Internal medicine

Question 1

Middle-aged patient has a bilateral action/postural tremor that improves with alcohol and worsens with outstretched arms. Most likely dx & first-line drug?

Answer 1

Essential tremor → propranolol (alt. primidone).

Question 2

Elderly patient exhibits a “pill-rolling” 4-6 Hz rest tremor that lessens with voluntary movement and is asymmetric. Likely dx & cornerstone therapy?

Answer 2

Parkinson disease → carbidopa-levodopa (antimuscarinic = trihexyphenidyl for tremor-predominant cases).

Question 3

Tremor absent at rest but worsens as the finger nears the target; exam shows ataxia/dysmetria. What type of tremor and typical lesion site?

Answer 3

Cerebellar (intention) tremor—lesion in ipsilateral cerebellar hemisphere (or its pathways).

Question 4

Patient develops a fine, low-amplitude action tremor after excess caffeine or thyrotoxicosis; it disappears at rest and is often invisible at baseline. Name this tremor type.

Answer 4

Enhanced physiological tremor (exaggerated normal tremor).

Question 5

Marked high-frequency tremor of legs/trunk only while standing; disappears on sitting or walking. Diagnosis and first-line treatment strategy?

Answer 5

Orthostatic tremor—treat with clonazepam or gabapentin (β-blockers often ineffective).

Question 6

List 4 physiologic / metabolic states and 4 medications that commonly exacerbate or unmask an action (physiologic or essential) tremor.

Answer 6

Physiologic / Metabolic:

Anxiety or acute emotional stress

Sleep deprivation / fatigue

Hyperthyroidism

Alcohol or benzodiazepine withdrawal

Medications:

β-agonists (e.g., albuterol)

Lithium

SSRIs/SNRIs

Systemic corticosteroids

Question 7

A 52-year-old develops painful, flaccid intra-epidermal bullae and oral erosions; the lesions shear with slight pressure (+Nikolsky). Which autoimmune blistering disorder is this, what is the pathogenic antibody & DIF pattern, and what is first-line treatment?

Answer 7

• Pemphigus vulgaris
• IgG against desmoglein 1 & 3 (desmosomes)
• DIF: “net-like”/chicken-wire intercellular IgG in epidermis
• Tx: High-dose systemic corticosteroids ± steroid-sparing agent; rituximab is now preferred long-term immunosuppressant.
  (Skin biopsy with DIF is gold-standard; serum desmoglein ELISA supports dx.)

Question 8

An itchy 76-year-old presents with tense, sub-epidermal bullae on trunk and flexor limbs, sparing the mouth; Nikolsky negative. Name the disease, its autoantibody target & DIF pattern, and initial therapy.

Answer 8

Bullous pemphigoid
* IgG against BP180/BP230 hemidesmosomes (dermal–epidermal junction)
* DIF: Linear IgG ± C3 along basement membrane
* Tx: High-potency topical clobetasol for limited disease; oral prednisone or doxycycline + nicotinamide for widespread/severe cases.

Question 9

1. Which thionamide is preferred in first-trimester pregnancy and during thyroid storm, and why?
2. Which is preferred otherwise?

Answer 9

1. Propylthiouracil (PTU) — less teratogenic than methimazole early in pregnancy and uniquely inhibits peripheral T₄ → T₃, so it’s first-line in thyroid storm.
2. Methimazole is preferred in most other settings (2nd/3rd trimester & non-pregnant adults) because it needs only once-daily dosing and has far lower risk of severe hepatotoxicity.

Question 10

Match each clinical setting with its most likely IE pathogen:

1. Acute, fulminant course in IV-drug user
2. Subacute course after dental work
3. Early (< 60 d) prosthetic-valve infection
4. IE with concomitant colonic cancer or IBD
5. Culture-negative IE after livestock exposure

Answer 10

1. Staphylococcus aureus (MRSA > MSSA)
2. Viridans group streptococci (S. sanguinis, mutans, mitis)
3. Staphylococcus epidermidis (coagulase-negative staph)
4. Streptococcus gallolyticus (bovis)—screen colon!
5. Coxiella burnetii (Q fever) – often serology-positive, culture-negative

Board pearl: HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella) cause culture-negative IE in patients with poor dentition.

Question 11

Empiric IV antibiotics for** native-valve** IE? For prosthetic-valve IE?

List 3 absolute indications for early valve surgery.

Answer 11

Native valve: Vancomycin + ceftriaxone (covers MRSA, Viridans, Enterococcus, HACEK).
Prosthetic valve: Vancomycin + gentamicin + cefepime (add rifampin once staph confirmed).

Operate early if ANY:

1. Refractory heart failure due to severe valve dysfunction
2. Uncontrolled infection (abscess, persistent bacteremia ≥ 7 d on proper antibiotics, fungal or highly resistant bug)
3. Prevent emboli: large mobile vegetation > 10 mm after embolic event or > 15 mm even without embolus

Question 12

Which population will need Dental IE prophylaxis

and Which Abx is given?

Answer 12

amoxicillin 2 gr is recommended only for high-risk cardiac lesions (prosthetic valve, prior IE, certain congenital defects) undergoing gingival or respiratory-incision procedures.

Question 13

A 72-year-old with painless, episodic melena undergoes colonoscopy showing tortuous, dilated, thin-walled vessels in the right colon. What is the most likely lesion, where else does it commonly occur, and what causes it?

Answer 13

Lesion: Angiodysplasia (vascular malformation)

Sites: Cecum & ascending colon > distal small bowel

Pathogenesis: Recurrent, intermittent venous obstruction in the muscularis propria → dilated submucosal veins & arteriovenous communications that bleed easily.

Question 14

Name the two systemic conditions that greatly increase the risk of bleeding from GI angiodysplasias and explain the mechanism for one of them.

Answer 14

End-stage renal disease (ESRD)

**Aortic stenosis **— turbulent jet destroys high-molecular-weight von Willebrand factor multimers, worsening mucosal bleeding (Heyde syndrome).

Question 15

1. Best diagnostic test if colonoscopy is nondiagnostic but bleeding persists?
2. First-line endoscopic therapy?
3. Two pharmacologic options for recurrent or multifocal disease?

Answer 15

1. Video capsule endoscopy (or CT angiography if brisk bleed).
2. Argon plasma coagulation (APC) or bipolar cautery via endoscope.
3. Octreotide (splanchnic vasoconstriction) or thalidomide/estrogen-progesterone as adjuncts when endoscopic therapy fails or lesions are diffuse.

Question 16

Digoxin’s two key physiologic actions and the two main Step 2 indications?

Answer 16

Inhibits Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → ↓ Na⁺/Ca²⁺ exchange → ↑ Ca²⁺ in myocytes → stronger contraction (positive inotropy).

↑ Vagal tone → slows AV-node conduction (negative chronotropy).

Indications

Symptomatic HFrEF (↑ contractility).

Rate control in atrial flutter/fibrillation, especially when hypotensive or in HF and β-blockers can’t be up-titrated.

Question 17

1. Classic early symptoms of digoxin toxicity?
2. Characteristic EKG changes?
3. Name four common precipitants.

Answer 17

1. GI (nausea, anorexia), neurologic (fatigue, confusion,** yellow-green vision**), and arrhythmias.
2. Scooped “Salvador-Dali” ST depression, prolonged PR, PVCs; severe: atrial tachy w/ AV block or bidirectional VT.

Precipitants: 1.Hypokalemia
2. hypomagnesemia
3. renal failure (↓ clearance),
4. drug interactions (amiodarone, verapamil, quinidine, macrolides).

Question 18

Stepwise treatment and the three board-favorite indications for digoxin-specific Fab fragments?

Answer 18

1. Stop digoxin → check electrolytes
2. Correct K⁺ & Mg²⁺, give activated charcoal if ingestion < 2 h.
3. Control bradyarrhythmia with atropine; use lidocaine or β-blockers for ventricular ectopy (avoid calcium).

Digoxin-specific antibody (Fab) if ANY:

1. Life-threatening arrhythmia (VT, VF, symptomatic brady-block).
2. Serum K⁺ > 5.5 mEq/L from acute overdose.
3. Hemodynamic instability or CNS symptoms with digoxin level > 10 ng/mL (acute) or > 6 ng/mL (chronic).

Question 19

A 28-year-old woman develops multiple tender, erythematous, non-ulcerating nodules on the anterior shins, accompanied by low-grade fever and arthralgias.

What is the most likely diagnosis?

What layer of skin is inflamed, and how would a biopsy describe the lesion?

Answer 19

Erythema nodosum (EN)

Immune-mediated septal panniculitis of the subcutaneous fat; biopsy shows septal inflammation without vasculitis.
(Epidemiology: F > M, peak age 20-40 yr.)

Question 20

Give at least five common underlying causes or associations of erythema nodosum that Step 2 loves to test.

Answer 20

N = No idea (idiopathic; ~50 %)

O = Oral contraceptives / pregnancy

D = Drugs (sulfonamides, penicillin)

O = Organisms → Strep pharyngitis, TB, Coccidioides, Histoplasma, Yersinia

S = Sarcoidosis (look for bilateral hilar adenopathy)

U = Ulcerative colitis / Crohn disease

M = Malignancy (Hodgkin lymphoma, leukemias)

(Boards also like Behçet disease and recent COVID or vaccines.)

Question 21

What initial tests should you order to screen for the most common secondary causes of EN?

Outline first-line treatment, and state the usual prognosis.

EN = erythema nodosum

Answer 21

Baseline labs & imaging:

1. Throat culture or ASO titer (post-Strep)
2. Chest X-ray (sarcoidosis, TB)
3. CBC, ESR/CRP; +/- stool studies (IBD) & pregnancy test
4. Further work-up guided by history/travel.

Treatment:

1. NSAIDs + leg elevation + compressive stockings (supportive)
2. Short course of oral prednisone or potassium iodide if severe or refractory
3. Treat underlying trigger (e.g., antibiotics for Strep, stop culprit drug).
4. Prognosis: Self-limited; nodules fade over 3-6 weeks without scarring, but recurrences possible if trigger persists.

* can leave residual hyperpigmentation

Question 22

How to confirm and Tx Conn syndrome (primary hyperaldo)

SaLTY mnemonic

Answer 22

S Saline suppression test IV NaCl or oral salt load fails to lower aldosterone → confirms autonomy
A Adrenal CT + AVS Localize: unilateral adenoma vs bilateral hyperplasia (adrenal-vein sampling if surgery planned)
L Laparoscopic adrenalectomy Definitive for unilateral Conn
Ty Type ‘e’ = Eplerenone / Spironolactone Mineralocorticoid antagonists for bilateral disease or non-surgical patients

Eplerenone- less endocrine effect (gnycomastia, decrease libido)

60% bi-lateral
Resistant HTN, hypokalemia w/ metabolic alkelosis.
Dgx- eleveted plasma aldosterone > 15 + low plasma renin.

Question 23

Use the word CONN to recall the cardinal triad and first diagnostic step for primary hyperaldosteronism.

Answer 23

C Cramps / muscle weakness From hypokalemia ↓K⁺
O Overwhelming blood pressure Resistant or early-onset hypertension
N Na⁺ up Hypernatremia (mild), expanded volume
N Negative renin PAC : PRA ≥ 20 → Screen test

Question 24

A kidney recipient at 3 weeks post-transplant shows rising creatinine, proteinura and graft tenderness.

Which two immune mechanisms cause acute rejection, and how are they recognized on biopsy?

Outline first-line therapy.

Answer 24

Acute cellular (T-cell) rejection → interstitial lymphocytic infiltrate + tubulitis, C4d-negative.

Acute antibody-mediated (humoral) rejection → peritubular capillaritis with bright C4d staining ± transplant glomerulopathy.

Tx- SALT
S = high-dose Steroids (IV methylprednisolone × 3–5 d).

A = Anti-thymocyte globulin for steroid-resistant cellular rejection.

L = “Lower antibodies” with plasmapheresis + IVIG ± rituximab/bortezomib for humoral rejection.

T = Tweak maintenance drugs (optimize tacrolimus trough, add mycophenolate).

Question 25

Compare chronic renal allograft rejection with acute rejection in terms of timing, pathology, clinical course, and management options.

Answer 25

**Chronic Rejection** * Timing – **usually after 1 year**; gradual rise in creatinine. * Pathology – intimal fibrous thickening and luminal narrowing (“transplant vasculopathy”); interstitial fibrosis/tubular atrophy (IF/TA); may show C4d-positive transplant glomerulopathy. * Pathogenesis – low-grade, mixed T-cell and antibody injury plus non-immune factors (hypertension, calcineurin-inhibitor toxicity, recurrent native disease). * Clinical Course – slowly progressive hypertension and proteinuria; largely irreversible. * Management – control BP and glucose, minimize calcineurin toxicity, consider switching to belatacept or mTOR inhibitor; eventual re-transplantation is the only definitive solution. **Acute Rejection (for comparison)** * Timing – **1 week to 6 months** (or any time if immunosuppression lapses). * Pathology – cellular tubulitis (T-cell) or peritubular capillaritis with C4d (antibody-mediated). * Clinical Course – often reversible when treated promptly. * Management – “S-A-L-T” regimen (high-dose steroids, anti-thymocyte globulin, plasmapheresis + IVIG for antibody cases, and adjustment of maintenance drugs). ## Footnote **Board Pearl:** Chronic rejection is the** leading cause of late graft failure;** there is no curative treatment—only risk-factor modification and eventual re-listing for transplant.

Question 26

A 16-year-old presents with headaches, epistaxis, and claudication when running. BP is 160/90 in both arms but 90/60 in the legs; femoral pulses are delayed. 1. What congenital lesion is this? 2. List three classic physical or imaging clues Step 2 loves. 3. Which test confirms the anatomy before surgery?

Answer 26

**Coarctation of the aorta** (usually just distal to the left subclavian, “juxta-ductal”). **High-yield clues:** *** Systolic murmur** best heard between scapulae * **“Figure-3 sign” ** and **rib notching** (collateral enlargment of the intercostal arteries) on CXR * **Radio-femoral delay **with upper->lower-extremity hypertension (arm BP > leg BP by ≥ 20 mm Hg) **Dgx-** CT angiography or MR angiography of the thoracic aorta (echo in infants). ## Footnote (**Board associations:** bicuspid aortic valve, Turn­er syndrome, intracranial berry aneurysm.)

Question 27

# Aorta coractation 1. Name four major complications if coarctation is left untreated. 2. What are first-line definitive treatments in infants versus older children/adults? 3. Which blood-pressure medication class is used short-term to control post-repair hypertension?

Answer 27

**Untreated coarctation** → accelerated HTN, heart failure or LV hypertrophy, aortic dissection/rupture, and intracranial hemorrhage from berry aneurysm. **Infants with critical coarctation:** keep ductus open with IV prostaglandin E₁, then surgical end-to-end anastomosis. **Older children/adults:** balloon angioplasty with stent or surgical repair depending on anatomy. **BP medications:** Beta-blockers (or ACE inhibitors) control residual hypertension until the aortic baroreceptors reset. ## Footnote Adolescents or adults with repaired or unrepaired CoA remain at increased lifetime risk of subarachnoid hemorrhage. Guidelines often recommend screening brain MRA in older teens/adults with CoA—especially if they have refractory hypertension, a family history of aneurysm, or plan to become pregnant.

Question 28

Match each thyroid cancer type to its usual definitive therapy and post-op surveillance marker.

Answer 28

**apillary & Follicular** → Total thyroidectomy (lobectomy if < 1 cm), **± radio-iodine ablation** and TSH suppression with levothyroxine. **Marker:** serum thyroglobulin (should be undetectable once gland removed). **Medullary** → Total thyroidectomy + prophylactic central-neck dissection; no role for iodine. **Marker:** calcitonin (and CEA). Screen for pheochromocytoma (MEN 2) before surgery. **Anaplastic** → Often unresectable; palliative tracheostomy, **external-beam radiation**, or targeted RET/BRAF therapy; poor prognosis ## Footnote **High-yield complication:** Post-thyroidectomy hypocalcemia from hypoparathyroidism—check ionized Ca²⁺, supplement as needed.

Question 29

# Which cancer is it? Histology: “Orphan-Annie-eye” nuclei + psammoma bodies Lymphatic spread to cervical nodes Often follows childhood neck radiation

Answer 29

Papillary thyroid carcinoma

Question 30

# Which type of cancer is it? Uniform micro- or macrofollicles that invade capsule & blood vessels Hematogenous metastases to bone and lung Cannot be diagnosed by FNA cytology alone (needs lobectomy)

Answer 30

Follicular thyroid carcinoma (Hurthle-cell variant included)

Question 31

# Which type of cancer? Tumor of parafollicular C cells with amyloid stroma on Congo-red Produces high serum calcitonin; flushing & diarrhea possible Associated with MEN 2 (RET mutation) — screen for pheochromocytoma

Answer 31

Medullary thyroid carcinoma

Question 32

# Which type of cancer? Elderly patient with rapidly enlarging neck mass, stridor, or dysphagia Pleomorphic giant cells; highly aggressive, poor prognosis Unresponsive to radio-iodine; usually requires palliative care

Answer 32

Anaplastic thyroid carcinoma

Answer 33

1. **TSH + neck ultrasound** first. 2. **Hyper- or subclinical hyper-thyroid?** → order **radio-iodine uptake scan**; a “hot” nodule is rarely cancer (treat for hyper-thyroidism). 3. **Normal / low TSH**: use ultrasound features & size: 4. **Suspicious US features** (solid hypoechoic, micro-calcifications, taller-than-wide, irregular margins, extrathyroidal extension) → **FNA if ≥ 1 cm**. Intermediate features → **FNA if ≥ 1 cm (solid) or ≥ 1.5 cm (mixed).** Spongiform or purely cystic → **observe unless > 2 cm or symptomatic.** **Bethesda cytology guides next step (surgery vs repeat FNA vs obs).**

Question 34

List the 6 NIH clinical criteria for Neurofibromatosis type 1 and state how many must be present for diagnosis.

Answer 34

Mnemonic **CAFÉ SPOT** – need ≥ 2 out of 7 1. **Café-au-lait macules** (≥ 6; > 5 mm pre-puberty, > 15 mm post-puberty). 2. **Axillary or inguinal freckling**. 3. **Family history** (first-degree relative with NF1). 4. **Éye lesion** – optic pathway glioma. 5. **Skeletal lesion** – sphenoid dysplasia or tibial pseudoarthrosis. 6.** Papules** – ≥ 2 cutaneous/subcutaneous neurofibromas or 1 plexiform neurofibroma. 7. **Ocular** – ≥ 2 Lisch nodules (iris hamartomas).

Question 35

What are the hallmark tumors and recommended surveillance for Neurofibromatosis type 2?

Answer 35

Multiple Inhherited Schwannomas, Meningiomas, Ependymomas. Classic lesion = bilateral vestibular schwannomas (sensorineural hearing loss, balance issues). Surveillance: annual audiogram & neuro exam; baseline brain/spine MRI in teens, then every 1–2 yr; prompt MRI if new neuro symptoms.

Question 36

**Match each clue to NF1 or NF2.** * Café-au-lait spots + axillary freckling. * Bilateral vestibular schwannomas. * Optic pathway glioma in childhood. * Chromosome 17, neurofibromin mutation. * Chromosome 22, merlin mutation.

Answer 36

* Café-au-lait spots + axillary freckling - **NF1** * Bilateral vestibular schwannomas. - **NF2** * Optic pathway glioma in childhood. - **NF1** * Chromosome 17, neurofibromin mutation. **NF1** * Chromosome 22, merlin mutation. **NF2**

Question 37

Middle-aged patient has progressive increase in shoe, glove, and hat size; coarse facial features; deep voice; and carpal-tunnel–type paresthesias. What hormone is overproduced, and by what lesion in > 95 % of cases? Name two classic systemic complications Step 2 loves to test.

Answer 37

**Excess growth hormone (GH),** almost always from a **pituitary somatotroph adenoma** (rarely ectopic GHRH). **Complications:** 1.** Cardiomyopathy / concentric LVH **→ leading cause of death. 2. **Colonic neoplasia (polyp or cancer)** → needs earlier colonoscopy. (Others: OSA, diabetes, arthropathy.)

Question 38

Outline the three-step work-up for suspected acromegaly, including the best initial test and the confirmatory test.

Answer 38

**Best initial test**: Serum insulin-like growth factor-1 (IGF-1). **If IGF-1 elevated** → **Oral glucose suppression test (75 g).** Failure of GH to fall < 1 ng/mL confirms biochemical acromegaly. **Pituitary MRI to localize** macro- or micro-adenoma. (If MRI negative, look for ectopic GHRH with chest/abd CT.)

Question 39

What is the first-line definitive therapy? List two medical options when cure is incomplete or surgery isn’t feasible. What labs and imaging are followed long-term?

Answer 39

**Trans-sphenoidal resection** of the pituitary adenoma. **Medical therapy:** 1. **Octreotide or lanreotide** (somatostatin analogs) to suppress GH. 2.** Pegvisomant** (GH-receptor antagonist) or **cabergoline** (dopamine agonist) as add-ons. **Surveillance:** IGF-1 (and random GH) at 3 months post-op, then every 6–12 mo; MRI of pituitary yearly for residual/recurrent tumor.

Question 40

Put these four alcohol-withdrawal syndromes in chronological order after the last drink and give their typical time windows: – Alcoholic hallucinosis – Delirium tremens – Tremulousness (“the shakes”) – Withdrawal seizures

Answer 40

**Tremulousness** (anxiety, diaphoresis, tachycardia, mild tremor) → 6–24 h **Withdrawal seizures** (generalized tonic-clonic, often multiple) → 12–48 h **Alcoholic hallucinosis** (visual > tactile; sensorium intact) → 12–48 h **Delirium tremens** (agitation, fever, HTN, disorientation, autonomic storm) → 48–96 h

Question 41

Name the four cornerstones of acute alcohol-withdrawal treatment using the mnemonic BATS.

Answer 41

**B = Benzodiazepines** — diazepam or chlordiazepoxide (long-acting); lorazepam or oxazepam if liver disease. **A = Assessment with CIWA-Ar score**; give meds symptom-triggered when CIWA ≥ 8–10. **T = Thiamine** 100 mg IV before any glucose to prevent Wernicke encephalopathy. **S = Supportive care** — IV fluids, electrolytes (correct ↓Mg²⁺ ↓K⁺), quiet room, vital-sign monitoring.

Question 42

Runner presents with sharp heel pain that is worst on the first few steps in the morning and after prolonged standing; pain reproducible by passive dorsiflexion of the toes. 1. Most likely diagnosis and anatomic structure involved? 2. Two first-line treatments?

Answer 42

1. **Plantar fasciitis** — micro-tearing and degeneration of the plantar fascia origin on the medial calcaneal tuberosity. 2. **Tx-** Ice-stretch-strengthen program (calf stretches, plantar fascia stretch) and orthotic heel cup/night splint; add NSAIDs, avoid steroid injection unless refractory.

Question 43

Endurance runner develops gradual forefoot pain on the dorsum, worse with impact and relieved by rest; focal bony tenderness over the 2nd metatarsal shaft. Most likely diagnosis and imaging of choice if X-ray is normal? Give one clinical clue that distinguishes this from medial tibial stress syndrome (“shin splints”).

Answer 43

**Metatarsal stress fracture** (2nd > 3rd > 5th); order MRI (or bone scan) when plain films are negative in first 2–3 weeks. Stress fracture pain is** point-tender over a single bone** and persists with non-impact activity, whereas shin splints cause diffuse posteromedial tibial pain that improves quickly with rest and lacks focal tenderness. ## Footnote Management tip: Stress fracture → relative rest & stiff-soled shoe/boot 4–6 weeks; shin splints → activity modification, calf stretching, and arch support.

Question 44

Runner complains of sharp, “stepping-on-a-pebble” pain and burning between the 3rd and 4th toes during toe-off phase; pain reproduced by squeezing the forefoot (Mulder click). What is the lesion and pathophysiology? Two modifiable shoe-related contributors? Stepwise management?

Answer 44

1. **Morton neuroma**—perineural fibrosis/entrapment of the common plantar digital nerve between the 3rd and 4th metatarsal heads. 2. **Tight toe box and high-heeled shoes** (excess met-head pressure). 3. **Wide shoes + metatarsal pad** → NSAIDs → ultrasound-guided corticosteroid or alcohol ablation; persistent disability → surgical excision of the neuroma.

Question 45

**Give the preferred first-line antiepileptic drug(s) for each of the following:** Focal (partial) seizures ± secondary generalization Generalized tonic–clonic (GTC) seizures Absence seizures Myoclonic seizures Acute status epilepticus (initial and definitive agents)

Answer 45

**Focal** → Lamotrigine or Levetiracetam (carbamazepine/oxcarbazepine are alternatives) **GTC** → Valproate, Lamotrigine, or Levetiracetam **Absence** → Ethosuximide (valproate second-line if mixed seizure types) **Myoclonic** → Valproate or Levetiracetam **Status epilepticus **→ IV lorazepam (or diazepam) for rapid control, followed by IV fosphenytoin or valproate/levetiracetam for definitive therapy; refractory cases may need propofol/phenobarbital

Question 46

# Match-the-Drug to Its Signature Toxicity **Name the antiepileptic associated with each “board-favorite” adverse effect:** * Gingival hyperplasia, hirsutism, cerebellar ataxia * Stevens–Johnson syndrome risk highest when dose escalated quickly * Pancreatitis, weight gain, neural-tube defects * Hyponatremia from SIADH * Acute angle-closure glaucoma and kidney stones * Agranulocytosis and aplastic anemia

Answer 46

* Gingival hyperplasia, hirsutism, cerebellar ataxia- **Phenytoin** * Stevens–Johnson syndrome risk highest when dose escalated quickly - **Lamotrigine** * Pancreatitis, weight gain, neural-tube defects - **Valporate** * Hyponatremia from SIADH - **Carbamazepine** * Acute angle-closure glaucoma and kidney stones **Topiramate** * Agranulocytosis and aplastic anemia **Carbamazepine**

Question 47

# Special Situations & Safety Pearls 1. Which two broad-spectrum AEDs are considered **safer in pregnancy** (lowest teratogenic risk)? 2. Which AED doubles as **first-line prophylaxis** for both **bipolar disorder and migraine**? 3. Name one AED preferred in **renal failure** because it is not renally cleared, and one that should be **avoided for the same reason**. | AED = anti epileptic drug

Answer 47

1.** Levetiracetam and Lamotrigine** (still give high-dose folic acid) 2.** Valproate** (contraindicated in pregnancy, however) 3. **Preferred in renal failure** → Valproate (hepatic clearance); **avoid** → Gabapentin or Pregabalin (require dose adjustment, accumulate).

Question 48

Fill in the blanks: * Neurologic findings (paresthesias, ataxia, dorsal-column loss) = _______ deficiency. * Both deficiencies raise homocysteine, but only _______ raises methylmalonic acid. * Main GI absorption site: terminal ileum for _______ and proximal jejunum for _______. * Pernicious anemia destroys _______ cells, eliminating intrinsic factor needed for absorption of _______. | B12, Folate

Answer 48

B12 deficiency causes neurologic damage. * B12 elevates both homocysteine and methylmalonic acid; folate elevates homocysteine only. * Terminal ileum absorbs B12; proximal jejunum absorbs folate. * Pernicious anemia destroys parietal cells, stopping intrinsic-factor production → B12 malabsorption.

Question 49

Name four non-dietary causes of B12 deficiency and three drugs that trigger folate deficiency. Why must you give B12 before folate when both are low? Expected reticulocyte response after correct therapy?

Answer 49

**B12 causes: **pernicious anemia, Crohn/ileal resection, tapeworm (Diphyllobothrium), chronic metformin or PPI use. **Folate-depleting drugs: ** methotrexate, phenytoin, trimethoprim (also chronic ethanol). **Folate** alone can correct anemia but **will worsen irreversible B12-related neurologic injury.** Reticulocyte count should rise **within 3–5 days**, hemoglobin normalizes in **~8 weeks**.

Question 50

A 55-year-old woman has months of sub-occipital headache, progressive gait ataxia, and new hand numbness. Exam reveals spastic weakness in all four limbs and diminished gag reflex on the left. * What dural-based tumour at the cranio-cervical junction explains these findings? * List two classic MRI clues and the definitive treatment.

Answer 50

* Foramen magnum meningioma compressing lower medulla and upper cervical cord. * MRI: (i) extra-axial, homogeneously enhancing mass with a “dural tail”; (ii) encasement of vertebral artery or dentate ligament displacement. Definitive therapy is microsurgical resection (often far-lateral approach); stereotactic radiosurgery if unresectable or in poor surgical candidates. ## Footnote Pearl: multiple meningiomas → screen for NF-2.

Question 51

Most common Skin malignancy in chronic immunosuppresion patients

Answer 51

SCC- more agressive with risk for regional metastasis.

Question 52

You see acute diarrhea on the wards. Which common organisms cause non-bloody, watery diarrhea and which cause bloody / inflammatory diarrhea?

Answer 52

**Watery:** Vibrio cholerae, enterotoxigenic E. coli (ETEC), Clostridium perfringens, Staph aureus toxin, Bacillus cereus, Norovirus, Rotavirus, Giardia. **Inflammatory (± blood):** Shigella, Salmonella (non-typhi), Campylobacter jejuni, enterohemorrhagic E. coli (EHEC / STEC), Yersinia, C. difficile, Entamoeba histolytica. Memory tip: “S.S.C.E.Y.C.D.E.” = inflammatory alphabet soup.

Question 53

Hospitalized patient develops profuse watery diarrhea after clindamycin. List two “severe-disease” markers that change therapy. First-line treatment for non-severe vs severe/fulminant infection. When do you consider fecal microbiota transplant (FMT)?

Answer 53

**Severe** if WBC ≥ 15 000 /µL or creatinine ≥ 1.5 mg/dL above baseline (fulminant if shock, ileus, megacolon). **Non-severe:** oral vancomycin 125 mg q6h (or fidaxomicin). **Severe/fulminant:** oral vancomycin 500 mg q6h + IV metronidazole; add rectal Vanco if ileus. **Third recurrence or refractory severe disease** → consider FMT.

Question 54

Backpacker in Mexico with abrupt watery stools, mild cramps, no blood. Most common pathogen and empiric oral antibiotic regimen?

Answer 54

Usually ETEC; give azithromycin 1 g once (first-line in Asia or pregnancy) or ciprofloxacin 500 mg BID x 3 days.

Question 55

Match each exposure to its protozoan and treatment: A. Day-care outbreaks, foul greasy stools B. Traveler drinking mountain-stream water, steatorrhea after 1-2 weeks C. AIDS patient with watery diarrhea, acid-fast oocysts in stool

Answer 55

A. **Entamoeba histolytica **– metronidazole + luminal agent (paromomycin). B. **Giardia lamblia** – metronidazole or tinidazole. C. **Cryptosporidium parvum** – nitazoxanide if immunocompetent; HAART and supportive care in AIDS.

Question 56

**Match each buzz-phrase to the most likely adult CNS tumour.** a. Ring-enhancing butterfly lesion crossing corpus callosum. b. Calcified parasagittal mass, seizures, hyperostosis of adjacent skull. c. CPA angle mass with ipsilateral sensorineural hearing loss. d. Pituitary mass, bitemporal hemianopia, hyperprolactinaemia.

Answer 56

a. Glioblastoma multiforme (grade IV astrocytoma) – very poor prognosis. b. Meningioma – benign, resectable; whorls & psammoma bodies on histology. c. Vestibular (schwannoma) neurilemmoma – think NF-2 if bilateral. d. Pituitary adenoma (most often prolactinoma) – treat with dopamine agonist first.

Question 57

How is the ankle-brachial index measured? Give the interpretation cut-offs every Step 2 student must know. List two clinical scenarios where ABI is most useful and one setting where it can be misleading.

Answer 57

**Technique** * Measure systolic pressure in each brachial artery with Doppler. * Measure dorsalis pedis or posterior tibial systolic pressure in each ankle. * Calculate ABI = (higher ankle pressure) / (higher brachial pressure) for each leg. **Interpretation** * 1.00 – 1.40 = Normal (compressible arteries) * 0.91 – 0.99 = Borderline * 0.41 – 0.90 = Mild–moderate PAD (peripheral arterial disease) * 0.00 – 0.40 = Severe PAD / critical limb ischemia * > 1.40 = Non-compressible, calcified vessels → order toe-brachial index or pulse-volume recording. **Clinical pearls** **Most useful for:** – Screening & risk stratification of PAD in diabetics, smokers, or patients with exertional calf pain. – Post-exercise ABI drop confirms exertional claudication when resting ABI is normal. **Misleading when: ** Arterial walls are medial-calcified (end-stage renal disease, long-standing diabetes, elderly) → falsely elevated ABI > 1.40; rely on toe pressures or duplex ultrasound instead. ## Footnote **An ABI < 0.90** doubles 10-year cardiovascular-mortality risk—treat aggressively with antiplatelets, statin, smoking cessation, and supervised exercise therapy.

Question 58

**A patient presents with hand pain. Fill in the blanks to name the likely disease:** Bony, non-tender enlargements at DIP and PIP (Heberden & Bouchard nodes); 1st-CMC squaring; asymmetric; stiffness < 30 min → ____? Symmetric swelling of MCPs, PIPs, and wrists but spares DIP; ≥ 60 min morning stiffness; possible ulnar deviation → ____?

Answer 58

Osteoarthritis (OA) – degenerative “wear-and-tear” arthritis. Rheumatoid arthritis (RA) – chronic autoimmune synovitis. Memory hook: “Outside joints = OA; Right-at-base (MCP) = RA.”

Question 59

**Match each finding to OA or RA:** a. Elevated ESR/CRP, positive anti-CCP; marginal erosions on x-ray. b. Normal labs; x-ray shows non-uniform joint-space loss, osteophytes, subchondral sclerosis. c. Swan-neck / boutonnière deformities with soft-tissue swelling. d. Heberden nodes at DIP, Bouchard nodes at PIP.

Answer 59

a.** RA** – inflammatory markers & erosive imaging. b. **OA** – “wear-and-tear” radiograph and normal serology. c. **RA** – tendon/ligament laxity from chronic synovitis. d. **OA** – bony nodules from osteophyte formation. **Key distinction**: RA = systemic inflammation + erosions; OA = mechanical degeneration + osteophytes.

Question 60

Long-term hemodialysis patient (> 5 years) develops bilateral carpal-tunnel syndrome, shoulder pain with limited range, and cystic lesions in the carpal bones on X-ray. Which amyloid protein causes these findings and why does it accumulate? List three other skeletal or peri-articular complications that should make you think of DRA.

Answer 60

**β-2-microglobulin (Aβ2M) amyloid**. It is normally cleared by healthy kidneys; conventional low-flux dialysis membranes remove it poorly, so serum levels climb and β2M deposits in osteo-articular tissues. **“S-BONE” mnemonic for DRA complications:** **S:** destructive Shoulder (rotator-cuff) arthropathy **B:** Bone cysts/geodes in carpal & femoral heads **O:** Osseous spine disease (cervical/lumbar spondyloarthropathy) **N:** Nerve entrapment syndromes (carpal- & tarsal-tunnel) **E:** Effusions with β2M crystals in large joints

Question 61

**Match each bedside vignette to the amyloid protein type most likely involved**. * 65-y/o with nephrotic-range proteinuria, macroglossia, easy bruising; serum light-chain spike on SPEP/IFE. * Long-standing rheumatoid arthritis patient develops hepatosplenomegaly and rising creatinine; no monoclonal band. * Elderly man with slowly progressive restrictive cardiomyopathy and bilateral carpal-tunnel syndrome; fat pad biopsy Congo-red positive, serum studies negative. * African-American age 45 with severe diastolic heart failure; genetic test shows Val122Ile mutation in transthyretin gene.

Answer 61

* **AL (light-chain) amyloidosis** — plasma-cell dyscrasia (λ > κ). * **AA (serum amyloid A) amyloidosis** — chronic inflammatory disease. * **Senile (wild-type) ATTR amyloidosis** — deposition of normal transthyretin, chiefly in heart & ligamentum carpi. * **Hereditary ATTR amyloidosis **— mutant transthyretin (e.g., Val122Ile in Afro-Caribbean; Val30Met in Portuguese).

Question 62

A 28-year-old woman presents with confusion, petechiae, fever, and creatinine 2.1 mg/dL. Labs: Hb 7 g/dL, platelets 16 k, schistocytes, normal PT/PTT. 1. Name the syndrome and recite its classic “pentad.” 2. What is the underlying molecular defect? 3. Which single lab test (if available) clinches the diagnosis?

Answer 62

**Thrombotic Thrombocytopenic Purpura (TTP).** **Pentad:** Microangiopathic hemolytic anemia (MAHA) + Thrombocytopenia + Neurologic symptoms + Renal injury + Fever (only the first two are required for diagnosis). **Severe deficiency of ADAMTS13 metalloprotease** (often from autoantibody) → ultra-large vWF multimers → platelet-rich microthrombi. **ADAMTS13 activity < 10 %** with or without anti-ADAMTS13 antibodies confirms TTP (send but do NOT wait to treat).

Question 63

1. Outline the immediate, definitive treatment for TTP and two adjunctive drugs. 2. How do you distinguish TTP from DIC on routine labs? 3. Why are platelet transfusions generally avoided?

Answer 63

**Urgent plasma exchange** (PEX) daily until platelets > 150 k for 2 days. **Adjuncts: ** IV corticosteroids (methylpred 1 mg/kg) and rituximab for refractory/relapsing disease; caplacizumab (anti-vWF nanobody) shortens time to platelet recovery. **TTP:** normal PT/PTT & fibrinogen, marked schistocytes. **DIC:** prolonged PT/PTT, low fibrinogen, ↑ D-dimer. Donor platelets feed the vWF “logjam,” worsening microthrombosis unless life-threatening hemorrhage mandates transfusion.

Question 64

List the major syndromes and disorders that present with microangiopathic hemolytic anemia (MAHA).

Answer 64

**Thrombotic Thrombocytopenic Purpura (TTP)** – ADAMTS13 deficiency → vWF-mediated platelet thrombi. *** Hemolytic Uremic Syndrome (HUS)** – Shiga-toxin (EHEC) or complement-mediated (atypical) → renal microthrombi. *** Disseminated Intravascular Coagulation (DIC)** – widespread fibrin deposition and schistocytes from sepsis, trauma, or malignancy. *** HELLP Syndrome (in pregnancy) **– Hemolysis, Elevated Liver enzymes, Low Platelets in pre-eclampsia → microvascular injury.

Question 65

A 30-year-old woman from rural Guatemala is brought to the ER after a first generalized tonic-clonic seizure. She reports intermittent headaches and mild abdominal discomfort over the past month. She recalls eating undercooked pork in her village before she immigrated. Physical exam is unremarkable except for mild right-sided weakness. Brain CT (noncontrast) shows multiple 1–2 cm, round cystic lesions in both cerebral hemispheres; some have a small hyperdense “dot” centrally. Routine labs are normal. A stool ova & parasite exam is pending. What parasitic infection explains her neurologic findings, and how did she acquire it? What stool finding (if positive) would confirm concurrent intestinal infection? Describe the key diagnostic test and findings for her brain lesions. Outline first-line treatment for both her intestinal tapeworm and neurocysticercosis, including any adjunctive measures.

Answer 65

**Neurocysticercosis from Taenia solium eggs.** She acquired cysticercosis by ingesting eggs (fecal–oral transmission) shed in the stool of a human carrier (often a family member or food handler with an adult tapeworm). Oncospheres hatched in her gut penetrated the bowel wall, traveled via bloodstream, and formed cysticerci in her brain. **Stool exam would show Taenia eggs or gravid proglottids** (yellowish segments). Eggs are oval with a thick shell and radial striations; proglottids have uterine branches and, if available, a scolex with hooklets. **Brain imaging – Characteristic findings on CT/MRI:** **“Dot sign”:** a 1–2 cm fluid-filled cyst with an eccentric hyperdense scolex **(pathognomonic).** Viable cysts appear as well-defined cystic lesions without surrounding edema; degenerating cysts enhance peripherally; chronic lesions are calcified nodules. Serology (enzyme-linked immunoelectrotransfer blot) supports the diagnosis if multiple active cysts are present. **Treatment:** **Intestinal Taeniasis** (adult tapeworm): *** Praziquantel **single dose 5–10 mg/kg (kills adult worm). * Counsel on hygiene to prevent egg spread; check and treat close contacts if stool is positive. **Neurocysticercosis:** *** Albendazole** 15 mg/kg/day in two divided doses for 10–28 days (first-line). * **Praziquantel** 50–75 mg/kg/day in three divided doses for 14–28 days if albendazole unavailable. * Give dexamethasone (0.1 mg/kg/day) starting 1 day before antiparasitic therapy and taper over 1–2 weeks to mitigate inflammatory response from dying cysts. * **Antiepileptic** (e.g., levetiracetam) for seizure control; duration depends on lesion resolution. * **Neurosurgical intervention if obstructive hydrocephalus (ventricular cysts) or large parenchymal cysts causing mass effect**—ventricular drainage or cyst excision.

Question 66

When suspecting refeeding syndrome, what lab changes confirm it, and how do you prevent and treat it?

Answer 66

**Key Lab Findings (after refeeding):** ** ↓ Serum phosphate** (often first and most severe). **↓ Serum potassium and ↓ serum magnesium**. **Thiamine deficiency **signs may appear (high-output cardiac failure, lactic acidosis). **Possible fluid overload** and edema from sodium/water retention. **Prevention & Treatment**: Assess risk before feeding; obtain baseline electrolytes (phosphate, potassium, magnesium), thiamine, and glucose. **Start low, go slow:** Begin calories at 10–20 kcal/kg/day (10 kcal/kg if very high risk), advancing over 4–7 days. **Supplement electrolytes & vitamins:** * Phosphate (e.g., 0.32–0.36 mmol/kg/day IV/PO). * Potassium and magnesium to keep in mid-normal range. * Thiamine 100–300 mg IV daily for first 3 days, then PO.

Question 67

A 35-year-old HIV-positive patient with CD4 120/mm³ presents with subacute (2-week) progressive dyspnea, nonproductive cough, and low‐grade fever. – Exam: tachypnea, bilateral crackles; oxygen saturation 88% on room air. – CXR: bilateral perihilar interstitial infiltrates; chest CT: diffuse ground‐glass opacities. * Which pathogen is likely, * how do you confirm the diagnosis, * what is the first‐line treatment (including adjuncts), * and what prophylaxis should have been given?

Answer 67

**Etiologic organism:** **Pneumocystis jirovecii** (formerly P. carinii), a yeast‐like fungus. **Diagnosis:** Induced sputum or **BAL fluid with silver stain** (methenamine silver) showing cysts or immunofluorescent DFA. Elevated serum LDH and (often) 1,3‐β-D-glucan support suspicion but are not definitive. **Treatment:** Trimethoprim–sulfamethoxazole** (TMP-SMX) high-dose for 21 days.** **Add prednisone if** A-a gradient ≥ 35 mm Hg or PaO₂ ≤ 70 mm Hg on room air: * Prednisone 40 mg BID days 1–5, 40 mg daily days 6–10, 20 mg daily days 11–21. If sulfa allergy: Pentamidine IV (second-line) or clindamycin + primaquine. **Prophylaxis (for CD4 < 200/mm³):** TMP-SMX single-strength daily (or three times weekly). **Alternatives**:** dapsone** (± pyrimethamine/leucovorin) **or atovaquone** if G6PD deficiency or sulfa intolerance.

Question 68

A 40-year-old firefighter is pulled from a smoke-filled building. He’s hypotensive, tachypneic, and confused with seizures. Vitals: HR 130, BP 170/90, RR 30, SpO₂ 98% on high-flow O₂. ABG shows pH 7.10, lactate 12 mmol/L. You detect a faint “bitter almond” odor. What toxin is most likely? Explain its mechanism of cellular injury. Which key lab finding helps distinguish it from carbon monoxide poisoning? Outline the first-line antidote regimen and its rationale.

Answer 68

Cyanide—commonly inhaled in smoke from burning plastics/nylon or in nitroprusside overdose. Mechanism: Binds cytochrome-a₃ (complex IV) in mitochondrial electron-transport chain → halts oxidative phosphorylation → histotoxic hypoxia → anaerobic metabolism → lactic acidosis. Lab clue: High mixed-venous O₂ saturation (poor tissue extraction) versus low in CO; severe metabolic acidosis with very elevated lactate. Antidote regimen: Hydroxocobalamin IV — binds cyanide to form cyanocobalamin for renal excretion. Sodium thiosulfate — sulfur donor for rhodanese-mediated conversion of cyanide to thiocyanate (less toxic). (Older nitrite-based kits use amyl/nitrite to induce methemoglobin, which sequesters cyanide, but these can worsen hypotension and are second-line.) ## Footnote **Key Step 2 pearl**: In any smoke-inhalation victim with neurologic changes, lactic acidosis, and normal pulse ox, suspect cyanide poisoning—don’t wait for confirmatory labs before starting hydroxocobalamin.

Question 69

Nitroprusside overdose can lead to?

Answer 69

Cyanide toxicity- Treat with 100% oxygen + hydroxycobalamin

Question 70

Question 71

Most commom cause for Charcot neuropathic arthropathy?

Answer 71

Dibetic neuropathy