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Episode Notes

Source / episode info

  • Episode: 29
  • Title: Divine Intervention Episode 29 – 3rd Year Medicine Shelf Review Part 1.
  • Published: 2018-05-18
  • Source: Episode page

One-liner

This comprehensive review covers critical board topics including cardiac murmurs (MS), metabolic emergencies (hypoglycemia, AI), infectious diarrhea differentials, nephritic/nephrotic syndromes, iron overload workup, and management of acute respiratory distress.

High-yield summary

  • Mitral Stenosis: Classic finding is an opening snap followed by a low-pitched diastolic rumble at the left 4th interspace; associated with elevated Jugular Venous Pressure (JVP) A waves.
  • Hypoglycemia Workup: Must differentiate causes using labs: Insulinoma (high insulin, low glucose), Factitious (excess exogenous insulin/sulfonylurea), or other drugs (e.g., sulfonylureas). Acute treatment is IV dextrose or glucagon.
  • Adrenal Insufficiency (AI): Primary AI involves low cortisol and low aldosterone; secondary AI involves low cortisol but normal aldosterone (due to preserved RAAS axis). Stress dosing requires hydrocortisone.
  • Iron Overload: Diagnosed by elevated ferritin/TIBC, confirmed by Prussian blue staining of bone marrow smears (basophilic inclusions); treated with chelation therapy (e.g., deferoxamine).
  • Acute Kidney Injury (AKI): Causes are multifactorial; prevention includes holding specific drugs (e.g., DM medications) before contrast C Ts, and recognizing nephrotoxins (NSAI Ds, aminoglycosides).
  • GI Diarrhea: Must differentiate bugs based on presentation: C. difficile (bloody/pseudomembranous after antibiotics), Giardia (watery, chronic), Shigella (bloody, high inoculum), Salmonella (fever, bloody).

Learning objectives

  • Differentiate common causes and acute management strategies for hypoglycemia.
  • Recognize the classic physical exam findings associated with valvular heart disease (e.g., Mitral Stenosis).
  • Apply knowledge of infectious diarrhea etiologies based on clinical presentation and travel history.
  • Compare primary versus secondary adrenal insufficiency, including appropriate diagnostic testing and stress dosing protocols.
  • Interpret bone marrow staining and iron studies to diagnose iron overload syndromes.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
Mitral Stenosis (MS)Opening snap + Diastolic rumbleHigh LA pressure, elevated JVP A wavesRemember the triad: opening snap, diastolic rumble, and high JVP.
HypoglycemiaResolution with glucose; high insulin/low glucoseInsulinoma, factitious ingestion of insulinAlways check for exogenous insulin use in a hypoglycemic patient.
Primary Adrenal Insufficiency (Addison's)Hyperpigmentation + Low Cortisol/AldosteroneAutoimmune destruction of adrenal cortexThe hyperpigmentation is due to high ACTH stimulating melanocytes.
Iron OverloadPrussian blue staining; elevated ferritinHemochromatosis, transfusional iron overloadChelation therapy (e.g., Deferoxamine) is the primary treatment.

Rapid review table

TopicKey PointContextExam Relevance
HypoglycemiaDifferentiate causes using labs (Insulinoma vs. Factitious).Acute presentation, often in diabetics or those on sulfonylureas.High-yield emergency; know the specific lab pattern for diagnosis.
Mitral StenosisOpening snap + Diastolic rumble.Physical exam finding indicating restricted valve opening and high LA pressure.Classic physical exam question; requires knowing the associated pathophysiology (LA dilation).
Adrenal InsufficiencyPrimary AI: Low Cortisol/Aldosterone, High ACTH. Secondary AI: Low Cortisol, Normal Aldosterone.Stress situations (surgery, infection) require immediate steroid replacement.Know which axis is failing to determine if aldosterone levels are preserved.
Iron OverloadPrussian blue stain of bone marrow; elevated ferritin.Chronic transfusions or genetic disorders (Hemochromatosis).Treatment involves removing iron via chelation therapy and phlebotomy.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
Opening snap with diastolic rumble at left 4th interspace.Mitral StenosisThis is the classic physical exam triad for MS due to restricted valve opening and high LA pressure.
Elevated AST/ALT, blistering lesions on dorsum of hands, severe hirsutism.Wilson's DiseaseThese findings represent hepatic failure (elevated LF Ts) combined with signs of copper deposition and endocrine dysfunction.
Hypoglycemia, resolution with glucose administration; labs show high insulin.InsulinomaThe combination of hypoglycemia and elevated insulin strongly points to an insulin-secreting tumor.
Flank pain with gross hematuria; shaped like a hexagon/radiolucent.Nephrolithiasis (Kidney Stones)These are classic descriptive findings for stones, requiring imaging (CT urogram).
Cherry red appearance of the skin in an unconscious patient.Syphilis (Tertiary)This is a classic sign of advanced syphilis, prompting immediate workup for systemic infection.

Differential diagnosis / distinguishing features

Causes of Hypoglycemia

Key FeaturesDistinguishing FindingsNext Step
InsulinomaLow glucose, high insulin (and often low C-peptide).Surgical resection of the tumor; Octreotide/Pancreatic somatostatin analogs.
Factitious HypoglycemiaLow glucose, high insulin, but normal or elevated C-peptide.History review for exogenous insulin use; N/A (requires cessation of drug).
Sulfonylurea OverdoseLow glucose, low insulin, often associated with diabetic history.Supportive care; discontinue the offending agent.

Adrenal Insufficiency

Key FeaturesDistinguishing FindingsNext Step
Primary AI (Addison's)Low Cortisol AND Low Aldosterone; High ACTH/High Renin.Cosyntropin stimulation test: Failure to raise cortisol. Treat with Hydrocortisone and Fludrocortisone.
Secondary AILow Cortisol BUT Normal Aldosterone; Low ACTH.Cosyntropin stimulation test: Failure to raise cortisol. Treat only with Hydrocortisone (Aldosterone is preserved).

Management pearls

  • Hypoglycemia: Always treat the acute emergency first (Dextrose/Glucagon) before pursuing the underlying cause.
  • Mitral Stenosis: The primary risk factor is Infective Endocarditis (leading to valve damage), and treatment involves anticoagulation (Warfarin).
  • Adrenal Crisis: Suspect in any patient with unexplained hypotension, hyponatremia, or hyperkalemia during illness/stress; treat immediately with IV Hydrocortisone.
  • Iron Overload: The definitive diagnosis requires Prussian blue staining of bone marrow smears and is managed by phlebotomy (for hemochromatosis) or chelation therapy.

Don't miss

🚨
When evaluating diarrhea, always consider the difference between bacterial pathogens ( Shigella , Salmonella ) vs. protozoa ( Giardia ).
🚨
The classic triad for Mitral Stenosis is: Opening snap, diastolic rumble, and elevated JVP A waves.
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In primary adrenal insufficiency (Addison's), the high ACTH leads to hyperpigmentation due to MSH co-secretion.

Integration & clinical reasoning

  • Endocrine/Cardio: Severe hypoglycemia can precipitate cardiac arrhythmias; AI causes volume depletion leading to hypotension and poor cardiac output.
  • GI/Nephro: Chronic diarrhea (e.g., Giardia ) can lead to malabsorption, contributing to electrolyte imbalances that stress the kidneys.
  • Hematology/Endocrine: Iron overload affects multiple organs, including the pituitary gland, which can contribute to secondary adrenal insufficiency.

OMM / COMLEX integration

🦴
For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Adrenal Crisis Management: In any acute setting where adrenal function is questionable (illness, surgery), assume AI and administer stress-dose steroids immediately.
  • Electrolyte Balance in CKD: Be prepared to manage the classic triad of metabolic acidosis, hyperkalemia, and phosphate retention as kidney function declines.

Concept connections / cross-references

  • No explicit cross-references.

High-yield association table

ConditionAssociationMechanismClinical Significance
Mitral StenosisOpening snap + Diastolic rumbleHigh left atrial pressure causes restricted opening of the valve leaflets.Requires anticoagulation to prevent thromboembolism (risk of stroke).
HypoglycemiaInsulinomaTumor secretes excess insulin autonomously, leading to profound hypoglycemia.Must differentiate from factitious ingestion; high-yield emergency diagnosis.
Primary Adrenal InsufficiencyHigh ACTH levelsLack of negative feedback on the pituitary gland due to adrenal failure.Causes hyperpigmentation (due to MSH) and electrolyte abnormalities (hyponatremia, hyperkalemia).
Iron OverloadHemochromatosisGenetic defect leading to excessive absorption and deposition of iron in organs.Requires regular monitoring of liver function and potential chelation therapy.

Key terms glossary

TermDefinitionContextExample
Opening SnapA high-pitched sound heard early in diastole.Mitral Stenosis (MS) exam finding; indicates restricted opening of the mitral valve leaflets.Heard best at the apex, often associated with a diastolic rumble.
Prussian Blue StainStaining that turns iron deposits blue/green.Diagnosis of systemic iron overload (e.g., Hemochromatosis).Used on bone marrow smears to visualize basophilic inclusions.
Cosyntropin TestSynthetic ACTH administered intravenously.Diagnostic test for adrenal insufficiency; measures the pituitary gland's ability to stimulate cortisol production.If cortisol fails to rise after cosyntropin, AI is suspected.
Opening Snap (Mitral)A distinct sound heard during early diastole.Indicates restricted movement of the mitral valve leaflets due to fibrosis/stenosis.Helps differentiate MS from other murmurs.

Study optimization

TopicStudy ApproachPriorityResources
Endocrine EmergenciesCreate flowcharts for hypoglycemia and adrenal crisis workup.High (Board-critical)Review the specific lab patterns (Insulinoma vs. Factitious).
Cardiology/Physical ExamPractice identifying classic murmurs and associated findings.Medium-HighFocus on the why behind the physical exam finding (e.g., why MS causes high JVP A waves).
GI Bugs & DiarrheaUse a table format to compare bugs, symptoms, and treatments.High (Step 2/3)Link travel history and antibiotic use to specific pathogens (C. diff, Giardia).

Question pattern recognition

  • The "Best Next Step" Pattern: Given a complex presentation (e.g., fever + abdominal pain), the question asks for the single most appropriate initial diagnostic test or management step.
  • Differential Diagnosis Pattern: Presenting symptoms that overlap multiple systems (e.g., fatigue, GI upset, skin changes) requires ruling out several possibilities systematically.
  • Classic Triad/Tetrad Pattern: Memorizing specific combinations of signs and symptoms (e.g., MS: Opening snap + rumble + high JVP).

Test yourself

Common mistakes to avoid

🚫
Mistaking the cause of hypoglycemia (e.g., assuming it's always due to insulinoma when factitious ingestion is possible).
🚫
Forgetting that primary AI involves both cortisol and aldosterone deficiency, leading to unique electrolyte abnormalities.
🚫
Confusing the signs of Mitral Stenosis with those of other valvular diseases.

Common traps

⚠️
The "Normal" Aldosterone Trap: In secondary adrenal insufficiency (due to pituitary failure), aldosterone levels are preserved because the RAAS axis is intact; this is a common distracter.
⚠️
The "Chronic Transfusion" Trap: Assuming all iron overload is due to hemochromatosis when it could be transfusional iron, requiring different management strategies.
⚠️
The "GI Bug" Trap: Overlooking the importance of antibiotic use history when diagnosing diarrhea (always suspect C. difficile ).

Original transcript with highlights

Original transcript with highlights

NBME Medicine Shelf Review Session 1 Some MS4 Introduction -This first review set contains 70 keyword slides. -The goal would be to spend 90s or less per slide (some will take < 30s). -Strongly encourage making notes with each slide. Study these notes for your shelf. Writing stuff down will help tremendously with retention. -Designed to be a more comprehensive but HY medicine shelf review. -Make sure you do all 4 practice NBM Es for the medicine shelf. If a topic is completely new to you, spend about 10 mins studying that topic as something similar may be tested on the shelf. -The medicine shelf is surprisingly not a huge departure from a lot of the material tested from the organ systems on Step 1. We will review some of this pertinent stuff. 1 Opening snap with diastolic rumble at left 4th interspace. Tall jugular venous A waves. How can we increase the intensity of this murmur? 2 Elevated AST/ALT, blistering lesions on the dorsum of the hands, severe hirsutism. What is the enzyme deficiency? How is this disease treated? 3 Hypoglycemia, hypoglycemic sxs, resolution with glucose administration. Differentiating 3 big causes of hypoglycemia based on labs. The acute treatment of hypoglycemia.

4 A Diarrhea (Bugs, associations, treatment) Pork consumption, Undercooked shellfish, Severe rice-water stools in a developing country, Bloody diarrhea with a super small inoculum, Bloody diarrhea after consuming eggs/poultry, Watery diarrhea 2 hrs after consuming potato salad, Bloody diarrhea with low plts/unconjugated hyperbilirubinemia/elevated creatinine. 4 B Diarrhea (Bugs, associations, treatment) Diarrhea upon return to the US from Mexico, Foul smelling watery diarrhea after recent treatment for an anaerobic bacterial pneumonia, Crampy abdominal pain after consumption of home canned veggies, Bloody diarrhea with ascending paralysis in a puppy owner, Watery diarrhea after eating fried rice at a Chinese restaurant. 5 Prussian blue staining of a bone marrow smear reveals basophilic inclusions around the nucleus in a 75 yo M that lives in a home built in the 1930s. What are the associated Fe lab values? How is this disease treated (+ potentially helpful vitamin supplementation)? 6 CXR showing diffuse, bilateral, ground glass infiltrates in a febrile patient taking high dose immunosuppressants. What is the bug? Relevant stain? Prophylaxis? Treatment? Who should get concomitant steroids? Diagnostic studies? Classically elevated marker from pulmonary fluid? 7 (Associations/Relevant Bugs/Risk factors) Flank pain with gross hematuria. Envelope shaped? Coffin shaped? Radiolucent? Shaped like a hexagon? What is the best diagnostic testing modality?

How is this presentation treated? 8 24 yo M presents with a painless, palpable bony mass on the left knee. Knee X ray reveals a contiguous mushroom shaped mass. What is the diagnosis? 9 66 yo F is found unconscious at home by her daughter in December. PE is notable for a cherry red appearance of the skin. Next best step in diagnosis? Treatment modalities? Pathophysiology and O2 delivery associations? Classic exam presentation and risk factors? 10 Elevated creatinine 24 hrs after getting a CT scan. How could this have been prevented? Skin fibrosis after getting a brain MRI. Is there a particular DM medication that should be held before getting a CT scan? 11 A common lower extremity side effect associated with hydralazine and Ca channel blockers. What is the pathophysiology? How is this condition treated? What is the pathophysiologic mechanism? 12 HIV patient with a 3 day history of fever presents with targetoid skin lesions, lip/mouth ulcerations, and visual impairment. PE is notable for skin sloughing (8% BSA). Nikolsky sign is +ve. He was placed on Allopurinol 10 days ago for chronic gout. What is your diagnosis? > 30% BSA involvement? 13 30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl, Bicarb is 21, pH is 7.35. Diagnosis? Pathophysiology? Risk factors? Treatment? Na balance? K balance? What is your dx if the patient becomes altered/comatose with rapid treatment? 14 49 yo F presents with wheezing and flushing.

PE is +ve for murmurs consistent with tricuspid regurgitation and pulmonic stenosis. Diagnosis? Diagnostic steps? Treatment (pharmacology)? Symptoms by location? Pellagra? 15 61 yo M presents with exertional dyspnea. CBC is notable for a Hct of 27%. What is the next best step in management? What would Fe studies dictate? What is our primary concern? When should transfusion be explored? What would your diagnosis be if the patient had a similar presentation and difficulty swallowing? 16 29 yo F with a recent trip to India (ate local foods). Returned 2 weeks ago and initially had fevers for 1 week. Now presents with severe abdominal pain and distension. PE is notable for salmon colored circular lesions on the trunk. Diagnosis? Treatment? 17 Septic arthritis ->what is the bug? (+most common cause, + in a sickle cell patient, + in a young F with purpuric skin lesions). Diagnostic step? Findings from diagnostic steps? Treatment (2 pronged approach). The Neisseria vs Chlamydia treatment difference. 18 Subconjunctival hemorrhage in a patient with nasty coughing episodes. Diagnosis? Treatment? Prophylaxis for close contacts? What would the next step in management be in a person that recently started Ramipril for the treatment of HTN who has a cough? 19 Reviewing first, second, and third degree AV blocks. Acute management in a symptomatic patient? Contraindicated medications? Who gets a pacemaker??

20 Reduced EF in a patient with coarse facial features and enlarging fingers. Diagnosis? Diagnostic steps (3)? Treatment options? Most common cause of death? 21 Dysphagia to solids and liquids in a patient with thick/thin blood smears (Giemsa) revealing what appears to be motile parasites. Diagnosis? Diagnostic steps (2)? Pathophysiology? Surgical/Non-Surgical treatment options? Potential sequelae of treatment/disease sequelae? 22 Reduced MCV in a patient with a long history of untreated rheumatoid arthritis. Diagnosis? What would the results of a CBC/Fe studies indicate? Pathophysiology? 23 25 yo M with nasal packing presents with a BP of 65/40, elevated Cr, respiratory distress, T of 104, and marginally elevated troponins. Diagnosis? Pathophysiology? Classic bug associations (2)? Treatment strategies? 24 Sequelae of CKD (acid-base anomalies, electrolyte anomalies, hematologic anomalies, Ca and P balance). Consequences of uremia. Management of CKD (drugs, electrolyte/hematologic fixes). How is kidney function preserved in DKD? Indications for dialysis. 25 Rb gene mutations, Paget’s disease, and Teriparatide administration increase risk of what primary bone malignancy? Associated radiological features? 26 Aspirin Exacerbated Respiratory Disease. Potential pathophysiology? Classic presentation? Treatment 27

28 Aspirin Exacerbated Respiratory Disease. Potential pathophysiology? Classic presentation? Treatment 29 Classic EKG presentation of a Supraventricular Tachycardia. Stepwise management of an SVT. What is the next best step in management if a patient has an SVT but is hemodynamically unstable? What is the most common EKG finding in a patient having a pulmonary embolus? 30 18 yo F presents with scaly, erythematous upper extremity lesions. She has a long history of allergic rhinitis. What is your diagnosis? How is this treated? What would your diagnosis be if these lesions also had umbilicated vesicles? How would this be treated? What is the classic CBC finding with these diagnoses? 31 A patient presents with the classic “stones, bones, groans, and psychic overtones”. PE is notable for skin tenting. What is the FIRST step in management? A quick overview of Ca pharmacology. 32 Testing modalities for H. Pylori infection (3). Triple therapy. Classic presentation/risk factors for peptic ulcer disease. 33 Alpha vs Beta Thalassemias. Pathophysiology. Compare and contrast (C/C) beta vs alpha thalassemia minor in terms of Hb electrophoresis results. C/C beta vs alpha thalassemia major in terms of presentation onset and Hb electrophoresis results. What is Hb H disease? What is Hb Barts? What is the classic smear finding in thalassemias? 34 Classic CBC findings in hemolytic anemias. Classic “gallbladder” pathology present in patients with hemolytic anemias.

These patients are at risk of aplastic crises with what bug? Do thalassemias present as a microcytic, normocytic, or macrocytic anemia? 35 23 yo M who recently returned from Tucson presents with a 2 week history of fever, ankle/knee pain, chest pain, and a painful, erythematous pretibial lesion. Diagnosis? Classic finding on microscopy? Treatment strategy? Classic geographical association. 36 Periorbital edema, hematuria, and HTN in a patient with a recent history of cellulitis. BUN and Cr are elevated. Diagnosis? Pathophysiology? Associated antibodies? This disease reflects what kind of hypersensitivity reaction? 37 11:22 translocation, X-Ray imaging reveals an “onion skin like” periosteal reaction, bone biopsy with histology reveals small, round, blue cells. What is your diagnosis? 38 What is a parapneumonic effusion (PNE)? Describe the following->Uncomplicated PNE, Complicated PNE, Empyema. What are the pH, LDH, glucose, and micro criteria that typify a “high risk” PNE? How do the available treatment modalities help you differentiate between the different parapneumonic effusion types? For Keyword 39 (next slide)

39 What is your diagnosis? How would you describe the rhythm? How would treat this rhythm in a patient that is stable/asymptomatic vs a patient that is hemodynamically unstable vs a patient that lacks a pulse? What is the most common cause of death in the immediate period following an MI? 40 Oral mucosal ulcerations + +ve Nikolsky sign (flaccid skin blisters) in a 45 yo M. Diagnosis? Pathophysiology? Type of hypersensitivity reaction? Diagnostic testing modality (super HY)? Treatment strategy? 41 Lab differentiation between primary and secondary hyperaldosteronism. Screening vs confirmatory testing for Conn Syndrome. Causes of secondary hyperaldosteronism. Treatment strategies with Conn Syndrome. Quick description of nephron physiology. 42 The Rome Criteria for Irritable Bowel Syndrome. Classic patient demographic. Are there lab abnormalities? IBS Classification. 43 Cold vs Warm Agglutinins (classic antibodies, bug associations). Treatment differences b/w warm and cold agglutinin disease. LDH, Bilirubin, and Haptoglobin levels in hemolytic anemia. 44 32 yo Egyptian immigrant presents with a 2 week history of abdominal pain, hepatosplenomegaly, and hematuria. He swam in The Nile 2 months ago. Diagnosis? Bug? Route of transmission? Classic CBC observation? Potential oncologic sequelae? Pharmacological management? 45 Synpharyngitic glomerulonephritis.

Compare and contrast with Post Infectious Glomerulonephritis wrt to->Timeline to onset of symptoms, complement levels, etc. Treatment strategies. Classic urine findings with the nephritic syndromes. 46 70 yo M with leg pain that is worsened by a back held in extension (but better when held in flexion). Diagnosis? Diagnostic testing? Treatment strategies? 47 Opening snap with a diastolic rumble heard best in the 4th intercostal space in the midclavicular line. Diagnosis? #1 risk factor? Diagnostic testing? Treatment strategies? 48 No oral mucosal lesions + Pruritus + Negative Nikolsky sign. Diagnosis? Pathophysiology? Best diagnostic test? Treatment strategies (contrast with initial management of the somewhat analogous Nikolsky +ve disease)? 49 Compare and contrast primary and secondary adrenal insufficiency (by classic cause, skin findings, levels of ACTH/Aldosterone/Renin, Cosyntropin testing, treatment strategy). Key labs/CBC findings in AI. AI with a history of nuchal rigidity and purpuric skin lesions. Discussion of adrenal physiology. Stress Steroid Dosing. 50 69 yo M with fever, leukocytosis, and LLQ pain. Diagnosis? Pathophysiology? Diagnostic testing? Contraindicated initial studies? GI Antibiotic strategies on the NBME (2)? What is your diagnosis if this patient presents weeks later with recurrent UT Is with urinalysis revealing air and fecal material?

Practice questions — USMLE style

Question 1 — Internal Medicine

A 30-year-old male presents to the emergency department with acute onset of generalized weakness, confusion, and diaphoresis. His blood glucose level is measured at 45 mg/dL. He has a history of poorly controlled Type 2 Diabetes Mellitus (T2 DM) and was last seen in his home several hours ago. Initial laboratory workup reveals the following: Glucose: 45 mg/dL Insulin: High C-peptide: Low Proinsulin: Normal Uric Acid: Elevated Based on this clinical presentation and lab profile, what is the most likely cause of his hypoglycemia?

  • A) Insulinoma secreting excess endogenous insulin.
  • B) Exogenous insulin administration or sulfonylurea overdose.
  • C) Increased hepatic glucose uptake due to severe sepsis.
  • D) Adrenal insufficiency leading to cortisol deficiency.

Answer: B. Explanation: The combination of low C-peptide and high insulin suggests that the patient's body is not producing the excess insulin; rather, it is likely receiving exogenous insulin (e.g., from accidental injection or overdose of sulfonylureas). Insulinomas would show high C-peptide levels because they are endogenous sources of insulin. Adrenal insufficiency typically causes hypoglycemia due to cortisol deficiency, but this specific lab pattern points strongly toward iatrogenic or drug-induced hypoglycemia.

Question 2 — Gastroenterology

A 45-year-old traveler returns from Mexico after a two-week stay. He presents with severe, foul-smelling, watery diarrhea and significant abdominal cramping. He reports that his symptoms began shortly after leaving the area and has no history of recent antibiotic use or consumption of home-canned foods. Stool studies are pending. Which of the following pathogens is most likely responsible for this patient's acute diarrheal illness?

  • A) Clostridioides difficile
  • B) Salmonella enteritidis
  • C) Campylobacter jejuni
  • D) Giardia lamblia

Answer: C. Explanation: The clinical picture of severe, foul-smelling watery diarrhea following travel is highly suggestive of an invasive bacterial gastroenteritis. While C. difficile causes pseudomembranous colitis (often after antibiotics), and Salmonella can cause bloody diarrhea, Campylobacter jejuni is the most common bacterial cause of acute, non-bloody or mildly bloody diarrheal illness acquired from contaminated sources during travel. Giardia lamblia typically causes more chronic, greasy, foul-smelling diarrhea (giardiasis), but the acute onset and severity described favor an invasive bacterium like Campylobacter.

Question 3 — Dermatology/Endocrinology

A 55-year-old HIV-positive male presents with a three-day history of fever, generalized malaise, and multiple targetoid skin lesions that are pruritic. He reports that he was started on Allopurinol 10 days ago for chronic gout management. On physical examination, the patient exhibits widespread skin sloughing (estimated >30% Body Surface Area) and a positive Nikolsky sign. What is the most likely diagnosis, and what mechanism best explains the severe cutaneous reaction?

  • A) Stevens-Johnson Syndrome; T-cell mediated cytotoxic response to the drug.
  • B) Toxic Epidermal Necrolysis (TEN); Direct drug toxicity leading to keratinocyte apoptosis.
  • C) Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS); Hypersensitivity involving delayed release of cytokines.
  • D) Erythema Multiforme Major; Type IV hypersensitivity reaction triggered by the medication.

Answer: B. Explanation: The combination of fever, targetoid lesions, widespread sloughing (>30% BSA), a positive Nikolsky sign, and recent initiation of an offending drug (Allopurinol) is classic for Toxic Epidermal Necrolysis (TEN). TEN is considered a severe form of cutaneous adverse drug reaction where the mechanism involves massive keratinocyte apoptosis. While SJS/TEN spectrum reactions are often grouped together, the severity described (>30% BSA involvement) points to TEN.

Question 4 — Nephrology

A 28-year-old female presents with acute onset of oliguria, generalized fatigue, and mild proteinuria following a recent upper respiratory infection (URI). Her blood work shows elevated creatinine and decreased serum complement levels (C3/C4). She has no history of autoimmune disease. Which of the following best describes the pathophysiology and typical timeline of this patient's condition?

  • A) Pathophysiology: Immune complex deposition in the glomerulus; Timeline: 1-2 weeks post-infection.
  • B) Pathophysiology: Direct viral damage to podocytes; Timeline: Acute onset, concurrent with infection.
  • C) Pathophysiology: Autoantibody attack on basement membrane components; Timeline: Weeks to months after initial trigger.
  • D) Pathophysiology: Minimal change in the glomerular filtration barrier; Timeline: Chronic and progressive over years.

Answer: A. Explanation: The clinical picture—acute onset of nephritic syndrome (hematuria, proteinuria, acute kidney injury) following an infection, coupled with low complement levels—is highly suggestive of Post-Infectious Glomerulonephritis (PIGN). PIGN is characterized by the formation and deposition of immune complexes (antigen/antibody complexes) within the glomeruli. The typical timeline for this process is 1 to 2 weeks following the initiating infection, distinguishing it from primary autoimmune GN or chronic causes.

Quick fire review

What are the three major causes of hypoglycemia that must be differentiated based on labs?

Insulin excess, increased glucose utilization (e.g., exercise), or impaired hepatic gluconeogenesis (e.g., fasting/starvation).

What is the classic finding associated with iron overload seen on bone marrow smear?

Basophilic inclusions around the nucleus when stained with Prussian blue.

In a patient presenting with targetoid skin lesions, lip/mouth ulcerations, and visual impairment after starting Allopurinol for gout, what is the likely diagnosis?

Drug-induced hypersensitivity syndrome (e.g., DRESS or fixed drug eruption).

What are the classic findings associated with nephrotic syndrome in a patient presenting with periorbital edema, hematuria, and hypertension following cellulitis?

Hypoalbuminemia, hypolipidemia, and proteinuria. The underlying mechanism is often immune complex deposition (e.g., post-infectious glomerulonephritis).

What are the key components of the "stones, bones, groans, and psychic overtones" mnemonic?

Stones (kidney stones), Bones (osteoporosis/bone pain), Groans (abdominal cramping/GI issues), and Psychic overtones (depression/mood changes) – all associated with chronic hypercalcemia.

What is the primary concern when managing a patient with severe anemia due to chronic blood loss or hemolysis?

Preventing iron deficiency, monitoring for signs of acute blood loss, and assessing the need for transfusion vs. supportive care.

What specific staining technique reveals basophilic inclusions around the nucleus in bone marrow suggesting iron overload?

Prussian blue stain.

Name two common causes of severe diarrhea associated with travel from Mexico or developing countries.

Shigella (bloody, small inoculum) and Campylobacter (foul-smelling/anaerobic association).

What is the primary risk factor for developing Mitral Stenosis?

Rheumatic heart disease (or chronic valve damage leading to restricted leaflet opening).

Which specific type of anemia presents with a "gallbladder" pathology, and what does this suggest about its etiology?

Hemolytic anemias. The gallbladder suggests increased bilirubin load/bilirubin metabolism issues.

What is the key difference in management between an unstable patient with SVT versus a stable patient?

Unstable requires immediate synchronized cardioversion (electrical), while stable allows for vagal maneuvers or pharmacologic agents (e.g., adenosine).

In the context of adrenal insufficiency, what hormone level would be low if the primary failure is due to lack of ACTH stimulation?

Cortisol and Aldosterone (if secondary/tertiary failure). If it's primary failure (Addison's), both are low.

What is the classic CBC finding in Thalassemia major compared to other anemias?

Microcytic, hypochromic anemia with elevated reticulocyte count (relative) and target cells.

Quick recall / Anki-style questions

What specific staining technique reveals basophilic inclusions around the nucleus in bone marrow suggesting iron overload?

Prussian blue stain.

Name two common causes of severe diarrhea associated with travel from Mexico or developing countries.

Shigella (bloody, small inoculum) and Campylobacter (foul-smelling/anaerobic association).

What is the primary risk factor for developing Mitral Stenosis?

Rheumatic heart disease (or chronic valve damage leading to restricted leaflet opening).

Which specific type of anemia presents with a "gallbladder" pathology, and what does this suggest about its etiology?

Hemolytic anemias. The gallbladder suggests increased bilirubin load/bilirubin metabolism issues.

What is the key difference in management between an unstable patient with SVT versus a stable patient?

Unstable requires immediate synchronized cardioversion (electrical), while stable allows for vagal maneuvers or pharmacologic agents (e.g., adenosine).

In the context of adrenal insufficiency, what hormone level would be low if the primary failure is due to lack of ACTH stimulation?

Cortisol and Aldosterone (if secondary/tertiary failure). If it's primary failure (Addison's), both are low.

What is the classic CBC finding in Thalassemia major compared to other anemias?

Microcytic, hypochromic anemia with elevated reticulocyte count (relative) and target cells.