CNS Pathology I Flashcards

1
Q

What are the major clinical presentations of raised intracranial pressure (ICP)?

A

Nausea, headache, and altered consciousness.

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2
Q

What are the two main processes involved in cerebrovascular disease?

A

Ischaemia (hypoxia) and haemorrhage.

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3
Q

What is the definition of a stroke?

A

Neurologic signs and symptoms explained by a vascular mechanism, with acute onset and lasting beyond 24 hours.

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4
Q

What are the causes of non-communicating hydrocephalus?

A

Obstruction between the ventricular and subarachnoid space due to space-occupying lesions, congenital malformations (e.g., Arnold-Chiari malformation), or mass lesions like tumors.

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5
Q

What are the common clinical symptoms of raised ICP?

A

Vomiting, nausea, headache, papilledema, and possibly cerebral herniation leading to life-threatening conditions.

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6
Q

How does hypertension affect cerebrovascular health?

A

Hypertension can lead to lacunar infarcts, hypertensive encephalopathy, and hypertensive intracerebral hemorrhage.

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7
Q

What is the typical cause of intracerebral haemorrhage in younger patients?

A

Ruptured arteriovenous malformation (AVM).

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8
Q

What is the key clinical sign of a subarachnoid hemorrhage?

A

Sudden, severe “thunderclap” headache.

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9
Q

What is the pathogenesis of raised intracranial pressure (ICP)?

A

Increased intracranial volume due to fluid (cerebral edema, hydrocephalus) or tissue (space-occupying lesions like tumors or hemorrhages).

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10
Q

What are the two types of hydrocephalus?

A

Non-communicating (obstruction between ventricles and subarachnoid space) and communicating (defective absorption, overproduction, or venous drainage insufficiency).

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11
Q

What is cerebral herniation and its most dangerous form?

A

Displacement of part of the brain into another compartment due to increased ICP. The most dangerous form is tonsillar herniation (“coning”), which can lead to cardiorespiratory arrest.

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12
Q

What is a lacunar infarct and its common location?

A

A small infarct (<15mm) due to occlusion of deep penetrating arteries or arterioles, commonly found in the basal ganglia, internal capsule, thalamus, or pons.

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13
Q

What are the two types of cerebral infarctions?

A

Pale/Non-haemorrhagic infarcts and Red/Haemorrhagic infarcts, which require different treatments (thrombolytics are avoided in haemorrhagic infarcts).

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14
Q

What is a “watershed infarct” and what causes it?

A

A type of infarction that occurs in the regions between major arteries (e.g., between MCA and ACA), caused by global hypoperfusion, such as in cardiac arrest or shock.

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15
Q

What are the characteristic microscopic changes in a brain infarction over time?

A

12 hours: Ischaemic neuronal change (red neurons)
24-48 hours: Neutrophil infiltration
2 days: Macrophages
1-3 weeks: Reactive gliosis and liquefactive necrosis.

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16
Q

What is Charcot-Bouchard aneurysm and its association with intracerebral hemorrhage?

A

Small aneurysms in the deep brain structures (e.g., basal ganglia) often caused by chronic hypertension, leading to intracerebral hemorrhage.

17
Q

What are the primary causes of subarachnoid hemorrhage?

A

Ruptured saccular (berry) aneurysms, often located in the Circle of Willis, or ruptured arteriovenous malformations (AVMs).

18
Q

What imaging feature distinguishes an epidural hematoma?

A

A biconvex (lenticular) appearance on a CT scan, often caused by the laceration of the middle meningeal artery following trauma.

19
Q

What is the clinical presentation of hypertensive encephalopathy?

A

Acute hypertensive encephalopathy presents with diffuse cerebral dysfunction, headaches, confusion, convulsions, and can progress to coma if ICP increases.

20
Q

What differentiates subdural from epidural hemorrhage?

A

Subdural hemorrhage is typically caused by tearing of bridging veins (due to acceleration-deceleration injuries), while epidural hemorrhage is caused by arterial injury (e.g., middle meningeal artery), often with a lucid interval followed by rapid deterioration.