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IPFC 4 > STROKE Patho > Flashcards

STROKE Patho Flashcards

1
Q

What is stroke?

A

A stroke occurs when a blood vessel that carries O2 and nutrients to the brain is either blocked by a clot or ruptures –> brain cannot get the blood (and O2) it needs, so brain cells die

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2
Q

How is stroke characterized?

A

Neurological deficit caused by an acute, focal injury to the CNS due to a vascular (blood vessels) cause

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3
Q

How is stroke classified?

A

Ischemic stroke, Hemorrhagic stroke (Intracerebral or Subarachnoid) and TIA

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4
Q

Ischemic stroke

A

Involves vascular injury (infarct) to the brain, SC or retina related to ischemia with sx persisting for >/= 24 hrs

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5
Q

TIA

A

A transient episode of neurological dysfunction caused by focal brain, SC or retinal ischemia without acute infarction

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6
Q

Hemorrhagic stroke

A

Intracerebral –> caused by focal collection of blood within the brain parenchyma or ventricles, not related to trauma (direct bleeding into brain)

Subarachnoid – caused due to bleeding into the subarachnoid space, not related to trauma

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7
Q

Stroke breakdown by gender

A
  • Upto 80 years old, men survive stroke more than women
  • After 80, women survive more
  • Stroke incidence is same till age 60
    -After age 60, men tend to get more strokes than women
    -After age 60, incidence of stroke doubles
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8
Q

Why does an ischemic stroke occur?

A
  • Occurs due to blockage resulting from in-situ thrombosis in a blood vessel or clot embolization
  • Embolization could occur from a proximal artery to a distal artery or from the heart
  • Lack of cerebral blood flow –> neuronal damage and cell death

(Loss of supply of O2 and glucose –> collapse of energy producing processes in neurons –> disintegration of cell structures and membranes leading to necrosis)

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9
Q

What is ischemic core and penumbra?

A

Ischemic core - tissue that has already experienced irreversible damage and cannot be salvaged

Penumbra –> tissue at risk –> hypo- perfused tissue surrounding the ischemic core –> may be salvaged by acute reperfusion therapy but delay in tx leads to permanent, irreversible damage

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10
Q

Signs of stroke

A

F - Is face drooping?
A - Can you raise both arms?
S - Is speech slurred or jumbled?
T - time to call 911 right away

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11
Q

What arteries supply blood to the brain?

A
  • Common carotid artery (Internal/anterior and External/various facial structures)
  • Vertebral artery (Basilar artery to create vertebrobasilar system - posterior BS)
  • Internal carotid arteries and vertebral arteries feed into the circle of willis
  • The arteries of the circle of willis connects circulation from the anterior to the posterior portion of the brain
  • This collateral circulation allows for blood flow to be redirected in the event of an obstruction –> blood redirected to damaged part of the brain (People with complete circle of willis tend to have better collateral circulation and smaller infarcts in stroke)
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12
Q

Stroke etiology

A

Ischemic stroke –> Large artery Atherosclerosis, Small artery disease, Cryptogenic, Cardiac embolism, Unusual

Hemmorhagic stroke –> ICH, SAH

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13
Q

Large artery atherosclerosis (patho/most affected areas)

A
  • Includes both extracranial (common and internal carotids, vertebral artery) and intracranial system (circle of willis and proximal branches)
  • Most common cause is build of plaque
  • May be caused due to in-situ thrombosis in the affected vessel or due to artery to artery embolization
  • Intermittent progression of sx –> over several mins to hours

Pathogenesis: plaque forms at branching points and curves of cerebral arteries

Most commonly affected areas-
1. Internal carotid artery at its origin from common carotid
2. Vertebral artery at origin from the subclavian vessels or at its junction to form the basilar artery
3. Main bifurcation of the middle cerebral artery

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14
Q

Cardiac embolism

A
  • Fragment broken away from a thrombus within the heart –> either one of the heart chambers or from a heart valve and blocks arteries in the brain

Thrombus formation may occur due to:
- pre-existing cardiac conditions (Afib)
- valvular heart disease
- patent foramen ovale (hole between left and right side of heart)

May affect any part of the brain
- embolus attaches to a bifurcation point or narrowed vessel

Sx develop rapidly within seconds

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15
Q

Small artery disease

A
  • Caused due to occlusion in the small penetrating branches of the cerebral arteries (0.2-15 mm in diameter) –> deeper parts of the brain
  • Necrotic tissue from the infarct is removed by macrophages resulting in the formation of a small cavity or lacune
  • Sx appear over few hrs to days and in some cases may be asymptomatic
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16
Q

Pathogenesis of lacunar stroke

A

Usually caused by:
- thickening of small vessel walls due to lipid build up in the wall structure –> lipohyalinosis (most common)
- atherosclerosis in larger blood vessels that occludes the origin of smaller blood vessels
- entry of small embolic material into smaller blood vessels (rare)

Strong relationship with vascular disease: HTN and Diabetes

17
Q

Non-modifiable risk factors of ischemic stroke

A

Age –> risk of stroke increases with age, men tend to have it more after 60
Gender
Ethnicity –> risk twice as high in african americans vs caucasians

18
Q

INTERSTROKE 2 study

A

PAR - contribution of risk factor to stroke

HTN –> increases risk of ischemic stroke and intracerebral haemorrhage (more ICH risk)

Good regular physical activity (4 hours of mod-severe in 1 week) will decrease risk of stroke

Smoking mostly increases risk of Ischemic stroke

High hip to waist ratio –> increased stroke

ApoB/A1 –> increases risk of ischemic stroke mostly

History of diabetes or HbA1C >/= 6.5% –> risk of ischemic stroke

Having a good diet decreases risk of stroke

Alcohol can increase risk of stroke but weak association

Psychosocial factors (stress and depression) increase risk of stroke

Cardiac causes (Afib, AFL) increases risk of stroke

Afib affects ischemic stroke

19
Q

S/S of Ischemic stroke

A

Depends on area of infarction in the brain but typically involve:

  • Numbness/weakness in the face, arm or leg esp on one side
  • Sudden confusion, trouble speaking, or difficulty understanding speech
  • Trouble seeing in one or both eyes
  • Trouble walking, dizziness, loss of balance or lack of coordination
20
Q

MCA stroke syndrome

A

MCA provides supply to the frontal, parietal and temporal lobes

Subdivided into 4 main dvisions: M1, M2, M3 and M4

Infarcts occur most commonly in the M1 and M2 sections

Superior division affects broca area(speech), motor and sensory

Inferior division affects visual cortex, wernicke area (language and comprehension), auditory area

21
Q

What happens if there is occlusion of the main stem? (MCA)

A

-contralateral hemiplegia involves face, arm and legs (paralaysis)
-contralateral hemianesthesia is the loss of sensation on contralateral side
-contralateral homonymous hemianopia: visual field loss on the same side of both eyes
-deviation of head and eyes to the side of the lesion
-dysarthria (if left hemisphere affected) –> slurred/slow speech

22
Q

ACA occlusion

A

Provides circulation to the medial portion of the frontal lobe and the superior medial portion of the parietal lobe

Common features:
- sensorimotor deficits in the contralateral foot and leg, less in upper extremities
-urinary incontinence
-language disturbances (dysarthria or mutism or speak in whispers)
-behavioural disturbances (abulia, distractibility and mood changes)

Abulia: slowness or lack of spontaneity in reactions, reduction in reflexes

23
Q

PCA occlusion

A

Provides circulation to the occipital lobe and the medial temporal lobe

Mainly visual field deficits
- contralateral homonymous hemianopia
-partial or complete vision loss and visual hallucinations

Anomia- inability to name objects but can describe them

Short term or long term memory loss due to temporal lobe involvement

24
Q

Subarachnoid Haemorrhage (SAH)

A

Extravasation of blood into the SA space resulting in mixing of blood and CSF

Typically occurs in younger pts

80% caused by aneurysmal rupture

Neurologic emergency if bleeding caused by trauma

25
Q

Risk factors for SAH

A

Ethnicity – African american or hispanic
2 or more first degree relatives with aneurysms or history of SAH

Modifiable – hypertension, smoking, sympathomimetic drug use, alcohol abuse or large aneurysms (>7 mm)

26
Q

S/S of SAH

A

Unruptured aneurysms are asymptomatic, sx begins after rupture

-Severe headache
-N/V
-Photophobia
-Neck stiffness
-Focal neurological deficits
-Loss of consciousness in severe cases

27
Q

Complications of SAH

A

Re-rupture
- risk highest within 24 hrs but remains elevated for the first 30 days in untreated pts
-mortality rate with re-rupture is higher

Delayed cerebral ischemia
- neurological deterioration after initial aneurysm rupture
-vasospam –> narrowing of large cerebral arteries
- starts around day 4 upto 21 days

Hydrocephalus
-blockage in normal flow of the CSF leading to increase in intracranial pressure
-leads to coma in severe cases
-requires replacement of CSF

28
Q

Intracerebral hemorrhage (ICH)

A

Rupture of the intracerebral vessel leading to bleeding within the parenchyma

Occurs more in older pts

High mortality rate - 35 to 45% in the first month

Neurologic emergency

29
Q

Pathophysiology of ICH

A

Uncontrolled HTN
- most common cause
- breakage in smaller penetrating arteries that branch off from larger vessels
-chronic untreated HTN leads to weakened vessel walls that are prone to rupture

Amyloid angiopathy
-deposition of amyloid beta-peptides within small to medium sized blood vessels
-results in degenerative changes in wall structure, leading to breakage
-genetic predisposition

Use of anticoagulants - secondary ICH

30
Q

S/S of ICH

A
  • occurs when pt is up and active
  • acute reactive HTN with SBP > 180 mmHg
    -severe headache
    -vomiting
    -rapid onset focal neurological deficit
    -decreased consciousness
31
Q

ICH complications

A

Hematoma expansion
-occurs within 24 hrs, rise in ICP (bleeding has to be controlled)
-can cause midline shift and cerebral herniation

Cerebral edema
-48 to 72 hrs after primary hemorrhage
-secondary neurologic injury due to compression of structures

Seizures
Respiratory depression
Coma

32
Q

Diagnosis of strokes

A

Complete physical and neurologic exam

NIHSS score – measures neurologic impairment using an 11 item scale
Each item rated from 0 (normal) to 4 (complete impairment) for a max score of 42
Predictive of long term outcomes post stroke
Higher the score, worse the outcomes (16+ has poor outcomes)

33
Q

TIA - ABCD score

A

Helps predict 2,7,30 and 90 day stroke risk post TIA

Age >/= 60 —> 1
BP >/= 140/90 –> 1

Clinical sx
- unilateral weakness –> 2
-speech impairment without weakness –> 1

Duration
>/= 60 mins —> 2
10-59 mins –> 1

Diabetes –> 1

5,6,7 score is the worst

34
Q

Neuroimaging

A

Brain imaging
- allows for differentiating between ischemia and hemorrhage
-rule out stroke mimics (ie tumour)
-assess status of large intracranial arteries
-guide acute tx

Computed tomography (CT)
-non contrast CT preferred in acute setting to rule out hemorrhage
-readily accessible

CT angiography
-uses contrast to help identify location of clots in larger intracranial vessels (dye doesn’t flow through –> block)

MRI
- provides high resolution images and allows for visualization of smaller vessels
-not readily accessible

Carotid doppler
- identify clots in carotid arteries (not gold standard anymore as CTA more sensitive)

35
Q

Cardiac monitoring

A

ECG
- identify abnormal heart rhythm in a snapshot of time
- look for AFIB!

Holter monitoring (most pts use this)
-identify abnormal heart rhythm over a period of time

Echocardiogram
-visualize heart chambers and valves to rule out clots

IPFC 4 (2 decks)

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