Edema mechanisms US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Edema mechanisms. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Edema mechanisms US Medical PG Question 1: A 41-year-old man comes to the emergency department because of fatigue, worsening abdominal discomfort, and progressive swelling of his legs for 3 months. The swelling is worse in the evenings. His only medication is ibuprofen for occasional joint pain. The patient does not smoke and drinks 2–3 beers each weekend. His temperature is 36°C (96.8°F), pulse is 88/min, respirations are 18/min, and blood pressure is 130/80 mm Hg. Pulmonary examination shows no abnormalities. Abdominal examination shows a mildly distended abdomen with shifting dullness. The liver is palpated 2–3 cm below the right costal margin. When pressure is applied to the right upper quadrant, the patient's jugular veins become visibly distended for 15 seconds. The 2nd and 3rd metacarpophalangeal joints of both hands are tender to palpation. There is 2+ edema in the lower extremities. Which of the following is the most likely underlying cause of this patient's edema?
- A. Reduced glomerular filtration rate
- B. Macrovesicular steatosis of the liver
- C. Dermal deposition of glycosaminoglycans
- D. Impaired hepatic protein synthesis
- E. Impaired relaxation of the right ventricle (Correct Answer)
Edema mechanisms Explanation: ***Impaired relaxation of the right ventricle***
- The presence of **fatigue**, **abdominal discomfort**, **leg swelling**, **ascites with shifting dullness**, **hepatomegaly**, and particularly a positive **hepatojugular reflux** (jugular vein distension with RUQ pressure) strongly suggests **right-sided heart failure** due to impaired right ventricular relaxation, such as in **constrictive pericarditis** or **restrictive cardiomyopathy**.
- **Ibuprofen (NSAID) use** and **joint tenderness** in the metacarpophalangeal joints hint at a potential underlying inflammatory condition like rheumatoid arthritis, which can be associated with **amyloidosis** causing restrictive cardiomyopathy.
*Reduced glomerular filtration rate*
- While a reduced GFR can cause edema, it typically leads to **generalized anasarca** and is often associated with symptoms of **uremia** or significant proteinuria, which are not described.
- The prominent **hepatomegaly** and **positive hepatojugular reflux** are not primary features of renal-induced edema.
*Macrovesicular steatosis of the liver*
- **Macrovesicular steatosis** (fatty liver) itself does not directly cause significant edema or ascites unless it progresses to **cirrhosis**, which would manifest with more distinct signs of **liver failure** and portal hypertension.
- While the patient has some alcohol intake, the clinical picture with prominent hepatojugular reflux points more towards cardiac than isolated liver pathology at this stage.
*Dermal deposition of glycosaminoglycans*
- Dermal deposition of **glycosaminoglycans** is characteristic of **myxedema** (hypothyroidism), which causes non-pitting edema and is usually associated with other symptoms like **cold intolerance**, **bradycardia**, and **dry skin**, none of which are mentioned.
- The pitting edema observed in this patient is inconsistent with myxedema.
*Impaired hepatic protein synthesis*
- Impaired hepatic protein synthesis, leading to **hypoalbuminemia**, can cause edema and ascites due to reduced **oncotic pressure**.
- However, the significant **hepatomegaly** and the distinct **hepatojugular reflux** are more indicative of a circulatory issue affecting the liver, rather than primary intrinsic liver failure.
Edema mechanisms US Medical PG Question 2: A 65-year-old man comes to the physician for the evaluation of a 2-month history of worsening fatigue and shortness of breath on exertion. While he used to be able to walk 4–5 blocks at a time, he now has to pause every 2 blocks. He also reports waking up from having to urinate at least once every night for the past 5 months. Recently, he has started using 2 pillows to avoid waking up coughing with acute shortness of breath at night. He has a history of hypertension and benign prostatic hyperplasia. His medications include daily amlodipine and prazosin, but he reports having trouble adhering to his medication regimen. His pulse is 72/min, blood pressure is 145/90 mm Hg, and respiratory rate is 20/min. Physical examination shows 2+ bilateral pitting edema of the lower legs. Auscultation shows an S4 gallop and fine bibasilar rales. Further evaluation is most likely to show which of the following pathophysiologic changes in this patient?
- A. Increased left ventricular compliance
- B. Decreased alveolar surface tension
- C. Increased potassium retention
- D. Increased tone of efferent renal arterioles (Correct Answer)
- E. Decreased systemic vascular resistance
Edema mechanisms Explanation: ***Increased tone of efferent renal arterioles***
- The patient's symptoms (fatigue, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, bilateral pitting edema, S4 gallop, rales, hypertension) are highly suggestive of **heart failure**, primarily left-sided due to his history of **uncontrolled hypertension**.
- In response to decreased cardiac output and renal perfusion in heart failure, the **renin-angiotensin-aldosterone system (RAAS)** is activated. This activation leads to **angiotensin II** production, which constricts **efferent renal arterioles**, increasing the glomerular filtration rate and maintaining renal perfusion pressure to sustain function.
*Increased left ventricular compliance*
- This patient's findings, particularly the **S4 gallop** and history of uncontrolled hypertension, indicate **diastolic dysfunction**, which is characterized by a **stiff, non-compliant left ventricle**.
- The S4 gallop is produced by the atria contracting against a **stiff ventricle**, reflecting reduced ventricular compliance.
*Decreased alveolar surface tension*
- **Decreased alveolar surface tension** (due to surfactant) is a normal physiological state that prevents alveolar collapse and facilitates gas exchange.
- In heart failure, the presence of **bibasilar rales** indicates **pulmonary edema** (fluid accumulation in the alveoli and interstitial spaces), which would *increase* the work of breathing and impair gas exchange, but does not directly relate to decreased surface tension.
*Increased potassium retention*
- Activation of the **renin-angiotensin-aldosterone system (RAAS)** leads to increased **aldosterone** secretion. Aldosterone promotes **sodium reabsorption** and **potassium excretion** in the renal collecting ducts.
- Therefore, chronic RAAS activation in heart failure typically leads to **potassium wasting**, not retention.
*Decreased systemic vascular resistance*
- In heart failure, especially due to chronic hypertension, the body attempts to compensate by activating the **sympathetic nervous system** and **RAAS**, leading to **vasoconstriction** and an *increase* in systemic vascular resistance to maintain blood pressure and perfusion to vital organs.
- **Decreased systemic vascular resistance** would typically worsen the low cardiac output state, and is not a compensatory mechanism in this context.
Edema mechanisms US Medical PG Question 3: Two weeks after undergoing low anterior resection for rectal cancer, a 52-year-old man comes to the physician because of swelling in both feet. He has not had any fever, chills, or shortness of breath. His temperature is 36°C (96.8°F) and pulse is 88/min. Physical examination shows a normal thyroid and no jugular venous distention. Examination of the lower extremities shows bilateral non-pitting edema that extends from the feet to the lower thigh, with deep flexion creases. His skin is warm and dry, and there is no erythema or rash. Microscopic examination of the interstitial space in this patient's lower extremities would be most likely to show the presence of which of the following?
- A. Neutrophilic, protein-rich fluid
- B. Lymphocytic, hemosiderin-rich fluid
- C. Lipid-rich, protein-rich fluid (Correct Answer)
- D. Protein-rich, glycosaminoglycan-rich fluid
- E. Acellular, protein-poor fluid
Edema mechanisms Explanation: ***Lipid-rich, protein-rich fluid***
- The presentation of bilateral non-pitting edema extending to the thigh, with deep flexion creases, in a patient post-**low anterior resection** for rectal cancer, strongly suggests **lymphedema**.
- Lymphedema results from impaired lymphatic drainage, leading to the accumulation of **protein-rich fluid**, **macromolecules**, and **adipose tissue** in the interstitial space, which eventually becomes lipid-rich due to chronic inflammation and fibroblasts stimulating adipogenesis.
*Neutrophilic, protein-rich fluid*
- This description is characteristic of **inflammatory edema** or **purulent exudate**, typically seen in infections.
- The patient's lack of fever, chills, erythema, or warmth makes an infectious or acute inflammatory process unlikely.
*Lymphocytic, hemosiderin-rich fluid*
- **Hemosiderin deposits** are indicative of chronic **venous insufficiency** or recurrent hemorrhages, leading to red blood cell extravasation and breakdown.
- While lymphocytes can be present in chronic inflammation, the primary issue here is lymphatic obstruction, not venous stasis or bleeding.
*Protein-rich, glycosaminoglycan-rich fluid*
- While lymphedema is indeed **protein-rich**, the primary accumulation in mature lymphedema involves **adipose tissue** and fibrosis.
- **Glycosaminoglycans** accumulate significantly in conditions like **myxedema** (hypothyroidism), which was ruled out by the normal thyroid examination.
*Acellular, protein-poor fluid*
- This describes a **transudate**, typically seen in conditions like **heart failure**, **liver cirrhosis**, or **nephrotic syndrome** where there's an imbalance of hydrostatic and oncotic pressures.
- The edema in this case is **non-pitting**, suggesting a higher protein content and tissue changes characteristic of lymphatic dysfunction, not systemic fluid overload leading to protein-poor fluid.
Edema mechanisms US Medical PG Question 4: A 72-year-old woman with hypertension comes to the physician because of swelling and pain in both legs for the past year. The symptoms are worse at night and improve in the morning. Current medications include losartan and metoprolol. Her temperature is 36°C (96.8°F), pulse is 67/min, and blood pressure is 142/88 mm Hg. Examination shows normal heart sounds; there is no jugular venous distention. Her abdomen is soft and the liver edge is not palpable. Examination of the lower extremities shows bilateral pitting edema and prominent superficial veins. The skin is warm and there is reddish-brown discoloration of both ankles. Laboratory studies show a normal serum creatinine and normal urinalysis. Which of the following is the most likely underlying cause of this patient's symptoms?
- A. Decreased arteriolar resistance
- B. Increased venous valve reflux (Correct Answer)
- C. Decreased intravascular oncotic pressure
- D. Decreased lymphatic flow
- E. Increased capillary permeability
Edema mechanisms Explanation: ***Increased venous valve reflux***
- The patient presents with **bilateral pitting edema**, **prominent superficial veins**, and **reddish-brown discoloration of the ankles**, which are classic signs of **chronic venous insufficiency**.
- **Venous valve reflux** leads to increased hydrostatic pressure in the capillaries, causing fluid transudation into the interstitial space, leading to edema that is worse at night and improves with elevation.
*Decreased arteriolar resistance*
- **Decreased arteriolar resistance** can lead to increased blood flow to the capillaries, but it typically causes edema that is **warm and erythematous**, often in the context of inflammation or certain medications (e.g., dihydropyridine calcium channel blockers), which is not the primary mechanism here.
- While some medications can cause edema, the full clinical picture points more specifically to venous stasis.
*Decreased intravascular oncotic pressure*
- **Decreased intravascular oncotic pressure** (e.g., due to low albumin from liver disease or nephrotic syndrome) causes **generalized edema** that is often symmetrical, but it would not typically cause prominent superficial veins or reddish-brown ankle discoloration.
- The patient's normal liver exam and creatinine/urinalysis make this less likely.
*Decreased lymphatic flow*
- **Decreased lymphatic flow** results in **lymphedema**, which is typically **non-pitting**, unilateral, and does not cause prominent superficial veins or pigment changes initially.
- Lymphedema often leads to a "woody" texture and can be associated with skin thickening over time.
*Increased capillary permeability*
- **Increased capillary permeability** can cause edema, often due to **inflammation**, allergic reactions, or sepsis, and typically presents with warmth, erythema, and localized swelling.
- This mechanism is usually acute and does not primarily explain the chronic skin changes and prominent veins seen in this patient.
Edema mechanisms US Medical PG Question 5: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?
- A. Lidocaine
- B. Verapamil
- C. Carvedilol (Correct Answer)
- D. Aspirin
- E. Ibutilide
Edema mechanisms Explanation: ***Carvedilol***
- The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**.
- **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function.
*Lidocaine*
- **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management.
- It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias.
- It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function.
*Aspirin*
- **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease).
- It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology.
*Ibutilide*
- **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm.
- It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.
Edema mechanisms US Medical PG Question 6: A 68-year-old man is brought to the emergency department 30 minutes after the onset of uncontrollable jerking movements of his arms and legs followed by loss of consciousness. His wife says that he seemed confused this morning and had a headache. Immediately before the shaking episode, he said that he smelled rotten eggs. He is unresponsive. Cerebrospinal fluid (CSF) analysis shows a leukocyte count of 700/μL (70% lymphocytes), a glucose concentration of 60 mg/dL, and a protein concentration of 80 mg/dL. Despite appropriate lifesaving measures, the man dies. Which of the following is most likely to be found on postmortem examination of this patient?
- A. Hemorrhage into the adrenal glands
- B. Spore-forming, obligate anaerobic rods
- C. Atrophy of the mammillary bodies
- D. Cytoplasmic inclusions in cerebellar Purkinje cells
- E. Necrosis of the temporal lobes (Correct Answer)
Edema mechanisms Explanation: ***Necrosis of the temporal lobes***
- The patient's symptoms (headache, confusion, seizure preceded by **olfactory aura** smelling rotten eggs) and CSF findings (**lymphocytic pleocytosis**, moderately elevated protein, normal glucose) are highly suggestive of **herpes simplex encephalitis (HSE)**.
- HSE typically causes severe **necrotizing encephalitis** with a predilection for the **temporal and frontal lobes**, especially the medial temporal lobes, leading to significant **tissue necrosis**.
*Hemorrhage into the adrenal glands*
- This finding, known as **Waterhouse-Friderichsen syndrome**, is typically associated with **fulminant meningococcemia**, which presents with rapid onset of sepsis, petechial rash, and profound shock, not primarily with encephalitis and seizures.
- The CSF analysis in meningococcemia would show **neutrophilic pleocytosis** and markedly low glucose, which differs from this patient's lymphocytic predominance and normal glucose.
*Spore-forming, obligate anaerobic rods*
- This describes **Clostridium** species, which are associated with conditions like **tetanus** or **botulism**, causing distinct neurological symptoms such as muscle spasms or flaccid paralysis, rather than focal seizures and encephalitis.
- These bacteria are not typical causative agents for acute viral encephalitis, and their presence would not be the primary finding in a postmortem examination related to the described illness.
*Atrophy of the mammillary bodies*
- **Atrophy of the mammillary bodies** is characteristic of **Wernicke-Korsakoff syndrome**, a neurological disorder caused by **thiamine deficiency**, often seen in chronic alcoholics.
- This syndrome presents with **ophthalmoplegia, ataxia, and confusion** (Wernicke encephalopathy) followed by memory impairment (Korsakoff psychosis), which does not align with the acute seizure and encephalitis presentation.
*Cytoplasmic inclusions in cerebellar Purkinje cells*
- **Cytoplasmic inclusions (Negri bodies)** are pathognomonic for **rabies encephalitis** and are classically found in **hippocampal pyramidal neurons**, though they can also occur in cerebellar Purkinje cells and cortical neurons.
- Rabies typically presents with prodromal symptoms followed by acute neurological dysfunction (e.g., hydrophobia, agitation, paralysis) and rapidly progresses to coma and death, which is a different clinical course and viral etiology than suggested by the temporal lobe involvement and olfactory aura.
Edema mechanisms US Medical PG Question 7: A 69-year-old white man comes to the physician because of a 15-day history of fatigue and lower leg swelling. Over the past 8 months, he has had a 3.8-kg (8.3-lb) weight loss. He has smoked one pack of cigarettes daily for 48 years. Vital signs are within normal limits. He appears thin. Examination shows 2+ pretibial edema bilaterally. An x-ray of the chest shows a right upper lobe density. Laboratory studies show:
Hemoglobin 11.3 g/dL
Leukocyte count 8600/mm3
Platelet count 140,000/mm3
Serum
Urea nitrogen 25 mg/dL
Glucose 79 mg/dL
Creatinine 1.7 mg/dL
Albumin 1.6 mg/dL
Total cholesterol 479 mg/dL
Urine
Blood negative
Glucose negative
Protein 4+
WBC 0–1/hpf
Fatty casts numerous
Light microscopic examination of a kidney biopsy reveals thickening of glomerular capillary loops and the basal membrane. Which of the following is the most likely diagnosis?
- A. Rapidly progressive glomerulonephritis
- B. Granulomatosis with polyangiitis
- C. Membranous nephropathy (Correct Answer)
- D. Focal segmental glomerulosclerosis
- E. Membranoproliferative glomerulonephritis
Edema mechanisms Explanation: ***Membranous nephropathy***
- The patient's presentation with **nephrotic syndrome** (edema, severe proteinuria 4+, hypoalbuminemia, hyperlipidemia, and fatigue) in an older adult, along with a **right upper lobe density** concerning for malignancy, strongly suggests secondary membranous nephropathy.
- The renal biopsy finding of **thickening of glomerular capillary loops and the basal membrane** is a hallmark of membranous nephropathy.
*Rapidly progressive glomerulonephritis*
- Characterized by a **rapid decline in renal function** over days to weeks, often with oliguria and symptoms of severe systemic illness.
- While proteinuria can be present, the classic biopsy finding is **crescent formation**, which is not described here.
*Granulomatosis with polyangiitis*
- This is a systemic vasculitis often involving the **upper and lower respiratory tracts** and kidneys, commonly presenting with **hemoptysis, sinusitis, and glomerulonephritis**.
- While a lung density is present, the absence of **hemoptysis** and the specific biopsy findings of membranous nephropathy make it less likely.
*Focal segmental glomerulosclerosis*
- This typically causes nephrotic syndrome but is characterized by **segmental sclerosis of glomeruli** on biopsy.
- While it can be idiopathic or secondary, the specific biopsy description and association with a potential malignancy point away from FSGS.
*Membranoproliferative glomerulonephritis*
- This condition presents with features of both **nephrotic and nephritic syndromes** and is characterized by a "tram-track" appearance on biopsy due to mesangial cell proliferation and basement membrane splitting.
- This specific microscopic finding is not mentioned in the patient's biopsy report.
Edema mechanisms US Medical PG Question 8: A 7-year-old girl is brought to her pediatrician by her mother because of puffiness under both eyes in the morning. The mother reports that the child has just recovered from a seasonal influenza infection a few days ago. Vital signs include: temperature 37°C (98.6°F), blood pressure 100/67 mm Hg, and pulse 95/min. On examination, there is facial edema and bilateral 2+ pitting edema over the legs. Laboratory results are shown:
Serum albumin 2.1 g/dL
Serum triglycerides 200 mg/dL
Serum cholesterol 250 mg/dL
Urine dipstick 4+ protein
Which of the following casts are more likely to be present in this patient’s urine?
- A. Waxy casts
- B. Fatty casts (Correct Answer)
- C. Red cell casts
- D. Granular casts
- E. White cell casts
Edema mechanisms Explanation: ***Fatty casts***
- The patient's presentation with **facial edema**, **pitting edema**, **hypoalbuminemia**, **hyperlipidemia** (increased triglycerides and cholesterol), and **heavy proteinuria** (4+ protein on urine dipstick) is highly suggestive of **nephrotic syndrome**.
- **Fatty casts** are pathognomonic for **nephrotic syndrome** because they are formed from renal tubular epithelial cells that have absorbed filtered lipids (cholesterol, triglycerides) and subsequently desquamated.
*Waxy casts*
- **Waxy casts** are typically associated with **chronic kidney disease** and indicate severe, longstanding tubular atrophy and dilation, often seen in end-stage renal disease.
- While they can be present in nephrotic syndrome if the kidney damage is severe and chronic, they are not the most characteristic cast *specifically* for the acute onset and hyperlipidemia seen here.
*Red cell casts*
- **Red cell casts** are indicative of **glomerulonephritis** (nephritic syndrome), where red blood cells leak through damaged glomerular capillaries into the renal tubules.
- This patient's presentation is characterized by **heavy proteinuria** and **edema** (nephrotic syndrome), without signs such as hematuria or hypertension that would typically suggest a nephritic picture.
*Granular casts*
- **Granular casts** are formed from degenerated cellular casts (e.g., granular breakdown products of renal tubular epithelial cells) or aggregated plasma proteins, and are non-specific indicators of **kidney damage** or **acute tubular necrosis**.
- While they can be seen in various kidney diseases, including nephrotic syndrome, they are not as specific as fatty casts for the constellation of symptoms presented.
*White cell casts*
- **White cell casts** are typically associated with **pyelonephritis** (kidney infection) or **interstitial nephritis**, indicating inflammation within the renal tubules or interstitium.
- There is no clinical or laboratory evidence of infection or inflammation suggesting pyelonephritis in this patient.
Edema mechanisms US Medical PG Question 9: A 36-year-old man comes to the physician for a 4-week history of swollen legs. He has difficulty putting on socks because of the swelling. Two years ago, he was diagnosed with sleep apnea. He takes no medications. He emigrated from Guatemala with his family when he was a child. He is 171 cm (5 ft 6 in) tall and weighs 115 kg (253 lb); BMI is 39 kg/m2. His pulse is 91/min and blood pressure is 135/82 mm Hg. Examination shows periorbital and bilateral lower extremity edema.
Serum
Albumin 3.1 g/dL
Total cholesterol 312 mg/dL
Urine
Blood negative
Protein +4
RBC 1-2/hpf
RBC cast negative
Fatty casts numerous
A renal biopsy is obtained. Which of the following is most likely to be seen under light microscopy of the patient's renal biopsy specimen?
- A. Diffuse thickening of glomerular capillaries
- B. Amyloid deposition in the mesangium
- C. Eosinophilic nodules within the glomeruli
- D. Fibrin crescents within the glomerular space
- E. Segmental sclerosis of the glomeruli (Correct Answer)
Edema mechanisms Explanation: ***Segmental sclerosis of the glomeruli***
- The patient presents with **nephrotic syndrome** (edema, proteinuria, hypoalbuminemia, hypercholesterolemia) and **obesity** (BMI 39 kg/m2), which are strong risk factors for **focal segmental glomerulosclerosis (FSGS)**.
- **FSGS** is characterized by **segmental sclerosis** within some glomeruli, often affecting juxtamedullary glomeruli initially.
*Diffuse thickening of glomerular capillaries*
- **Diffuse thickening of glomerular capillaries** (due to subepithelial immune complex deposition causing SPIKES on silver stain) is characteristic of **membranous nephropathy**, which typically presents with nephrotic syndrome but is not directly linked to obesity in the way FSGS is.
- While membranous nephropathy could cause nephrotic syndrome, the association with **morbid obesity** makes FSGS a stronger consideration.
*Amyloid deposition in the mesangium*
- **Amyloid deposition** typically presents with nephrotic syndrome and is associated with chronic inflammatory conditions or plasma cell dyscrasias, not primarily with obesity or the specific presentation described.
- On light microscopy, amyloid appears as **acellular, eosinophilic congophilic deposits** in the mesangium and capillary walls, showing apple-green birefringence under polarized light, which is not suggested by the clinical picture.
*Eosinophilic nodules within the glomeruli*
- **Eosinophilic nodules within the glomeruli** (Kimmelstiel-Wilson lesions) are characteristic of **diabetic nephropathy**, which commonly causes nephrotic syndrome.
- While the patient is obese, there is no information about diabetes or hyperglycemia to suggest diabetic nephropathy as the primary cause.
*Fibrin crescents within the glomerular space*
- **Fibrin crescents within the glomerular space** are indicative of **rapidly progressive glomerulonephritis (RPGN)**, which typically presents as nephritic syndrome (hematuria, hypertension, azotemia) rather than pure nephrotic syndrome.
- The patient's urine microscopic findings show only 1-2 RBC/hpf and no RBC casts, making RPGN unlikely.
Edema mechanisms US Medical PG Question 10: A 41-year-old African American woman presents to her primary care physician with a 3-week history of lower extremity edema and shortness of breath. She says that she has also noticed that she gets fatigued more easily and has been gaining weight. Her past medical history is significant for sickle cell disease and HIV infection for which she is currently taking combination therapy. Physical exam is significant for periorbital and lower extremity edema. Laboratory testing is significant for hypoalbuminemia, and urinalysis demonstrates 4+ protein. Which of the following would most likely be seen on kidney biopsy in this patient?
- A. Birefringence under polarized light
- B. Segmental scarring (Correct Answer)
- C. Subepithelial deposits
- D. Expansion of the mesangium
- E. Normal glomeruli
Edema mechanisms Explanation: ***Segmental scarring***
- The patient's history of **HIV infection**, symptoms of **nephrotic syndrome** (edema, weight gain, fatigue, hypoalbuminemia, 4+ proteinuria), and African American ethnicity are highly suggestive of **HIV-associated nephropathy (HIVAN)**.
- HIVAN is a form of **collapsing focal segmental glomerulosclerosis (FSGS)**, a condition characterized by **segmental scarring** and collapse of the glomerular tuft. In HIVAN, this scarring is severe and progressive.
*Birefringence under polarized light*
- This finding is characteristic of **amyloidosis**, where protein deposits (amyloid) accumulate in tissues and exhibit apple-green birefringence under Congo red stain and polarized light.
- While amyloidosis can cause nephrotic syndrome, it is not the most common kidney pathology in an HIV-positive patient with these specific features.
*Subepithelial deposits*
- **Subepithelial deposits** with a characteristic "spike and dome" appearance on electron microscopy are pathognomonic for **membranous glomerulonephritis**.
- This type of glomerulonephritis is not typically associated with HIV infection, nor does it typically present with the rapidly progressive decline seen in HIVAN.
*Expansion of the mesangium*
- **Mesangial expansion** is a common feature in several glomerular diseases, including **diabetic nephropathy** and early-stage IgA nephropathy.
- While it can be present in some forms of FSGS, it is not the primary or most characteristic finding for HIVAN, which is better described by collapsing glomeruli and segmental scarring.
*Normal glomeruli*
- Given the patient's profound **proteinuria (4+)**, hypoalbuminemia, and symptoms of **nephrotic syndrome**, it is highly unlikely that the glomeruli would appear normal on biopsy.
- Normal glomeruli would not explain the significant kidney dysfunction and proteinuria observed in this patient.
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