Free PANCE and PANRE Practice Exam

Acute tubular necrosis is death of the kidney's tubular cells and the most common cause of intrinsic acute kidney injury. It is usually caused by ischemia (hypotension, sepsis, major surgery) or nephrotoxins (aminoglycosides, contrast, cisplatin). Damaged tubules can no longer reabsorb sodium, so sodium spills into the urine and the fractional excretion of sodium (FENa) rises above 2%. The dead cells slough off and clump into muddy brown granular casts. Treatment is supportive: stop nephrotoxins, manage volume and potassium, and use dialysis only if needed. This woman had repeated intraoperative hypotension during bypass surgery, then oliguria, a FENa of 2.8%, and muddy brown casts: classic ischemic acute tubular necrosis. The trap is prerenal azotemia, which comes from the same low blood flow but leaves the tubules alive, so they hold on to sodium (FENa below 1%) and the sediment stays bland.

Board-Level Insight: Read the urine: muddy brown casts + FENa above 2% = the tubules are dead (acute tubular necrosis). FENa below 1% with bland sediment = kidneys still saving sodium (prerenal).

Gonococcal ophthalmia neonatorum is a conjunctivitis of the newborn caused by Neisseria gonorrhoeae picked up from the mother's cervix during delivery. The organism multiplies fast and triggers an intense pus-forming response, so it typically appears 2 to 5 days after birth with severe eyelid swelling and copious purulent discharge, and a Gram stain shows gram-negative intracellular diplococci. Untreated, it can perforate the cornea and cause blindness, and it can spread through the bloodstream to cause sepsis, arthritis, or meningitis. That is why treatment must be systemic: a single intravenous or intramuscular dose of ceftriaxone, per the Centers for Disease Control and Prevention. This unprophylaxed, non-jaundiced term infant with day-3 hyperpurulent conjunctivitis and gram-negative diplococci needs ceftriaxone. The trap is topical therapy: drops or ointment alone never cure it.

Board-Level Insight: Newborn with pus pouring from both eyes on day 2 to 5 and gram-negative diplococci = gonorrhea: systemic ceftriaxone, because drops alone never cure it. Later, milder onset suggests chlamydia, treated with oral erythromycin.

Deep venous thrombosis (DVT) is a blood clot in a deep vein, most often in the legs or pelvis. It forms when blood slows (bed rest after surgery), the vein wall is injured (orthopedic surgery), and the blood clots more easily, the three parts of Virchow triad. The clots that matter most sit in the proximal deep veins (popliteal, femoral, and iliac). These are large veins, so a fragment that breaks off is big enough to lodge in the pulmonary arteries and cause a pulmonary embolism (PE). Calf-vein clots usually cause a large embolus only after they climb into the thigh, and superficial veins rarely embolize. This woman, 3 days after knee replacement with sudden pleuritic chest pain, tachycardia, and hypoxemia, most likely has a clot in the proximal femoral veins. Do not be fooled by the negative calf-pain sign on dorsiflexion (Homans sign): it is neither sensitive nor specific.

Board-Level Insight: Ask two questions about the vein: deep or superficial, and above or below the knee? PE comes from deep veins at or above the knee; calf clots embolize only after they climb, and superficial clots almost never do.

Corneal abrasion is a scratch that strips away part of the thin surface layer (epithelium) of the cornea. The cornea is packed with pain nerves, so even a tiny defect causes a foreign-body sensation, tearing, redness, and pain in bright light. Fluorescein dye sticks to the bare spot and glows green under cobalt-blue light, which is how the diagnosis is made. Before calling it a simple abrasion, you evert the lids to find a hidden particle and check the Seidel test to rule out a full-thickness leak. This worker had a low-speed sawdust injury, one well-defined area of green uptake, no retained particle, and a negative Seidel test, so this is a simple corneal abrasion. The trap is corneal foreign body: that diagnosis needs something actually embedded, and lid eversion found nothing.

Board-Level Insight: Green dye uptake with nothing stuck in the eye is an abrasion. Multiple vertical linear scratches mean a particle is hiding under the upper lid, and high-speed metal grinding or hammering needs a CT scan for an intraocular foreign body.

Compartment syndrome is a dangerous rise in pressure inside a closed muscle compartment, a space wrapped in tough fascia that cannot stretch. After a fracture or crush injury, bleeding and swelling fill that space until the pressure squeezes shut the small vessels feeding the muscles and nerves, and the tissue starts to die. In an awake patient the first warning is pain out of proportion to the injury that worsens with passive stretch. When the patient cannot report pain, or the picture is unclear, you measure the compartment pressure directly with a needle-based monitor; a compartment pressure within about 30 mm Hg of the diastolic blood pressure confirms it. This sedated man with a tibial fracture and tense compartments cannot give that history, so compartment pressure measurement decides whether he needs a fasciotomy. The trap is his palpable pulses: pulses are lost late, so they never rule it out.

Board-Level Insight: The patient's mental status picks the path: awake with pain out of proportion and pain on passive stretch → straight to fasciotomy; sedated, obtunded, or equivocal → measure compartment pressures. Palpable pulses never rule it out.

Wolff-Parkinson-White (WPW) syndrome is an extra electrical wire (an accessory pathway) between the atria and ventricles, plus episodes of tachycardia that use it. Because the wire skips the normal delay in the atrioventricular (AV) node, part of the ventricle is activated early, producing the short PR interval, the slurred delta wave, and the wide QRS. The same wire lets an impulse loop between atria and ventricles, causing a reentrant supraventricular tachycardia. Medicines only suppress the loop, but catheter ablation destroys the wire itself, cures most patients, and is the preferred long-term treatment. This young woman has recurrent symptomatic episodes and a preexcited ECG (PR 0.10 seconds, delta wave, QRS 0.13 seconds), so she should be referred for ablation. The trap is choosing an AV nodal blocker, which can be dangerous if she ever develops atrial fibrillation.

Board-Level Insight: Symptomatic WPW gets the wire burned, not the node slowed: catheter ablation cures it, while digoxin, verapamil and other AV nodal blockers can drive preexcited atrial fibrillation down the bypass tract into ventricular fibrillation.

Obstructive sleep apnea is repeated collapse of the throat (pharyngeal) airway during sleep, which causes pauses in breathing, drops in oxygen, and brief arousals that fragment sleep. That explains this man's loud snoring, witnessed apneas, morning headaches, and dangerous daytime sleepiness, and obesity with a thick neck is the biggest risk factor. Polysomnography grades severity by the apnea-hypopnea index (AHI): 5 to 15 events per hour is mild, 15 to 30 moderate, and more than 30 severe, so his AHI of 42 is severe disease. Nasal continuous positive airway pressure (CPAP) is first-line for moderate-to-severe obstructive sleep apnea because the steady air pressure splints the floppy airway open, stopping apneas and desaturations from the first night of proper titration. Weight loss, alcohol avoidance, and side sleeping are prescribed alongside CPAP, not instead of it.

Board-Level Insight: Read the apnea-hypopnea index before picking therapy: severe obstructive sleep apnea (more than 30 events per hour) gets CPAP first; weight loss, alcohol avoidance, and oral appliances are add-ons or fallbacks, and oxygen alone never fixes the obstruction.

Bipolar II disorder is a mood disorder defined by at least one hypomanic episode plus at least one major depressive episode, with no lifetime manic episode. Hypomania and mania share the same symptoms (elevated mood, less need for sleep, rapid speech, distractibility, extra goal-directed activity); what separates them is severity. Hypomania lasts at least 4 days and causes no marked impairment, no psychosis, and no hospitalization. Mania lasts at least 7 days or causes any of those three. This man's 6 days of little sleep, rapid speech, distractibility, and new business ventures, while he keeps working and attending class, is hypomania. Two months ago he had a full major depressive episode (at least 2 weeks with five or more symptoms). Hypomania plus major depression equals bipolar II. The trap is bipolar I: that requires true mania, and he has no impairment, psychosis, or hospitalization.

Board-Level Insight: Hypomania versus mania is a severity call, not a symptom list: marked impairment, psychosis, or hospitalization makes it mania (bipolar I). Functioning normally, plus a past major depressive episode, means bipolar II.

Acute epidural hematoma is bleeding between the skull and the dura, usually from the middle meningeal artery torn by a temporal bone fracture. The first blow causes a brief loss of consciousness, and then the patient wakes up and seems fine (the lucid interval) while the artery keeps bleeding. Because arterial blood fills the space fast, pressure climbs quickly and pushes the temporal lobe toward herniation, compressing the oculomotor nerve (a dilated pupil on the same side) and the cerebral peduncle (weakness on the opposite side). On noncontrast computed tomography (CT) it looks lens-shaped. This boy had a left temporal blow, a brief loss of consciousness, a lucid interval, then rapid decline with a blown left pupil and right-sided weakness: a left epidural hematoma that needs emergency neurosurgery. The trap is acute subdural hematoma, which is venous, crescent-shaped, and usually leaves the patient depressed from the start.

Board-Level Insight: Talk, then crash = epidural: arterial bleeding (middle meningeal artery) fills fast after a lucid interval and looks lens-shaped. Down from the start after a fall = subdural: venous bridging-vein bleeding that looks crescent-shaped.

Secondary hyperparathyroidism is overproduction of parathyroid hormone (PTH) by normal parathyroid glands reacting to a low calcium signal, most often from chronic kidney disease. Failing kidneys cause two problems. They make less calcitriol (active vitamin D), so the gut absorbs less calcium and calcium falls. They also cannot excrete phosphate, so phosphate rises. Both changes drive the glands to pump out more PTH, and because the diseased kidney cannot respond by dumping phosphate, phosphate stays high. The result is high PTH, low (or low-normal) calcium, and high phosphate. Over time the excess PTH pulls calcium out of bone (renal osteodystrophy), which explains this man's bone pain and elevated alkaline phosphatase with stage 4 chronic kidney disease. The trap is primary hyperparathyroidism (high PTH, high calcium, low phosphate), where a healthy kidney still clears phosphate.

Board-Level Insight: With a high PTH, let phosphate tell you where the problem is: low phosphate means the gland is the problem (primary, healthy kidney dumps phosphate); high phosphate means the kidney is the problem (secondary, failed kidney keeps it).

Stevens-Johnson syndrome (SJS) is a severe, life-threatening immune reaction, most often to a medication, in which the top layer of skin and the mucous membranes die and peel away. It usually starts 1 to 3 weeks after a new drug, with sulfonamide antibiotics and antiseizure medications among the most common triggers. A flu-like prodrome comes first, then dusky macules and atypical targets merge into flaccid blisters that slough, and the mucous membranes erode (mouth, eyes, and genitals). SJS and toxic epidermal necrolysis (TEN) are one disease named by how much skin detaches: under 10% of body surface area (BSA) is SJS, 10 to 30% is overlap, and over 30% is TEN. This man took a sulfonamide 10 days ago and now has a prodrome, sloughing targets, three eroded mucosal sites, and 6% BSA detachment, which makes this SJS.

Board-Level Insight: Count the detached skin: under 10% BSA is SJS, 10 to 30% overlap, over 30% TEN. Mucosa spared points to scalded skin syndrome; raised targets on hands and feet after a cold sore point to erythema multiforme.

Medical malpractice is negligence in clinical care: a failure to meet the standard of care that injures a patient. The plaintiff must prove all four elements, the 4 Ds. Duty comes from a clinician-patient relationship. Dereliction is breach of the standard of care, meaning what a reasonably prudent physician assistant (PA) would have done in similar circumstances, usually established by expert testimony. Direct causation means the breach actually caused the harm, and it is the element that most often sinks a claim. Damages are real, measurable injury; a near miss caught in time is a quality problem, not a lawsuit. For this missed myocardial infarction, the patient must show a duty, care below the standard, and that the miss itself caused measurable harm. The trap is adding intent: negligence is an unintentional tort, so intent to harm or deceive belongs to battery or fraud.

Board-Level Insight: Negligence needs no intent: an answer choice that includes intent to harm or deceive describes an intentional tort or fraud. Look for the 4 Ds: duty, dereliction, direct causation, damages.

Placental abruption is premature separation of a normally implanted placenta from the uterine wall before delivery. Blood dissecting behind the placenta irritates the uterine muscle, producing constant pain, dark-red bleeding, and a rigid, tender, hypertonic uterus with frequent low-amplitude contractions. Losing placental surface starves the fetus of oxygen, which shows up as fetal tachycardia, minimal variability, and late decelerations. The biggest risk factors are maternal hypertension and cocaine use (intense vasoconstriction), along with smoking and abdominal trauma. Abruption is a clinical diagnosis: a normal ultrasound never rules it out. This patient used cocaine, is hypertensive, and has painful dark bleeding, a board-like uterus, and a nonreassuring tracing, while her fundal placenta excludes previa. She needs stabilization, coagulation studies (fibrinogen first), and expedited delivery. The trap is placenta previa, which bleeds bright red and painlessly from a soft uterus.

Board-Level Insight: Third-trimester bleeding fork: painful bleeding with a rigid uterus = abruption; painless bright-red bleeding with a soft uterus = previa; painless bleeding at membrane rupture with fetal bradycardia = vasa previa.

Central diabetes insipidus (DI) is a shortage of antidiuretic hormone (ADH, vasopressin), the hormone made in the hypothalamus and released from the posterior pituitary that tells the kidneys to hold on to water. Without it, the kidneys cannot concentrate urine, so the patient passes large volumes of dilute urine, becomes thirsty, and drinks to keep up; if intake falls behind, serum sodium climbs. Damage to the hypothalamus or pituitary stalk causes it, and pituitary surgery, sellar or suprasellar tumors, and skull-base fractures are classic causes. The water deprivation test proves it: urine stays dilute while water is withheld, then concentrates sharply once desmopressin replaces the missing hormone. This man's polyuria after transsphenoidal surgery, high-normal sodium, urine osmolality of 110 mOsm/kg, and 80% rise after desmopressin fit central DI.

Board-Level Insight: Dilute polyuria has three suspects and the water deprivation test sorts them: urine concentrates with thirst alone → primary polydipsia; concentrates only after desmopressin → central DI; never concentrates → nephrogenic DI.

Gestational trophoblastic disease is a group of pregnancy-related growths of placental (trophoblast) cells, ranging from the benign hydatidiform mole to malignant gestational trophoblastic neoplasia, including choriocarcinoma. Trophoblast cells make human chorionic gonadotropin (hCG), and the amount tracks how much abnormal tissue remains, so hCG works as a tumor marker. After the mole is evacuated, the level should fall steadily to undetectable; if tissue persists or turns malignant, hCG plateaus or rises. That is why every patient gets serial quantitative serum hCG measurements, weekly until undetectable and then monthly for a period afterward, with reliable contraception so a new pregnancy does not muddy the signal. About 15 to 20% of complete moles progress to neoplasia, so this woman needs exactly this surveillance. The trap is a qualitative urine test, which reads only positive or negative and cannot show whether the level is falling, flat, or rising.

Board-Level Insight: After a molar evacuation, hCG is the tumor marker: follow quantitative serum hCG down to undetectable. A plateau or rise means gestational trophoblastic neoplasia, and a new pregnancy would hide that signal, so require contraception.

Mitral valve prolapse (MVP) is a billowing of the mitral leaflets back into the left atrium during systole, most often from myxomatous degeneration that makes the leaflets floppy and redundant. As the ventricle contracts, the loose leaflets and their chordae tendineae are suddenly pulled tight, like a sail catching the wind, and that snap is the crisp midsystolic click, best heard at the apex. If the leaflets no longer seal, a late systolic murmur of regurgitation follows the click. MVP travels with connective-tissue traits such as a slender build, pectus excavatum, Marfan syndrome, and Ehlers-Danlos syndrome, and symptomatic patients describe palpitations and atypical chest pain. This slender young woman with pectus excavatum and billowing mitral leaflets on echocardiography fits perfectly, so a midsystolic click is the expected finding. The trap is reaching for mitral stenosis sounds (opening snap, diastolic rumble) just because the mitral valve is involved.

Board-Level Insight: Anything that shrinks the left ventricle (standing, Valsalva) moves the MVP click earlier and lengthens the murmur; anything that fills it (squatting, handgrip) delays the click; only MVP and hypertrophic cardiomyopathy get louder when you stand.

Number needed to treat (NNT) is the number of patients who must receive a treatment for a stated period to prevent one additional bad outcome. It is calculated as 1 divided by the absolute risk reduction (ARR), the simple difference in event rates between the control and treatment groups. Here events fell from 8% with placebo to 6% with the statin, so ARR = 8% minus 6% = 2 percentage points = 0.02, and NNT = 1/0.02 = 50: treat 50 patients for 5 years to prevent one cardiovascular event. The same data give a relative risk reduction of 2/8 = 25%, which sounds more impressive but hides the baseline risk, and that 25 is the trap. The p value only says the effect is probably real; the NNT says whether it is worth it. Always quote an NNT with its time frame and round up to a whole patient.

Board-Level Insight: Don't let 25 fool you: 8% to 6% is a 25% relative risk reduction but only a 2-point absolute drop. Subtract the rates first, then invert: NNT = 1/ARR.

Hypercholesterolemia is an elevated blood cholesterol, mainly low-density lipoprotein (LDL) cholesterol, the particle that deposits cholesterol in artery walls and builds atherosclerotic plaque. More LDL means more plaque, so lowering LDL lowers heart attack and stroke risk. Statins cut LDL the most and reduce cardiovascular events, and a high-intensity statin (atorvastatin or rosuvastatin) lowers LDL by 50% or more. It is the starting drug for patients with clinical atherosclerotic cardiovascular disease (ASCVD) and for anyone with an LDL of 190 mg/dL or higher. This man fits both groups: calf pain relieved by rest with weak foot pulses is peripheral artery disease, exertional chest pressure with ECG changes is coronary disease, and his LDL is 210 mg/dL. That makes this secondary prevention, so no risk calculator is needed. The trap is thinking lifestyle changes deserve a trial first.

Board-Level Insight: Before you reach for a risk calculator, ask two questions: does the patient already have ASCVD (heart, brain, or leg arteries), or is LDL 190 or higher? Either "yes" means high-intensity statin, no score needed.

Immune thrombocytopenia (ITP) is an autoimmune disorder in which the body makes antibodies against its own platelets, most often against the surface protein glycoprotein IIb/IIIa. Coated platelets are cleared by macrophages in the spleen, and the same antibodies slow platelet production in the marrow. Because only platelets are hit, the picture is isolated thrombocytopenia: normal hemoglobin, white count, PT, and aPTT, with large, young platelets on the smear as the marrow tries to keep up. Bleeding is mucocutaneous: petechiae, purpura, gum bleeding, and nosebleeds. ITP is a diagnosis of exclusion, and hepatitis C, HIV, and Helicobacter pylori are classic secondary triggers. This woman has isolated severe thrombocytopenia, big platelets, no schistocytes, no heparin, and chronic hepatitis C, which fits anti-GPIIb/IIIa ITP. The trap is ADAMTS13, the target in thrombotic thrombocytopenic purpura, which would bring schistocytes and hemolysis.

Board-Level Insight: Low platelets alone, big platelets, normal PT/aPTT, no schistocytes = ITP (anti-GPIIb/IIIa). Add schistocytes and hemolysis = TTP (anti-ADAMTS13). Add recent heparin and new clots = HIT (anti-PF4).

Duodenal atresia is a complete blockage of the duodenum present at birth, caused by failure of the embryonic duodenum to hollow out (recanalize). Because the fetus cannot pass swallowed amniotic fluid down the gut, the pregnancy often shows polyhydramnios. The blockage usually sits just below where bile enters, so feeds come back up as bilious vomiting on the first day while the lower abdomen stays flat. On a radiograph, air trapped in the stomach and proximal duodenum makes the double bubble sign, and a complete atresia leaves no gas beyond it. About a quarter to 40% of affected infants have Down syndrome. This newborn has every piece: polyhydramnios, Down syndrome features, day-1 bilious vomiting, and a double bubble with a gasless distal bowel. The main trap is malrotation with midgut volvulus, which also causes bilious vomiting but usually lets some gas through.

Board-Level Insight: Bilious vomiting on day 1: a double bubble with NO gas beyond it, plus Down syndrome or polyhydramnios, is duodenal atresia; a double bubble with some distal gas keeps malrotation with midgut volvulus on the table.

Salter-Harris fractures are fractures of a child's growth plate (physis), the band of growing cartilage between the metaphysis and the epiphysis. In children the physis is weaker than the nearby ligaments and bone, so an injury that would sprain an adult's joint often breaks through the growth plate instead. The system sorts these fractures by which structures the fracture line crosses, and the risk to future growth rises from Type I to Type V. A Type II fracture runs through the physis and then exits through the metaphysis, leaving a triangular metaphyseal corner fragment (the Thurston Holland fragment). It is the most common type and usually heals well with closed reduction and immobilization. This boy's fracture crosses the physis and exits through the metaphysis with the epiphysis and joint spared, which is a Type II injury.

Board-Level Insight: Classify by what the line crosses (SALTR): Straight across the plate = I; exits Above into the metaphysis (corner fragment) = II; exits Lower into the epiphysis and joint = III; Through all three = IV; Rammed (crushed) = V.

Thyroid nodules are discrete lumps within the thyroid gland; they are very common, and the great majority are benign. The workup follows a fixed order. TSH comes first: a low TSH suggests a hyperfunctioning nodule, which is almost never cancer, and sends you to a radionuclide scan. With a normal TSH, ultrasonography sizes the nodule and looks for suspicious features, and fine-needle aspiration (FNA) samples nodules that meet size and appearance criteria. FNA cytology is the decision point. When cytology is benign, the chance of cancer is low, so no treatment is needed; the American Thyroid Association recommends periodic ultrasound surveillance, with repeat FNA only if the nodule grows significantly or develops suspicious features. This euthyroid, asymptomatic woman with no red flags, a bland ultrasound, and benign cytology needs reassurance and follow-up ultrasound, not surgery or medication.

Board-Level Insight: TSH picks the path, FNA picks the treatment: low TSH → uptake scan (hot nodule rarely cancer); normal TSH → ultrasound → FNA. Benign cytology → watch with ultrasound; malignant or suspicious → surgery.

Fournier gangrene is a necrotizing soft-tissue infection of the perineum and genitals caused by a mix of aerobic and anaerobic bacteria that kill the tissue under the skin. It usually starts from a nearby source such as a perirectal abscess, recent surgery, or a urethral infection, and people with diabetes are at particular risk. The infection races along the fascia beneath skin that still looks fairly normal, so the patient has pain out of proportion to the exam, and gas made by the bacteria produces crepitus. Dead tissue has no blood supply, so antibiotics cannot reach it; the only way to stop the spread is to cut it out. That is why treatment is emergent surgical debridement alongside broad-spectrum antibiotics, without waiting for imaging. This septic diabetic man with perineal crepitus after a perirectal abscess needs the operating room now.

Board-Level Insight: Perineal pain out of proportion + crepitus = Fournier gangrene. Antibiotics run alongside, but dead tissue has no blood flow, so only the scalpel is definitive: go straight to the operating room and never wait for a CT.

Foreign body aspiration is the inhalation of an object, most often food such as nuts or seeds, into the airway, and it peaks between ages 1 and 3 years. A lodged object in a bronchus can act as a ball valve: air slips past it on inspiration but cannot escape on expiration, so the lung beyond it becomes trapped with air. That explains this toddler's focal expiratory wheeze, decreased breath sounds on the right, and right-sided hyperlucency with mediastinal shift away from the blocked side, all after a witnessed choking episode while eating peanuts. A stable child with a bronchial foreign body needs prompt removal under general anesthesia, and rigid bronchoscopy is the procedure of choice because the rigid tube secures the airway, allows ventilation, and fits grasping forceps and suction for crumbly organic material like peanuts. Delay risks complete obstruction, pneumonia, and bronchiectasis.

Board-Level Insight: Choking history plus a focal, one-sided wheeze in an afebrile toddler is a mechanical problem: take the object out with rigid bronchoscopy. Bronchodilators, racemic epinephrine, and a flexible scope are the tempting detours.

Sickle cell anemia is an inherited disease in which a person carries two copies of the gene for hemoglobin S (HbS). When HbS gives up its oxygen, it clumps into long rods that bend red cells into stiff sickle shapes. Those cells break apart early, causing a hemolytic anemia with a high reticulocyte count and jaundice, and they jam small vessels, causing repeated painful vaso-occlusive crises. A smear or a solubility test can show that HbS is present, but only hemoglobin electrophoresis (or high-performance liquid chromatography) separates and measures each hemoglobin type: sickle cell anemia shows HbS with some fetal hemoglobin (HbF) and no normal adult hemoglobin (HbA), while sickle trait shows more HbA than HbS. This unscreened young man with lifelong pain crises, hemolysis, and sickled cells needs electrophoresis to confirm the diagnosis. The trap is the solubility test, which cannot separate trait from disease.

Board-Level Insight: The smear and the solubility test only say “HbS is here”; they cannot split trait from disease. Electrophoresis counts the hemoglobins: all S (plus some F) = sickle cell anemia; more A than S = trait.

Cluster headache is a primary headache disorder of brief, severe, one-sided attacks around the eye that come in daily bouts lasting weeks to months, then disappear for months or years. The hypothalamus acts as the trigger, which is why attacks strike at the same time each day or night. During an attack the trigeminal nerve and nearby autonomic fibers fire together, so the pain brings same-side tearing, red eye, runny nose, and a droopy eyelid with a small pupil. Attacks peak fast and last only 15 to 180 minutes, so treatment must work within minutes: 100% oxygen by nonrebreather mask aborts many attacks quickly and carries no cardiac risk. This restless man, in the middle of a nightly bout with alcohol as the trigger, is mid-attack, so high-flow oxygen is the right first move. The trap is reaching for a preventive (verapamil, prednisone) or a slow oral drug while the attack is happening.

Board-Level Insight: Split cluster therapy into “stop this attack” vs “stop the next ones”: abort = 100% oxygen or an injected/nasal triptan; prevent = verapamil, with prednisone as a short bridge. Anything oral and slow loses to a 45-minute attack.

Ménière disease is an inner ear disorder caused by endolymphatic hydrops, a buildup of fluid (endolymph) inside the inner ear's membranes. When that pressure spikes, the balance organ and the hearing organ misfire together, so each attack brings episodic vertigo lasting 20 minutes to 12 hours, fluctuating low-frequency sensorineural hearing loss, tinnitus, and ear fullness. Early on, hearing recovers between attacks. The tuning forks locate the problem: a positive Rinne on both sides (air conduction louder than bone) rules out a conductive loss, and in sensorineural loss the Weber lateralizes to the better ear, so a Weber to the left puts the damage in the right ear. This man's hours-long recurrent attacks with right-sided fullness, tinnitus, and sensorineural loss, plus a normal MRI that excludes a tumor, fit Ménière disease.

Board-Level Insight: Time the vertigo: under a minute with head turns = benign positional vertigo; 20 minutes to 12 hours with low-tone hearing loss and ear fullness = Ménière; one continuous spell lasting days = neuritis (hearing spared) or labyrinthitis (hearing lost).

Opioid use disorder is a chronic brain disease of compulsive opioid use despite harm, and its greatest danger is not withdrawal but fatal overdose after relapse once tolerance is lost. That is why treatment means long-term medication, not just riding out withdrawal. Buprenorphine is a high-affinity partial mu-opioid agonist with a ceiling on respiratory depression, so it relieves withdrawal and craving with low overdose risk and can be started in an office-based primary care clinic. It is started only once the patient is in objective withdrawal; otherwise it knocks the remaining full agonist off the receptor and precipitates withdrawal. This man is 14 hours out from heroin, with yawning, rhinorrhea, piloerection, dilated pupils, and a withdrawal score of 14, and he wants to keep working, so buprenorphine-naloxone is the right start. The trap is methadone: equally effective, but dispensed for this disorder only through a licensed opioid treatment program.

Board-Level Insight: Match the medication to the setting and the timing: office start in active withdrawal = buprenorphine; methadone only through an opioid treatment program; naltrexone only after about 7 opioid-free days.

Rabies is a viral brain infection (encephalitis) spread in the saliva of an infected mammal, usually through a bite. The virus creeps slowly along nerves from the wound to the brain, so symptoms start weeks later; the incubation period averages 1 to 2 months. It begins with a vague prodrome of fever, headache, and malaise. Once the virus reaches the brain, most patients develop furious rabies: agitation, confusion that comes and goes, excessive salivation, and hydrophobia, painful throat spasms when they try to drink. Even a breeze on the face can set off spasms (aerophobia). This man has an untreated stray-dog bite a month ago, a nonspecific prodrome, and now hydrophobia, aerophobia, drooling, and fluctuating confusion: classic furious rabies. The trap is tetanus, which also follows a wound and causes painful spasms, but the mind stays clear.

Board-Level Insight: Two wound-linked spasm diseases split on the mind and the trigger: rabies = spasms set off by drinking or a breeze, with agitation and confusion; tetanus = constant rigidity and trismus (lockjaw) with a clear mind.

Suspected small bowel bleeding (formerly called obscure gastrointestinal bleeding) is bleeding from the digestive tract when a good-quality upper endoscopy and colonoscopy are both normal. Those two scopes see the esophagus, stomach, and proximal duodenum from above and the colon and terminal ileum from below, but they cannot reach the long middle stretch of small intestine, where angioectasias (small abnormal vessels), NSAID ulcers, and small-bowel tumors hide. Capsule endoscopy is a swallowed pill-sized camera that photographs the whole small bowel, and it is the first-line test once upper and lower sources are excluded in a stable patient. This man has melena (which points above the colon), stable vital signs, a normal EGD, and innocent diverticula, so the next step is a capsule. The trap is blaming the diverticula: diverticular bleeding is painless, bright hematochezia, not black stool.

Board-Level Insight: Normal upper scope plus normal colonoscopy means the blood is in the small bowel: stable patient → capsule endoscopy; actively bleeding and unstable → angiography. Diverticula with no blood or clot are bystanders, not the source.