Cerebrovascular diseases US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Cerebrovascular diseases. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Cerebrovascular diseases US Medical PG Question 1: A 48-year-old man presents to the ER with a sudden-onset, severe headache. He is vomiting and appears confused. His wife, who accompanied him, says that he has not had any trauma, and that the patient has no relevant family history. He undergoes a non-contrast head CT that shows blood between the arachnoid and pia mater. What is the most likely complication from this condition?
- A. Hemorrhagic shock
- B. Arterial Vasospasm (Correct Answer)
- C. Renal failure
- D. Bacterial Meningitis
- E. Blindness
Cerebrovascular diseases Explanation: **Arterial Vasospasm**
- **Arterial vasospasm** is a major delayed complication of **subarachnoid hemorrhage (SAH)**, typically occurring 3-14 days after the initial bleed.
- The presence of blood products in the subarachnoid space can irritate cerebral arteries, leading to their narrowing and subsequent **delayed cerebral ischemia** or infarction.
*Hemorrhagic shock*
- **Subarachnoid hemorrhage (SAH)** typically involves bleeding within the confines of the skull, which is usually not extensive enough to cause systemic **hypovolemia** or **hemorrhagic shock**.
- **Hemorrhagic shock** would require significant external blood loss or internal bleeding into a large body cavity, which is not characteristic of an isolated SAH.
*Renal failure*
- **Renal failure** is not a direct or common complication of **subarachnoid hemorrhage (SAH)**.
- While systemic complications can sometimes arise in critically ill patients, there is no direct pathophysiological link between SAH and primary kidney injury.
*Bacterial Meningitis*
- The presence of blood in the **subarachnoid space** can cause a **chemical meningitis** due to irritation, mimicking some symptoms of bacterial meningitis.
- However, it does not typically predispose to **bacterial infection** unless there's an iatrogenic cause (e.g., lumbar puncture contamination).
*Blindness*
- While damage to the **optic nerves** or visual pathways can occur with severe neurological events or increased intracranial pressure, **blindness** is not a common or direct complication specifically arising from the bleed itself or its immediate sequelae in SAH.
- Visual disturbances are possible due to elevated **intracranial pressure** or specific anatomical lesion, but not primary blindness.
Cerebrovascular diseases US Medical PG Question 2: A 61-year-old man is brought to the emergency room with slurred speech. According to the patient's wife, they were watching a movie together when he developed a minor headache. He soon developed difficulty speaking in complete sentences, at which point she decided to take him to the emergency room. His past medical history is notable for hypertension and hyperlipidemia. He takes aspirin, lisinopril, rosuvastatin. The patient is a retired lawyer. He has a 25-pack-year smoking history and drinks 4-5 beers per day. His father died of a myocardial infarction, and his mother died of breast cancer. His temperature is 98.6°F (37°C), blood pressure is 143/81 mmHg, pulse is 88/min, and respirations are 21/min. On exam, he can understand everything that is being said to him and is able to repeat statements without difficulty. However, when asked to speak freely, he hesitates with every word and takes 30 seconds to finish a short sentence. This patient most likely has an infarct in which of the following vascular distributions?
- A. Proximal middle cerebral artery
- B. Inferior division of the middle cerebral artery
- C. Middle cerebral artery and posterior cerebral artery watershed area
- D. Superior division of the middle cerebral artery (Correct Answer)
- E. Anterior cerebral artery and middle cerebral artery watershed area
Cerebrovascular diseases Explanation: ***Superior division of the middle cerebral artery***
- The patient's inability to speak spontaneously coupled with intact comprehension and repetition is characteristic of **Broca's aphasia**, which results from damage to **Broca's area** in the dominant frontal lobe.
- Broca's area is supplied by the **superior division of the middle cerebral artery (MCA)**.
*Proximal middle cerebral artery*
- An infarct in the proximal MCA, or the main stem, would typically lead to global aphasia if the dominant hemisphere is affected, characterized by **severe deficits in comprehension, repetition, and speech production**.
- This presentation does not align with the patient's ability to understand and repeat statements.
*Inferior division of the middle cerebral artery*
- The inferior division of the MCA supplies Wernicke's area in the dominant hemisphere.
- Damage here causes **Wernicke's aphasia**, characterized by **fluent but nonsensical speech** with **impaired comprehension** and **repetition**, which is contrary to the patient's symptoms.
*Middle cerebral artery and posterior cerebral artery watershed area*
- Watershed infarcts, especially between the MCA and posterior cerebral artery (PCA), can cause **transcortical sensory aphasia** if in the dominant hemisphere.
- This type of aphasia involves impaired comprehension but **intact repetition**, which differs from Broca's aphasia where spontaneous speech is the main deficit.
*Anterior cerebral artery and middle cerebral artery watershed area*
- Infarcts in the watershed area between the anterior cerebral artery (ACA) and MCA can result in **transcortical motor aphasia** if in the dominant hemisphere.
- This condition presents with **non-fluent speech** and **intact repetition**, similar to Broca's aphasia, but Broca's area itself is located specifically within the MCA superior division territory.
Cerebrovascular diseases US Medical PG Question 3: A 76-year-old woman with hypertension and coronary artery disease is brought to the emergency department after the sudden onset of right-sided weakness. Her pulse is 83/min and blood pressure is 156/90 mm Hg. Neurological examination shows right-sided facial drooping and complete paralysis of the right upper and lower extremities. Tongue position is normal and she is able to swallow liquids without difficulty. Knee and ankle deep tendon reflexes are exaggerated on the right. Sensation to vibration, position, and light touch is normal bilaterally. She is oriented to person, place, and time, and is able to speak normally. Occlusion of which of the following vessels is the most likely cause of this patient's current symptoms?
- A. Ipsilateral anterior cerebral artery
- B. Contralateral middle cerebral artery
- C. Anterior spinal artery
- D. Contralateral lenticulostriate artery (Correct Answer)
- E. Ipsilateral posterior inferior cerebellar artery
Cerebrovascular diseases Explanation: ***Contralateral lenticulostriate artery***
- The patient presents with **pure motor hemiparesis** affecting the face, arm, and leg equally on the right side, with **no sensory deficits, aphasia, or cognitive impairment**.
- This clinical pattern is classic for a **lacunar stroke** affecting the **internal capsule**, which is supplied by the **lenticulostriate arteries** (branches of the middle cerebral artery).
- The internal capsule contains tightly packed corticospinal and corticobulbar fibers; a small infarct here causes complete contralateral motor deficits without cortical signs.
- The **absence of cortical findings** (normal speech, cognition, and sensation) distinguishes this from cortical MCA stroke.
*Contralateral middle cerebral artery*
- A **cortical MCA stroke** would typically present with **cortical signs** such as aphasia (if left hemisphere), neglect (if right hemisphere), sensory loss, and visual field defects.
- MCA strokes usually show **arm and face > leg** weakness (the leg area is supplied by ACA).
- This patient's **pure motor syndrome** without cortical signs points to a subcortical lesion, not cortical MCA occlusion.
*Ipsilateral anterior cerebral artery*
- First, the lateralization is incorrect - symptoms are right-sided, indicating left hemisphere pathology, so it would be **contralateral** ACA.
- ACA occlusion causes weakness predominantly in the **contralateral leg > arm**, with relative sparing of the face.
- This patient has equal involvement of face, arm, and leg, which is inconsistent with ACA territory.
*Anterior spinal artery*
- The **anterior spinal artery** supplies the anterior two-thirds of the spinal cord, including the corticospinal tracts and anterior horn cells.
- Occlusion causes **bilateral** motor weakness below the lesion level and bilateral loss of pain/temperature sensation.
- It does not cause **unilateral facial weakness** or the distribution of deficits seen in this patient.
*Ipsilateral posterior inferior cerebellar artery*
- Again, lateralization is incorrect - symptoms would be from **contralateral** PICA for motor findings, but PICA supplies the lateral medulla and inferior cerebellum.
- PICA occlusion causes **lateral medullary syndrome (Wallenberg syndrome)**: ataxia, vertigo, dysphagia, dysarthria, Horner syndrome, and contralateral pain/temperature loss.
- The patient's **pure motor hemiparesis** without cerebellar or brainstem signs is incompatible with PICA occlusion.
Cerebrovascular diseases US Medical PG Question 4: A 67-year old woman is brought to the emergency department after she lost consciousness while at home. Her daughter was with her at the time and recalls that her mother was complaining of a diffuse headache and nausea about 2 hours before the incident. The daughter says that her mother has not had any recent falls and was found sitting in a chair when she lost consciousness. She has hypertension. Current medications include amlodipine, a daily multivitamin, and acetaminophen. She has smoked 1/2 pack of cigarettes daily for the past 45 years. Her pulse is 92/min, respirations are 10/min, and blood pressure is 158/100 mm Hg. She is disoriented and unable to follow commands. Examination shows nuchal rigidity. She has flexor posturing to painful stimuli. Fundoscopic examination is notable for bilateral vitreous hemorrhages. Laboratory studies are within normal limits. An emergent non-contrast CT scan of the head is obtained and shows a diffuse hemorrhage at the base of the brain that is largest over the left hemisphere. Which of the following is the most likely cause of this patient's symptoms?
- A. Intracranial arterial dissection
- B. Ruptured saccular aneurysm (Correct Answer)
- C. Ruptured mycotic aneurysm
- D. Spinal arteriovenous malformation
- E. Intracranial arteriovenous malformation
Cerebrovascular diseases Explanation: ***Ruptured saccular aneurysm***
- The sudden onset of a "thunderclap" headache, **nuchal rigidity**, diffuse hemorrhage at the base of the brain, and **vitreous hemorrhages (Terson syndrome)** are all highly suggestive of a **subarachnoid hemorrhage (SAH)**, most commonly caused by a ruptured saccular aneurysm. Her history of **hypertension and smoking** are significant risk factors for aneurysm formation and rupture.
- The disorientation and flexor posturing indicate severe neurological compromise due to increased **intracranial pressure** and brainstem involvement, consistent with a large SAH.
*Intracranial arterial dissection*
- While an intracranial arterial dissection can cause hemorrhage, it typically presents with neck pain, lower cranial nerve palsies, or ischemic stroke symptoms due to **thromboembolism**, which are not prominent features here.
- The **diffuse hemorrhage at the base of the brain** and bilateral vitreous hemorrhages are more characteristic of a ruptured aneurysm than a dissection.
*Ruptured mycotic aneurysm*
- A mycotic aneurysm results from an **infectious embolus** lodging in an artery, leading to vessel wall weakening and rupture. This would typically be seen in the context of **endocarditis** or other systemic infections, for which there is no evidence in this patient.
- The patient's presentation lacks systemic signs of infection (e.g., fever, new heart murmur, or elevated inflammatory markers) that would point to an infectious etiology.
*Spinal arteriovenous malformation*
- A spinal arteriovenous malformation (AVM) would present with **spinal cord symptoms** such as back pain, weakness, sensory deficits, or bladder/bowel dysfunction, not primarily with a diffuse intracranial hemorrhage or severe headache.
- While it could theoretically cause a hemorrhage, the clinical presentation and CT findings are unequivocally localized to the **brain**, making a spinal origin unlikely.
*Intracranial arteriovenous malformation*
- An intracranial AVM can cause **intracerebral hemorrhage** or, less commonly, subarachnoid hemorrhage, but the hemorrhages tend to be more localized within the brain parenchyma or along the AVM itself.
- Though an AVM could be a differential, the classic presentation including **thunderclap headache**, Terson syndrome, and diffuse basilar hemorrhage is a more classic presentation of a **ruptured saccular aneurysm**.
Cerebrovascular diseases US Medical PG Question 5: A 47-year-old man presents as a new patient at an outpatient clinic. He has never seen a physician before, but was motivated by his 40-year-old brother's recent heart attack and seeks to optimize his health. In particular, he read that uncontrolled atherosclerosis can lead to a heart attack. Which molecule is downregulated in response to the advent of atherosclerosis?
- A. Tumor necrosis factor
- B. Serotonin
- C. Nitric oxide (Correct Answer)
- D. Interleukin 1
- E. Thromboxane A2
Cerebrovascular diseases Explanation: ***Nitric oxide***
- **Nitric oxide (NO)** is a potent **vasodilator** and **anti-inflammatory** molecule produced by endothelial cells. In atherosclerosis, endothelial dysfunction leads to reduced NO bioavailability.
- Decreased NO production contributes to vasoconstriction, increased platelet aggregation, and enhanced smooth muscle cell proliferation, all of which promote **atherosclerotic plaque formation** and progression.
*Tumor necrosis factor*
- **Tumor necrosis factor-alpha (TNF-α)** is a **pro-inflammatory cytokine** that plays a significant role in the pathogenesis of atherosclerosis.
- It is **upregulated** in response to atherosclerotic plaque formation, contributing to endothelial activation, leukocyte recruitment, and smooth muscle cell proliferation.
*Serotonin*
- **Serotonin (5-hydroxytryptamine)** is primarily known for its role as a neurotransmitter but also acts as a **vasoconstrictor** and promotes platelet aggregation.
- While it can be released from activated platelets in the context of vascular injury, it is not consistently **downregulated** in atherosclerosis; rather, its effects can contribute to disease progression.
*Interleukin 1*
- **Interleukin-1 (IL-1)**, particularly IL-1β, is a major **pro-inflammatory cytokine** critically involved in the immune response in atherosclerosis.
- It is **upregulated** in atherosclerotic plaques, contributing to systemic inflammation, endothelial dysfunction, and vascular smooth muscle cell activation.
*Thromboxane A2*
- **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and **platelet aggregator** produced by activated platelets.
- Its levels are **increased** in atherosclerosis, contributing to hypercoagulability and increased risk of thrombotic events like myocardial infarction.
Cerebrovascular diseases US Medical PG Question 6: A 72-year-old man comes to the physician because of a 6-month history of intermittent dull abdominal pain that radiates to the back. He has smoked one pack of cigarettes daily for 50 years. His blood pressure is 145/80 mm Hg. Abdominal examination shows generalized tenderness and a pulsatile mass in the periumbilical region on deep palpation. Further evaluation of the affected blood vessel is most likely to show which of the following?
- A. Obliterative inflammation of the vasa vasorum
- B. Formation of giant cells in the tunica media
- C. Necrotizing inflammation of the entire vessel wall
- D. Fragmentation of elastic tissue in the tunica media (Correct Answer)
- E. Accumulation of foam cells in the tunica intima
Cerebrovascular diseases Explanation: ***Fragmentation of elastic tissue in the tunica media***
- This patient's presentation with **intermittent dull abdominal pain radiating to the back**, a **pulsatile periumbilical mass**, and a history of **heavy smoking** is highly suggestive of an **abdominal aortic aneurysm (AAA)**.
- The pathological hallmark of AAA is **degradation and fragmentation of elastic tissue in the tunica media**, caused by chronic inflammation and increased activity of **matrix metalloproteinases (MMPs)**.
- This medial degeneration leads to **weakening of the vessel wall** and progressive **dilation**, ultimately forming an aneurysm.
- While atherosclerosis initiates the process, the actual aneurysm formation is characterized by this elastic tissue destruction in the media.
*Accumulation of foam cells in the tunica intima*
- This describes the **early lesion of atherosclerosis**, which is a **risk factor** for AAA development.
- However, when examining an **established AAA**, the predominant finding is not intimal foam cells but rather **medial degeneration** with elastic tissue fragmentation.
- Atherosclerosis is the underlying cause, but the question asks about findings in the affected vessel (the aneurysm itself).
*Obliterative inflammation of the vasa vasorum*
- This is characteristic of **syphilitic aortitis** (tertiary syphilis), which typically affects the **ascending thoracic aorta**.
- While syphilis can cause aneurysms, the patient's presentation and demographics are more consistent with atherosclerotic AAA.
*Formation of giant cells in the tunica media*
- This finding is associated with **giant cell arteritis** (temporal arteritis), which affects large and medium-sized arteries, particularly the temporal and ophthalmic arteries.
- It presents with headache, jaw claudication, and visual disturbances—features absent in this case.
*Necrotizing inflammation of the entire vessel wall*
- This describes **necrotizing vasculitis** such as **polyarteritis nodosa**, which affects medium-sized muscular arteries.
- While vasculitis can cause aneurysms, the clinical picture of AAA in an elderly smoker with atherosclerotic risk factors points to atherosclerotic pathogenesis, not primary vasculitis.
Cerebrovascular diseases US Medical PG Question 7: A 42-year-old man with systolic heart failure secondary to amyloidosis undergoes heart transplantation. The donor heart is obtained from a 17-year-old boy who died in a motor vehicle collision. Examination of the donor heart during the procedure shows a flat, yellow-white discoloration with an irregular border on the luminal surface of the aorta. A biopsy of this lesion is most likely to show which of the following?
- A. Apoptotic smooth muscle cells
- B. Necrotic cell debris
- C. Proteoglycan accumulation
- D. Collagen deposition
- E. Lipoprotein-laden macrophages (Correct Answer)
Cerebrovascular diseases Explanation: ***Lipoprotein-laden macrophages***
- The description of a flat, yellow-white discolored lesion with an irregular border on the luminal surface of the aorta in a 17-year-old is classic for a **fatty streak**, the earliest lesion of **atherosclerosis**.
- Fatty streaks are histologically characterized by the accumulation of **macrophages that have ingested oxidized lipoproteins**, appearing as foam cells within the intima.
*Apoptotic smooth muscle cells*
- While apoptosis of various cell types, including smooth muscle cells, can occur in advanced atherosclerotic lesions, it is not the primary or defining feature of an early **fatty streak**.
- **Apoptosis** contributes to the necrotic core formation in later stages of plaque development, not the initial yellow-white discoloration of a fatty streak.
*Necrotic cell debris*
- **Necrotic cell debris** is a prominent feature of more advanced, **complicated atherosclerotic plaques**, forming the necrotic core.
- In a **fatty streak**, the cells are primarily viable foam cells, and significant necrosis is not yet present.
*Proteoglycan accumulation*
- **Proteoglycan accumulation** occurs in the arterial intima and is involved in the retention of lipoproteins, contributing to the development of atherosclerosis.
- However, the immediate and most characteristic histological finding of the **yellow-white discoloration** in a fatty streak is the lipid-laden macrophage.
*Collagen deposition*
- **Collagen deposition** is a key feature of the fibrous cap in **advanced atherosclerotic plaques**, laid down by migrating smooth muscle cells.
- It is not the primary histological characteristic of an early, flat, yellow-white **fatty streak**.
Cerebrovascular diseases US Medical PG Question 8: A 53-year-old woman presents to her physician for evaluation of sudden onset respiratory distress for the past few hours. The past medical history includes a myocardial infarction 2 years ago. The vital signs include a blood pressure 70/40 mm Hg, pulse 92/min, respiratory rate 28/min, and SpO2 92% on room air. The physical examination reveals bilateral basal crepitations on auscultation. The echocardiogram reveals an ejection fraction of 34%. She is admitted to the medical floor and started on furosemide. The urine output in 24 hours is 400 mL. The blood urea nitrogen is 45 mg/dL and the serum creatinine is 1.85 mg/dL. The fractional excretion of sodium is 2.4%. Urinalysis revealed muddy brown granular casts. Which of the following is the most likely cause of the abnormal urinalysis?
- A. Acute interstitial nephritis
- B. Acute tubular necrosis (Correct Answer)
- C. Acute pyelonephritis
- D. Chronic kidney disease
- E. Acute glomerulonephritis
Cerebrovascular diseases Explanation: ***Acute tubular necrosis***
- The presence of **muddy brown granular casts** on urinalysis is pathognomonic for **acute tubular necrosis (ATN)**, indicating damage to the renal tubules.
- The patient's history of **cardiogenic shock** (low BP 70/40 mm Hg, respiratory distress, low SpO2, low ejection fraction of 34%) led to **renal hypoperfusion** and ischemic tubular injury.
- The **fractional excretion of sodium (FENa) of 2.4%** (>2%) is characteristic of **intrinsic renal injury** (ATN), as damaged tubules cannot effectively reabsorb sodium.
- **Oliguria** (400 mL/24 hours), elevated **BUN (45 mg/dL)** and **creatinine (1.85 mg/dL)** further support acute kidney injury from ATN.
*Acute interstitial nephritis*
- This condition is typically associated with **drug hypersensitivity** (e.g., NSAIDs, antibiotics, PPIs) or **infections** and is characterized by inflammatory infiltrate in the renal interstitium.
- Urinalysis typically shows **white blood cell casts** and **eosinophiluria**, not muddy brown granular casts.
*Acute pyelonephritis*
- This is an **infection of the kidney** parenchyma, usually caused by bacterial ascension from the urinary tract.
- Symptoms often include **fever, flank pain, dysuria**, and urinalysis reveals **leukocyturia** (white blood cells) and **bacterial casts**, not muddy brown granular casts.
*Chronic kidney disease*
- While the patient has elevated creatinine and BUN, **chronic kidney disease (CKD)** develops over months to years and is characterized by persistent kidney damage or decreased function.
- Urinalysis in CKD often shows **broad waxy casts** and typically does not present with such **acute, sudden onset** of severe renal dysfunction with muddy brown granular casts.
*Acute glomerulonephritis*
- This condition involves inflammation of the glomeruli and typically presents with **hematuria, proteinuria, and red blood cell casts** (dysmorphic RBCs).
- The patient's clinical picture, including the absence of significant hematuria and the presence of **muddy brown granular casts**, does not fit acute glomerulonephritis.
Cerebrovascular diseases US Medical PG Question 9: A 73-year-old man with coronary artery disease and hypertension is brought to the emergency department by ambulance 90 minutes after the acute onset of substernal chest pain and dyspnea. He has smoked 2 packs of cigarettes daily for 52 years. Shortly after arriving at the hospital, he loses consciousness and is pulseless. Despite attempts at cardiopulmonary resuscitation, he dies. Examination of the heart at autopsy shows complete occlusion of the left anterior descending artery with a red thrombus overlying a necrotic plaque. Which of the following pathophysiologic mechanisms is most likely responsible for this patient's acute coronary condition?
- A. Influx of lipids into the endothelium
- B. Secretion of matrix metalloproteinases (Correct Answer)
- C. Release of platelet-derived growth factor
- D. Type III collagen deposition
- E. Proliferation of smooth muscle cells
Cerebrovascular diseases Explanation: ***Secretion of matrix metalloproteinases***
- **Matrix metalloproteinases (MMPs)** degrade the **extracellular matrix** within the fibrous cap of an atherosclerotic plaque, leading to its **destabilization and rupture**.
- Plaque rupture then exposes the highly thrombogenic lipid core, initiating thrombus formation and acute coronary events like the **red thrombus** seen in the **left anterior descending artery (LAD)**.
*Influx of lipids into the endothelium*
- This process is characteristic of the **initial stages of atherosclerosis**, leading to **fatty streak formation**, not the acute plaque rupture and thrombosis described.
- While essential for plaque development, lipid influx alone does not directly explain aggressive plaque rupture and acute thrombus formation.
*Release of platelet-derived growth factor*
- **Platelet-derived growth factor (PDGF)** is primarily involved in **smooth muscle cell proliferation** and migration, contributing to plaque growth and thickening.
- Its role is more chronic and proliferative, not immediate plaque destabilization and rupture leading to acute thrombosis.
*Type III collagen deposition*
- **Type III collagen** is characteristic of early, developing atherosclerotic plaques and granulation tissue, contributing to plaque stability.
- Plaque vulnerability associated with rupture involves a **thin fibrous cap** with reduced **collagen content**, often due to increased collagen degradation.
*Proliferation of smooth muscle cells*
- **Smooth muscle cell proliferation** occurs during chronic atherosclerosis, contributing to the **fibrous cap formation** and overall plaque stability.
- In the context of acute plaque rupture, it is the *erosion* of the fibrous cap, often due to degradation, rather than proliferation, that is the immediate cause.
Cerebrovascular diseases US Medical PG Question 10: A 35-year-old woman presents with headaches and seizures. MRI shows a well-circumscribed, calcified frontal lobe mass. Histology reveals oligodendroglioma with 1p/19q codeletion and IDH1 mutation. She undergoes gross total resection. Two years later, surveillance MRI shows a new enhancing nodule at the resection margin. Biopsy shows increased mitotic activity, microvascular proliferation, and retained 1p/19q codeletion but new CDKN2A/B homozygous deletion. What is the most critical factor in determining management strategy?
- A. The tumor has progressed to anaplastic oligodendroglioma requiring combined chemoradiation with temozolomide and RT
- B. CDKN2A/B deletion indicates transformation to glioblastoma requiring maximal therapy
- C. Retained 1p/19q codeletion predicts continued chemosensitivity to PCV regimen (Correct Answer)
- D. Loss of IDH1 mutation suggests new primary tumor requiring re-resection only
- E. Microvascular proliferation mandates anti-angiogenic therapy with bevacizumab
Cerebrovascular diseases Explanation: ***Retained 1p/19q codeletion predicts continued chemosensitivity to PCV regimen***
- The preservation of **1p/19q codeletion** in a recurrent tumor is the strongest predictor of clinical response to alkylating chemotherapy, specifically the **PCV (Procarbazine, Lomustine, Vincristine)** regimen.
- While the tumor shows histological progression, the underlying molecular subtype remains an **oligodendroglioma**, which generally carries a better prognosis and higher chemosensitivity than non-codeleted gliomas.
*The tumor has progressed to anaplastic oligodendroglioma requiring combined chemoradiation with temozolomide and RT*
- While the histology suggests a higher grade, the standard of care for 1p/19q codeleted tumors frequently favors **PCV** over **Temozolomide** due to more robust long-term survival data from clinical trials like RTOG 9402.
- Grading alone does not dictate management as much as the **molecular profile** does in modern neuro-oncology guidelines.
*CDKN2A/B deletion indicates transformation to glioblastoma requiring maximal therapy*
- Under the current WHO classification, **glioblastoma** is defined as an **IDH-wildtype** tumor; since this tumor has an **IDH1 mutation**, it cannot be classified as a glioblastoma.
- **CDKN2A/B homozygous deletion** is a marker of high-grade malignancy (WHO Grade 4) in IDH-mutant astrocytomas, but its presence in an **oligodendroglioma** does not change the lineage-defining 1p/19q status.
*Loss of IDH1 mutation suggests new primary tumor requiring re-resection only*
- **IDH1 mutations** are early, trunk events in gliomagenesis and are almost never
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