PANCE Exam Flashcards

Q: How is PANCE content weighted in the current NCCPA blueprint?

The blueprint effective January 2025 weights 15 content areas: cardiovascular 11%, pulmonary 9%, gastrointestinal/nutrition 8%, musculoskeletal 8%, infectious diseases 7%, neurologic 7%, psychiatry/behavioral science 7%, reproductive 7%, endocrine 6%, eyes/ears/nose/throat 6%, professional practice 6%, hematologic 5%, renal 5%, dermatologic 4%, and genitourinary 4%. Medical content is 94% of the exam and professional practice is the other 6%. NCCPA also states that 8-10% of the exam covers general surgical topics and 12-15% covers pediatric patients.

Q: What are the PANCE task categories?

Every medical content question is also coded to a task category. In the January 2025 blueprint those are: formulating the most likely diagnosis 18%, history taking and performing physical examination 16%, clinical intervention 16%, pharmaceutical therapeutics 15%, health maintenance/patient education/preventive measures 11%, using diagnostic and laboratory studies 10%, applying basic scientific concepts 8%, and professional practice 6%. Roughly half the exam is diagnosis plus management, which is why cards that teach a discriminator or a first-line treatment pay off more than cards that only define a term.

Q: How many questions are on the PANCE and how long is it?

NCCPA administers PANCE as five blocks of 60 questions, 300 multiple-choice questions in total, with 60 minutes to complete each block. That is 5 hours of exam time. You also get 45 minutes of break time to use between blocks and 15 minutes for a tutorial, so plan on roughly a 6-hour appointment. Break time used beyond the 45 minutes is deducted from your exam time.

Q: What is the PANCE passing score?

PANCE is reported as a scaled score, not a percentage. The scale runs from 200 to 800 and the passing score is 350, set by an Angoff standard-setting panel of certified PAs and approved by the NCCPA Board of Directors. Because scaled scores are equated across test forms, candidates of equal ability receive the same score regardless of which form they take, so there is no fixed number of correct answers that guarantees a pass.

Q: What is the PANCE first-time pass rate?

NCCPA's five-year pass-rate table reports a 91.5% first-time pass rate for 2025 across 13,145 first-time test takers, with a mean scaled score of 458.65. The rate across all 14,669 exams administered that year, including repeat attempts, was 88.4%. First-time rates in the preceding four years were 92.4% (2024), 92.0% (2023), 91.9% (2022), and 93.2% (2021).

Q: What is the PANCE retake policy if I fail?

NCCPA allows PANCE to be taken one time in any single 90-day period or three times in a calendar year, whichever is fewer, so the minimum wait after a failed attempt is 90 days. There is no separate longer waiting period published for a fourth attempt, but once you have used three attempts in one calendar year you must wait until the next calendar year. Separately, the six-years-six-attempts rule caps you at six attempts within six years of completing your PA program; when either limit is exhausted you lose eligibility permanently unless you complete another ARC-PA accredited program.

Q: How are these 50 PANCE flashcards distributed?

Cards are allocated in proportion to the January 2025 NCCPA content weights: cardiovascular 6; pulmonary 5; gastrointestinal/nutrition, musculoskeletal, infectious diseases, and neurologic 4 each; endocrine, EENT, psychiatry, reproductive, and professional practice 3 each; and dermatologic, genitourinary, hematologic, and renal 2 each. Because 50 cards cannot land exactly on weights that work out to half a card, categories tied at the same percentage were separated by a documented rounding rule, so eight areas sit exactly 1 percentage point above or below their official share and the other seven match it exactly.

Q: Are flashcards enough preparation for the PANCE?

No. Flashcards are best used for the discriminators the exam rewards: which crystal, which murmur, which CSF pattern, which first-line drug. Half of PANCE is diagnosis and management under time pressure, so pair recall work with full 60-question timed blocks to build the stamina five back-to-back blocks demand. Most candidates report 180-320 hours of total preparation, and your score report's content-area subscores are the most reliable guide to where to spend the next block of study time.

Question 1

STEMI versus NSTEMI: what separates them, and how does that change the first hour of care?

Accepted Answer

Both raise troponin. STEMI requires new ST elevation at the J point in two contiguous leads: at least 1 mm in most leads, or at least 2 mm in V2-V3 for men 40 and older (2.5 mm under 40, 1.5 mm in women). STEMI needs immediate reperfusion - primary PCI within 90 minutes of first medical contact, or within 120 minutes if transfer is required, and fibrinolysis within 30 minutes of arrival when PCI is unavailable. NSTEMI shows ST depression, T-wave inversion, or no change; it is treated with antithrombotic therapy and risk-stratified angiography. Fibrinolysis is harmful in NSTEMI and must not be given.

Question 2

Which four drug classes form guideline-directed therapy for heart failure with reduced ejection fraction, and which of them actually reduce mortality?

Accepted Answer

All four reduce mortality in HFrEF (ejection fraction 40% or less): an angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan, preferred over an ACE inhibitor or ARB); an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol); a mineralocorticoid receptor antagonist (spironolactone or eplerenone); and an SGLT2 inhibitor (dapagliflozin or empagliflozin). Loop diuretics relieve congestion and symptoms but do not improve survival. Never start an ARNI within 36 hours of the last ACE inhibitor dose - the overlap causes angioedema.

Question 3

At the bedside, how do you tell the murmur of aortic stenosis from mitral regurgitation?

Accepted Answer

Aortic stenosis is a crescendo-decrescendo systolic ejection murmur, loudest at the right second intercostal space, radiating to the carotids, with a delayed and diminished carotid upstroke (pulsus parvus et tardus) and a soft or absent S2. Mitral regurgitation is holosystolic, loudest at the apex, and radiates to the axilla. Maneuvers settle it: handgrip raises afterload and makes mitral regurgitation louder while softening aortic stenosis. Valsalva reduces preload and softens both - but makes hypertrophic obstructive cardiomyopathy louder, which is the classic trap.

Question 4

What does the CHA2DS2-VASc score measure, and at what score do you anticoagulate in nonvalvular atrial fibrillation?

Accepted Answer

It estimates annual stroke risk: Congestive heart failure, Hypertension, Age 75 or older (2 points), Diabetes, prior Stroke/TIA/thromboembolism (2 points), Vascular disease, Age 65-74, and Sex category female - maximum 9. Anticoagulate at 2 or more in men and 3 or more in women; a single non-sex risk factor is a shared-decision zone. Direct oral anticoagulants are preferred over warfarin in nonvalvular atrial fibrillation, but warfarin is still required for a mechanical valve or moderate-to-severe mitral stenosis, where DOACs are contraindicated.

Question 5

Hypertensive emergency versus hypertensive urgency: what defines each, and how fast should the pressure come down?

Accepted Answer

The number alone never decides it - acute target-organ damage does. Emergency means severe hypertension (usually above 180/120) WITH encephalopathy, intracranial hemorrhage, acute coronary syndrome, pulmonary edema, aortic dissection, eclampsia, acute kidney injury, or papilledema: use IV agents and lower mean arterial pressure by no more than 25% in the first hour, because faster drops cause cerebral and renal hypoperfusion. Urgency means the same numbers without organ damage: oral agents over 24-48 hours, no IV push, no ICU. The exception is aortic dissection, which needs systolic pressure under 120 and heart rate under 60 within about 20 minutes, using an IV beta-blocker such as esmolol BEFORE any vasodilator.

Question 6

When does a D-dimer help in suspected pulmonary embolism, and when will it mislead you?

Accepted Answer

D-dimer is a rule-out test only, and only at low or intermediate pretest probability (for example Wells 4 or less, or a PERC-negative low-risk patient). In that setting a negative high-sensitivity D-dimer excludes pulmonary embolism without imaging. At high pretest probability, skip it and go straight to CT pulmonary angiography - a negative D-dimer does not exclude PE there. D-dimer also rises nonspecifically with age, pregnancy, malignancy, infection, recent surgery, and trauma, so use an age-adjusted threshold (age times 10 ng/mL FEU) above age 50 to cut false positives.

Question 7

Which spirometry findings separate asthma from COPD, and which point to restrictive disease instead?

Accepted Answer

Both asthma and COPD reduce the FEV1/FVC ratio. Asthma is reversible: FEV1 improves by at least 12% AND at least 200 mL after a bronchodilator. COPD is defined by a post-bronchodilator FEV1/FVC below 0.70 that persists; severity (GOLD 1-4) is then graded by post-bronchodilator FEV1 percent predicted at 80 or above, 50-79, 30-49, and below 30. Restrictive disease is the opposite pattern - FVC falls with a normal or high ratio - and spirometry alone cannot confirm it; you need lung volumes showing a reduced total lung capacity.

Question 8

A previously healthy adult with community-acquired pneumonia, no comorbidities and no recent antibiotics: what is first-line outpatient therapy?

Accepted Answer

Amoxicillin 1 g three times daily, doxycycline, or a macrolide - the macrolide only where local pneumococcal macrolide resistance is under 25%. If the patient has chronic heart, lung, liver or renal disease, diabetes, alcohol use disorder, malignancy, or asplenia, escalate to a beta-lactam plus a macrolide or doxycycline, or a respiratory fluoroquinolone alone. Treat for a minimum of 5 days and only stop once the patient has been afebrile and clinically stable for 48 hours. CURB-65 (confusion, BUN above 19 mg/dL, respiratory rate 30 or more, systolic under 90 or diastolic 60 or less, age 65 or older) of 0-1 supports outpatient management.

Question 9

Which pneumothorax must be decompressed before any chest x-ray is obtained?

Accepted Answer

Tension pneumothorax - hypotension, distended neck veins, absent breath sounds with hyperresonance, and tracheal deviation AWAY from the affected side. It is a clinical diagnosis; waiting for imaging can be fatal because the mediastinal shift obstructs venous return. Decompress immediately with a large-bore needle or catheter - in adults the fourth or fifth intercostal space at the anterior axillary line is now preferred over the second intercostal space at the midclavicular line - then place a chest tube. A simple pneumothorax with stable vital signs can be imaged first.

Question 10

Which paraneoplastic syndromes point to small cell lung cancer rather than squamous cell carcinoma?

Accepted Answer

Small cell (central, strongly smoking-related, rarely resectable) produces SIADH with hyponatremia, ectopic ACTH causing Cushing syndrome, and Lambert-Eaton myasthenic syndrome - weakness that IMPROVES with repeated use, the reverse of myasthenia gravis. Squamous cell (central, cavitates) produces PTHrP-mediated hypercalcemia. Adenocarcinoma is the most common type overall and in never-smokers, is usually peripheral, and is linked to hypertrophic pulmonary osteoarthropathy. A Pancoast tumor at the apex causes Horner syndrome and arm pain regardless of histology.

Question 11

Why is short-acting beta-agonist-only rescue no longer recommended in asthma?

Accepted Answer

SABA alone relieves bronchoconstriction but treats none of the underlying inflammation, and SABA-only regimens are associated with more exacerbations and asthma deaths. Current guidance for adults and adolescents 12 and older is an inhaled-corticosteroid-containing reliever: as-needed low-dose ICS-formoterol, used either alone in mild disease or as both maintenance and reliever therapy (MART/SMART) at higher steps. Judge control by daytime symptoms, night waking, reliever frequency, and activity limitation over the past 4 weeks - not by peak flow alone, and not by how good the patient says they feel today.

Question 12

Which reflux symptoms require endoscopy instead of an empiric PPI trial?

Accepted Answer

The alarm features: dysphagia, odynophagia, unintentional weight loss, GI bleeding or iron-deficiency anemia, persistent vomiting, a palpable mass or lymphadenopathy, and new-onset symptoms after age 60. Without them, treat empirically with 8 weeks of a once-daily PPI taken 30-60 minutes BEFORE a meal - timing matters because PPIs only bind actively secreting proton pumps. Long-standing reflux risks Barrett esophagus, a metaplastic change from squamous to intestinal-type columnar epithelium that raises the risk of esophageal adenocarcinoma and warrants surveillance.

Question 13

How do you confirm that Helicobacter pylori has been eradicated, and what must the patient stop first?

Accepted Answer

Test-of-cure with a urea breath test or stool antigen assay at least 4 weeks after finishing therapy. Serology cannot be used - IgG stays positive for years after successful treatment. False negatives are the trap: hold PPIs for 1-2 weeks and antibiotics or bismuth for 4 weeks before testing, because suppressed bacterial load reads as cure. First-line therapy has shifted to 14 days of bismuth quadruple therapy (PPI, bismuth, tetracycline, metronidazole) because clarithromycin resistance has made older triple therapy unreliable.

Question 14

Which two of three criteria establish acute pancreatitis, and does the enzyme level predict severity?

Accepted Answer

Diagnosis needs two of three: characteristic epigastric pain radiating to the back; lipase or amylase at least three times the upper limit of normal; or characteristic findings on imaging. Lipase is more sensitive and specific than amylase and stays elevated longer. The enzyme level does NOT correlate with severity or prognosis, so do not use it to triage. Gallstones and alcohol cause most cases. Manage with goal-directed fluid resuscitation using lactated Ringer at moderate rather than aggressive rates, analgesia, and early oral feeding as tolerated. Prophylactic antibiotics are not indicated in the absence of infected necrosis.

Question 15

Crohn disease versus ulcerative colitis: which features reliably separate them?

Accepted Answer

Crohn disease can involve anywhere from mouth to anus, with skip lesions, transmural inflammation, non-caseating granulomas, and the complications that follow full-thickness disease - fistulas, strictures, and perianal disease. The terminal ileum is the most common site and smoking makes it worse. Ulcerative colitis is continuous from the rectum proximally, limited to mucosa and submucosa, shows crypt abscesses, presents with bloody diarrhea and tenesmus, is associated with primary sclerosing cholangitis, and is paradoxically less common in smokers. Both raise colorectal cancer risk enough to require surveillance colonoscopy beginning about 8 years after diagnosis.

Question 16

How do synovial fluid crystals distinguish gout from pseudogout?

Accepted Answer

Gout: needle-shaped, NEGATIVELY birefringent monosodium urate crystals that appear yellow when aligned parallel to the polarizer. Pseudogout: rhomboid, POSITIVELY birefringent calcium pyrophosphate crystals that appear blue when parallel. Gout classically strikes the first metatarsophalangeal joint (podagra); pseudogout favors the knee and wrist and shows chondrocalcinosis - linear cartilage calcification - on x-ray. Serum uric acid is unreliable during an acute flare: it is often normal or low, so it neither confirms nor excludes gout. Arthrocentesis is the diagnostic test.

Question 17

A hot, swollen, painful single joint: what forces urgent arthrocentesis and empiric antibiotics?

Accepted Answer

Acute monoarthritis with fever or an inability to bear weight - septic arthritis destroys articular cartilage within days. A synovial white cell count above 50,000/microL with more than 90% neutrophils strongly favors infection, but crystal disease can overlap that range and the two can coexist, so a positive crystal result never rules out infection. Staphylococcus aureus is the most common organism overall; Neisseria gonorrhoeae dominates in young sexually active adults, presenting with migratory polyarthralgia, tenosynovitis, and pustular skin lesions. Aspirate BEFORE the first antibiotic dose, then drain the joint.

Question 18

Which hand joints and stiffness pattern separate rheumatoid arthritis from osteoarthritis?

Accepted Answer

Rheumatoid arthritis is symmetric and involves the MCP and PIP joints and wrists while SPARING the DIP joints; morning stiffness lasts more than an hour and improves with use. Anti-cyclic citrullinated peptide antibody is the most specific serology, and a DMARD - methotrexate first-line - should start early to prevent irreversible erosion. Osteoarthritis involves the DIP joints (Heberden nodes) and PIP joints (Bouchard nodes) asymmetrically along with weight-bearing joints; stiffness lasts under 30 minutes and worsens with use through the day. Its x-ray shows joint-space narrowing, osteophytes, subchondral sclerosis, and subchondral cysts.

Question 19

Which low back pain red flags override the usual rule of no early imaging?

Accepted Answer

Cauda equina syndrome - saddle anesthesia, urinary retention with overflow incontinence, bilateral leg weakness - demands emergent MRI and surgical decompression. Also image for suspected infection (fever, injection drug use, recent bacteremia), suspected malignancy (cancer history, unexplained weight loss, night pain), significant trauma or osteoporosis with possible compression fracture, and any progressive neurologic deficit. Without red flags, acute low back pain needs no imaging at all: stay active, use NSAIDs, and expect resolution in 4-6 weeks. Early imaging in uncomplicated cases finds incidental degenerative changes that lead to unnecessary procedures.

Question 20

What must happen in the first hour after recognizing sepsis with hypotension or a lactate of 4 or more?

Accepted Answer

The Surviving Sepsis one-hour bundle: measure lactate and remeasure if elevated; obtain blood cultures BEFORE antibiotics; give broad-spectrum antibiotics; start 30 mL/kg of crystalloid for hypotension or lactate at or above 4 mmol/L; and add vasopressors if fluid alone will not maintain a mean arterial pressure of at least 65 mmHg. Norepinephrine is the first-line vasopressor. The sequencing trap is cultures before antibiotics - true when it costs no time, but in septic shock antibiotics must never be delayed waiting for a culture draw.

Question 21

Bacterial versus viral meningitis: what does the CSF show, and when does dexamethasone have to be given?

Accepted Answer

Bacterial CSF shows neutrophil predominance (often more than 1,000 white cells), glucose below 40 mg/dL or a CSF-to-serum ratio under 0.4, markedly elevated protein, and high opening pressure. Viral CSF shows lymphocyte predominance, normal glucose, and only mildly elevated protein. Dexamethasone must be given BEFORE or with the first antibiotic dose in suspected pneumococcal meningitis - it reduces mortality and hearing loss but loses that benefit if given afterward. Get a head CT before lumbar puncture only for immunocompromise, known CNS disease, new seizure, papilledema, or focal deficit, and give antibiotics first if imaging will cause delay.

Question 22

At which CD4 counts do the classic HIV opportunistic infection prophylaxes begin?

Accepted Answer

Below 200 cells/microL: start Pneumocystis jirovecii prophylaxis with trimethoprim-sulfamethoxazole. Below 100 with a positive Toxoplasma gondii IgG: the same TMP-SMX regimen also covers toxoplasmosis. Below 50: azithromycin for Mycobacterium avium complex was the traditional threshold, but it is no longer routine when effective antiretroviral therapy is started promptly. The larger current principle is that antiretroviral therapy is recommended for everyone living with HIV regardless of CD4 count, ideally on the same day as diagnosis - a change from the older practice of waiting for a threshold.

Question 23

When do you treat Lyme disease clinically without waiting for serology?

Accepted Answer

When erythema migrans appears in a patient with plausible exposure in an endemic area. The rash is diagnostic on its own and serology is frequently still negative in early localized disease, so a negative test must not delay treatment. Doxycycline is preferred - short courses are now considered safe in children of any age - with amoxicillin or cefuroxime used in pregnancy. Serologic testing (an immunoassay confirmed by a second test) is for later manifestations: carditis with AV block, cranial nerve VII palsy that may be bilateral, meningitis, or arthritis. A single erythema migrans lesion needs no lumbar puncture or imaging.

Question 24

What is the time window for IV thrombolysis in acute ischemic stroke, and what must be excluded first?

Accepted Answer

Alteplase - or tenecteplase, now an accepted alternative - within 4.5 hours of last known well. Mechanical thrombectomy for large-vessel occlusion can extend to 24 hours when perfusion imaging shows salvageable tissue. A non-contrast head CT must exclude hemorrhage before any lytic. Absolute contraindications include intracranial hemorrhage, intracranial or spinal surgery or serious head trauma within 3 months, active internal bleeding, and blood pressure above 185/110 that cannot be lowered. Blood pressure targets diverge: below 185/110 for thrombolysis candidates, but permissive hypertension up to 220/120 for those not receiving it.

Question 25

First-line drug for convulsive status epilepticus, and what follows if seizures persist?

Accepted Answer

A benzodiazepine, adequately dosed and repeated once: IV lorazepam, IM midazolam when there is no IV access, or IV diazepam. If seizure activity continues at about 20 minutes, give a second-line IV agent - levetiracetam, fosphenytoin, or valproate - which the ESETT trial showed to be equally effective, so choose on contraindications and availability. Check a fingerstick glucose immediately; in suspected alcohol use disorder or malnutrition give thiamine before or with glucose to avoid precipitating Wernicke encephalopathy. Status epilepticus is now defined as 5 minutes or more of continuous seizure activity, not the older 30-minute threshold, because underdosed and delayed benzodiazepines are the most common treatment failure.

Question 26

Which headache presentation requires a non-contrast head CT and possibly a lumbar puncture?

Accepted Answer

A thunderclap headache - maximal within seconds to a minute - suggests subarachnoid hemorrhage. Non-contrast CT within 6 hours of onset is highly sensitive; beyond that window, a negative CT should be followed by lumbar puncture looking for xanthochromia, or by CT angiography. Other red flags: new headache after age 50, headache with fever and neck stiffness, papilledema, focal deficit, immunosuppression or known cancer, and headache reproduced by Valsalva or positional change. In a patient over 50 with jaw claudication, scalp tenderness, and a raised ESR, start high-dose corticosteroids for giant cell arteritis BEFORE temporal artery biopsy - waiting risks irreversible vision loss.

Question 27

How do you distinguish the tremor of Parkinson disease from essential tremor?

Accepted Answer

Parkinson disease produces a resting tremor of about 3-5 Hz, classically pill-rolling, that dampens with voluntary movement and begins asymmetrically, accompanied by bradykinesia, cogwheel rigidity, and later postural instability; it responds to levodopa. Essential tremor is an action or postural tremor - worse holding a cup or writing, absent at rest - usually bilateral and symmetric, often involving the head or voice, frequently with a family history, temporarily improved by alcohol, and treated with propranolol or primidone. The decisive point is that bradykinesia is required for a Parkinson diagnosis; tremor alone does not make it.

Question 28

Which numbers separate diabetic ketoacidosis from hyperosmolar hyperglycemic state, and what is the single most dangerous ordering error?

Accepted Answer

DKA: glucose usually above 250 mg/dL, arterial pH below 7.3, bicarbonate below 18 mEq/L, positive ketones, and an elevated anion gap - more often type 1 diabetes. HHS: glucose often above 600 mg/dL, serum osmolality above 320 mOsm/kg, pH above 7.3, bicarbonate above 18, minimal ketosis, profound dehydration and altered mental status - more often type 2, with higher mortality. Both start with IV fluids, then an insulin infusion, with potassium replacement. The lethal error is starting insulin before checking potassium: hold insulin until potassium is above 3.3 mEq/L, because insulin drives potassium intracellularly and can cause fatal hypokalemia and arrhythmia.

Question 29

Which lab pattern confirms primary hypothyroidism, and how would central hypothyroidism differ?

Accepted Answer

Primary hypothyroidism: TSH high with free T4 low. Subclinical disease is a high TSH with a normal free T4. Central hypothyroidism from pituitary or hypothalamic disease shows a low free T4 with a TSH that is low or inappropriately normal - which is why TSH-only screening misses it, and why any suspicion of pituitary disease requires a free T4. Hashimoto thyroiditis with anti-thyroid peroxidase antibodies is the most common cause in iodine-sufficient regions. Levothyroxine is taken on an empty stomach and separated by 4 hours from calcium, iron, and proton pump inhibitors; recheck TSH 6-8 weeks after any dose change, since it takes that long to re-equilibrate.

Question 30

Primary versus secondary adrenal insufficiency: which electrolyte and skin findings tell them apart?

Accepted Answer

Primary insufficiency (Addison disease) destroys the adrenal cortex, so BOTH cortisol and aldosterone fail: hyponatremia WITH hyperkalemia, hypotension, and hyperpigmentation of skin creases and buccal mucosa driven by the high ACTH precursor molecule. Secondary insufficiency comes from deficient pituitary ACTH - most often abrupt withdrawal of exogenous glucocorticoids - and the renin-angiotensin system keeps aldosterone intact, so potassium is normal and there is no hyperpigmentation. Confirm with an early-morning cortisol and cosyntropin stimulation test, but in suspected adrenal crisis give IV hydrocortisone and saline immediately; treatment must never wait for the result.

Question 31

A painful red eye with a fixed mid-dilated pupil and halos around lights - what is it, and what must you avoid giving?

Accepted Answer

Acute angle-closure glaucoma: severe eye pain, headache, nausea and vomiting that can be mistaken for a GI illness, blurred vision with halos, a hard globe, ciliary flush, and a mid-dilated, poorly reactive pupil. Measure intraocular pressure and get the patient to ophthalmology immediately - vision loss is measured in hours. Avoid mydriatic drops and systemic anticholinergics, which dilate the pupil and worsen the block. Contrast with conjunctivitis (no true pain, normal pupil, normal vision) and anterior uveitis (photophobia with a small, constricted pupil and cells and flare in the anterior chamber).

Question 32

Which single exam finding separates otitis externa from acute otitis media?

Accepted Answer

Pain on tragal traction or auricle manipulation, with a swollen erythematous canal, indicates otitis externa; treat with topical drops such as ciprofloxacin-dexamethasone and keep the ear dry, reserving oral antibiotics for spread beyond the canal. Acute otitis media shows a bulging, opaque tympanic membrane with reduced mobility on pneumatic otoscopy - the mobility check, not erythema alone, is what confirms effusion. High-dose amoxicillin is first-line, and observation for 48-72 hours is reasonable for nonsevere unilateral disease over age 2. In a diabetic or immunocompromised patient with severe pain and granulation tissue at the bony-cartilaginous junction, suspect malignant (necrotizing) otitis externa from Pseudomonas.

Question 33

When do Centor criteria justify testing for group A streptococcus, and which sore throat should never be examined with a tongue depressor?

Accepted Answer

Centor/McIsaac points: tonsillar exudate, tender anterior cervical adenopathy, fever, and absence of cough, adjusted for age (add 1 for ages 3-14, subtract 1 for 45 and older). A score of 0-1 needs no testing and no antibiotics. A score of 2 or more warrants a rapid antigen test, backed by throat culture in children. Treat confirmed strep with penicillin or amoxicillin - the point is preventing acute rheumatic fever, not shortening the sore throat. But a drooling, tripoding patient with a muffled hot-potato voice and stridor may have epiglottitis: do not examine the pharynx or use a tongue depressor, because it can precipitate complete airway obstruction. Secure the airway first.

Question 34

What must be present to diagnose major depressive disorder, and what must be ruled out before prescribing?

Accepted Answer

At least five of nine symptoms present for 2 weeks or more, and at least one must be depressed mood or anhedonia. The rest: Sleep change, loss of Interest, Guilt or worthlessness, low Energy, poor Concentration, Appetite or weight change, Psychomotor agitation or retardation, and Suicidal ideation (SIG E CAPS). Symptoms must cause functional impairment and not be better explained by a substance or another medical condition, so check TSH and substance use. Always screen for a past manic or hypomanic episode first: an unopposed antidepressant in undiagnosed bipolar disorder can precipitate mania.

Question 35

Serotonin syndrome versus neuroleptic malignant syndrome: which physical findings separate them fastest?

Accepted Answer

Neuromuscular tone is the discriminator. Serotonin syndrome begins within hours of a serotonergic drug or dose increase and produces HYPERreflexia with inducible clonus - worst in the lower limbs - plus tremor, mydriasis, diarrhea, and agitation; stop the agent, give benzodiazepines and cooling, and add cyproheptadine in severe cases. Neuroleptic malignant syndrome evolves over days after an antipsychotic, or after abrupt dopamine agonist withdrawal, and produces lead-pipe rigidity with HYPOreflexia and bradykinesia, markedly elevated creatine kinase, and autonomic instability; stop the antipsychotic, give supportive care, and consider dantrolene or bromocriptine. Clonus versus rigidity, and hours versus days, will settle most cases.

Question 36

How long must psychotic symptoms last before the diagnosis is schizophrenia rather than something else?

Accepted Answer

Brief psychotic disorder lasts at least 1 day but under 1 month with full return to baseline. Schizophreniform disorder lasts 1 to 6 months. Schizophrenia requires 6 months or more of continuous disturbance, including at least 1 month of active-phase symptoms - delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, or negative symptoms - with at least one of those being delusions, hallucinations, or disorganized speech. Schizoaffective disorder requires a concurrent major mood episode PLUS at least 2 weeks of delusions or hallucinations in the ABSENCE of prominent mood symptoms, which is what separates it from a mood disorder with psychotic features.

Question 37

What defines preeclampsia with severe features, and which drug prevents the seizure?

Accepted Answer

New-onset hypertension at or after 20 weeks (at least 140/90 on two occasions 4 hours apart) with proteinuria - or, in the absence of proteinuria, with any severe feature: blood pressure at or above 160/110, platelets under 100,000, creatinine above 1.1 mg/dL or doubled, transaminases at twice normal, pulmonary edema, or new cerebral or visual symptoms. IV magnesium sulfate prevents and treats eclamptic seizures; it is a neuroprotective anticonvulsant, NOT an antihypertensive, so severe hypertension still needs labetalol, hydralazine, or nifedipine. Loss of deep tendon reflexes is the first sign of magnesium toxicity, and calcium gluconate is the antidote. Delivery is the only definitive treatment.

Question 38

A positive pregnancy test with no intrauterine gestational sac on ultrasound - what does the hCG discriminatory zone tell you?

Accepted Answer

When beta-hCG exceeds the discriminatory zone - roughly 3,500 mIU/mL by transvaginal ultrasound - and no intrauterine gestational sac is visible, ectopic pregnancy becomes likely. That threshold was deliberately raised to reduce the risk of interrupting a viable intrauterine pregnancy. Below it the scan is indeterminate, so trend serial hCG levels: a normal early intrauterine pregnancy rises by at least about 35% in 48 hours, while a plateau or a slow rise suggests ectopic or failing pregnancy. Methotrexate is an option only in a stable, unruptured patient meeting criteria; hemodynamic instability or rupture means the operating room.

Question 39

What are the Rotterdam criteria for polycystic ovary syndrome, and what must be excluded first?

Accepted Answer

Two of three, after excluding thyroid disease, hyperprolactinemia, and non-classic congenital adrenal hyperplasia: oligo-ovulation or anovulation; clinical or biochemical hyperandrogenism (hirsutism, acne, elevated free testosterone); and polycystic ovarian morphology on ultrasound. Ultrasound is unnecessary when the other two are present and should not be used within 8 years of menarche, because multifollicular ovaries are normal in adolescence. Screen for impaired glucose tolerance and dyslipidemia. Chronic anovulation leaves the endometrium under unopposed estrogen, raising hyperplasia and carcinoma risk. First-line management is lifestyle change plus a combined hormonal contraceptive; letrozole is first-line for ovulation induction when pregnancy is desired.

Question 40

What four elements must a patient demonstrate to have decision-making capacity?

Accepted Answer

Communicate a choice; understand the relevant information; appreciate how that information applies to their own situation; and reason logically among the options. Capacity is a clinical determination made by a clinician, is specific to the decision at hand, and can fluctuate - a delirious patient may regain it. Competency, by contrast, is a global legal determination made by a court. A patient with capacity may refuse even life-saving treatment. Informed consent additionally requires disclosure of the diagnosis, the proposed intervention, its risks and benefits, the alternatives including doing nothing, and voluntariness; a signed form by itself is documentation, not consent.

Question 41

When may protected health information be disclosed without the patient's authorization?

Accepted Answer

For treatment, payment, and health care operations, and under specific required-by-law exceptions: reportable communicable diseases, suspected child or elder abuse, certain injury reporting such as gunshot wounds, valid court orders and subpoenas, and a serious imminent threat to an identifiable person - the Tarasoff duty to warn and protect. Every disclosure is limited to the minimum necessary information. What does NOT qualify: a family member being present in the room, a spouse or adult child asking about the patient, or an employer inquiring - none of those create an exception, and disclosing to them without authorization is a violation.

Question 42

Why does a highly specific test confirm disease while a highly sensitive test rules it out?

Accepted Answer

A sensitive test has few false negatives, so a Negative result rules OUT disease (SnNout) - useful for screening. A specific test has few false positives, so a Positive result rules IN disease (SpPin) - useful for confirmation. Sensitivity and specificity are properties of the test itself and do not change with disease prevalence. Predictive values DO change: as prevalence falls, positive predictive value falls and negative predictive value rises, which is exactly why screening a low-risk population generates a flood of false positives. Likelihood ratios combine sensitivity and specificity and remain prevalence-independent, which makes them the better tool for revising pretest probability.

Question 43

Which pigmented lesion features require biopsy, and which biopsy technique is the wrong choice?

Accepted Answer

ABCDE: Asymmetry, Border irregularity, Color variation, Diameter above 6 mm, and Evolution or change - plus the ugly duckling sign, a lesion that simply does not resemble the patient's other nevi. Perform a full-thickness excisional biopsy with narrow margins. A shave biopsy is the wrong choice because it can transect the lesion base and destroy the Breslow depth measurement, which is the single strongest prognostic factor in melanoma and determines surgical margins and staging. For comparison: basal cell carcinoma is the most common skin cancer, a pearly papule with telangiectasias that rarely metastasizes; squamous cell carcinoma is scaly or ulcerated, arises from actinic keratosis, and does metastasize.

Question 44

Which drug rash is a dermatologic emergency, and what body-surface-area cutoff separates SJS from TEN?

Accepted Answer

Stevens-Johnson syndrome and toxic epidermal necrolysis: painful skin rather than itchy, dusky targetoid lesions, involvement of two or more mucosal sites, and a positive Nikolsky sign where lateral pressure shears the epidermis. SJS involves under 10% of body surface area, TEN over 30%, and 10-30% is called SJS/TEN overlap. Common triggers are sulfonamides, allopurinol, anticonvulsants such as lamotrigine, carbamazepine, and phenytoin, and NSAIDs. Stop the culprit drug immediately and transfer to a burn unit; systemic corticosteroids are not standard therapy. Distinguish from DRESS, which appears 2-8 weeks after exposure with fever, facial edema, eosinophilia, and internal organ involvement.

Question 45

Acute scrotal pain: which findings mean testicular torsion, and what is the time limit?

Accepted Answer

Sudden severe pain with nausea and vomiting, a high-riding testis with a transverse lie, an ABSENT cremasteric reflex, and a negative Prehn sign (elevating the testis does not relieve pain). Testicular salvage rates fall sharply after roughly 6 hours, so when suspicion is high, go to surgical exploration rather than waiting for Doppler ultrasound - imaging is for equivocal cases only. Epididymitis is the main alternative: gradual onset, fever and dysuria, an INTACT cremasteric reflex, and pain relieved by elevation. Treat epididymitis under age 35 for gonorrhea and chlamydia with ceftriaxone plus doxycycline, and over 35 for enteric organisms with a fluoroquinolone.

Question 46

Which medication class relieves BPH symptoms fastest, which one shrinks the gland, and how does that affect PSA?

Accepted Answer

Alpha-1 blockers such as tamsulosin and alfuzosin relax prostatic smooth muscle and work within days; watch for orthostatic hypotension, dizziness, retrograde ejaculation, and intraoperative floppy iris syndrome in patients heading for cataract surgery. 5-alpha-reductase inhibitors such as finasteride and dutasteride actually reduce glandular volume, but take 3-6 months and lower serum PSA by roughly 50% - so a measured PSA must be doubled when interpreting cancer screening in a treated patient. Anatomy explains the exam findings: BPH arises in the transition zone around the urethra, while prostate cancer usually arises in the peripheral zone, which is why it is palpable as a hard nodule on digital rectal exam.

Question 47

Iron deficiency, anemia of chronic disease, or thalassemia trait: which iron studies separate the three microcytic anemias?

Accepted Answer

Iron deficiency: ferritin low, serum iron low, TIBC/transferrin HIGH, transferrin saturation low, RDW elevated. Ferritin is the single most useful test, but it is an acute-phase reactant that rises with inflammation, so a normal ferritin does not exclude deficiency in an inflamed patient. Anemia of chronic disease: ferritin normal or high with a LOW TIBC - iron is sequestered, not absent. Thalassemia trait: normal or high iron studies with an MCV disproportionately low for the degree of anemia and a normal RDW; confirm with hemoglobin electrophoresis. New iron deficiency in an adult male or a postmenopausal female is a GI malignancy until proven otherwise and requires endoscopic evaluation.

Question 48

Thrombocytopenia with schistocytes and neurologic changes - why is transfusing platelets the wrong move?

Accepted Answer

This is thrombotic thrombocytopenic purpura from ADAMTS13 deficiency: microangiopathic hemolytic anemia, thrombocytopenia, fever, neurologic changes, and renal impairment. Platelets are being consumed by widespread microthrombi, so transfusing more platelets feeds the process and can worsen ischemic injury. Treatment is urgent plasma exchange, with corticosteroids and caplacizumab in current practice. Contrast with immune thrombocytopenia (ITP): isolated thrombocytopenia, no schistocytes, normal PT and aPTT, and treatment with corticosteroids or IVIG reserved for bleeding or a very low platelet count. The blood smear is what separates them.

Question 49

Which urine indices separate prerenal azotemia from acute tubular necrosis, and when do they fail?

Accepted Answer

Prerenal: BUN-to-creatinine ratio above 20:1, fractional excretion of sodium under 1%, urine sodium under 20 mEq/L, urine osmolality above 500 mOsm/kg, and bland sediment with hyaline casts - the tubules are intact and avidly reabsorbing sodium and water. Acute tubular necrosis: ratio closer to 10-15:1, FENa above 2%, urine sodium above 40, urine osmolality near 300 (isosthenuric because concentrating ability is lost), and muddy brown granular casts. The failure mode: FENa is unreliable in a patient who has taken a diuretic, since the drug forces sodium excretion. Use the fractional excretion of urea instead, where under 35% suggests prerenal.

Question 50

Hyperkalemia with peaked T waves: what do you give first, and what does it actually accomplish?

Accepted Answer

IV calcium gluconate (or calcium chloride through a central line). It does NOT lower the potassium at all - it stabilizes the cardiac myocyte membrane within minutes to prevent arrhythmia, buying time. Then shift potassium into cells with insulin plus dextrose and with nebulized albuterol; sodium bicarbonate helps only when there is a concurrent metabolic acidosis. Only three approaches actually remove potassium from the body: dialysis, loop diuretics, and gut binders such as patiromer or sodium zirconium cyclosilicate. Know the ECG progression - peaked T waves, then a prolonged PR with flattened P waves and a widening QRS, then a sine-wave pattern and cardiac arrest.

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