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PDF - CVD Flashcards

1
Q

Definition TIA?

A

Sudden, focal neurological deficits which completely resolve in 24 hours

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2
Q

Definition Stroke?

A

Sudden, focal neurological deficit which does not completely resolve within 24 hours
- May variably improve over several weeks to months

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3
Q

Where do atherosclerotic changes predominate in vessels?

A

Bifurcation points of arteries, due to more turbulent blood flow at these sites

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4
Q

Process of plaque development?

A

lipid deposition, smooth muscle proliferation, and fibrosis

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5
Q

Why do some patients with cerebral artery occlusion not have stroke?

A

Congenitally “complete” circle of Willis at the base of brain
- Have collaterals from external carotid artery, vertebrobasilar arteries, or both

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6
Q

How does brain appear after infarct?

A
  • Cortex appears soft and swollen
  • Less distinction of gray-white matter
  • Spotty hyperemia from extravasated blood
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7
Q

Microscopic appearance of brain within 12 to 36 hours of the clinical stroke? Days?

A

Hours: ischemic neurons shrink and appear eosinophilic
Days:macrophages scavenge necrotic debris and cyst formation occurs with astrocytes at periphery of infarction

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8
Q

Thrombotic or embolic cause lacunar infarct?

A

Thrombosis

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9
Q

What do the lenticulostriate arteries supply?

A

Deeper structures: basal ganglia, internal capsule, thalamus, and corona radiata
- Ischemia here causes lacunar infarcts

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10
Q

What is Amaurosis fugax?

A

Monocular blindness: type of carotid TIA involving ophthalmic artery or its retinal branches
- Often describe “lowered dark shade” in one eye which gradually lightens up

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11
Q

What do Vertebrobasilar territory TIAs cause?

A

Ischemia of brain stem, cerebellum, or visual cortex:

  1. Ataxia,
  2. Homonymous hemianopsia
  3. Hemiparesis associated with “crossed” brainstem syndromes.
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12
Q

What is Homonymous hemianopsia?

A

Visual field loss on L or R side of vertical midline

- Can affect one eye but usually affects both eyes

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13
Q

What does hemiparesis with greater weakness of face and upper limb suggests?

A

Infarct in the precentral MCA

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14
Q

How does MCA infarct present?

A

Hemiparesis with greater weakness of face and upper limb

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15
Q

What does hemiparesis with greater weakness of lower limb suggest?

A

Infarct in precentral ACA

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16
Q

How does Infarct in precentral ACA present?

A

Hemiparesis with greater weakness of lower limb

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17
Q

What does sensory deficits limited to face and upper limb suggest?

A

Infarct in postcentral MCA

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18
Q

What does sensory deficits limited to the lower limb suggest?

A

Infarct in the postcentral ACA

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19
Q

How does Infarct in postcentral MCA present?

A

Sensory deficits limited to face and upper limb suggest

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20
Q

How does Infarct in the postcentral ACA present?

A

Sensory deficits limited to the lower limb

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21
Q

What does a pure sensory stroke suggest?

A

Lacunar syndrome from small vessel occlusion involving thalamus

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22
Q

Type of investigation to do in lacunar infarct?

A

These are thrombotic; do not need to look for an embolic source

23
Q

Neuro exam in TIA?

A

Usually normal

24
Q

Can you repair 100% stenosis of carotid?

25
How to reduce risk stroke in TIA patients?
Antiplatelet drugs such: 1. Aspirin 50-325 mg daily 2. Clopidogrel 75 mg daily 3. Aspirin 25 mg/dipyridamole 200 mg twice daily 4. Statin: reduce risk even in absence of hyperlipidemia 5. Control BP/Diabetes 6. Cessation of smoking
26
Rx option if tPA contraindicated?
Endovascular thrombectomy
27
Impacts high sugars on stroke outcomes?
Worse outcomes: 1. Saline w/o dextrose is preferred 2. Use insulin / orals
28
BP requirement if using tPA?
185/110 or lower
29
Warfarin indication in stroke other than Afiv?
1. Antiphospholipid syndrome | 2. Cerebral venous thrombosis
30
How to decrease ICP?
1. Mechanical hyperventilation to a PCO2 of 30-35 - Hypocapnia induced cerebral constriction which reducing cerebral blood volume 2. Mannitol 3. Hypertonic saline
31
When can emergent surgical removal of herniating ischemic or hemorrhagic brain be used?
Cerebellar lesions
32
When do Corticosteroids help in ICP?
``` Do not work in: 1. Ischemic infarction or 2. Hemorrhage Do work in elevated ICP from: 1. Tumor 2. Infection. ```
33
What happens to ICP in hemorrhage?
1. Arterial BP normally exceeds ICP 2. Sudden rupture of arterial blood into brain parenchyma abruptly increases ICP causing: - Severe HA - LOC - Neurological deficit
34
What does location of hemorrhage?
1. Deeply located hemorrhage: hypertension as cause | 2. Superficial hemorrhages: trauma
35
How does clot from stroke appear pathologically?
- Dark red clot with surrounding edema - Occasional dissection into ventricular system - Clot gradually liquefies, edema resolves, and remaining cyst or slit appears peripherally stained brown from hemosiderin
36
Who is bleeding from venous source problem in?
Elderly with brain atrophy - Bridging cortical veins tear, emptying into venous sinuses - Accumulates in subdural space, not brain parenchyma
37
What happens as large subdural expands?
- Impaired cognition and consciousness, can create neurological deficits
38
What do do if bleeding disorder has caused hemorrhage?
- Infusions of platelets or plasma clotting factors
39
Drugs that can cause hemorrhage?
- Cocaine or other sympathomimetic drugs which abruptly increase blood pressure
40
Most common cause cerebral hemorrhage?
Hypertension | - Weakened small, lenticulostriate arteries rupture, bleeding most often into striatum (putamen/caudate) and thalamus
41
When is surgical evacuation of hematoma warranted?
Only for worsening cerebellar hemorrhages, where brain stem herniation is prevented with minimal residual neurological deficits
42
What appears white on CT?
1. Bones | 2. Acute blood
43
What causes leads recurrent lobar hemorrhages usually in posterior cerebral hemispheres?
Cerebral amyloid angiopathy - Hereditary condition whereby arterial walls are weakened by amyloid deposits
44
Congenital vascular abnormalities carrying risk of rupture and hemorrhage?
AVM | - Abnormal connection of cerebral artery to vein, without intervening capillary bed, enlarging slowly over time
45
How to treat small AVM?
May be successfully resected surgically, or occluded by intravascular procedures, to prevent future bleeding
46
How can ischemia cause hemorrhage?
Damaged, ischemic endothelium may leak or ooze | blood if reperfusion occurs in ischemic infarction
47
Most common cause bleeding into subarachnoid space?
1. Trauma | 2. Ruptured congenital berry aneurysm
48
What is a Berry aneurysm?
A rise in the circle of Willis at base of brain, especially anteriorly, beginning as bulges or thinned out-pouchings at arterial bifurcations - Greater risk of rupture beyond 7 to 10 mm in size
49
Presentation SAH?
1. Nuchal rigidity 2. Meningeal signs are 3. Nausea / vomiting 4. Impaired consciousness 5. Localizing neurological signs often absent, since hemorrhage does not involve brain parenchyma
50
What does 3rd cranial (oculomotor) nerve palsy | suggests in SAH?
That aneurysm is near PCA
51
What to do if CT negative in suspected SAH?
LP necessary to exclude a small volume of subarachnoid blood
52
How to locate small aneurysm if LP positive?
Emergent angiography, preferably conventional catheter | angiography
53
Complication of clipped/coiled aneurysm? Rx?
Cerebral vasospasm - reduced flow from vasospasm creates ischemic infarctions, and is more likely after a large SAH Rx (nimodipine): hypertensive therapy, using vasopressors to sdpreserve cerebral flow

Neurology (37 decks)

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