Keywords in the Stem to identify correct option 

• “Acute chest pain” → suggests a sudden cardiovascular event (possible MI or dissection).
• “Unequal blood pressure in both arms” → classic clue for aortic dissection due to involvement of major branches of the aorta.

Classic Triad (Aortic Dissection):

1. Sudden tearing chest pain
   2. Radiation to the back
   3. Unequal pulses or blood pressure in arms

These keywords and triad point directly toward Aortic Dissection as the correct diagnosis.

Explanation 

(Option D) Aortic Dissection:

• Severe, tearing or ripping chest pain radiating to the back.
• Unequal blood pressure or pulses in upper limbs due to involvement of subclavian arteries.
• Often occurs in hypertensive or Marfan syndrome patients.
• Diagnosis confirmed by CT angiography or transesophageal echocardiography (TEE).
• Medical emergency due to risk of rupture and cardiac tamponade.

(Option A) Acute Myocardial Infarction (MI):

• Presents with severe, crushing substernal chest pain that may radiate to the left arm, jaw, or neck.
• Pain usually lasts >20 minutes and is not relieved by rest or nitrates.
• No significant BP difference between arms.

 (Option B) Acute Pericarditis:

• Causes sharp, pleuritic chest pain that improves when sitting up and leaning forward.
• Often accompanied by a pericardial friction rub.
• BP equal in both arms; no pulse deficit.

 (Option C) Gastroesophageal Reflux Disease (GERD):

• Produces retrosternal burning pain after meals or lying down.
• Relieved by antacids; not associated with hemodynamic instability or BP difference.
• Not an acute vascular emergency.

 (Option E) Spontaneous Pneumothorax:

• Causes sudden unilateral pleuritic chest pain and shortness of breath.
• On exam: hyperresonance and decreased breath sounds on affected side.
• No BP difference between arms.

Key Concept 

Acute tearing chest pain with unequal arm blood pressures is characteristic of aortic dissection, caused by an intimal tear in the aorta leading to separation of its layers. It’s a life-threatening vascular emergency requiring urgent imaging and stabilization.

Subject: Medicine / Internal Medicine / Emergency Medicine

System: Cardiovascular System – Acute Chest Pain (aorta (vascular system)) - Differential Diagnosis – Aortic Dissection

Topic: Cardiovascular System – Aortic Dissection (Acute Chest Pain Differential Diagnosis)

• Competency Domain: Diagnosis
• Cognitive Level (Bloom’s): Application
• Clinical Skill: Reasoning and Decision-making
• Difficulty Level: Moderate

Cardiovascular System – Aortic Dissection 

(Acute Chest Pain Differential Diagnosis)

Differential Diagnosis of Acute Chest Pain

(Where Aortic Dissection is a key consideration)

Summary

Aortic dissection must be differentiated from MI, PE, Pericarditis, Pneumothorax, and GERD — all causes of acute chest pain, but unequal arm BP uniquely points to aortic dissection.

Aortic Dissection – Acute Chest Pain Differential Diagnosis

This diagram visually highlights aortic dissection as a central cause of acute chest pain and contrasts it with other major differentials such as MI, pericarditis, pulmonary embolism, pneumothorax, and GERD. It emphasizes key distinguishing symptoms to help medical graduates rapidly differentiate life-threatening cardiovascular emergencies.

Keywords in the Stem to identify correct option

1. Recurrent jaundice – indicates chronic hemolysis.
2. Mild splenomegaly – suggests extravascular hemolysis due to splenic sequestration.
3. Spherocytes on peripheral smear – hallmark of Hereditary Spherocytosis (HS).

Classic Triad (Present in Stem):

Anemia + Jaundice + Splenomegaly → Classic triad of Hereditary Spherocytosis.

The combination of spherocytes with the triad of hemolytic anemia (jaundice + splenomegaly) directly points to Hereditary Spherocytosis, for which the confirmatory test is the Osmotic Fragility Test.

Explanation 

(Option A) Osmotic Fragility Test:

• This test measures the resistance of red blood cells (RBCs) to hemolysis when placed in increasingly hypotonic saline solutions. 
• Spherocytes, which are characteristic of Hereditary Spherocytosis, have a reduced surface-area-to-volume ratio due to a membrane defect. This makes them less flexible and less able to accommodate water influx in hypotonic solutions compared to normal, biconcave RBCs. 
• Consequently, spherocytes lyse (hemolyze) at higher, less hypotonic salt concentrations than normal RBCs, showing increased osmotic fragility. This test provides the most specific and functional confirmation of the membrane defect in HS.
• Confirmatory and diagnostic for HS; modern variant: Eosin-5-maleimide (EMA) binding test by flow cytometry.

(Option B) Direct Coombs Test:

• Detects autoantibodies or complement attached to RBCs, used to diagnose autoimmune hemolytic anemia (AIHA).
• In HS, this test is negative, helping to differentiate from AIHA.

(Option C) Hemoglobin Electrophoresis:

• Used to identify abnormal hemoglobin variants (e.g., HbS, HbC, thalassemia).
• Not useful in membrane defects like HS where hemoglobin structure is normal.

(Option D) Iron Studies:

• Evaluate serum iron, ferritin, TIBC to assess iron deficiency or overload.
• HS is a hemolytic disorder, not related to iron metabolism directly.

(Option E) Schilling Test:

• Assesses vitamin B₁₂ absorption to diagnose pernicious anemia or B₁₂ malabsorption.
• Not related to hemolytic anemia or spherocytosis.

Key Concept 

Hereditary Spherocytosis presents with Coombs-negative hemolytic anemia, jaundice, and splenomegaly. The Osmotic Fragility Test confirms the diagnosis by demonstrating increased RBC lysis in hypotonic saline due to a membrane cytoskeletal defect.

Subject: Medicine + Pathology

System: Hematology – Anemias – Hemolytic Anemias / Hereditary Spherocytosis 

Topic: Hematology – Hemolytic Anemias – Hereditary Spherocytosis

• Competency Domain: Diagnosis
• Cognitive Level: Application
• Clinical Skill: Interpretation
• Difficulty Level: Moderate

Hematology – Hemolytic Anemias – 

Hereditary Spherocytosis

Differential Diagnosis of 

Hereditary Spherocytosis in Pediatric Patients

Key Point

HS is Coombs-negative hemolytic anemia with spherocytes, chronic jaundice, and splenomegaly—classic triad.

Hereditary Spherocytosis – 

Pathophysiology and Key Clinical Features

The diagram visually explains how hereditary spherocytosis results from a red cell membrane defect causing transformation of a normal biconcave RBC into a spherocyte. It highlights the classic clinical features (anemia, jaundice, splenomegaly) and shows the typical peripheral blood smear appearance used in

Keywords in the Stem to identify correct option

1. “3 days of severe diarrhea” → Indicates volume depletion, classic cause of pre-renal azotemia.
2. “Low blood pressure” → Suggests renal hypoperfusion, supporting pre-renal etiology.
3. “Decreased urine output” → Part of classic triad of pre-renal AKI: hypoperfusion, oliguria, and reversible azotemia.

Classic Triad (Pre-renal AKI): 

Volume depletion/hypoperfusion + Oliguria + Reversible azotemia.

Explanation 

(Option A) Pre-renal azotemia:

Rationale:

• Pre-renal AKI is caused by decreased renal perfusion, often due to volume depletion (like severe diarrhea).
• Lab findings in pre-renal AKI:
  • Low urine Na⁺ (<20 mEq/L) → kidney is conserving sodium
  • High urine creatinine concentration → concentrated urine
  • Fractional excretion of sodium (FENa) <1%
• This patient's history (hypotension, diarrhea), low urine Na⁺ (15 mEq/L), and concentrated urine support pre-renal AKI.

Explanation
This patient has volume depletion from diarrhea, leading to renal hypoperfusion. The kidney responds by maximally conserving sodium, reflected in low urine Na⁺ (15 mEq/L) and concentrated urine. These findings are classic for pre-renal AKI, which is reversible if perfusion is restored.

• Key distinguishing feature: low urine Na⁺ (<20 mEq/L) and concentrated urine differentiate pre-renal AKI from ATN.

(Option B) Intra-renal azotemia (Acute Tubular Necrosis, ATN):

Rationale:

• ATN usually follows ischemic or nephrotoxic injury.
• Lab features:
  • Urine Na⁺ >40 mEq/L (impaired sodium reabsorption)
  • FENa >2%
  • Muddy brown granular casts in urine
• Patient does not show these features; urine Na⁺ is low, suggesting kidneys are still able to conserve sodium → less likely ATN at this stage.

(Option C) Post-renal azotemia:

Rationale:

• Caused by obstruction of urine flow (e.g., stones, BPH).
• Lab findings:
  • Early urine Na⁺ may be low, but obstruction usually presents with bladder distension, hydronephrosis, or oliguria despite normal perfusion.
• Patient has no history or imaging evidence of obstruction → unlikely.

(Option D) Hepatorenal syndrome:

Rationale:

• Occurs in severe liver disease with renal vasoconstriction.
• Labs: low urine Na⁺ (<20 mEq/L), high serum creatinine
• Patient has no liver disease history → unlikely.

(Option E) Cardiorenal azotemia:

Rationale:

• Seen in heart failure, decreased cardiac output → renal hypoperfusion
• Labs may mimic pre-renal AKI
• Patient has no heart failure symptoms → less likely.

Key Concept 

Pre-renal azotemia occurs due to decreased renal perfusion; lab hallmark is low urine sodium (<20 mEq/L) and concentrated urine, whereas intrinsic AKI (like ATN) shows high urine sodium (>40 mEq/L) and impaired concentration ability. Early recognition is important because it is reversible with volume resuscitation.

Subject: Medicine / Internal Medicine 

System: Nephrology – Acute Renal Failure - Pre renal azotemia

Topic: Acute Kidney Injury – Pre-renal Azotemia

• Competency Domain: Diagnosis
• Cognitive Level: Application
• Clinical Skill: Interpretation
• Difficulty Level: Moderate

Acute Kidney Injury – Pre-renal Azotemia

Differential Diagnosis of Pre-renal Acute Kidney Injury

Key Point

The most important differential is ATN, because pre-renal AKI can progress to ATN if hypoperfusion persists.

Acute Kidney Injury – Pre-renal Azotemia 

This diagram visually summarizes the essential elements of pre-renal acute kidney injury, including its common causes (mainly volume depletion), key lab markers (low urine sodium, concentrated urine), clinical presentation (hypotension, oliguria), and the reversible nature of the condition when promptly treated. It provides a clear, high-yield snapshot tailored for medical graduates studying nephrology.

Keywords in the Stem to identify correct option

• Rifampicin – Indicates a drug known for CYP450 induction, which is the central mechanism affecting OCPs.
• Combined oral contraceptives (ethinylestradiol + levonorgestrel) – Specifies the drug class affected by rifampicin, pointing toward metabolic drug interaction.
• Unintended pregnancy after 3 months – Suggests reduced contraceptive efficacy over time, consistent with enzyme induction.

Explanation 

(Option B) Rifampicin induces hepatic CYP450 enzymes → increased metabolism of OCPs:

• Rifampicin is a potent inducer of several hepatic cytochrome P450 (CYP450) enzymes, particularly CYP3A4. 
• These enzymes are crucial for metabolizing the steroid hormones in combined oral contraceptives (OCPs), such as ethinylestradiol and levonorgestrel. 
• By accelerating the metabolism of these contraceptive hormones, rifampicin significantly lowers their concentration in the bloodstream, often below the therapeutic level needed to reliably prevent ovulation. 
• This leads to a loss of contraceptive efficacy and, as in this patient's case, an unintended pregnancy.

Additional explanation: 

• The induction effect occurs over weeks, which explains why contraceptive failure may be noticed after 2–3 months of therapy. 

• Women on rifampicin are advised to use alternative or additional non-hormonal contraception during treatment.

(Option A) Rifampicin inhibits hepatic CYP450 enzymes → decreased metabolism of OCPs:

• Rifampicin does not inhibit CYP450; it induces it. 
• Inhibition would actually increase OCP levels, which could increase side effects, not cause contraceptive failure.

(Option C) Rifampicin binds estrogen in plasma → decreased free estrogen levels:

• Rifampicin does not bind estrogen in plasma. 
• The main interaction is metabolic, not protein-binding.

(Option D) Rifampicin inhibits enterohepatic recirculation of OCPs → increased drug levels:

• Rifampicin may affect enterohepatic recirculation slightly, but the net effect is decreased OCP levels, not increased. 
• The main mechanism is still CYP450 induction.

(Option E) Rifampicin competes with levonorgestrel at progesterone receptor:

• Rifampicin does not act at hormone receptors. 
• It affects drug metabolism, not receptor binding.

Key Concept

Rifampicin is a potent CYP450 (mainly CYP3A4) inducer, which accelerates the metabolism of combined oral contraceptives, lowering their plasma levels and reducing contraceptive efficacy, leading to unintended pregnancy. Always consider alternative or backup contraception with enzyme-inducing drugs.

Subject: Medicine 

System: Pulmonology (Female Reproductive System) – Tuberculosis - Pharmacology & Drug Interactions

Topic: Drug–Drug Interaction: Rifampicin and Combined Oral Contraceptives

• Competency Domain: Mechanism
• Cognitive Level: Application
• Clinical Skill: Decision-making
• Difficulty Level: Moderate

Drug–Drug Interaction: Rifampicin and Combined Oral Contraceptives

Drug–Drug Interaction: 

Rifampicin and Combined Oral Contraceptives

This diagram illustrates how rifampicin strongly induces hepatic CYP3A4 enzymes, leading to increased metabolism of ethinylestradiol and progestins in combined oral contraceptives. As a result, plasma hormone levels fall, causing reduced contraceptive efficacy and risk of unintended pregnancy.

Keywords in the Stem to identify correct option

1. Glucose 1400 mg/dL (Extreme Hyperglycemia) → Points toward HHS rather than DKA or euglycemic DKA.
2. Serum osmolality 345 mOsm/kg (High Osmolality) → Classic feature of HHS; not typical in DKA.
3. Negative urine ketones / Bicarbonate 22 (Minimal or No Ketosis, Near-Normal pH) → Rules out DKA, confirms HHS.

Classic Triad in Stem (HHS):

• Extreme hyperglycemia + High serum osmolality + Neurological symptoms (confusion) → This is the classic HHS triad.

Explanation

(Option D) Hyperosmolar hyperglycemic state (HHS); begin aggressive IV fluids, then insulin:

Patient Features Supporting HHS:

• Age >60, type 2 diabetes.
• Severe hyperglycemia (glucose 1400 mg/dL).
• High serum osmolality (345 mOsm/kg).
• Minimal or absent ketosis (negative urine ketones).
• Mildly decreased bicarbonate (22 mEq/L) → not enough for DKA.
• Clinical dehydration and neurological symptoms (confusion).

Management Rationale:

• Step 1: Aggressive intravenous fluids (usually 0.9% NaCl) to restore intravascular volume and improve renal perfusion.
• Step 2: Start insulin infusion after initial fluid resuscitation to gradually reduce blood glucose and avoid rapid osmotic shifts that can cause cerebral edema.
• Step 3: Monitor and correct electrolytes, especially potassium, before insulin therapy if needed.

(Option A) Diabetic ketoacidosis; start insulin and correct ketoacidosis:

• DKA usually presents with glucose <600–800 mg/dL, serum ketones positive, and metabolic acidosis (bicarbonate <18). 
• This patient has normal/mildly low bicarbonate and no ketones.

(Option B) Euglycemic DKA; stop SGLT2 inhibitor immediately:

• Euglycemic DKA is rare, associated with SGLT2 inhibitors, with normal/near-normal glucose (<250 mg/dL) and ketosis. 
• This patient has extreme hyperglycemia and no history mentioned of SGLT2 inhibitor use.

(Option C) Lactic acidosis; initiate urgent dialysis:

• Lactic acidosis usually presents with severe metabolic acidosis, elevated lactate, and systemic hypoperfusion. 
• Here, bicarbonate is near normal and lactate is not mentioned.

(Option E) Mixed DKA and HHS; start combined therapy with fluids and insulin:

• Mixed DKA/HHS shows both significant hyperglycemia and ketosis/metabolic acidosis. 
• This patient lacks ketosis and significant acidosis.

Key Concept 

HHS occurs in type 2 diabetes, presenting with extreme hyperglycemia, high osmolality, and minimal ketosis. Initial management is aggressive IV fluid resuscitation, followed by insulin therapy, with careful electrolyte monitoring to prevent complications.

Subject: Medicine (Internal Medicine / Emergency Medicine)

System: Endocrinology (Metabolic System) – Diabetes Mellitus - Diabetic Emergencies

Topic: Hyperglycemic Emergencies in Diabetes – HHS vs DKA

• Competency Domain: Diagnosis & Management
• Cognitive Level: Application
• Clinical Skill: Decision-making
• Difficulty Level: Moderate

Hyperglycemic Emergencies in Diabetes – 

HHS vs DKA

Key Point

• DKA: Ketosis + metabolic acidosis dominate; moderate hyperglycemia.
• HHS: Extreme hyperglycemia + hyperosmolality dominate; minimal ketosis; neurological symptoms prominent.

Differential Diagnosis of Hyperglycemic Emergencies 

(HHS vs Mimics)

Key Point

• HHS is distinguished by extreme hyperglycemia, high osmolality, minimal ketosis, and neurological symptoms.
• DKA is the most common differential; other conditions mainly mimic altered mental status or dehydration.

Hyperglycemic Emergencies in Diabetes —

DKA vs HHS (Clinical Comparison Diagram)

This diagram visually contrasts Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS) for medical graduates. It highlights the key differences in pathophysiology, clinical presentation, laboratory findings, and management priorities. The graphic helps learners quickly differentiate the two major hyperglycemic emergencies using a side-by-side format.

Keywords in the Stem to identify correct option

• HIV-positive – Indicates the patient has confirmed HIV infection, which is the condition requiring ART.
• CD4 count 420/µL – Shows immune status is not severely compromised, hinting that guidelines no longer delay ART based on CD4.
• Asymptomatic – Highlights that the patient has no clinical symptoms, ruling out options that depend on symptoms or opportunistic infections.

Explanation 

(Option E) Immediately after diagnosis:

• Current WHO, DHHS, and local HIV treatment guidelines recommend starting ART in all HIV-positive patients regardless of CD4 count or symptoms.
• Early initiation of ART reduces morbidity, mortality, and transmission risk.
• Even patients with high CD4 counts (like 420/µL here) benefit from early therapy.
• Early ART improves long-term survival, immune recovery, and reduces HIV transmission.
• Patients should be counseled, baseline labs done, and therapy started promptly.
• This is often referred to as "Treat All" or "Test and Treat."

(Option A) Only if symptomatic:

• Outdated practice. ART should not be delayed until symptoms appear, because patients may progress silently and early ART prevents complications.

(Option B) When CD4 <350/µL:

• Previous guidelines suggested starting ART at this threshold, but modern guidelines recommend treatment regardless of CD4.

(Option C) After first opportunistic infection:

• Waiting for opportunistic infections increases morbidity and mortality. 
• Prophylactic ART prevents such infections.

(Option D) Delay until CD4 <200/µL:

• Extremely outdated. Delaying therapy until severe immunosuppression is harmful and increases risk of infections and HIV progression.

Key Concept

• All HIV-positive patients should start ART immediately after diagnosis, regardless of CD4 count or symptoms.
• Early therapy prevents opportunistic infections, slows disease progression, and reduces transmission.

Subject: Medicine (Internal Medicine)

System: Infectious diseases – HIV - Management & ART

Topic: HIV Infection – Timing of Antiretroviral Therapy (ART) Initiation

• Competency Domain: Management
• Cognitive Level: Application
• Clinical Skill: Guideline-based action
• Difficulty Level: Easy

HIV Infection – Timing of Antiretroviral Therapy (ART) Initiation

HIV Infection – Antiretroviral Therapy (ART) Initiation

This diagram illustrates the guideline-based approach to initiating ART in an HIV-positive patient. It highlights that treatment should begin immediately after diagnosis, regardless of CD4 count or the presence of symptoms, ensuring early immune protection and reduced transmission.

Keywords in the Stem to identify correct option

1. SLE → Indicates autoimmune disease where immune complex-mediated flares occur.
2. Rising anti-dsDNA antibodies → Classic marker of disease activity; strongly associated with complement consumption.
3. Worsening joint pain → Suggests clinical flare, part of the classic SLE triad (joint pain, anti-dsDNA rise, ↓ complement).

Classic Triad in Stem (if applicable):

• Clinical flare triad: ↑ anti-dsDNA, ↓ C3/C4, clinical symptoms (e.g., joint pain).
• This triad directly points to Option C (↓ C3/C4) as the correct answer.

Explanation 

(Option C) ↓ C3 and C4:

• An SLE disease flare is characterized by active systemic inflammation and immune complex formation, which is strongly suggested by the patient's worsening joint pain and rising anti-dsDNA antibodies.
• In active SLE, the immune complexes (formed by the patient's antibodies, such as anti-dsDNA, binding to antigens) get deposited in various tissues (like joints, kidneys, and skin). 
• These immune complexes activate the classical complement pathway. The activation of this pathway consumes complement proteins, including C3 and C4, leading to their depletion in the serum. Therefore, a significant decrease (↓) in serum C3 and C4 levels is the most consistent laboratory finding accompanying an SLE flare.
• Rising anti-dsDNA antibodies plus low complement is a classic marker of active disease.
• Monitoring C3, C4, and anti-dsDNA helps assess disease activity and risk of organ involvement.
• Most reliable lab indicator of an SLE flare alongside clinical symptoms and rising dsDNA.

(Option A) ↑ C3 and C4:

• Opposite of what happens in a flare. 
• Complement proteins are consumed, not increased.

(Option B) Normal C3 and C4:

• Could be seen in quiescent disease or minor activity, but not typical in a flare.

(Option D) ↑ CRP only:

• CRP is usually normal in SLE flares unless infection or serositis is present.
• Not a sensitive marker for lupus activity.

(Option E) Normal ESR:

• ESR can be elevated in SLE flares but is nonspecific.
• Normal ESR does not rule out flare.

Key Concept

• SLE flares are marked by rising anti-dsDNA antibodies and decreased complement levels (C3, C4).
• Complement consumption is a direct result of immune complex formation, making it a sensitive marker for disease activity.
• CRP and ESR are less reliable for detecting lupus flare compared to dsDNA and complement levels.

Subject: Medicine (Internal Medicine)

System: Rheumatology (Immune system (autoimmunity), Musculoskeletal system) – Multi-system Immunological diseases – Systemic Lupus Erythematosus (SLE)

Topic: Rheumatology – SLE Disease Flare: Laboratory Indicators

• Competency Domain: Diagnosis
• Cognitive Level (Bloom’s): Application
• Clinical Skill: Interpretation
• Difficulty Level: Moderate

Rheumatology – SLE Disease Flare: 

Laboratory Indicators

Differential Diagnosis of 

SLE Flare Presenting with Joint Pain

Rheumatology – SLE Disease Flare

This diagram visually summarizes the key clinical and laboratory indicators of an SLE flare, highlighting worsening joint pain, rising anti-dsDNA antibodies, and decreased complement levels (C3, C4). It shows the immunological mechanism of immune-complex formation leading to complement consumption and depicts classic markers used to assess lupus disease activity.

Keywords in the Stem to identify correct option

1. Flaccid / easily rupturing blisters → Indicates intraepidermal blister typical of pemphigus vulgaris.
2. Oral mucosa involvement → Classic feature; bullous pemphigoid usually spares mucosa.
3. Nikolsky sign positive → Strong diagnostic clue for pemphigus vulgaris.

Classic triad in stem:

• Flaccid blisters + oral mucosal erosions + positive Nikolsky sign → Triad characteristic of pemphigus vulgaris.

This triad alone is usually sufficient to differentiate PV from other blistering disorders.

Explanation 

(Option B) Pemphigus vulgaris:

• Pemphigus vulgaris is an autoimmune blistering disorder caused by IgG antibodies against desmoglein 3 (and sometimes desmoglein 1) in the epidermis, leading to loss of keratinocyte adhesion (acantholysis).
• Clinically presents with flaccid, easily rupturing blisters and painful erosions, most commonly involving the oral mucosa.
• The positive Nikolsky sign (the superficial layer of the skin shears off easily when rubbed) is a key feature indicating the superficial, intraepidermal nature of the blister formation in PV due to the loss of cell-to-cell adhesion (acantholysis).
• Typically affects middle-aged adults (40–60 years), which fits this patient.
• Complications include secondary infection and fluid/electrolyte imbalance in severe cases.

(Option A) Bullous pemphigoid:

• Autoimmune subepidermal blistering disease.
• Tense blisters that are less fragile, rarely affect oral mucosa.
• Nikolsky sign usually negative.
• More common in elderly (>60 years).

(Option C) Dermatitis herpetiformis:

• Chronic, pruritic vesicles and papules on extensor surfaces.
• Associated with celiac disease.
• Mucosal involvement rare; blisters are small and grouped (“herpetiform”).

(Option D) Linear IgA disease:

• Autoimmune subepidermal blistering disorder with IgA deposition along the basement membrane.
• Lesions may appear as “string of pearls”; mucosal involvement is less frequent.
• Can mimic bullous pemphigoid in adults.

(Option E) Epidermolysis bullosa:

• Inherited disorder of skin fragility; usually presents in infancy or childhood.
• Blisters form after minor trauma, often congenital.
• Adult-onset presentation extremely rare.

Key Concept 

Pemphigus vulgaris is characterized by flaccid blisters, mucosal erosions, and positive Nikolsky sign due to autoantibodies against desmogleins causing intraepidermal acantholysis. Differentiation from bullous pemphigoid and other blistering diseases relies on blister type, mucosal involvement, and age of onset.

Subject: Medicine + Pathology

System: Dermatology – Skin Diseases (skin and mucosa) - Bullous Disorders

Topic: Autoimmune Blistering Disorders – Pemphigus Vulgaris

• Competency Domain: Diagnosis
• Cognitive Level: Application
• Clinical Skill: Interpretation
• Difficulty Level: Moderate

Autoimmune Blistering Disorders – 

Pemphigus Vulgaris

Differential Diagnosis of 

Pemphigus Vulgaris

AUTOIMMUNE BLISTERING DISORDERS: PEMPHIGUS VULGARIS

The diagram illustrates the key clinical and histological features of Pemphigus Vulgaris, a severe autoimmune blistering disorder.

• It shows a patient with painful, easily rupturing blisters on the face.
• A cross-section of the skin demonstrates the characteristic feature of Flaccid blisters that result from acantholysis (loss of cell-to-cell adhesion) above the basal layer of the epidermis.
• Clinical signs include erosions in the oral mucosa and a Nikolsky sign positive finding on the arm, where the outer layer of skin separates easily when rubbed.

Keywords in the Stem to identify correct option

• “Heavy alcohol consumption over the weekend” → Direct, classic trigger for alcohol-induced pancreatitis.
• “Severe epigastric pain radiating to the back” → Classic pain pattern of acute pancreatitis.
• “Ultrasound shows no gallstones” → Excludes the most common competing cause (gallstones), making alcohol the lead culprit.

Classic Triad in Stem

• Epigastric pain + radiates to back + elevated amylase/lipase

Explanation 

(Option D) Alcohol consumption:

• This guy has classic alcoholic pancreatitis: mid-50s male, heavy binge drinking, sudden severe epigastric pain → radiates to the back.
• Heavy alcohol use is the second most common cause (after gallstones) of acute pancreatitis and the most common cause of chronic pancreatitis. The patient's history of heavy consumption "over the weekend" immediately preceding the symptoms makes this the most likely cause.
• Labs show significantly raised amylase/lipase, and ultrasound shows no gallstones, which rules out the big competitor.
• Alcohol increases the secretion of protein-rich pancreatic fluid and causes spasm of the sphincter of Oddi, leading to obstruction, premature activation of pancreatic enzymes, and autodigestion of the pancreas.

(Option A) Gallstones:

• Usually the most common cause overall.
• BUT ultrasound shows no gallstones, and the patient had an alcohol binge → makes gallstones unlikely here.

(Option B) Hypertriglyceridemia:

• Typically causes pancreatitis when levels > 1000 mg/dL.
• No triglyceride value provided, and patient has a classic alcohol trigger instead.

(Option C) Drug-induced:

• Possible but uncommon (<2% cases).
• Needs a known culprit drug (e.g., azathioprine, valproate, thiazides). No such drug history provided.

(Option E) Post-ERCP:

• Happens after recent endoscopy with ERCP.
• No such history here, so ruled out immediately.

Key Concept 

Acute pancreatitis is most commonly due to gallstones and alcohol. In a patient with a clear history of heavy binge drinking and no gallstones on imaging, alcohol becomes the leading cause. Elevated amylase/lipase with typical pain confirms the diagnosis.

Subject: Medicine (Internal Medicine / Emergency Medicine)

System: Hepatology (Gastrointestinal system) – Pancreas - Acute pancreatitis

Topic: Acute Pancreatitis – Alcohol-Induced Etiology

• Competency Domain: Diagnosis
• Bloom’s Level: Application
• Clinical Skill: Reasoning
• Difficulty Level: Easy

Acute Pancreatitis – Alcohol-Induced Etiology

Differential Diagnosis of Acute Pancreatitis

Acute Pancreatitis – Alcohol-Induced Etiology

This diagram illustrates the clinical presentation, investigation findings, and etiology of a case of Acute Pancreatitis induced by alcohol.

• It features an illustration of a male patient presenting with typical symptoms (epigastric pain radiating to the back).
• It outlines key Presentation points: severe epigastric pain, nausea/vomiting, and a history of heavy alcohol use.
• It lists crucial Investigations results: elevated amylase and lipase, and an ultrasound showing no gallstones (ruling out the most common alternative cause).
• The image also visually reinforces the etiology by including an alcoholic beverage bottle alongside the inflamed pancreas.

Keywords in the Stem to identify correct option

1. “Non-healing ulcer for 2 months” – Chronicity (>2 weeks) is highly suggestive of malignancy.
2. “Indurated, raised margins, firm base” – Classic physical feature of oral squamous cell carcinoma.
3. “Chronic smoker for 30 years” – Major risk factor for oral SCC.

Classic triad in stem (high-yield for SCC):

• Chronic ulcer + Induration + Risk factor (smoking/tobacco) → Strongly points toward oral SCC.

Explanation 

(Option A) Squamous cell carcinoma (SCC):

• Chronic, non-healing ulcer (>2 weeks), especially in a long-term smoker, is highly suspicious for malignancy.
• Indurated, raised margins and firm base are classic features of SCC in the oral cavity.
• Buccal mucosa is a common site in smokers and betel quid/tobacco users.
• SCC often presents as persistent, painful or painless ulcer with gradual progression.

(Option B) Traumatic ulcer:

• Usually related to mechanical irritation (e.g., sharp tooth, denture).
• Heals within 1–2 weeks once the cause is removed.
• Rarely has indurated margins unless chronic irritation persists.

(Option C) Aphthous ulcer:

• Small, painful, round or oval ulcers with a yellowish base and erythematous halo.
• Typically heal within 1–2 weeks.
• Often recurrent and not associated with induration.

(Option D) Herpetic ulcer:

• Usually multiple small ulcers with vesicular prodrome.
• Rapid onset and heal within 7–10 days.
• Induration is absent.

(Option E) Syphilitic chancre:

• Painless, firm ulcer, usually on genital mucosa.
• Single ulcer, but oral involvement is uncommon.
• Regional lymphadenopathy may be present.

Key Concept 

Persistent, non-healing oral ulcers (>2 weeks) with indurated margins, especially in older patients with tobacco exposure, are highly suggestive of oral squamous cell carcinoma. Early recognition is critical for prognosis.

Subject: Medicine (Internal Medicine)

System: Gastroenterology - Oral cavity & Esophagus - Oral Cavity – Malignant Lesions

Topic: Oral Cavity – Squamous Cell Carcinoma

• Competency Domain: Diagnosis
• Cognitive Level: Application
• Clinical Skill: Reasoning
• Difficulty Level: Moderate

Oral Cavity – Squamous Cell Carcinoma

Differential Diagnosis of 

Non-Healing Oral Cavity Ulcers

Note

• The most important differentiation is chronicity (>2 weeks) + induration + risk factors, which points toward SCC.
• Biopsy is definitive for diagnosis.

Oral Cavity - Squamous Cell Carcinoma

This diagram illustrates a case of Oral Cavity - Squamous Cell Carcinoma (SCC).

• Visual Focus: The image displays an open human mouth, focusing on the oral cavity.
• Pathology Shown: A prominent, reddish, irregular, and raised ulcer is visible on the floor of the mouth/ventral tongue/gingiva area.
• Key Label: An arrow specifically points to this growth, labeling it as an "Ulcer," which is a common presentation of SCC in the oral cavity.

Keywords in the Stem to identify correct option 

1. Bilateral optic disc swelling (papilledema) – Indicates early raised ICP, key finding for option E.
2. Alert and oriented – Shows no late signs of ICP, ruling out Cushing’s triad or herniation.

Classic triad

None present in the stem. Cushing’s triad (hypertension, bradycardia, irregular respiration) is not mentioned, confirming this is an early ICP case.

Explanation 

(Option E) Papilledema indicates early raised ICP:

• The headache is often worse in the morning or with positional changes (like bending over), and vomiting is frequently non-projectile, occurring without nausea. The finding of papilledema (optic disc swelling due to raised ICP) is a critical objective sign confirming this diagnosis.
• Reason: Papilledema is optic disc swelling due to raised intracranial pressure. It is often the first detectable sign of chronically elevated ICP, occurring before changes in consciousness, vital signs, or cranial nerve palsies.
• Additional explanation: Mild bilateral optic disc swelling, as in this patient, is a hallmark of early ICP elevation. The patient’s alertness and absence of cranial nerve deficits indicate that this is an early, not late, stage.

(Option A) Early Cushing’s triad is present:

• Reason: Cushing’s triad (hypertension, bradycardia, irregular respiration) occurs late in raised ICP, typically when herniation is imminent. The patient is alert and oriented, so this is not present.

(Option B) Diplopia confirms cranial nerve involvement:

• Reason: Diplopia occurs with cranial nerve III, IV, or VI palsies from mass effect. This patient has no cranial nerve deficits, so diplopia is not relevant here.

(Option C) Altered consciousness indicates imminent herniation:

• Reason: Altered mental status is a late sign of raised ICP, signaling impending brain herniation. The patient is alert, so this does not apply.

(Option D) Bradycardia is an early sign:

• Reason: Bradycardia is part of Cushing’s triad, which is a late manifestation of raised ICP, not early.

Key Concept 

• Papilledema is an early sign of raised intracranial pressure, detectable on fundoscopy.
• Late signs include Cushing’s triad, cranial nerve palsies, bradycardia, and altered consciousness.
• Recognizing papilledema allows early diagnosis and intervention, preventing complications like herniation.

Subject: Medicine (Internal Medicine)

System: Central Nervous System - Intracranial mass, lesions and raised intracranial pressure (ICP) - Raised intracranial pressure

Topic: Raised Intracranial Pressure (ICP) – Early Clinical Signs

• Competency Domain: Diagnosis
• Cognitive Level: Application
• Clinical Skill: Interpretation
• Difficulty Level: Moderate

Raised Intracranial Pressure (ICP) – 

Early Clinical Signs

Differential Diagnosis of 

Early Raised Intracranial Pressure (ICP) with Papilledema

Raised Intracranial Pressure (ICP) Early Clinical Signs

The diagram illustrates the early clinical signs of Raised Intracranial Pressure (ICP). The main symptoms highlighted are:

• Headache
• Vomiting (shown with a curved arrow indicating direction of causality or association, and a standalone circle icon)
• Papilledema (swelling of the optic disc, shown in the circular image on the right)
• Decreased Alertness

The image serves as a quick visual guide for recognizing the initial symptoms of increased pressure within the skull.

Keywords in the Stem to identify correct option 

1. “After 48 hours of therapy” – indicates monitoring therapeutic response, not diagnosis.
2. “Neonate / suspected sepsis” – context specifies neonatal sepsis, guiding towards standard monitoring methods.
3. “Monitor response” – directly points to trend-based, non-invasive markers rather than invasive tests.

Classic triad in stem

• Fever, lethargy, and poor feeding → common clinical triad for neonatal sepsis.

These keywords help immediately focus on serial CRP/procalcitonin as the correct method for monitoring response.

Explanation 

(Option B) Serial C-reactive Protein (CRP) or procalcitonin measurements:

• CRP and procalcitonin are sensitive biomarkers for infection and inflammation.
• These are acute-phase reactants that become elevated in response to inflammation and infection. Following their levels serially (e.g., every 12-24 hours) provides an objective measure of the inflammatory response. 
• A decrease in CRP or procalcitonin over 24-48 hours after starting antibiotics strongly suggests a good clinical and therapeutic response, allowing for de-escalation or discontinuation of empirical therapy
• Serial measurements allow clinicians to monitor trend, helping to decide duration of antibiotics.

(Option A) Daily blood cultures:

• Repeating blood cultures daily is not recommended.
• Once antibiotics are started, cultures often become negative; daily sampling is invasive and rarely changes management.

(Option C) Daily lumbar puncture:

• Lumbar puncture is diagnostic, not for daily monitoring.
• Repeating LP daily is invasive and unnecessary, and is only indicated if meningitis is suspected or treatment failure occurs.

(Option D) Daily chest X-ray:

• Chest X-rays are only indicated if respiratory involvement is present.
• Routine daily imaging is not useful for monitoring sepsis response.

(Option E) Monitor platelet counts only:

• Platelets can reflect severity of sepsis, but changes are nonspecific.
• Platelet count alone is insufficient to assess treatment response.

Key Concept 

• In neonatal sepsis, therapeutic response is best monitored by trends in biomarkers such as CRP or procalcitonin, rather than repeated invasive tests or imaging.
• A falling CRP/procalcitonin trend indicates effective antibiotic therapy.

Subject: Medicine (Internal Medicine)

System: Pediatric Medicine (Hematologic & Immune / Infectious System) – The Newborn - Neonatal sepsis

Topic: Neonatal Sepsis – Monitoring Therapeutic Response

• Competency Domain: Management
• Cognitive Level (Bloom’s): Application
• Clinical Skill: Decision-making
• Difficulty Level: Moderate

Neonatal Sepsis – Monitoring Therapeutic Response

Differential Diagnosis of Neonatal Sepsis

Note

Neonatal sepsis is often a diagnosis of exclusion, confirmed with clinical signs plus laboratory markers (CRP, procalcitonin, blood culture).

Neonatal Sepsis – Key Clinical Features and Monitoring

This diagram visually summarizes the essential elements of neonatal sepsis, including hallmark symptoms (fever, lethargy, poor feeding), key diagnostic biomarkers (CRP, procalcitonin), and core management components such as antibiotic therapy. It provides a quick, high-yield snapshot for medical graduates to understand recognition and early monitoring of neonatal sepsis.

Keywords in the Stem to identify correct option 

1. “8-month history” – Duration >6 months, crucial to differentiate schizophrenia from schizophreniform (<6 months) or brief psychotic disorder (<1 month).
2. “Hearing voices” & “delusions” – Presence of positive symptoms (hallucinations + delusions) characteristic of schizophrenia.
3. “Social withdrawal, flat affect, neglect of personal hygiene” – Negative symptoms, which support schizophrenia over delusional disorder or brief psychotic disorder.

Classic Triad:

• Positive symptoms + Negative symptoms + Functional impairment – This triad helps confirm schizophrenia in chronic presentations.

Explanation 

(Option A) Schizophrenia:

• Explanation: The patient has symptoms for >6 months, including positive symptoms (auditory hallucinations, delusions) and negative symptoms (flat affect, social withdrawal, poor self-care), along with functional impairment. These criteria fit schizophrenia per DSM-5.
• Schizophrenia requires at least 6 months of continuous signs of illness, with at least 1 month of active-phase symptoms. The combination of hallucinations, delusions, and negative symptoms makes this the most likely diagnosis.

(Option B) Schizophreniform disorder:

• Duration of symptoms is 1–6 months, often with good premorbid functioning and without marked functional decline. 
• This patient has had symptoms for 8 months, which exceeds the time frame.

(Option C) Brief psychotic disorder:

• Characterized by sudden onset of psychotic symptoms lasting less than 1 month with eventual full return to baseline. 
• The duration in this case is much longer, so this is unlikely.

(Option D) Delusional disorder:

• In delusional disorder, delusions are the primary feature, without prominent hallucinations, negative symptoms, or significant functional impairment. 
• This patient has hallucinations and negative symptoms, ruling this out.

(Option E) Schizoaffective disorder:

• Requires mood episode (depressive or manic) concurrent with psychotic symptoms. 
• Here, there is no evidence of mood symptoms, so this diagnosis does not fit.

Key Concept 

Schizophrenia is a chronic psychotic disorder characterized by positive and negative symptoms lasting >6 months with functional impairment. Differentiation from schizophreniform, brief psychotic disorder, delusional disorder, and schizoaffective disorder is primarily based on duration, symptom profile, and presence of mood symptoms.

Subject: Psychiatry

System/Title: SCHIZOPHRENIA - Central Nervous System (CNS) / Brain – specifically the psychotic and cognitive functional pathways

Topic: Schizophrenia – First-Episode Psychosis

• Competency Domain: Diagnosis
• Cognitive Level: Application
• Clinical Skill: Reasoning
• Difficulty Level: Moderate

Schizophrenia – First-Episode Psychosis

Differential Diagnosis of 

First-Episode Psychosis / Schizophrenia

This table helps differentiate schizophrenia from other psychotic disorders based on duration, symptom profile, and functional impact.

Schizophrenia – First-Episode Psychosis

The diagram illustrates the key features used to diagnose Schizophrenia, specifically in the context of a First-Episode Psychosis.

It organizes the symptoms into two main categories:

1. Positive Symptoms: These are additions to normal experience. The diagram highlights Hallucinations (shown by an ear illustration).
2. Negative Symptoms: These are deficits in normal emotional responses or other thought processes. The diagram lists Social withdrawal, Flat affect, and Poor self-care (shown by a silhouette of a person sitting alone).

Finally, the diagram specifies the required Duration & Function criteria for diagnosis:

• Symptoms must last 6 months.
• There must be Impaired functioning.