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Neurology > PDF - CVD > Flashcards

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?

A

No

25
Q

How to reduce risk stroke in TIA patients?

A

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
Q

Rx option if tPA contraindicated?

A

Endovascular thrombectomy

27
Q

Impacts high sugars on stroke outcomes?

A

Worse outcomes:

  1. Saline w/o dextrose is preferred
  2. Use insulin / orals
28
Q

BP requirement if using tPA?

A

185/110 or lower

29
Q

Warfarin indication in stroke other than Afiv?

A
  1. Antiphospholipid syndrome

2. Cerebral venous thrombosis

30
Q

How to decrease ICP?

A
  1. Mechanical hyperventilation to a PCO2 of 30-35
    - Hypocapnia induced cerebral constriction which reducing cerebral blood volume
  2. Mannitol
  3. Hypertonic saline
31
Q

When can emergent surgical removal of herniating ischemic or hemorrhagic brain be used?

A

Cerebellar lesions

32
Q

When do Corticosteroids help in ICP?

A 
Do not work in:
1. Ischemic infarction or
2. Hemorrhage
Do work in elevated ICP from: 
1. Tumor 
2. Infection.
33
Q

What happens to ICP in hemorrhage?

A
  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
Q

What does location of hemorrhage?

A
  1. Deeply located hemorrhage: hypertension as cause

2. Superficial hemorrhages: trauma

35
Q

How does clot from stroke appear pathologically?

A
  • 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
Q

Who is bleeding from venous source problem in?

A

Elderly with brain atrophy

  • Bridging cortical veins tear, emptying into venous sinuses
  • Accumulates in subdural space, not brain parenchyma
37
Q

What happens as large subdural expands?

A
  • Impaired cognition and consciousness, can create neurological deficits
38
Q

What do do if bleeding disorder has caused hemorrhage?

A
  • Infusions of platelets or plasma clotting factors
39
Q

Drugs that can cause hemorrhage?

A
  • Cocaine or other sympathomimetic drugs which abruptly increase blood pressure
40
Q

Most common cause cerebral hemorrhage?

A

Hypertension

- Weakened small, lenticulostriate arteries rupture, bleeding most often into striatum (putamen/caudate) and thalamus

41
Q

When is surgical evacuation of hematoma warranted?

A

Only for worsening cerebellar hemorrhages, where brain stem herniation is prevented with minimal residual neurological deficits

42
Q

What appears white on CT?

A
  1. Bones

2. Acute blood

43
Q

What causes leads recurrent lobar hemorrhages usually in posterior cerebral hemispheres?

A

Cerebral amyloid angiopathy
- Hereditary condition whereby arterial walls are
weakened by amyloid deposits

44
Q

Congenital vascular abnormalities carrying risk of rupture and hemorrhage?

A

AVM

- Abnormal connection of cerebral artery to vein, without intervening capillary bed, enlarging slowly over time

45
Q

How to treat small AVM?

A

May be successfully resected surgically, or occluded by intravascular procedures, to prevent future bleeding

46
Q

How can ischemia cause hemorrhage?

A

Damaged, ischemic endothelium may leak or ooze

blood if reperfusion occurs in ischemic infarction

47
Q

Most common cause bleeding into subarachnoid space?

A
  1. Trauma

2. Ruptured congenital berry aneurysm

48
Q

What is a Berry aneurysm?

A

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
Q

Presentation SAH?

A
  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
Q

What does 3rd cranial (oculomotor) nerve palsy

suggests in SAH?

A

That aneurysm is near PCA

51
Q

What to do if CT negative in suspected SAH?

A

LP necessary to exclude a small volume of subarachnoid blood

52
Q

How to locate small aneurysm if LP positive?

A

Emergent angiography, preferably conventional catheter

angiography

53
Q

Complication of clipped/coiled aneurysm? Rx?

A

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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