Stroke (Ischemic) Flashcards

1
Q

Transient Ischemic Attack is a temporary focal loss of neurological function last less than

A

24 hours

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2
Q

Carotid arteries involvement

A

Transient loss of vision on one eye

Hemiparesis

Inability to speak

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3
Q

Vertebrobasilar arteries involvement

A

Tinnitus

Vertigo and blurring vision

Hemiparesis

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4
Q

Definition of Ischemia

A

a reduction in blood flow that can last for several seconds to a
few minutes

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5
Q

Infarction

A

If there is cessation of flow for than a few minutes, infarction of
brain tissue occurs

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6
Q

Pathophysiology in Ischemic Stroke

A

 Reduce blood flow in the arteries can be thrombosis or embolism

 Reduction in blood flow deprives the cells of O2 and glucose

 Lack of energy causes membrane dysfunction and entry of ions

 Edema of cells occurs, followed by death of cells

 Vascular changes aggravate edema

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7
Q

Causes of thrombosis

A

Arterial disease
 Atherosclerosis, arteritis

Blood disorders
 Thrombocytosis, polycythemia

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8
Q

Definition of Embolism

A

Thrombosis occurs in other parts of the body

A part of the thrombus detaches and travel to the brain through the
arteries

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9
Q

Causes of embolism

A

Embolic strokes are usually caused by a blood clot that forms elsewhere
in the body (embolus) and travels through the bloodstream to the brain.

Embolic strokes often result from heart disease or heart surgery and
occur rapidly and without any warning signs.

About 15% of embolic
strokes occur in people with atrial fibrillation, a type of abnormal heart
rhythm in which the upper chambers of the heart do not beat effectively

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10
Q

Clinical presentation of Ischemic stroke

A

Transient Ischemic Attacks (TIA)

Any neurological dysfunction that lasts for a few seconds to a
few minutes

Should recover within 24 hours

 Pathogenesis of TIA

 Low-flow states in vascular obstruction

 Small emboli which get dissolved later

 Recognition of TIA helps in prevention of major stroke

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11
Q

Established stroke

A

Infarction of brain tissue occurs due lack of blood. Deficit is permanent

 Increasing obstruction may involve a proximal branch of the artery and increase the deficit: stroke-in-evolution

 Edema occurs in surrounding tissue

 Resolution of edema after the acute stage may restore some
function

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12
Q

Clinical presentation of Ischemic stroke (site)

A

Depend on the site of obstruction

 the artery or its branch involved
 the brain area supplied by the artery

Depend on the state of circulation

 Presence of good arteries in the adjacent area may provide collateral
circulation
 Also on the state of general circulation

Onset
 Embolism - sudden, during exertion
 Thrombosis - slow, during rest time

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13
Q

Anterior Cerebral Artery

Involvement of Superficial branches signs and symptoms

A

Prefrontal lobe: confusion, disorientation

 Medial surface: paralysis and sensory loss in the opposite leg

 Apraxia, abulia and urinary incontinence in bilateral lesions

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14
Q

Anterior Cerebral Artery

Involvement of Deep Branches

A

Obstruction is well tolerated because of collateral flow

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15
Q

Middle Cerebral Artery

 Involvement Deep branches

A

Corticospinal fibers in internal
capsule - paralysis of opposite side

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16
Q

Middle Cerebral Artery

Involvement of Superficial
branches

Superior division:

A

Superior division: paralysis of face
and hand, conjugate gaze paralysis,
motor aphasia

17
Q

Middle Cerebral Artery

Involvement of Superficial
branches

Inferior division:

A

Inferior division: conduction or
sensory aphasia, construction or
dressing apraxia

18
Q

Vertebro-basilar territory

 Presence of cerebellar symptoms

What are the cerebellar sx?

Presence of brain lesion

What are the brain lesion sx?

A

Presence of cerebellar symptoms
 Ataxia, Intention tremor, In-coordination

Presence of brain lesion
 Crossed paralysis and sensory loss

19
Q

Posterior cerebral artery

Superficial branches

Deep branches

A

Visual loss, memory loss, agraphia

Thalamic syndromes

20
Q

Ipsilateral lesion

A

Cerebellar ataxia

 Wide-based, staggering unsteady gait

 Vermis lesions produce truncal ataxia

Intention tremor

 Incoordination of arm and leg on voluntary movement

 Worse when approaching target, diminishes with rest

 Finger-nose test, heel-shin test

Dysmetria

 Error in judging distance resulting in overshooting

 May be accompanied by tremor

Rebound phenomenon

 Difficulty in stopping the movement when resistance is withdrawn suddenly

21
Q

Dysdiadochokinesia

A

Inability to perform rapid alternating opposite movements

Pronation-supination, ankle flexion-extension

22
Q

Decomposition of movements

A

Inability to perform actions that involve more than one joint
simultaneously

Movement are broken into many components, one joint at a
time

Robotic movement

23
Q

Nystagmus

A

due to incoordination of extraocular muscles

24
Q

Scanning speech

A

Words are broken into many component sounds

‘Staccato’ speech

25
Q

Hypotonia

A

Decreased muscle tone and tendon reflexes

26
Q

Asthenia

A

Muscles affected are weaker and tire more easily than normal muscles

27
Q

Treatment for Ischemic stroke

A

Clot busters

IV tissue Plasminogen
Activator (tPA)

28
Q

Preventive Treatment for Ischemic stroke

A

Anticoagulants/Antiplatelets

 Antiplatelet: aspirin

 Anticoagulants: warfarin

 Carotid Endarterectomy
-Surgically remove plaque

Angioplasty/Stents
- Use balloon angioplasty
- Implant stents reduce fatty buildup

29
Q

Warfarin Counseling

A

blood thinner

 Prevent formational of blood clots

 Treatment duration varies

 Modification diet: Be consistent, avoid sudden reduction
of Vit K in diet

 Need monitor INR and make sure within therapeutic
range 2-3

 Monitor for side effects

 Special precautions

30
Q
A