A 49-year-old woman presents to the emergency room with bloody stool and malaise. She developed a fever and acute left lower quadrant abdominal pain earlier in the day. She has had 2 bowel movements with bright red blood. Her past medical history is notable for hyperlipidemia, hypertension, and diabetes mellitus. She takes lovastatin, hydrochlorothiazide, metformin, glyburide, and aspirin. Her temperature is 102.9°F (39.4°C), blood pressure is 101/61 mmHg, pulse is 110/min, and respirations are 22/min. On exam, she is fully alert and oriented. She is tender in the left lower quadrant. A computerized tomography (CT) scan is performed demonstrating acute diverticulitis. She is admitted and started on broad-spectrum antibiotics. 48 hours later, her urine output is significantly decreased. Her abdominal pain has improved but she has started vomiting and appears confused. She has new bilateral lower extremity edema and decreased breath sounds at the lung bases. Laboratory analysis upon admission and 48 hours later is shown below:
Admission:
Hemoglobin: 11.9 g/dl
Hematocrit: 34%
Leukocyte count: 11,500/mm^3
Platelet count: 180,000/ mm^3
Serum:
Na+: 141 mEq/L
Cl-: 103 mEq/L
K+: 4.5 mEq/L
HCO3-: 23 mEq/L
BUN: 21 mg/dL
Glucose: 110 mg/dL
Creatinine: 0.9 mg/dL
48 hours later:
Hemoglobin: 10.1 g/dl
Hematocrit: 28%
Leukocyte count: 11,500 cells/mm^3
Platelet count: 195,000/ mm^3
Serum:
Na+: 138 mEq/L
Cl-: 100 mEq/L
K+: 5.1 mEq/L
HCO3-: 24 mEq/L
BUN: 30 mg/dL
Glucose: 120 mg/dL
Creatinine: 2.1 mg/dL
Which of the following findings would most likely be seen on urine microscopy?
Q62
A 55-year-old man presents to the hospital with chief complaints of unintentional weight loss, anorexia, fever, and sweating. The patient has pleuritic chest pain, progressive dyspnea, and dry cough. There is no history of orthopnea or paroxysmal nocturnal dyspnea. On examination, the patient is afebrile and pericardial friction rub is noted. ECG shows diffuse ST-segment elevation in V1-V4 along with T wave inversion. Chest X-ray and CT scan show anterior and inferior pericardial eggshell calcification. Echocardiography reveals thickened pericardium and signs of diastolic right ventricular collapse. Pericardial fluid is sent for Ziehl-Neelsen staining to detect acid-fast bacilli. Mycobacterium tuberculosis is detected by PCR. What is the most likely mechanism associated with the patient’s condition?
Q63
A 22-year-old woman presents to the emergency department with a 2-day history of severe blistering. She says that she woke up 2 days ago with a number of painful blisters in her mouth and has since been continuing to develop blisters of her cutaneous skin all over her body and the mucosa of her mouth. She has no past medical history and has never experienced these symptoms before. Physical exam reveals a diffuse vesicular rash with painful, flaccid blisters that separate easily with gentle rubbing. The function of which of the following proteins is most likely disrupted in this patient?
Q64
A 57-year-old man comes to the physician for a follow-up evaluation of chronic, retrosternal chest pain. The pain is worse at night and after heavy meals. He has taken oral pantoprazole for several months without any relief of his symptoms. Esophagogastroduodenoscopy shows ulcerations in the distal esophagus and a proximally dislocated Z-line. A biopsy of the distal esophagus shows columnar epithelium with goblet cells. Which of the following microscopic findings underlie the same pathomechanism as the cellular changes seen in this patient?
Cell injury US Medical PG Practice Questions and MCQs
Question 61: A 49-year-old woman presents to the emergency room with bloody stool and malaise. She developed a fever and acute left lower quadrant abdominal pain earlier in the day. She has had 2 bowel movements with bright red blood. Her past medical history is notable for hyperlipidemia, hypertension, and diabetes mellitus. She takes lovastatin, hydrochlorothiazide, metformin, glyburide, and aspirin. Her temperature is 102.9°F (39.4°C), blood pressure is 101/61 mmHg, pulse is 110/min, and respirations are 22/min. On exam, she is fully alert and oriented. She is tender in the left lower quadrant. A computerized tomography (CT) scan is performed demonstrating acute diverticulitis. She is admitted and started on broad-spectrum antibiotics. 48 hours later, her urine output is significantly decreased. Her abdominal pain has improved but she has started vomiting and appears confused. She has new bilateral lower extremity edema and decreased breath sounds at the lung bases. Laboratory analysis upon admission and 48 hours later is shown below:
Admission:
Hemoglobin: 11.9 g/dl
Hematocrit: 34%
Leukocyte count: 11,500/mm^3
Platelet count: 180,000/ mm^3
Serum:
Na+: 141 mEq/L
Cl-: 103 mEq/L
K+: 4.5 mEq/L
HCO3-: 23 mEq/L
BUN: 21 mg/dL
Glucose: 110 mg/dL
Creatinine: 0.9 mg/dL
48 hours later:
Hemoglobin: 10.1 g/dl
Hematocrit: 28%
Leukocyte count: 11,500 cells/mm^3
Platelet count: 195,000/ mm^3
Serum:
Na+: 138 mEq/L
Cl-: 100 mEq/L
K+: 5.1 mEq/L
HCO3-: 24 mEq/L
BUN: 30 mg/dL
Glucose: 120 mg/dL
Creatinine: 2.1 mg/dL
Which of the following findings would most likely be seen on urine microscopy?
A. Waxy casts
B. Muddy brown casts (Correct Answer)
C. White blood cell casts
D. Fatty casts
E. Hyaline casts
Explanation: ***Muddy brown casts***
- The patient's presentation with **acute kidney injury** (creatinine rising from 0.9 to 2.1 mg/dL in 48 hours) along with signs of **sepsis** (fever, hypotension, altered mental status, decreased urine output) strongly suggests **acute tubular necrosis (ATN)**, a common cause of intrinsic renal failure.
- **Muddy brown casts** composed of degenerating renal tubular epithelial cells and granular material are pathognomonic for **acute tubular necrosis** and indicate significant tubular damage.
*Waxy casts*
- **Waxy casts** are typically associated with **chronic renal failure** and advanced renal disease, indicating prolonged tubular stasis and severe urine flow reduction.
- While the patient has acute kidney injury, her history does not suggest pre-existing chronic kidney disease to this extent.
*White blood cell casts*
- **White blood cell casts** are characteristic of **interstitial nephritis** or **pyelonephritis**, indicating inflammation or infection within the kidney parenchyma.
- Although the patient has a possible infection (diverticulitis, sepsis), the rapid decline in renal function with a clear rise in creatinine points more directly to ATN rather than primarily interstitial inflammation.
*Fatty casts*
- **Fatty casts** are typically seen in **nephrotic syndrome**, a condition characterized by massive proteinuria, hypoalbuminemia, and significant edema.
- The patient's symptoms are more consistent with acute kidney injury due to sepsis, and there is no information to suggest nephrotic-range proteinuria.
*Hyaline casts*
- **Hyaline casts** can be found in **healthy individuals** from concentrated urine or after exercise and are non-specific, indicating only mild tubular protein aggregation.
- They are not indicative of significant renal pathology like ATN and would not explain the patient's acute and severe renal deterioration.
Question 62: A 55-year-old man presents to the hospital with chief complaints of unintentional weight loss, anorexia, fever, and sweating. The patient has pleuritic chest pain, progressive dyspnea, and dry cough. There is no history of orthopnea or paroxysmal nocturnal dyspnea. On examination, the patient is afebrile and pericardial friction rub is noted. ECG shows diffuse ST-segment elevation in V1-V4 along with T wave inversion. Chest X-ray and CT scan show anterior and inferior pericardial eggshell calcification. Echocardiography reveals thickened pericardium and signs of diastolic right ventricular collapse. Pericardial fluid is sent for Ziehl-Neelsen staining to detect acid-fast bacilli. Mycobacterium tuberculosis is detected by PCR. What is the most likely mechanism associated with the patient’s condition?
A. Age-related amyloidosis
B. Metastatic calcifications
C. Dystrophic calcification (Correct Answer)
D. Primary amyloidosis
E. Secondary amyloidosis
Explanation: ***Dystrophic calcification***
- The presence of **Mycobacterium tuberculosis** in the pericardial fluid indicates an underlying tuberculous infection, which can lead to **caseous necrosis** and, subsequently, dystrophic calcification in the pericardium.
- **Dystrophic calcification** occurs in damaged or necrotic tissues (like inflamed pericardium in tuberculosis) despite normal serum calcium levels, fitting the *eggshell calcification* described.
*Age-related amyloidosis*
- This typically involves the **deposition of amyloid fibrils** in organs, often associated with aging, particularly in the heart with **transthyretin amyloidosis**.
- While it can cause restrictive cardiomyopathy, it does not typically present with **pericardial eggshell calcification** or a direct association with tuberculosis.
*Metastatic calcifications*
- **Metastatic calcification** occurs in otherwise normal tissues due to **hypercalcemia** (elevated serum calcium levels), which is not indicated in this patient's presentation.
- Conditions like **hyperparathyroidism** or certain malignancies can cause hypercalcemia, which is not suggested by the clinical picture or the finding of tuberculosis.
*Primary amyloidosis*
- This form of amyloidosis, usually associated with **plasma cell dyscrasias** (e.g., multiple myeloma), involves deposition of **light chain (AL) amyloid**.
- It primarily affects organs like the heart, kidneys, and liver, causing organ dysfunction but not typically **pericardial calcification** or being directly caused by tuberculosis.
*Secondary amyloidosis*
- Also known as **AA amyloidosis**, this type is associated with **chronic inflammatory diseases** such as rheumatoid arthritis, inflammatory bowel disease, or chronic infections.
- While tuberculosis can theoretically cause chronic inflammation, **secondary amyloidosis** presents with systemic amyloid deposition and not the specific **pericardial eggshell calcification** seen here, nor is it the primary mechanism of calcification in infected tissue.
Question 63: A 22-year-old woman presents to the emergency department with a 2-day history of severe blistering. She says that she woke up 2 days ago with a number of painful blisters in her mouth and has since been continuing to develop blisters of her cutaneous skin all over her body and the mucosa of her mouth. She has no past medical history and has never experienced these symptoms before. Physical exam reveals a diffuse vesicular rash with painful, flaccid blisters that separate easily with gentle rubbing. The function of which of the following proteins is most likely disrupted in this patient?
A. T-cell receptor
B. Cadherin (Correct Answer)
C. Keratin
D. Collagen
E. Integrin
Explanation: ***Cadherin***
- The patient's presentation with **diffuse flaccid blisters** that separate easily with gentle rubbing (a positive **Nikolsky sign**) and **oral mucosal involvement** is highly suggestive of **pemphigus vulgaris**.
- **Pemphigus vulgaris** is an autoimmune blistering disease where autoantibodies target **desmoglein 1 and 3**, which are types of **cadherin cell adhesion proteins** responsible for cell-to-cell adhesion in the epidermis. Their disruption leads to **intraepidermal blistering**.
*T-cell receptor*
- **T-cell receptors** are involved in immune recognition and T-cell activation, but their primary disruption is not directly responsible for the blistering seen in pemphigus vulgaris, which is mediated by **autoantibodies against desmogleins**.
- Conditions involving T-cell receptor dysfunction typically manifest as **immunodeficiencies**, **autoimmune responses** directed at self-antigens via cellular immunity, or **lymphomas**, not primary blistering diseases of this type.
*Keratin*
- **Keratin** is an intermediate filament protein that provides structural integrity to epithelial cells. While disruptions in keratin can lead to blistering disorders (e.g., **epidermolysis bullosa simplex**), these often present with **intact, tense blisters** (due to basal cell layer separation) or mechanical fragility, unlike the flaccid blisters of pemphigus vulgaris.
- **Genetic defects in keratin** would typically present earlier in life and are not usually associated with an autoimmune mechanism causing acute onset flaccid blistering.
*Collagen*
- **Collagen** is a primary component of the extracellular matrix and is crucial for skin strength and integrity. Disorders involving collagen, such as **epidermolysis bullosa acquisita** or certain types of **dystrophic epidermolysis bullosa**, typically disrupt the **dermal-epidermal junction**, leading to **subepidermal blistering** and often **scarring**.
- The flaccid, intraepidermal blisters and positive Nikolsky sign described are not characteristic of collagen-related blistering disorders.
*Integrin*
- **Integrins** are cell surface receptors involved in cell-to-extracellular matrix adhesion, particularly in forming **hemidesmosomes** that anchor basal keratinocytes to the basement membrane.
- Disruption of integrins or other hemidesmosomal components (e.g., in **bullous pemphigoid**) leads to **subepidermal blistering**, where blisters are typically tense and do not easily rupture with gentle pressure, which is distinct from the flaccid blisters of pemphigus vulgaris.
Question 64: A 57-year-old man comes to the physician for a follow-up evaluation of chronic, retrosternal chest pain. The pain is worse at night and after heavy meals. He has taken oral pantoprazole for several months without any relief of his symptoms. Esophagogastroduodenoscopy shows ulcerations in the distal esophagus and a proximally dislocated Z-line. A biopsy of the distal esophagus shows columnar epithelium with goblet cells. Which of the following microscopic findings underlie the same pathomechanism as the cellular changes seen in this patient?
A. Squamous epithelium in the bladder (Correct Answer)
B. Branching muscularis mucosa in the jejunum
C. Paneth cells in the duodenum
D. Pseudostratified columnar epithelium in the bronchi
E. Disorganized squamous epithelium in the endocervix
Explanation: ***Squamous epithelium in the bladder***
- The patient has **Barrett's esophagus**, characterized by **columnar epithelium with goblet cells** in the distal esophagus, which is an example of **metaplasia**.
- **Squamous metaplasia in the bladder** can occur due to chronic irritation (e.g., stones, recurrent infections) and represents a similar adaptive cellular change where one differentiated cell type is replaced by another.
*Branching muscularis mucosa in the jejunum*
- **Branching muscularis mucosa** is a normal anatomical variant sometimes seen in the jejunum, not a pathological cellular change.
- This finding does not represent a change in cell type due to chronic stress or adaptation.
*Paneth cells in the duodenum*
- **Paneth cells** are a normal component of the small intestine, including the duodenum, and are responsible for antimicrobial defense through the secretion of **lysozyme** and **defensins**.
- Their presence in the duodenum is physiological and not a metaplastic change.
*Pseudostratified columnar epithelium in the bronchi*
- **Pseudostratified columnar epithelium with cilia and goblet cells** is the normal and healthy lining of the bronchi, responsible for mucociliary clearance.
- This is a normal histological finding, not an abnormal cellular adaptation like metaplasia.
*Disorganized squamous epithelium in the endocervix*
- **Disorganized squamous epithelium** in the endocervix suggests **dysplasia** or **carcinoma in situ**, which is a pre-malignant or malignant change, not simple metaplasia.
- While metaplasia (e.g., squamous metaplasia in the transformation zone of the cervix) can precede dysplasia, the term "disorganized" indicates a higher grade of cellular abnormality and a different pathomechanism.
