, STOP oxytocin, correct maternal hypotension (ephedrine or phenylephrine), consider tocolysis for tachysystole.
Card 134Fetal Monitoring
Recurrent late decelerations persist after fluids, oxygen, repositioning, and stopping oxytocin. Next step?
Deliver. Emergency cesarean unless the patient meets ALL criteria for operative vaginal delivery.
Card 135Fetal Monitoring
What cervical exam finding is REQUIRED before forceps or vacuum delivery?
COMPLETE cervical dilation (10 cm). At 9 cm, operative vaginal delivery is contraindicated and the answer becomes cesarean.
Card 136Fetal Monitoring
List the prerequisites for operative vaginal (forceps or vacuum) delivery.
Complete dilation, ruptured membranes, engaged head at or below +2 station, known fetal position, adequate maternal anesthesia, empty bladder, no cephalopelvic disproportion, and a willingness to abandon for cesarean.
Card 137Fetal Monitoring
Define the three categories of fetal heart tracing.
Category I: normal baseline 110 to 160, moderate variability, no late or variable decels. Category II: everything in between (indeterminate). Category III: absent variability WITH recurrent late decels, recurrent variables, or bradycardia, OR a sinusoidal pattern. Category III requires prompt delivery.
Card 138Fetal Monitoring
What is the normal fetal heart rate baseline, and what defines brady and tachycardia?
Baseline 110 to 160/min. Bradycardia under 110, tachycardia over 160, each sustained for 10 minutes or more.
Card 139Fetal Monitoring
What defines a fetal ACCELERATION?
At or after 32 weeks: rise of 15 bpm above baseline lasting 15 seconds. Before 32 weeks: 10 bpm for 10 seconds. Accelerations indicate fetal well-being and rule out acidemia.
Card 140Fetal Monitoring
What is a PROLONGED deceleration, and what causes it?
A fall of 15 bpm or more lasting 2 to 10 minutes. Causes: cord prolapse, uterine rupture, placental abruption, maternal hypotension (often post-epidural), or tachysystole.
Card 141Fetal Monitoring
A SINUSOIDAL fetal heart rate pattern means what?
Fetal anemia. Think fetomaternal hemorrhage, Rh alloimmunization, or parvovirus B19. This is a Category III tracing requiring urgent delivery.
Card 142Fetal Monitoring
Define uterine tachysystole and its treatment.
More than 5 contractions in 10 minutes averaged over 30 minutes. Stop or reduce oxytocin. If decelerations persist, give a tocolytic such as subcutaneous terbutaline.
Card 143Fetal Monitoring
Sudden severe variable or prolonged decelerations with a palpable cord in the vagina. Management?
Umbilical cord prolapse. Elevate the presenting part with a gloved hand, place in Trendelenburg or knee-chest position, do NOT reduce the cord, and go to IMMEDIATE cesarean.
Card 144Fetal Monitoring
When is amnioinfusion used in labor?
For recurrent VARIABLE decelerations from cord compression, especially with oligohydramnios. It does not treat late decelerations.
Flashcards: Incontinence16 cards
Card 145Incontinence
Name the five types of urinary incontinence and the core mechanism of each.
Stress: urethral hypermobility or intrinsic sphincter deficiency. Urge (overactive bladder): detrusor overactivity. Overflow: detrusor underactivity or outlet obstruction. Mixed: both stress and urge. Functional: cognitive or mobility barrier with a normal urinary tract.
Card 146Incontinence
Leaks with coughing, sneezing, laughing, or lifting. Which type, and what is the mechanism?
Stress incontinence. Urethral hypermobility or intrinsic sphincter deficiency lets abdominal pressure exceed urethral closure pressure.
Card 147Incontinence
Sudden overwhelming urgency with leakage on the way to the bathroom, plus nocturia. Which type?
Urge incontinence, from detrusor overactivity. Also called overactive bladder.
Card 148Incontinence
Continuous dribbling with a sense of incomplete emptying. Which type, and what test confirms it?
Overflow incontinence. Confirm with a POSTVOID RESIDUAL, which is elevated. PVR is the single test that separates overflow from every other type.
Card 149Incontinence
Which incontinence treatment is first-line for STRESS, URGE, and MIXED types alike?
Pelvic floor muscle training (Kegel exercises). It is most associated with stress incontinence but is first-line across all three, which is why it can be the answer in more than one setting.
Card 150Incontinence
Give the full treatment ladder for STRESS incontinence.
1) Pelvic floor muscle training plus weight loss. 2) Pessary (incontinence or ring) to support the urethrovesical junction. 3) Urethral bulking agents for poor surgical candidates. 4) MIDURETHRAL SLING, the definitive and most effective treatment.
Card 151Incontinence
What is the definitive surgical treatment for stress incontinence?
Midurethral sling.
Card 152Incontinence
What is the non-surgical MECHANICAL device used for stress incontinence?
A pessary (incontinence or ring pessary). It supports the urethrovesical junction and is the usual answer when pelvic floor training has already been tried or is already listed.
Card 153Incontinence
Give the treatment ladder for URGE incontinence / overactive bladder.
1) Behavioral: bladder training, timed voiding, fluid and caffeine reduction, pelvic floor exercises. 2) Pharmacologic: antimuscarinic (oxybutynin, tolterodine) or mirabegron. 3) Refractory: intravesical botulinum toxin, sacral neuromodulation, percutaneous tibial nerve stimulation.
Card 154Incontinence
Why is mirabegron preferred over oxybutynin in elderly patients?
Mirabegron is a beta-3 agonist with no anticholinergic burden. Antimuscarinics cause confusion, falls, dry mouth, constipation, urinary retention, and carry an association with dementia risk. Monitor blood pressure on mirabegron.
Card 155Incontinence
What must be excluded BEFORE diagnosing or treating overactive bladder?
Urinary tract infection. Check a urinalysis, and obtain a URINE CULTURE if nitrites or leukocyte esterase are positive. UTI is a common and fully reversible cause of urgency and urge incontinence.
Card 156Incontinence
What does a POSITIVE urine NITRITE indicate, and how sensitive is it?
Nitrate-reducing bacteria (Enterobacteriaceae: E. coli, Klebsiella, Proteus). Highly SPECIFIC for bacteriuria but poorly sensitive, so a positive result is meaningful and a negative one does not exclude infection.
Card 157Incontinence
What does the DIAPPERS mnemonic cover, and when do you use it?
Reversible causes of incontinence to clear before labeling a chronic type: Delirium, Infection, Atrophic vaginitis, Pharmaceuticals, Psychological, Excess urine output, Restricted mobility, Stool impaction.
Card 158Incontinence
When is urodynamic testing indicated in incontinence?
Second line only: diagnostic uncertainty, mixed or refractory symptoms, or planning before surgical intervention. Never before infection has been excluded and conservative measures tried.
Card 159Incontinence
When is urine CYTOLOGY indicated in a patient with urinary symptoms?
When there is HEMATURIA, to screen for urothelial carcinoma. Cytology has no role in evaluating urgency or incontinence by itself.
Card 160Incontinence
Why can starting an anticholinergic be harmful if a UTI has not been excluded?
Anticholinergics impair bladder emptying and raise postvoid residual, which can worsen an untreated infection, while treating the wrong problem entirely.
Flashcards: Exanthems16 cards
Card 161Exanthems
Which rashes classically involve the PALMS AND SOLES?
Mnemonic CARS: Coxsackie (hand-foot-and-mouth), And Rocky Mountain spotted fever, Syphilis (secondary). Also Kawasaki, toxic shock, erythema multiforme, and the desquamation phase of scarlet fever.
Card 162Exanthems
Rash starting on the WRISTS AND ANKLES and spreading CENTRALLY. Diagnosis and treatment?
Rocky Mountain spotted fever (Rickettsia rickettsii). Treat with DOXYCYCLINE at any age including children. Treat empirically; serology is retrospective. Untreated mortality 20 to 25 percent.
Card 163Exanthems
Why is doxycycline given to children for RMSF despite the tetracycline rule?
Short courses do not cause clinically significant tooth staining, and untreated RMSF is frequently fatal. Withholding doxycycline in suspected RMSF is a documented cause of preventable pediatric death. Chloramphenicol is the pregnancy alternative.
Card 164Exanthems
Diffuse NON-PRURITIC copper-colored papulosquamous rash including palms and soles. Diagnosis?
Secondary syphilis. Appears diffusely rather than spreading directionally. Look for condyloma lata, generalized lymphadenopathy, and a preceding painless chancre.
Card 165Exanthems
FIRST disease: name, rash pattern, and key discriminator.
Measles (rubeola). Rash begins at the hairline and behind the ears, spreads CEPHALOCAUDALLY, becomes confluent. Discriminators: the 3 Cs (cough, coryza, conjunctivitis), KOPLIK SPOTS, high fever, and a sick-appearing child. Spares palms and soles.
Card 166Exanthems
SECOND disease: name, rash pattern, and key discriminator.
Scarlet fever (group A Streptococcus). SANDPAPER-textured rash on trunk and flexures. Discriminators: circumoral pallor, strawberry tongue, PASTIA LINES in skin folds, preceding pharyngitis. Acute rash spares palms and soles, but they DESQUAMATE during recovery.
Card 167Exanthems
THIRD disease: name, rash pattern, and key discriminator.
Rubella (German measles). Pink rash spreading face to downward, fading in about 3 days. Discriminators: POSTERIOR AURICULAR, OCCIPITAL, and posterior cervical LYMPHADENOPATHY; Forchheimer spots; the child looks WELL. Spares palms and soles.
Card 168Exanthems
FIFTH disease: name, organism, rash pattern, and contagiousness.
Erythema infectiosum, parvovirus B19. SLAPPED CHEEK appearance followed by a lacy reticular rash on the extremities. The rash appears as viremia resolves, so the child is NO LONGER CONTAGIOUS once the rash is visible and needs no school exclusion. Spares palms and soles.
Card 169Exanthems
SIXTH disease: name, organism, and the defining SEQUENCE.
Roseola infantum, HHV-6. High fever for 3 to 5 days in a WELL-APPEARING infant, then the FEVER BREAKS AND THE RASH APPEARS. Trunk to extremities, spares the face. The order of events is the diagnosis.
Card 170Exanthems
Which childhood exanthem shows lesions in DIFFERENT STAGES simultaneously?
Varicella. Macules, papules, vesicles, and crusts coexist in crops. Classic description: "dew drop on a rose petal." Spares palms and soles.
Card 171Exanthems
What is the contagious period for VARICELLA?
From 1 to 2 days BEFORE the rash appears until ALL lesions have crusted over, roughly 5 days after onset. Airborne plus contact transmission; secondary attack rate near 90 percent in susceptible household contacts.
Card 172Exanthems
Name three complications of parvovirus B19 beyond the rash.
1) APLASTIC CRISIS in sickle cell disease or chronic hemolysis, since B19 infects erythroid progenitors. 2) HYDROPS FETALIS in pregnancy. 3) Symmetric POLYARTHROPATHY in adults, mimicking rheumatoid arthritis.
Card 173Exanthems
Fever 5+ days, conjunctivitis, strawberry tongue, cervical node, and swollen hands. Diagnosis and why palms matter?
Kawasaki disease. Palms and soles show erythema and edema acutely, then DESQUAMATION in week 2. Requires fever 5 days plus 4 of 5 criteria. Treat with IVIG and aspirin; obtain echocardiography for coronary aneurysms.
Card 174Exanthems
Distinguish measles conjunctivitis from Kawasaki conjunctivitis.
Measles: EXUDATIVE conjunctivitis with discharge, plus cough and coryza. Kawasaki: bilateral NONEXUDATIVE (limbic-sparing) conjunctival injection, no respiratory prodrome.
Card 175Exanthems
What is the management of measles?
Report to the health department immediately, AIRBORNE isolation (not droplet), and VITAMIN A for all children, which reduces morbidity and mortality. Supportive care otherwise. Post-exposure prophylaxis: MMR within 72 hours or immune globulin within 6 days.
Card 176Exanthems
Vesicles on the palms, soles, and oral ulcers in a child under 5. Diagnosis?
Hand-foot-and-mouth disease, coxsackievirus A16. One of the few pediatric exanthems that DOES involve palms and soles. Self-limited; supportive care.
Flashcards: EPS / Movement15 cards
Card 177EPS / Movement
Antipsychotic side effect appearing within HOURS TO DAYS: name, features, treatment.
Acute dystonia. Sustained muscle contraction: torticollis, oculogyric crisis, trismus, laryngospasm (can be fatal). Treat with IM or IV benztropine or diphenhydramine (anticholinergic or antihistamine).
Card 178EPS / Movement
Antipsychotic side effect appearing within DAYS TO WEEKS: name, features, treatment.
Akathisia. Subjective inner restlessness with an inability to sit still, often pacing or leg rocking. First-line propranolol; alternatives benzodiazepine or mirtazapine. LOWER the antipsychotic dose.
Card 179EPS / Movement
Antipsychotic side effect appearing within WEEKS TO MONTHS: name, features, treatment.
Drug-induced parkinsonism. Bradykinesia, cogwheel rigidity, resting tremor, masked facies. Treat with benztropine or amantadine, reduce the dose, or switch to a lower-potency or second-generation agent.
Card 180EPS / Movement
Antipsychotic side effect appearing after MONTHS TO YEARS: name, features, treatment.
Tardive dyskinesia. Choreoathetoid orofacial movements: lip smacking, tongue thrusting, grimacing. Treat with a VMAT2 inhibitor (valbenazine or deutetrabenazine) and/or switch to clozapine.
Card 181EPS / Movement
Give the full timeline of antipsychotic movement side effects in order of onset.
Hours to days: acute dystonia. Days to weeks: akathisia. Weeks to months: parkinsonism. Months to years: tardive dyskinesia. NMS can occur at ANY time but often within the first 2 weeks or after a dose increase.
Card 182EPS / Movement
Three exam features that identify tardive dyskinesia on physical examination.
Movements DISAPPEAR during sleep, can be briefly SUPPRESSED voluntarily, and are EXACERBATED by distraction or by performing a task with the other hand.
Card 183EPS / Movement
Which antipsychotic carries the LOWEST risk of tardive dyskinesia and EPS, and why?
Clozapine. It has minimal D2 receptor occupancy. It may also improve existing TD, making it the preferred switch for a patient who still needs antipsychotic coverage.
Card 184EPS / Movement
What are the FDA-approved first-line drugs for tardive dyskinesia?
VMAT2 inhibitors: valbenazine and deutetrabenazine. They deplete presynaptic dopamine. Usually started while CONTINUING the antipsychotic, since abrupt withdrawal can transiently worsen the dyskinesia.
Card 185EPS / Movement
Why is carbidopa-levodopa wrong for tardive dyskinesia?
It increases dopaminergic tone, which worsens the dyskinesia and can exacerbate psychosis. TD treatment goes the opposite direction: deplete or block dopamine.
Card 186EPS / Movement
Name the tetrad of neuroleptic malignant syndrome.
Fever, LEAD-PIPE rigidity, autonomic instability (labile BP, tachycardia, diaphoresis), and altered mental status. Labs show a markedly elevated creatine kinase, leukocytosis, and myoglobinuria.
Card 187EPS / Movement
What is the treatment for neuroleptic malignant syndrome?
Stop the antipsychotic immediately, aggressive cooling and IV fluids, then dantrolene (ryanodine receptor blocker) and/or bromocriptine or amantadine (dopamine agonists). ICU-level care.
Card 188EPS / Movement
Distinguish neuroleptic malignant syndrome from serotonin syndrome.
NMS: onset over days, LEAD-PIPE rigidity, hyporeflexia, normal pupils, follows a dopamine ANTAGONIST. Serotonin syndrome: onset within hours, CLONUS and HYPERreflexia (lower limbs worse), mydriasis, diarrhea, follows a serotonergic agent. Treat serotonin syndrome with cyproheptadine.
Card 189EPS / Movement
Distinguish tardive dyskinesia from acute dystonia.
TD: months to years, choreoathetoid and writhing, orofacial, suppressible, treated by REMOVING the drug and adding a VMAT2 inhibitor. Acute dystonia: hours to days, sustained painful contraction, NOT suppressible, treated with an anticholinergic.
Card 190EPS / Movement
Which antipsychotics carry the HIGHEST risk of extrapyramidal symptoms?
High-potency first-generation agents: haloperidol, fluphenazine, trifluoperazine. Mnemonic: high potency equals high EPS, low anticholinergic and sedating effects. Low-potency agents (chlorpromazine, thioridazine) invert that.
Card 191EPS / Movement
Why is an anticholinergic like benztropine NOT used for tardive dyskinesia?
Anticholinergics treat acute dystonia and drug-induced parkinsonism but can WORSEN tardive dyskinesia. Knowing which EPS syndrome you are treating changes the drug class entirely.
Flashcards: Study Design8 cards
Card 192Study Design
Define INTERNAL validity and name its main threats.
Whether the study accurately measures what it claims WITHIN its own sample, i.e. the observed effect is truly caused by the intervention. Threatened by confounding, selection bias, information bias, and attrition.
Card 193Study Design
Define EXTERNAL validity and what determines it.
Generalizability: whether results apply to populations OUTSIDE the study. Determined by WHO you enrolled (inclusion/exclusion criteria, setting, demographics), not by how you assigned them.
Card 194Study Design
Why does RANDOMIZATION protect internal validity specifically?
It distributes KNOWN AND UNKNOWN confounders evenly across arms. Statistical adjustment can only control variables you measured; randomization controls the ones nobody thought to measure.
Card 195Study Design
Match the study design: RARE DISEASE.
Case-control. It samples ON THE OUTCOME, so you can deliberately assemble enough cases. Yields an ODDS RATIO. Vulnerable to recall bias and control selection bias.
Card 196Study Design
Match the study design: RARE EXPOSURE.
Cohort study. Sample on the exposure and follow forward. Yields incidence and RELATIVE RISK.
Card 197Study Design
Match the study design: need PREVALENCE or a quick burden estimate for health services planning.
Cross-sectional (survey). Measures exposure and outcome at ONE point in time. Cannot establish temporality. Fails for rare diseases because you take whatever the population gives you.
Card 198Study Design
Match the study design: strongest evidence that an intervention WORKS, no ethical or resource barrier.
Randomized controlled trial. Randomization controls known and unknown confounders. A systematic review with meta-analysis of RCTs ranks above a single RCT.
Card 199Study Design
Which measure of association comes from each design?
Cohort and RCT: RELATIVE RISK (and incidence). Case-control: ODDS RATIO. Cross-sectional: prevalence and prevalence odds ratio.
Flashcards: Statistics12 cards
Card 200Statistics
When is a confidence interval statistically significant?
RATIO measures (RR, OR, HR): significant when the CI EXCLUDES 1.0. DIFFERENCE measures (risk difference, mean difference): significant when the CI excludes 0.
Card 201Statistics
An odds ratio of 1.77 with 95% CI 0.82 to 4.91. Is it significant, and what does the width tell you?
NOT significant, because the interval crosses 1.0. The very wide interval signals few events and poor precision. A large point estimate with a wide interval tells you nothing.
Card 202Statistics
Distinguish STATISTICAL from CLINICAL significance.
Statistical significance = the effect is distinguishable from no effect; determined by whether the CI crosses the null. Clinical significance = the effect is large enough to matter; determined by MAGNITUDE. An OR of 1.04 with CI 1.01-1.07 is statistically significant but clinically trivial.
Card 203Statistics
What does a p value of 0.049 actually mean?
The probability of observing a result this extreme or more extreme IF THE NULL HYPOTHESIS WERE TRUE. It is the probability of the data given the null, NOT the probability that the null is true.
Card 204Statistics
Which statistical test: 2 groups, CONTINUOUS outcome?
t-test. (Paired data: paired t-test. Non-normal or ordinal: Mann-Whitney U.)
Card 205Statistics
Which statistical test: 3 or more groups, CONTINUOUS outcome?
ANOVA. Running multiple pairwise t-tests inflates the type I error rate. A significant ANOVA needs a post-hoc test (Tukey, Bonferroni) to identify WHICH pair differs.
Card 206Statistics
Which statistical test: CATEGORICAL outcome, any number of groups?
Chi-square. Use FISHER EXACT test when expected cell counts are under 5.
Card 207Statistics
Which statistical test: non-normal or ordinal data?
Mann-Whitney U for 2 groups; Kruskal-Wallis for 3 or more.
Card 208Statistics
State the EMPIRICAL RULE for a normal distribution.
68 percent within 1 SD, 95 percent within 2 SD, 99.7 percent within 3 SD. For an exact 95 percent confidence interval use 1.96 SD, not 2.
Card 209Statistics
Distinguish standard DEVIATION from standard ERROR of the mean.
SD describes the spread of individual data points. SEM describes the precision of the sample mean and equals SD divided by the square root of n. SEM builds confidence intervals around a mean; SD tells you where individuals fall.
Card 210Statistics
Define POWER, and what increases it.
Power = 1 minus beta, the probability of detecting a true effect. Conventionally set at 80 percent or higher. Increased by larger sample size, larger effect size, lower variability, and a higher alpha.
Card 211Statistics
Distinguish type I from type II error.
Type I (alpha): rejecting a true null, i.e. a FALSE POSITIVE conclusion. Type II (beta): failing to reject a false null, i.e. a FALSE NEGATIVE. Mnemonic: type I is convicting an innocent person.
Flashcards: Bias6 cards
Card 212Bias
Distinguish SELECTION bias from INFORMATION bias.
Selection bias: the distortion comes from WHO GOT INTO the study (referral/Berkson bias, healthy worker effect, loss to follow-up). Information bias: the distortion comes from HOW DATA WERE COLLECTED on those already enrolled (recall, observer, misclassification).
Card 213Bias
Define RECALL bias and which design it plagues.
Cases remember past exposures more thoroughly than controls, because illness prompts them to search their memory. Essentially confined to CASE-CONTROL studies.
Card 214Bias
A tertiary referral center reports an inflated rate of a procedure. Name the bias.
Selection bias, specifically REFERRAL bias (Berkson bias when it involves hospitalized patients). The denominator is enriched for high-risk cases and is not representative.
Card 215Bias
Define CONFOUNDING and how each design handles it.
A third variable associated with both exposure and outcome that distorts the apparent relationship. Handled at DESIGN stage by randomization, restriction, or matching; at ANALYSIS stage by stratification or multivariable regression. Only randomization controls UNMEASURED confounders.
Card 216Bias
Define LEAD-TIME bias and LENGTH-TIME bias.
Lead-time bias: screening detects disease earlier, so survival TIME appears longer without changing the date of death. Length-time bias: screening preferentially detects SLOW-GROWING, indolent disease, making screen-detected cases look more survivable.
Card 217Bias
Define the HEALTHY WORKER EFFECT.
Employed populations are healthier than the general population, so occupational cohorts show artificially LOW disease rates. A form of selection bias; also causes cross-sectional studies to miss workers who left because of illness.