Cellular Pathology of the Nervous System — MCQs

10 questions

A 21-year-old woman incurs a blow to her head from a fall while mountain biking. She then has loss of consciousness for 5 minutes. On examination her deep tendon reflexes are diminished. A head CT scan 6 hours later shows no abnormalities. She recovers over the next week, with no neurologic deficits, but cannot remember this event. During the next year she has irritability, headache, difficulty sleeping, trouble concentrating, and fatigue. Which of the following is the most likely consequence from her injury?

What are Gitter cells?

Which of the following statements about peripheral nerve injury is false?

What is the appropriate fluid management in the case of an intracerebral hemorrhage?

Two or more oligoclonal bands in cerebrospinal fluid are most often positive in-

What is not a feature of raised ICP

Neurological complications of meningitis include all of the following except:

Irreversible cell injury is indicated by

Histopathological feature of HIV encephalitis is/are-

Q10

What is the primary pathological mechanism in classical Guillain-Barré syndrome affecting the peripheral nervous system?

Cellular Pathology of the Nervous System Indian Medical PG Practice Questions and MCQs

Question 1: A 21-year-old woman incurs a blow to her head from a fall while mountain biking. She then has loss of consciousness for 5 minutes. On examination her deep tendon reflexes are diminished. A head CT scan 6 hours later shows no abnormalities. She recovers over the next week, with no neurologic deficits, but cannot remember this event. During the next year she has irritability, headache, difficulty sleeping, trouble concentrating, and fatigue. Which of the following is the most likely consequence from her injury?

A. Hydrocephalus
B. Concussion (Correct Answer)
C. Leukoencephalopathy
D. Arteriolosclerosis

Explanation: ***Concussion*** - The patient's presentation with **loss of consciousness** after a head injury [2], followed by persistent symptoms like **irritability, headache, difficulty sleeping, trouble concentrating, and fatigue** over the next year, is highly characteristic of **post-concussive syndrome**. - A normal head CT scan is common in concussion, as it primarily involves **functional brain disturbances** rather than structural damage visible on imaging [1]. *Hydrocephalus* - **Hydrocephalus** typically presents with symptoms such as headache, nausea, vision changes, and gait disturbances due to **increased intracranial pressure**. - It usually involves **ventricular enlargement** visible on imaging, which was not seen in this case. *Leukoencephalopathy* - **Leukoencephalopathy** refers to diffuse disease of the **white matter** of the brain, often associated with demyelination or vascular issues. - It would likely present with more profound and progressive neurological deficits, and usually has specific findings on **MRI**. *Arteriolosclerosis* - **Arteriolosclerosis** is a disease of small cerebral arteries, often seen in older individuals with **hypertension** or **diabetes**, and rarely seen in a 21-year-old. - It typically causes symptoms related to reduced blood flow, such as **stroke** or **vascular dementia**, which do not fit this clinical picture.

Question 2: What are Gitter cells?

A. Microglia
B. Modified macrophages in the CNS (Correct Answer)
C. Astrocytic cells
D. Oligodendrocytic cells

Explanation: ***Modified macrophages in CNS*** - Gitter cells are **modified macrophages** that have phagocytized lipid and other debris in the central nervous system (CNS), particularly in response to injury or disease [1][2]. - They play a crucial role in **cleaning up cellular debris** and are involved in the inflammatory response within the CNS [2]. *Macroglia* - Macroglia refers to **supportive cells** in the CNS, including astrocytes and oligodendrocytes, rather than being specifically modified macrophages. - It does not specifically describe the **phagocytic role** characteristic of Gitter cells. *Oligodendrocytes* - Oligodendrocytes primarily function to **myelinate axons** in the CNS and do not possess the same phagocytic capabilities as Gitter cells. - They are involved in **insulation** of neuronal axons rather than debris clearance. *Astrocytes* - Astrocytes are the principal **supportive glial cells** in the CNS and do not exhibit the characteristics of Gitter cells. - Their functions include **maintaining blood-brain barrier**, regulating blood flow, and supporting neuronal metabolism, not phagocytosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.

Question 3: Which of the following statements about peripheral nerve injury is false?

A. Wallerian degeneration starts in axonotmesis
B. Neuropraxia is irreversible (Correct Answer)
C. Neurotmesis is the most severe form of injury
D. Epineurium is intact in axonotmesis

Explanation: This question asks which statement is **FALSE** about peripheral nerve injury. ***Neuropraxia is irreversible*** - This statement is **FALSE** (making it the correct answer to this question). - Neuropraxia represents the **mildest form** of peripheral nerve injury, characterized by local **demyelination** or temporary conduction block without axonal damage [2]. - Recovery from neuropraxia is typically **complete and rapid**, usually within **weeks to months**, as axonal continuity is preserved. - **No Wallerian degeneration** occurs because the axon remains intact. *Epineurium is intact in axonotmesis* - This statement is **TRUE**. In **axonotmesis**, there is disruption of the axon and myelin sheath, but the **connective tissue sheaths** (epineurium, perineurium, and endoneurium) remain intact. - The intact connective tissue provides a guide for **axonal regeneration**, which makes recovery possible, although often incomplete [1]. - Recovery occurs at approximately **1 mm/day** or **1 inch/month**. *Neurotmesis is the most severe form of injury* - This statement is **TRUE**. **Neurotmesis** involves complete severance of the nerve fiber, including the axon, myelin, and **all supporting connective tissue structures** (epineurium, perineurium, and endoneurium). - This type of injury has the **poorest prognosis** for recovery and usually requires **surgical intervention** to attempt repair [1]. *Wallerian degeneration starts in axonotmesis* - This statement is **TRUE**. **Wallerian degeneration** is a process that occurs when a nerve fiber is severed or severely injured, affecting the segment **distal to the injury** [1]. - In **axonotmesis**, the axon is disrupted, leading to degeneration of the distal axonal segment and its myelin sheath, which is characteristic of Wallerian degeneration. - Wallerian degeneration also occurs in **neurotmesis** but NOT in **neuropraxia**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 109-110. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1232.

Question 4: What is the appropriate fluid management in the case of an intracerebral hemorrhage?

A. Normal saline (Correct Answer)
B. Colloids
C. Blood transfusion
D. Hypertonic fluids

Explanation: **Normal saline** - **Normal saline (0.9% NaCl)** is the preferred fluid for volume maintenance in patients with **intracerebral hemorrhage (ICH)** as it is an isotonic crystalloid. - It helps maintain an adequate **cerebral perfusion pressure (CPP)** and avoids hypotonic effects that could worsen cerebral edema. *Colloids* - **Colloids** are generally avoided in ICH as they can potentially **increase intracranial pressure (ICP)** due to their osmotic effects within the damaged blood-brain barrier. - They are also associated with **increased risk of cerebral edema** and poor neurological outcomes in stroke patients. *Blood transfusion* - **Blood transfusions** are indicated only in cases of significant **anemia** (typically hemoglobin < 7-8 g/dL) or active bleeding where oxygen delivery to the brain is compromised. - Routine blood transfusion without clear indication is not part of standard fluid management for ICH and carries risks. *Hypertonic fluids* - **Hypertonic saline (e.g., 3% NaCl)** or **mannitol** are used specifically for the acute management of **elevated intracranial pressure (ICP)**, not for routine fluid maintenance. - While they improve cerebral perfusion by reducing brain edema, their continuous use as maintenance fluid can lead to severe electrolyte imbalances and dehydration.

Question 5: Two or more oligoclonal bands in cerebrospinal fluid are most often positive in-

A. Acute bacterial meningitis
B. Multiple sclerosis (Correct Answer)
C. Subarachnoid hemorrhage
D. Polyneuropathy

Explanation: Multiple sclerosis - The presence of two or more oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) is a hallmark finding in multiple sclerosis (MS), indicating intrathecal immunoglobulin synthesis [1]. - OCBs are found in over 90% of MS patients, reflecting a chronic inflammatory process within the central nervous system [1]. Acute bacterial meningitis - CSF analysis in acute bacterial meningitis typically shows elevated white blood cell count (neutrophils), decreased glucose, and elevated protein, but not characteristic OCBs [2]. - While there may be a generalized immune response, it does not typically produce the specific, persistent OCB pattern seen in MS. Subarachnoid hemorrhage - CSF findings in subarachnoid hemorrhage are characterized by xanthochromia (yellow discoloration due to bilirubin), red blood cells, and elevated protein, but OCBs are not a diagnostic feature [2]. - OCBs are related to intrathecal immunoglobulin production, not the breakdown products of blood. Polyneuropathy - Polyneuropathies, such as Guillain-Barré syndrome, are characterized by albuminocytological dissociation (elevated protein with normal cell count) in CSF, or other findings depending on the specific cause. - While some inflammatory neuropathies can have CSF abnormalities, they do not typically present with the same diagnostic pattern of OCBs as observed in MS.

Question 6: What is not a feature of raised ICP

A. Vomiting
B. Tachycardia (Correct Answer)
C. Blurring of vision
D. Hypertension

Explanation: ***Tachycardia*** - **Bradycardia**, not tachycardia, is a classic component of the **Cushing's triad**, which is a physiological response to increased ICP. - The elevated ICP triggers a reflex arc that causes a decrease in heart rate as the body attempts to maintain cerebral perfusion. *Vomiting* - **Vomiting**, especially projectile and without nausea, is a common symptom of increased ICP due to activation of the **chemoreceptor trigger zone** in the medulla. - The pressure directly stimulates this area, leading to emesis. *Blurring of vision* - **Blurring of vision** is a frequent symptom of raised ICP, often associated with **papilledema** (swelling of the optic disc). - The elevated pressure is transmitted to the optic nerve sheath, impeding venous return and causing nerve swelling. *Hypertension* - **Hypertension** is part of the **Cushing's triad** in response to increased ICP, where the body raises systemic blood pressure to overcome resistance and maintain cerebral blood flow [2]. - This is a compensatory mechanism to ensure adequate perfusion to the brain [1].

Question 7: Neurological complications of meningitis include all of the following except:

A. Increased intracranial pressure
B. Brain abscess
C. Subdural effusions
D. Cerebral hamartoma (Correct Answer)

Explanation: Cerebral hamartoma - A cerebral hamartoma is a benign, tumor-like malformation of abnormally organized mature brain tissue; it is a developmental anomaly and not a complication of meningitis. - Unlike the other options, it does not represent an inflammatory, infectious, or pressure-related sequela of meningeal infection. Increased intracranial pressure - Increased intracranial pressure (ICP) is a common and serious complication of meningitis due to cerebral edema, hydrocephalus, or vasodilation. - Elevated ICP can lead to herniation, neurological deficits, and even death if not managed promptly. Brain abscess - A brain abscess is a localized collection of pus within the brain parenchyma that can develop as a focal complication of bacterial meningitis, particularly in cases of hematogenous spread or direct extension of infection [1]. - This serious condition causes focal neurological deficits and requires aggressive treatment. Subdural effusions - Subdural effusions are accumulations of sterile or infected fluid in the subdural space, most commonly seen in infants and young children with bacterial meningitis. - While they can be asymptomatic, large effusions may cause increased ICP or focal neurological signs requiring drainage.

Question 8: Irreversible cell injury is indicated by

A. Calcium accumulation in cells (Correct Answer)
B. Myelin figures
C. Decreased ATP levels
D. Loss of ribosomal attachment

Explanation: ***Myelin figures*** - Myelin figures are indicative of **irreversible cell injury** and are formed during **cellular degeneration**, representing the breakdown of cell membranes [3]. - Their presence suggests severe damage, which often leads to **cell death** and loss of function [2]. *ATP depletion* - While **ATP depletion** occurs early in cell injury, it does not solely indicate irreversible damage, as cells may recover if ATP levels are restored [3]. - It's associated with **reversible injury**, particularly in conditions like ischemia [5]. *Shifting of Ribosomes* - The **shifting of ribosomes** from the rough endoplasmic reticulum is a sign of **reversible injury**, indicating stress or sublethal damage rather than irreversible damage [5]. - Cells can return to normal function if the stressor is removed [2]. *Accumulation of calcium in endoplasmic reticulum* - Accumulation of calcium often indicates **cellular stress** or **early injury**, but does not confirm irreversible injury by itself [4]. - It can lead to cell damage, but can also be a part of **reversible injury mechanisms** in certain contexts [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 53-55. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 53. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 61-62. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 60-61. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 51-53.

Question 9: Histopathological feature of HIV encephalitis is/are-

A. Microglial nodules (Correct Answer)
B. Lewy body
C. Fibrillary plaque
D. Negri body

Explanation: ***Microglial nodules*** - **Microglial nodules** are a hallmark histopathological feature of **HIV encephalitis**, representing clusters of activated microglia and macrophages in the brain parenchyma [2]. - These nodules often contain **multinucleated giant cells**, which are believed to be formed by the fusion of HIV-infected macrophages and are pathognomonic for HIV encephalitis [1]. *Lewy body* - **Lewy bodies** are abnormal aggregates of protein (primarily **alpha-synuclein**) that develop inside nerve cells, primarily associated with **Parkinson's disease** and **Lewy body dementia**. - They are not characteristic of HIV encephalitis or other viral infections of the brain. *Fibrillary plaque* - **Fibrillary plaques**, specifically **amyloid plaques**, are extracellular deposits of aggregated **beta-amyloid protein** found in the brains of individuals with **Alzheimer's disease**. - These are a key feature of neurodegenerative conditions but are not seen in HIV encephalitis. *Negri body* - **Negri bodies** are eosinophilic, sharply demarcated neuronal cytoplasmic inclusions found in the pyramidal cells of the hippocampus and Purkinje cells of the cerebellum in individuals with **rabies**. - They are specific to rabies infection and are not associated with HIV encephalitis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 711-712. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256.

Question 10: What is the primary pathological mechanism in classical Guillain-Barré syndrome affecting the peripheral nervous system?

A. It blocks neurotransmitter release.
B. It causes demyelination of peripheral nerves. (Correct Answer)
C. It inhibits muscle contraction.
D. It leads to axonal degeneration.

Explanation: ***It causes demyelination of peripheral nerves.*** - Classical Guillain-Barré syndrome (AIDP - Acute Inflammatory Demyelinating Polyneuropathy) is an autoimmune disorder where the immune system attacks the **myelin sheath** surrounding peripheral nerves. - This **demyelination** impairs nerve signal conduction, leading to weakness and paralysis. - AIDP represents the most common form of GBS in Western countries (~85-90% of cases). *It blocks neurotransmitter release.* - Conditions like **Lambert-Eaton myasthenic syndrome** primarily involve antibodies targeting presynaptic voltage-gated calcium channels, thereby reducing neurotransmitter release. - While GBS affects nerve conduction, its primary mechanism is not the blockage of neurotransmitter release at the synapse. *It inhibits muscle contraction.* - Inhibition of muscle contraction is a downstream effect of impaired nerve innervation, but the fundamental problem in GBS is with the **nerve itself**, not the muscle's ability to contract directly. - Conditions like **myasthenia gravis** directly affect neuromuscular transmission by blocking acetylcholine receptors on muscle fibers. *It leads to axonal degeneration.* - While **axonal variants** of GBS exist (AMAN - Acute Motor Axonal Neuropathy; AMSAN - Acute Motor-Sensory Axonal Neuropathy), particularly common in Asia, the **classical and most common form** is characterized by **primary demyelination** (AIDP). - Pure axonal degeneration as a primary pathology is seen in specific GBS variants, not the classical presentation. - Secondary axonal damage can occur in severe or prolonged cases.

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