Irreversible cell injury (necrosis) US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Irreversible cell injury (necrosis). These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Irreversible cell injury (necrosis) US Medical PG Question 1: A 78-year-old man dies suddenly from complications of acute kidney failure. An autopsy is performed and microscopic evaluation of the kidneys shows pale, swollen cells in the proximal convoluted tubules. Microscopic evaluation of the liver shows similar findings. Which of the following is the most likely underlying mechanism of these findings?
- A. Double-stranded DNA breakage
- B. Impaired Na+/K+-ATPase pump activity (Correct Answer)
- C. Free radical formation
- D. Cytochrome C release
- E. Cytoplasmic triglyceride accumulation
Irreversible cell injury (necrosis) Explanation: ***Impaired Na+/K+-ATPase pump activity***
- **Acute kidney failure** leads to **hypoxia** and ATP depletion, which impairs the function of the **Na+/K+-ATPase pump** on the cell membrane.
- Failure of this pump results in **intracellular accumulation of sodium** and water, causing **cellular swelling** and pallor as seen in the kidneys and liver.
*Double-stranded DNA breakage*
- This is primarily associated with **apoptosis** or **radiation injury**, which would lead to nuclear fragmentation and cellular death rather than simple cellular swelling.
- While cell death can occur in acute kidney failure, the initial changes described (pale, swollen cells) are characteristic of **reversible cell injury** before extensive DNA damage.
*Free radical formation*
- **Free radical formation** (oxidative stress) can cause cellular injury, but it primarily leads to **lipid peroxidation of membranes** and damage to proteins and DNA, not directly to the widespread intracellular water accumulation described.
- While part of the injury cascade, it's not the most direct mechanism for the initial gross and microscopic findings of swelling.
*Cytochrome C release*
- **Cytochrome C release** from mitochondria is a critical step in the **intrinsic pathway of apoptosis**, leading to programmed cell death.
- The findings described (pale, swollen cells) are more indicative of **reversible cellular injury** or early necrosis, prior to the widespread activation of apoptosis.
*Cytoplasmic triglyceride accumulation*
- **Cytoplasmic triglyceride accumulation** (steatosis or fatty change) is often seen in conditions like **alcoholic liver disease** or **metabolic syndrome**.
- While it can be a sign of cellular injury, it does not directly explain the generalized "pale, swollen cells" observed in both the kidneys and liver following acute kidney failure, which points to water influx.
Irreversible cell injury (necrosis) US Medical PG Question 2: A 72-year-old female is brought to the emergency department by ambulance because she was unable to walk. She says that she cut her leg while falling about a week ago. Since then, the wound has started draining fluid and become progressively more painful. She is found to have necrotizing fasciitis and is taken emergently to the operating room. Histological examination of cells along the fascial planes reveal cells undergoing necrosis. Which of the following represents the earliest sign that a cell has progressed to irreversible damage in this patient?
- A. Fragmentation of the nucleus
- B. Membrane blebbing from organelles
- C. Chromatin dissolution and disappearance
- D. Ribosomal detachment from the endoplasmic reticulum
- E. Condensation of DNA into a basophilic mass (Correct Answer)
Irreversible cell injury (necrosis) Explanation: ***Condensation of DNA into a basophilic mass***
- **Karyopyknosis**, or the **condensation of nuclear chromatin into a dense, shrunken mass**, is an early microscopic sign of irreversible cell injury leading to necrosis. It indicates the cell has committed to a death pathway.
- This nuclear change is characterized by the nucleus appearing as a **small, dense, and deeply basophilic structure** due to chromatin clumping.
*Fragmentation of the nucleus*
- **Karyorrhexis**, the fragmentation of the pyknotic nucleus, occurs *after* karyopyknosis, indicating a later stage of irreversible injury.
- This process involves the breakdown of the condensed nuclear fragments, leading to their subsequent disappearance.
*Membrane blebbing from organelles*
- **Membrane blebbing** can occur in both reversible and irreversible injury, but its presence on *organelles* specifically doesn't necessarily represent the *earliest* sign of irreversible damage compared to nuclear changes.
- While significant blebbing points towards severe damage, **nuclear changes** are often considered more definitive early markers of irreversible commitment.
*Chromatin dissolution and disappearance*
- **Karyolysis**, the dissolution and fading of the nucleus due to enzymatic degradation, represents a *later* stage of irreversible injury, occurring after karyopyknosis and karyorrhexis.
- In this stage, the nucleus eventually completely disappears, leaving only an anucleated ghost cell.
*Ribosomal detachment from the endoplasmic reticulum*
- **Ribosomal detachment** from the endoplasmic reticulum is an early sign of **reversible cell injury**, leading to decreased protein synthesis.
- It indicates initial cellular stress but not necessarily a commitment to irreversible damage or necrosis.
Irreversible cell injury (necrosis) US Medical PG Question 3: A 54-year-old man was brought to the emergency room due to acute onset of slurred speech while at work, after which he lost consciousness. The patient's wife says this occurred approximately 30 minutes ago. Past medical history is significant for poorly controlled hypertension and type 2 diabetes mellitus. His blood pressure is 90/50 mm Hg, respiratory rate is 12/min, and heart rate is 48/min. The patient passes away shortly after arriving at the hospital. At autopsy, bilateral wedge-shaped strips of necrosis are seen in this patient's brain in the medial temporal lobe structures. Which of the following is the most likely location of these necrotic cells?
- A. Frontal lobe
- B. Hippocampus (Correct Answer)
- C. Cortex or cerebral hemisphere
- D. Substantia nigra
- E. Caudate nucleus
Irreversible cell injury (necrosis) Explanation: ***Hippocampus***
- The description of wedge-shaped necrosis just below the **medial temporal lobes** points directly to the **hippocampus**, which is highly susceptible to **ischemic injury**.
- The patient's **hypotension** and subsequent death suggest an event causing global cerebral hypoperfusion, making the hippocampus vulnerable due to its high metabolic demand and sensitivity to oxygen deprivation.
*Frontal lobe*
- While the frontal lobe can be affected by ischemia, its location is not consistent with "just below the **medial temporal lobes**" and the necrotic pattern described is more characteristic of specific vulnerable regions.
- Involvement of the frontal lobe would typically present with different focal neurological deficits depending on the specific area affected, such as motor weakness or personality changes.
*Cortex or cerebral hemisphere*
- **Wedge-shaped necrosis** is a pattern often seen in watershed areas or specific vulnerable regions, not a general description for global cortical ischemia.
- While the cortex is broadly affected by global ischemia, the specific localization described is much more precise than "cortex or cerebral hemisphere."
*Substantia nigra*
- The substantia nigra is located in the **midbrain** and is primarily involved in motor control, not typically implicated in the described **wedge-shaped necrosis** pattern associated with global ischemia below the medial temporal lobes.
- Damage to the substantia nigra is more commonly associated with conditions like **Parkinson's disease**.
*Caudate nucleus*
- The caudate nucleus is part of the **basal ganglia**, located deep within the cerebral hemispheres, and is not described as being "just below the **medial temporal lobes**."
- Ischemic damage to the caudate nucleus would cause different symptoms and typically not present with the specific necrotizing pattern described.
Irreversible cell injury (necrosis) US Medical PG Question 4: An 87-year-old woman is admitted to the intensive care unit after a neighbor found her lying on the floor at her home. Her respirations are 13/min and shallow. Despite appropriate therapy, the patient dies. Gross examination of the brain at autopsy shows neovascularization and liquefactive necrosis without cavitation in the distribution of the left middle cerebral artery. Histological examination of a brain tissue sample from the left temporal lobe shows proliferation of neural cells that stain positive for glial fibrillary acidic protein. Based on these findings, approximately how much time has most likely passed since the initial injury in this patient?
- A. 2 days
- B. 2 hours
- C. 10 days (Correct Answer)
- D. 25 days
- E. 12 hours
Irreversible cell injury (necrosis) Explanation: ***10 days***
- **Neovascularization** and the absence of cavitation with **liquefactive necrosis** are indicative of a subacute phase of ischemic injury, typically seen around 1-3 weeks.
- The proliferation of **glial fibrillary acidic protein (GFAP)** positive neural cells (astrocytes) signifies **astrogliosis**, a repair response common after approximately one week, peaking around 2-3 weeks post-injury.
*2 days*
- At 2 days, the primary histological findings would be **neutrophilic infiltration** and initial stages of neuronal necrosis.
- **Neovascularization** and significant astrogliosis are generally not prominent until later in the recovery phase.
*2 hours*
- Within 2 hours, there would be minimal to no gross changes, and microscopic examination might show only **red neurons** (eosinophilic neurons with pyknotic nuclei) reflecting early irreversible neuronal damage.
- There would be no signs of inflammation, tissue breakdown, or repair processes like neovascularization or astrogliosis.
*25 days*
- By 25 days (approximately 3-4 weeks), **cavitation** with a **cystic astrocytic glial scar** would likely be prominent at the site of liquefactive necrosis, which is explicitly stated as absent in the question.
- While astrogliosis would still be present, the lack of cavitation points to an earlier stage of repair.
*12 hours*
- At 12 hours, gross changes are typically still absent or subtle, and microscopic findings would primarily involve **edema** and early signs of neuronal injury (e.g., changes in Nissl bodies, mild eosinophilia).
- Inflammatory cell infiltration and reparative processes like neovascularization or astrogliosis would not yet be significant.
Irreversible cell injury (necrosis) US Medical PG Question 5: A 21-year-old medical student is studying different types of necrosis and tissue injuries. In the pathology laboratory, he observes different dead tissues under the microscope and notices the changes that are occurring as a function of time. After serial observations, he deduced that coagulation necrosis is...?
- A. The result of denaturation of glucose
- B. Characterized by the preservation of cellular shape (Correct Answer)
- C. Characteristic of brain ischemia
- D. Commonly associated with acute pancreatic necrosis
- E. The result of hydrolytic enzymes
Irreversible cell injury (necrosis) Explanation: ***Characterized by the preservation of cellular shape***
* **Coagulation necrosis** results from **protein denaturation**, which prevents the breakdown of the cell's structural proteins and enzymes.
* This preserves the **outline of the cell** and tissue architecture for a period of time, even after cell death, giving it a ghost-like appearance.
*The result of denaturation of glucose*
* **Glucose** is a simple sugar and does not undergo denaturation in the context of necrosis; rather, **proteins** are denatured.
* Denaturation refers to the disruption of the three-dimensional structure of proteins, not carbohydrates.
*Characteristic of brain ischemia*
* **Brain ischemia** typically results in **liquefactive necrosis**, not coagulation necrosis.
* This is due to the brain's high lipid content and the abundance of hydrolytic enzymes that rapidly digest the tissue.
*Commonly associated with acute pancreatic necrosis*
* **Acute pancreatitis** is primarily associated with **fat necrosis** (due to lipase activity) and **hemorrhagic necrosis**, not classic coagulation necrosis.
* The release of activated pancreatic enzymes leads to the digestion of local adipose tissue and blood vessels.
*The result of hydrolytic enzymes*
* While hydrolytic enzymes are involved in various forms of necrosis, **coagulation necrosis** is characterized by the **denaturation of structural proteins and enzymes**, which initially inhibits their proteolytic activity.
* **Liquefactive necrosis**, conversely, is largely driven by the release of powerful hydrolytic enzymes.
Irreversible cell injury (necrosis) US Medical PG Question 6: An 84-year-old man is brought to the physician by the staff of a group home where he resides because of worsening confusion and decreased urinary output. His nurse reports that the patient has not been drinking much for the last 3 days. Examination shows a decreased skin turgor and dry oral mucosa. His pulse is 105/min and blood pressure is 100/65 mm Hg. His serum creatinine is 3.1 mg/dL and a urea nitrogen is 42 mg/dL. Urine studies show multiple brownish granular casts. Which of the following processes is most likely involved in the pathogenesis of this patient's condition?
- A. Immune complex deposition in mesangium
- B. Leukocytic infiltration of renal interstitium
- C. Necrosis of renal papillae
- D. Necrosis of tubular epithelial cells (Correct Answer)
- E. Disruption of glomerular podocytes
Irreversible cell injury (necrosis) Explanation: ***Necrosis of tubular epithelial cells***
- The patient presents with classic signs of **acute kidney injury (AKI)**, including confusion, decreased urinary output, decreased skin turgor, dry oral mucosa, tachycardia, hypotension, elevated creatinine (3.1 mg/dL), and urea nitrogen (42 mg/dL).
- The presence of **brownish granular casts** in the urine is highly suggestive of **acute tubular necrosis (ATN)**, secondary to ischemia caused by severe dehydration and hypoperfusion.
*Immune complex deposition in mesangium*
- This typically points to a **glomerular pathology**, such as IgA nephropathy or post-infectious glomerulonephritis.
- These conditions would usually present with **hematuria** and **proteinuria**, not necessarily brownish granular casts or the acute dehydration found here.
*Leukocytic infiltration of renal interstitium*
- This finding is characteristic of **acute interstitial nephritis**, which is often caused by drug hypersensitivity or infection.
- The clinical presentation with dehydration and granular casts is not typical for acute interstitial nephritis.
*Necrosis of renal papillae*
- **Renal papillary necrosis** is often associated with analgesic abuse, sickle cell disease, diabetes, or obstruction.
- While it can cause AKI, it typically presents with **flank pain** and **hematuria**, and the urine sediment would show ghost cells or fragments of necrotic papillae, not specifically brownish granular casts.
*Disruption of glomerular podocytes*
- **Podocyte disruption** is seen in primary glomerular diseases like minimal change disease or focal segmental glomerulosclerosis.
- These conditions primarily cause **nephrotic syndrome** (heavy proteinuria, edema), which is not the main presentation here.
Irreversible cell injury (necrosis) US Medical PG Question 7: A 34-year-old woman comes to the physician a week after noticing a lump in her left breast. Three months ago, she was discharged from the hospital after treatment of multiple injuries sustained in a motor vehicle collision. Her only medication is an oral contraceptive. Her mother died of ovarian cancer. Examination shows a 2.5-cm, nontender mass in the upper outer quadrant of the left breast. Mammography shows a circumscribed radiolucent lesion with a rim of peripheral calcification. A photomicrograph of tissue from a biopsy of the mass is shown. Which of the following is the most likely cause of the breast swelling?
- A. Defect in DNA repair
- B. Obstruction of lactiferous ducts
- C. Stimulation of estrogen receptors
- D. Thrombophlebitis of subcutaneous veins
- E. Release of cytoplasmic triglycerides (Correct Answer)
Irreversible cell injury (necrosis) Explanation: ***Release of cytoplasmic triglycerides***
- This patient's history of **trauma** followed by a new breast lump and mammographic findings of a **circumscribed radiolucent lesion with peripheral calcification** are classic for **fat necrosis**. The image shows necrotic fat cells, inflammatory infiltrates, and foamy macrophages, consistent with fat necrosis.
- Fat necrosis occurs when **adipocytes** are damaged, causing the release of **triglycerides** and free fatty acids. These then incite an inflammatory response, followed by calcification and fibrosis.
*Defect in DNA repair*
- A defect in DNA repair is associated with an increased risk of **malignancy**, such as breast cancer, especially given the family history of ovarian cancer (BRCA gene mutations). However, the histologic image and the description of a **radiolucent lesion with rim calcification** are not characteristic of malignancy.
- While the family history is relevant for cancer risk, the clinical and histological findings point away from a primary malignancy and towards a benign reactive process.
*Obstruction of lactiferous ducts*
- Obstruction of lactiferous ducts typically leads to conditions like **mastitis**, **duct ectasia**, or **galactocele**. These would present with different radiographic features, often with inflammation or fluid-filled cysts, and different histological patterns.
- The image does not show features of ductal obstruction, such as dilated ducts, inspissated secretions, or periductal inflammation characteristic of duct ectasia.
*Stimulation of estrogen receptors*
- Stimulation of estrogen receptors is relevant in conditions like **fibroadenoma**, **fibrocystic changes**, or certain types of **breast cancer**. While the patient is on oral contraceptives (estrogenic), the clinical picture and biopsy findings are not consistent with these estrogen-mediated conditions.
- Fibroadenomas often appear as well-defined masses on mammography but histologically consist of glandular and stromal proliferation, which is not seen here. Fibrocystic changes involve cysts and fibrosis.
*Thrombophlebitis of subcutaneous veins*
- Thrombophlebitis of subcutaneous veins, also known as **Mondor's disease**, presents as a palpable cord-like structure with pain and tenderness localized along the affected vein. It typically resolves spontaneously.
- This condition is unlikely given the description of a **2.5-cm, nontender mass** and the specific histological findings of necrotic fat and inflammation, which are not characteristic of venous thrombosis.
Irreversible cell injury (necrosis) US Medical PG Question 8: A 62-year-old man presents to the emergency room with an acute myocardial infarction. Twenty-four hours after admission to the cardiac intensive care unit, he develops oliguria. Laboratory tests show that his serum BUN is 59 mg/dL and his serum creatinine is 6.2 mg/dL. Renal biopsy reveals necrosis of the proximal tubules and thick ascending limb of Henle's loop. Which of the following would you most likely observe on a microscopic examination of this patient's urine?
- A. White blood cell casts
- B. Broad waxy casts
- C. Fatty casts
- D. Hyaline casts
- E. Muddy brown casts (Correct Answer)
Irreversible cell injury (necrosis) Explanation: ***Muddy brown casts***
- The patient's presentation of **acute myocardial infarction** followed by **oliguria**, elevated **BUN** and **creatinine**, and necrosis of the **proximal tubules** and **thick ascending limb** of Henle's loop is characteristic of **acute tubular necrosis (ATN)**.
- **Muddy brown casts** composed of **granular material** and **renal tubular epithelial cells** are the classic finding in the urine sediment of patients with ATN.
*White blood cell casts*
- **White blood cell casts** are typically associated with **pyelonephritis** or **interstitial nephritis**, indicating renal inflammation or infection.
- While infection can exacerbate kidney injury, the primary pathology described here is **ischemic ATN**, not an infectious process.
*Broad waxy casts*
- **Broad waxy casts** indicate severe, **chronic kidney disease** with significant **tubular dilation** and **stasis**, often end-stage renal disease.
- The patient's clinical picture depicts **acute kidney injury**, not chronic kidney failure.
*Fatty casts*
- **Fatty casts** are characteristic of **nephrotic syndrome**, which involves significant proteinuria and hyperlipidemia.
- This patient's presentation does not describe the features of **nephrotic syndrome**, such as **massive proteinuria** or **edema**.
*Hyaline casts*
- **Hyaline casts** are composed of **Tamm-Horsfall protein** and can be found in healthy individuals, especially after exercise or dehydration.
- While they can be present in various kidney conditions, they are **non-specific** and not indicative of the specific **tubular epithelial cell injury** seen in ATN.
Irreversible cell injury (necrosis) US Medical PG Question 9: A 46-year-old Caucasian female presents with cold intolerance, weight gain, and constipation. She has also noticed that her nails have become thinner recently but denies any fever or neck pain. Which of the following is NOT an expected histological finding in the thyroid?
- A. Hurthle cells
- B. Lymphocytic infiltration
- C. Multinucleate giant cells (Correct Answer)
- D. Several germinal centers
- E. Fibrosis
Irreversible cell injury (necrosis) Explanation: ***Multinucleate giant cells***
- The patient's symptoms (cold intolerance, weight gain, constipation, thin nails) are highly suggestive of **hypothyroidism**, most commonly caused by **Hashimoto's thyroiditis**.
- **Multinucleate giant cells** are typically associated with **subacute granulomatous (de Quervain's) thyroiditis**, which presents with painful thyroid enlargement and a biphasic course (transient hyperthyroidism followed by hypothyroidism).
*Hurthle cells*
- These are **eosinophilic, granular follicular cells** that represent metaplastic changes within the thyroid.
- They are a common histological finding in **Hashimoto's thyroiditis**, often seen alongside chronic inflammation.
*Lymphocytic infiltration*
- This is a hallmark feature of **Hashimoto's thyroiditis**, characterized by extensive infiltration of the thyroid parenchyma by **lymphocytes**, plasma cells, and macrophages.
- The immune response targets thyroid peroxidases and thyroglobulin, leading to gradual destruction of thyroid follicles.
*Several germinal centers*
- The presence of **germinal centers** within the thyroid is a characteristic histopathological feature of **Hashimoto's thyroiditis**.
- These centers indicate active B-cell proliferation and are part of the autoimmune process in the gland.
*Fibrosis*
- Over time, chronic inflammation in **Hashimoto's thyroiditis** often leads to **fibrosis** within the thyroid gland.
- Extensive fibrosis can result in a firm, enlarged thyroid and contribute to impaired thyroid function.
Irreversible cell injury (necrosis) US Medical PG Question 10: During an experiment, an investigator attempts to determine the rates of apoptosis in various tissue samples. Injecting cytotoxic T cells into the cell culture of one of the samples causes the tissue cells to undergo apoptosis. Apoptosis is most likely due to secretion of which of the following substances in this case?
- A. Cytochrome C
- B. TNF-α
- C. Granzyme B (Correct Answer)
- D. Caspases
- E. Bcl-2
Irreversible cell injury (necrosis) Explanation: ***Granzyme B***
- **Granzyme B** is a serine protease released by **cytotoxic T cells** and **natural killer cells** that directly initiates apoptosis by cleaving and activating caspases within the target cell.
- Upon entry into the target cell, granzyme B activates executioner caspases, such as caspase-3 and caspase-7, leading to the **proteolytic cascade** that dismantles the cell.
*Cytochrome C*
- **Cytochrome c** is a mitochondrial protein that, when released into the cytoplasm, can trigger the **intrinsic pathway of apoptosis** by forming the apoptosome.
- While it's crucial for the intrinsic pathway, cytotoxic T cells primarily induce the **extrinsic pathway** of apoptosis.
*TNF-α*
- **TNF-α (Tumor Necrosis Factor-alpha)** is a cytokine that can induce apoptosis by binding to its receptor (TNFR1), activating adaptor proteins like TRADD and FADD, and subsequently initiating the extrinsic apoptotic pathway.
- However, while TNF-α can induce apoptosis, the scenario specifically mentions **cytotoxic T cells** as the cause, whose primary mechanism involves granzymes and perforin rather than TNF-α secretion.
*Caspases*
- **Caspases** are a family of cysteine proteases that are central to the apoptotic process, acting as both initiator and executioner enzymes.
- They are the *effectors* of apoptosis but are not the direct substances *secreted by cytotoxic T cells* to initiate the process in the target cell.
*Bcl-2*
- **Bcl-2** is an anti-apoptotic protein that inhibits the release of cytochrome c from mitochondria, thereby preventing the activation of the intrinsic pathway of apoptosis.
- It is a regulator *within the target cell* that prevents apoptosis, not a substance secreted by cytotoxic T cells to *induce* it.
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