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Clinical Medicine III > Stroke > Flashcards

Stroke Flashcards

1
Q

Define stroke or cerebrovascular accident

A
  • acute onset of neurological dysfunction due to abnormality in cerebral circulation
  • rapidly developing clinical signs of focal or global disturbance or cerebral function lasting 24hrs or longer
  • destruction of surrounding brain tissue
  • consequence of changes in both the function of the heart & in the integrity of the vessels providing blood to the brain
    -Transient ischemic attack (TIA)/ministroke = when neurological symptoms resolve within 24hrs, a warning sign for a stroke in the near future
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2
Q

Vascular requirements of the brain

A
  • the brain makes up 2% of the body & receives 20% of the body’s O2 & glucose of cardiac output
  • cerebral blood flow (CBF) transports O2 & glucose across the blood brain barrier
  • CBF is maintained by a coordinated action of interconnected blood vessels
  • CBF if interrupted: brain function stops in seconds while cell damaged occurs in minutes
  • CBF is controlled/regulated automatically without being affected much by changes in: arterial pressure, intracranial pressure, arterial blood gases, neural activity, & metabolic demand
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3
Q

Death rates from stroke/CVA

A
  • 5th leading cause of death & one of the leading causes of disability
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4
Q

Incidence rates of stroke/CVA

A
  • responsible for 1 in every 20 deaths, every 4 min someone dies from stroke
  • someone in the US has a stroke every 40 secs
  • 16 million suffer a 1st time stroke each year
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5
Q

Non-modifiable risk factors for stroke/CVA

A
  • Age: doubles every decade after 55 yrs
  • Sex: men > women
  • Family Hx: certain genes
  • Race: Latin American/African descent
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6
Q

Modifiable risk factors for stroke/CVA

A
  • Hypertension: >160/95 mm Hg
  • Pre-Hypertension: 120-139/80-89
  • Cardiac conditions
  • Fibrinogen (coagulation factor): increased fibrin deposition
  • Diabetes
  • Dyslipidemia: low HDL, high LDL
  • Sedentary lifestyle
  • Obesity: abdominal
  • Smoking: increases risk by 50%
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7
Q

Types of stroke

A
  • Ischemic stroke (87%): thrombotic or embolic occlusion of an artery stopping blood flow to a cerebral area
  • Hemorrhagic stroke (13%): bleeding from a blood vessel due to leakage/rupture
  • TIA (transient ischemic attack): temporary occlusion of cerebral vessel which gets resolved within 24hrs
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8
Q

Early warning signs of a stroke

A
  • sudden weakness or numbness of the face, arm, or leg
  • sudden dimness or loss of vision, particularly in one eye
  • sudden difficulty speaking (slurred) or understanding speech
  • sudden severe headache with no known cause
  • unexplained dizziness, unsteadiness, or sudden falls
  • BE FAST: balance, eyesight, face, arm, speech, time
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9
Q

Chances of TIA progressing to stroke

A
  • ABCD prediction scale
  • age ≥ 60 yrs
  • BP ≥140/≥90 mmHg
  • unilateral weakness
  • speech impairment w/o weakness
  • diabetes mellitus
  • duration of TIA: ≥ 60 minutes = 2 points; 10-59 minutes = 1 point
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10
Q

Pathogenesis of an ischemic stroke

A
  • Occlusion of major arteries: thrombus formation narrowing vessel or embolus which has been carried in the bloodstream to lodge in another vessel obstructing blood flow
  • Vascular Causes: atherosclerosis or artery to artery embolism
  • Cardiogenic Causes: A-fib, MI, or valve disease
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11
Q

Cerebral blood flow (CBF) impairments following ischemia

A
  • normal CBF = 50 ml/100g/min
  • average cerebral perfusion pressure (CPP) = ~60 mmHg
  • CBF falls below 20 ml/100mg/min = neuronal functioning impairments
  • CBF falls below 8-10 ml/100mg/min = tissue death occurs
  • time is tissue: brain ages 3.6 yrs each hour w/o treatment
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12
Q

What is the primary goal for treatment of an ischemic stroke

A
  • immediate recovery of adequate perfusion in the penumbra to stop progression of infarct zone
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13
Q

Events causing secondary neural damage in stroke

A
  • mitochondrial energy failure due to lack of O2 in penumbra
  • Increased glutamate release -> Ca2+ ions -> excitotoxicity
  • Hypoxia-induced free radical production
  • Release of degradative enzymes
  • Inflammatory responses – leukocytes, cytokines/chemokines
  • Activation of glial cells (macrophages, astrocytes) following inflammation
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14
Q

Clinical syndrome of ischemic stroke

A
  • depends on arterial distribution of the region
  • depends on the functional areas affected in the occluded region: need to know the location of the functional areas in the brain
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15
Q

Describe the circle of Willis

A
  • joins blood supply from 2 arteries to provide collateral circulation to all of brain
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16
Q

Describe the middle cerebral artery distribution

A
  • biggest distribution
  • supplies. the dorsolateral regions of frontal/parietal lobes, temporal lobe, basal ganglia nuclei, & internal capsule
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17
Q

Describe the anterior cerebral artery supply distribution

A
  • medial regions of frontal & parietal lobes
  • anterior region of frontal lobe
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18
Q

Describe the posterior cerebral artery supply distribution

A
  • occipital lobe
  • inferior regions of temporal lobe (hippocampus)
  • midbrain (cerebral peduncles)
  • thalamus
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19
Q

Describe the brainstem & cerebellar artery distributions

A
  • collateral circulation provided by a pair of vertebral arteries, to form the basilar artery (vertebrobasilar system supplies brainstem & cerebellum)
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20
Q

Describe the SCA supply distribution

A
  • SCA (superior cerebellar artery)
  • cerebellar cortex
  • cerebellar nuclei
  • superior cerebellar peduncle
  • a small portion of midbrain
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21
Q

Describe the AICA supply distribution

A
  • AICA (anterior inferior cerebellar artery)
  • supplies inferior surface of the cerebellum, cerebellar nuclei, & portions of the pons & medulla
  • CN nuclei 5/7/8
  • vestibular & hearing organs (helps with differential diagnosis)
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22
Q

Describe the PICA supply distribution

A
  • PICA (posterior inferior cerebellar artery)
  • arises from vertebral arteries
  • supplies dorsolateral medulla
  • posterior portion of the cerebellar hemispheres
  • central nuclei of the cerebellum
  • CN nuclei 5/9/10
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23
Q

describe the prefrontal area of the cortex

A
  • supplied by the ACA (anterior cerebral artery) & MCA (middle cerebral artery)
  • behaviors, judgement, foresight, problem solving, social appropriateness
  • Lesion = apathy, poor motivation, flat affect, social inappropriateness, perseveration, poor judgement
  • due to connections between dorsolateral prefrontal cortex to basal ganglia may have difficulty with dual tasking & motor planning
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24
Q

Describe the premotor area of the cortex

A
  • supplied by the MCA (middle cerebral artery)
  • motor planning area (externally guided movements): reaching, grasping
  • Lesion = ideomotor apraxia (inability to perform a task in response to a verbal command or imitate gestures; pt knows what they want to do but cannot plan the muscle coordination needed to complete a task; problems with bimanual tasks
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25
Q

Describe the supplementary motor area of the cortex

A
  • supplied by the ACA
  • motor planning area (internally guided movements)
  • Lesion = ideomotor apraxia
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26
Q

Describe the primary motor area in the cortex

A
  • supplied by the ACA & MCA
  • execution of voluntary skilled movements
  • Lateral cortex = UE, upper trunk & face
  • Medial cortex = LE, lower trunk
  • Lesion = lack of voluntary skilled movements
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27
Q

Describe the primary sensory area of the cortex

A
  • supplied by the ACA & MCA
  • detection & localization of sensation from the opposite side of the body & face
  • Lateral cortex = UE, upper trunk & face
  • Medial cortex = LE, lower trunk
  • Lesion = loss of sensation, impaired balance
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28
Q

Describe the sensory association area of the cortex

A
  • supplied by the ACA & MCA
  • sensory processing & sensory perception
  • Lesion = ideational apraxia (failure to conceptualize, plan, & execute complex sequences or motor actions involved in using tool bc of loss of perception of the object’s purpose)
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29
Q

Describe the frontal eye fields area of the cortex

A
  • supplied by the MCA
  • controls voluntary saccadic eye movements & smooth pursuits
  • Lesion = eyes deviate towards the lesion (look away from paralysis)
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30
Q

Describe Wernicke’s area of the cortex

A
  • supplied by the MCA & PCA 9dominant hemisphere usually left)
  • language comprehension
  • Lesion = pt cannot comprehend speech, pt can speak fluently, but output makes no sense, fluent/receptive aphasia
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31
Q

Describe the Broca’s area of the cortex

A
  • supplied by the MCA (dominant hemisphere usually left)
  • expressive language (speak, write, sign, etc.)
  • Lesion = inability to express one’s self through language (but comprehension is intact), nonfluent/expressive aphasia
32
Q

Describe the primary visual area of the cortex

A
  • supplied by the PCA
  • perceives visual info coming from the retina
  • Lesion = cortical blindness, loss of vision in contralateral 1/2 of the visual field, but pt may not feel the loss (visual agnosia)
33
Q

Describe the visual associations area & taste/gustatory area of the cortex

A
  • Visual association area: supplied by the PCA; makes sense of vision, recognizes faces & objects
  • Taste/gustatory area: supplied by the MCA; insular cortex & frontal operculum; detects & discriminates between tastes
34
Q

Describe the internal capsule of the sub-cortical regions

A
  • supplied by the MCA (Lenticulostriate arteries)
  • Sensory:contralateral loss of pain, temperature, touch and proprioception from entire extremities and face (remember where they relay?)
  • Motor: contralateral weakness of all muscles of the body
35
Q

Describe the midbrain of the sub-cortical regions

A
  • supplied by the basilar artery, PCA, & SCA
  • Sensory: Spinal Lemniscus (Pain and temp), Medial Lemnicus (touch and proprio)
  • Motor: Cranial nerve nuclei III, IV, MLF (causes internuclear ophthalmopegia), corticobulbar tract, corticospinal tract
36
Q

Describe the pons of the sub-cortical regions

A
  • supplied by the vertebrobasillar system (pontine, AICA, & sub cerebellar)
  • Sensory: Spinal Lemniscus (Pain and temp), Medial Lemniscus (touch and proprio), superior olivary nucleus (hearing), main sensory nucleus (sensation from V, VII, IX, X), ½ of the vestibular nucleus
  • Motor: Cranial nerve nuclei V, VI, VII, PPRF, corticospinal tract, reticulospinal tract
37
Q

Describe the medulla of the sub-cortical regions

A
  • supplied by the PICA & vertebral arteries

Open medulla:
- Sensory: Spinal Lemniscus (Pain and temp), Medial Lemniscus (touch and proprio), cochlear nuclei, spinal trigeminal nucleus (Pain and temperature from V, VII, IX, X)
- Motor: nucleus ambiguous (IX, X), hypoglossal nucleus (XII), lateral vestibulospinal tract, corticospinal tract

Closed medulla:
- Sensory: nucleus cuneatus (touch and proprioception from UE) & nucleus gracilis (touch and proprioception from LE), lateral spinothalamic tract (pain and temp)
- motor: nuclus ambiguous (IX, X), hypoglossal nucleus (XII), lateral vestibulospinal tract, corticospinal tract

38
Q

Clinical manifestations of an MCA syndrome (63% of ischemic strokes)

A
  • supplies primary motor & sensory cortices, Broca’s area, & Wernicke’s area
  • contralateral weakness (UE & face)
  • contralateral sensory impairment (UE & face)
  • aphasia (L/dominant hemisphere): expressive, receptive, global
  • neglect (R/nondominant hemisphere)
39
Q

Clinical manifestations of an ACA syndrome (6-7% ischemic strokes)

A
  • supplies the primary motor & sensory (LE), supplementary motor, & prefrontal cortex
  • sensory impairment in contralateral LE
  • weakness in contralateral LE
  • altered mental status: frontal lobe behavioral abnormalities (poor judgement, decreased attention, decreased motivation, difficulty registering emotions)
  • speech perseveration (aphasia)
  • abulia (a lack of drive/will power
40
Q

Clinical manifestations of a posterior cerebral artery (12-13% of ischemic strokes)

A
  • supplies the occipital lobe, inferior & lateral parts of temporal lobe (hippocampus), diencephalon structures (thalamus & sub thalamus), cerebral peduncles & midbrain
  • Contralateral homonymous hemianopsia
  • Contralateral limb weakness
  • Thalamic pain syndrome (abnormal sensations of temperature/proprioception/touch, tingling, paresthesia, intractable pain, allodynia)
  • Disruption of anterior supply – apathy, amnesia
  • Disruption of posterior supply – neglect (R hemisphere), aphasia
  • Visual agnosia, anomia
41
Q

Clinical manifestations fo a Lacunar syndrome (5-8%)

A
  • affects the basal ganglia, internal capsule, thalamus, & brainstem
  • small infarcts at the end of deep penetrating arteries, often affecting white matter
  • Pure contralateral weakness (posterior limb of internal capsule)
  • Pure contralateral sensory loss (posterolateral thalamus or posterior limb of internal capsule)
  • Parkinsonism (basal ganglia)
  • Large majority are asymptomatic
42
Q

Clinical manifestations of a vertebrobasillar artery syndrome (9%)

A
  • supplies corticospinal tracts, corticobulbar tracts, medial & superior cerebellar peduncles, spinothalamic tracts, & several cranial nerve nuclei
    -Deficits in sensory and motor cranial nerve functions
  • Headache, D/N/V, diplopia, nystagmus, dysarthria, dysphagia
  • Ipsilateral ataxia (possibly due to double-crossing over of pathways), Hemiparesis, dysmetria
  • Bilateral effects if trunk of basilar artery occluded
  • Locked in syndrome is due to stroke in basilar artery causing damage to pons/caudal midbrain; total body paralysis, while sparing vertical ocular movement, eye blinking; all sensation is greatly decreased if not absent; cognition and hearing intact
43
Q

Clinical manifestations of a superior cerebellar artery syndrome

A
  • supplies the superior cerebellar cortex, superior cerebellar peduncle, cerebellar nuclei, small portions of midbrain/pons
  • Headache, D/N/V, Nystagmus, diplopia, dysarthria
  • Dysmetria
  • Ipsilateral limb/gait ataxia
  • Ipsilateral Horner’s syndrome – damage to sympathetic nerves arising from superior cervical ganglion
  • Contralateral loss of touch/pain/temp in extremities, torso, and face if any
  • Contralateral mild hemiparesis if any
44
Q

Clinical manifestations of an anterior inferior cerebellar artery syndrome

A
  • supplies the anterior inferior surface of the cerebellum, cerebellar nuclei, portions of the pons & medulla (CN 5/7/8), vestibular & hearing organs in inner ear
  • symptoms referred to as Lateral Pontine Syndrome
  • D/N/V, nystagmus, diplopia, dysarthria, dysmetria
  • Ipsilateral deafness
  • Ipsilateral ataxia, ipsilateral loss of balance
  • Ipsilateral Horner’s syndrome (decreased sweating on face, ptosis, constricted pupil)
  • Ipsilateral loss of touch/pain/temp and weakness in face
  • Contralateral loss of pain/temp and weakness in limbs if any
45
Q

Clinical manifestations of a posterior inferior cerebellar artery syndrome (8%)

A
  • supplies the posterior inferior portion of the cerebellar hemispheres, the central nuclei of the cerebellum and dorsolateral medulla (cranial nerve nuclei V/VIII, IX, X)
  • Results in Lateral medullary syndrome or Wallenberg Syndrome
  • D/N/V, nystagmus, dysarthria (due to both cerebellar and CN IX/X reasons), dysmetria
  • Ipsilateral ataxia, ipsilateral loss of balance
  • Ipsilateral Horner’s Syndrome
  • Dysphagia (CN nuclei IX, X)
  • Hoarseness of voice (CN nuclei IX, X)
  • Ipsilateral loss of touch/pain/temp on face (CN V nucleus)
  • Contralateral loss of pain/temp on body if any
46
Q

Clinical manifestations of a spinal artery & vertebral arteries syndrome

A
  • results in medial medullary syndrome
  • supplies medial medulla
  • paresis of contralateral UE & LE
  • contralateral loss of touch & proprioception
  • ipsilateral tongue deviation (hypoglossal nucleus)
47
Q

Diagnosis of an ischemic stroke using CT scan

A
  • quickly know ‘nature’ of stroke, trade off between increased information about perfusion & the time needed to acquire such information
  • CT is the imaging of choice, used due to quickly determine ischemic vs hemorrhagic stroke
48
Q

What is important to know for diagnosing an ischemic stroke

A
  • know location & severity of stroke
  • quickly know nature of stroke - trade off between increased information about perfusion & the time needed to acquire such info
  • CT is imaging of choice to quickly determine ischemic vs hemorrhagic stroke
49
Q

What is the purpose of quick CT for stroke

A
  • to make decision about administering r-tPA
  • if CT reveals ischemic stroke administer IV tPA within 3 hrs of last known normal and to more selective groups within 4.5 hrs of last known normal
  • hemorrhagic stroke would contraindicate use of clot-busting drugs
50
Q

Describe early administration of NIHSS (NIH stroke scale)

A
  • not used for diagnosing nature or location of stroke but to assess severity of stroke
  • helps with consistent communication
  • allows objective measurement of changing clinical status
51
Q

NIHSS scoring

A
  • 0 = no stroke
  • 0-4 = minor stroke
  • 5-15 = moderate stroke
  • 16-20 = moderate to severe stroke
  • 21-42 = severe stroke
52
Q

Describe diagnosis of stroke using an MRI/PET scan

A
  • helps with localizing = lobe, structures that are damaged
  • severity/area of damage
  • detects the area of ischemic penumbra
  • determine who would be a good candidate for continued use of thrombolytic drugs
53
Q

Primary goal of acute care interventions for stroke

A
  • reperfusion/recanalization of the occluded vessels using pharmacologic management, end-vascular management, or a combination approach
54
Q

KNOW BP management guidelines (AHA) for acute care interventions for stroke

A
  • After rt-PA administration, keep BP less than 180/105
  • Not treated with t-PA & plan for mechanical thrombectomy: BP ≤185/110 before procedure and ≤180/105 first 24 hrs after procedure
  • Mechanical thrombectomy performed = control BP < 180/105
  • Not treated with t-PA or mechanical thrombectomy = permissive HTN up to 220/120, if >220/120 decrease by 15% in first 24hrs post-stroke
55
Q

KNOW Oxygen saturation and surgical intervention guidelines (AHA) for acute intervention for stroke

A
  • O2 Sat: maintain ≥94% and supplement O2 if needed to maintain >94%
  • Surgical: mechanical endovascular thrombectomy (stent placement) up to 8hrs after Sx onset
56
Q

Blood glucose from new slides***Other acute care pharmacologic interventions for stroke

A
  • Once neurologically stable obtain BP 140/90 with use of diuretics & ß–blockers
  • Use of anti-thrombotic/thrombolytic agents if indicated but avoid for 24hrs after rt-PA
  • Mannitol for edema management as it can increase ICP & put pressure on the cerebellum/brainstem (most common fatal complication)
  • Hypoglycemia should be assessed and treated to keep blood glucose between 140-
    180 mg/dL as hypoglycemia is related to worse outcome
57
Q

Most common fatal complication of stroke

A
  • Edema causing ICP and increased pressure on cerebellum and brainstem
58
Q

Prophylactic interventions for stroke

A
  • Anticoagulation
  • Lipid-lowering Agents (statins)
  • Neuroprotection
  • Nerve growth factor
  • Surgical intervention
59
Q

Describe anticoagulation as a stroke intervention

A
  • Goad standard for prevention of ischemic stroke
  • should not be used if at risk of hemorrhagic stroke
  • Aspirin, Clopidogrel (Plavix), Warfarinn sodium (Coumadin, Panwarfin), Dabigatran (Pradaxa), Rivaroxaban (Xarelto), Apixaban (Eliquis)
60
Q

Describe neuroprotection as a stroke intervention

A
  • compounds that decrease excitotoxicity by reducing glutamate levels
  • Magnesium ion, Minocycline
61
Q

Describe nerve growth factor as a stroke intervention

A
  • neurotrophic factor that supports the survival & growth of neural cells
  • Noggin
62
Q

Describe surgical intervention for stroke

A
  • Carotid endarterectomy
  • needs to be considered if stenosis is >70% & patient is younger than 80 y/o
63
Q

Describe sub-acute interventions for control of stroke symptoms

A
  • Spasticity: Baclofen & benzodiazepines work at the level of the spinal cord; Dantrolene works on the muscle fibers; Botulinum toxin A (Botox) spot specific to muscle injected
  • Urinary incontinence: Urge incontinence (anticholinergics); Areflexic bladder (self catheterization or Foley catheter
  • Depression: Tricyclic antidepressants, SSRI, SNRI
64
Q

Prognosis based on the NIH stroke scale score

A
  • ≥16 suggests a high probability of death or severe debility
  • ≤6 suggests good recovery
65
Q

Types of hemorrhagic strokes

A
  • Hemorrhagic stroke = bleeding from an arterial source
  • Intracerebral hemorrhage
  • Subarachnoid Hemorrhage
  • Subdural Hemorrhage
  • Epidural Hematoma
66
Q

Describe intracerebral hemorrhage stroke

A
  • Bleeding into brain parenchyma
  • Most deadly subtype of stroke with a 40-50%
    mortality
  • Incidence low among young people, increases
    dramatically after 65 years of age
  • Risk factors – chronic HTN, alcohol abuse,
    substance abuse, chronic thrombolytic therapy, smoking, eclampsia during pregnancy
67
Q

Pathogenesis of an intracerebral hemorrhage (ICH) stroke

A
  • Dysfunction in cerebral microvasculature secondary to chronic HTN
  • Replacement of smooth muscle cells by collagen/fat/amyloid, weakening of arterial walls, formation of aneurysms prone to rupture/leakage,
  • Mostly in smaller deep penetrating arteries – lenticulostriates, arteries entering thalamus, brainstem
  • Expansion of hematoma – grey matter more prone to compression than white matter
  • Blood can be reabsorbed in weeks/months, leaving a cavity surrounded by necrotic tissue
  • Damage to brain tissue from lack of blood supply, edema, inflammation, necrosis
68
Q

Clinical manifestations of an ICH (intracerebral hemorrhage) stroke

A
  • Similar types of clinical presentation as ischemic stroke
  • Initial symptoms are related to area where bleed occurs
  • Additional neurologic symptoms occur gradually representing expansion of hematoma
  • As bleed enlarges ICP may increase causing headache, vomiting and decreased alertness
  • Seizures are possible with cerebral cortex causing the most seizure activity
69
Q

Diagnosis of an ICH (intracerebral hemorrhage) stroke

A
  • CT scan: allows prompt diagnosis of ICH; size & location of hematoma; presence & extent of any mass effect
  • MRI: limited usefulness in first 24hrs
  • Angiograph: performed if patient is young & not hypertensive; cocaine use; to rule out AVM/Aneurysm/Vasculitis or Tumor
  • PT/INR & Platelet count: rule out bleeding disorder
70
Q

Treatment for stroke

A
  • Needs rapid transport to emergency department due to decreased consciousness & may require intubation
  • Decrease elevated BP through use of rapid acting, potent antihypertensive medication; maintain systolic BP <140 (recommend if BP >160-180/105
  • Reduce increased ICP using Mannitol in case of cerebral edema
  • Anticonvulsants for seizure management
  • Emergent surgical draining if neurological condition deteriorates to reduce ICP (especially for cerebellar hemorrhage), may suddenly deteriorate to coma/death
  • If on Vit K antagonist (Warfarin), correct INR/PT with Vit K (takes 12-24hrs); fresh frozen plasma (FFP) or prothrombin complex concentrates (PCCs) work immediately
71
Q

Prognosis of a stroke

A
  • Mortality is high but functional recovery of survivors is also high if person survives initial changes in ICP
  • Size of hemorrhage is greatest predictor of outcome, second is location
  • Coma leads to poorer prognosis
72
Q

Describe a subarachnoid hemorrhage

A
  • Bleeding into subarachnoid space
  • Mostly in older women: >70 y/o
  • Risk factors: HTN, alcohol abuse, smoking
  • Etiology: Aneuryms and vascular malformations
73
Q

Etiology of subarachnoid hemorrhage (SAH)

A
  • Berry aneurysms: abnormal local dissension occurring at vessel bifurcations
  • About 90% of SAH are due to berry aneurysms
  • Aneurysms are caused by congenital defects & degenerative changes in vessel walls
  • Vascular malformations
  • Venous malformations
  • Arteriovenous malformations (AVMs): direct communication b/w artery to vein; abnormal fetal development
74
Q

Clinical manifestations of SAH (subarachnoid hemorrhage)

A
  • Sudden onset with severe thunderclap headache/sentinel headache; sudden intense & persistent, preceding spontaneous subarachnoid hemorrhage (SAH) by days or wks
  • Sentinel headache: warning sign of leaks from aneurysm
  • At the time of rupture, Sx include nausea/vomiting, altered mental status (syncope, confusion, coma), lethargy, seizure, neck pain, nuchal rigidity
  • Focal neurological signs like hemiplegia or hemianopia are absent, unless bleeding into brain parenchyma
75
Q

Medical management of SAH (subarachnoid hemorrhage)

A
  • Diagnosis: CT scan, Angio, MRI
  • Treatment: Immediate neurosurgery to isolate the aneurysm or rupture site, evacuate hematoma to prevent further damage
  • Prognosis: Mortality is high in elderly; If hematoma is <3cm, prognosis is good
76
Q

Describe subdural hemorrhage

A
  • Result of tearing of bridging veins b/w brain surface & dural sinuses
  • Mostly occur in elderly after falls 2ndy to increased movement of brain inside skulls (due to brain atrophy, fragility of bridging veins)
  • If blood accumulates, compression of brain tissue can result in herniation of cortex into adjoining spaces
77
Q

Describe an epidural hemorrhage

A
  • Result of tearing of meningeal arteries that run in b/w the dura
  • Can be torn 2ndy to trauma
  • Medical emergency, need immediate evacuation to prevent compression of brainstem structures, which may cause death

Clinical Medicine III (20 decks)

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