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STEP 5: NEURO SHELF > Stroke_StepUp_Pre-Test > Flashcards

Stroke_StepUp_Pre-Test Flashcards

1
Q

What is the MOST COMMON etiology of a TIA/CVA? Does the risk of stroke in a pt with TIA history increase?

A

EMBOLI

YES, risk of stroke in a preceding TIA pt is 10%, with 30% 5-year risk of stroke

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2
Q

What are the risk factors of an ISCHEMIC stroke?

A

MOST IMPORTANT - Age>40yo, HTN
Others - DM, HL, Obesity, Smoking
Afib, CAD, Carotid bruits, previous stroke/TIA

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3
Q

What are other rare causes/risk factors of an ISCHEMIC stroke in particularly younger pts?

A

VASCULAR - Vasospasm (amphetamines, cocaine), Vasculitis
METABOLIC - Sickle cell disease, Hypercoagulable states (Protein C, S deficiency, Factor V leiden mutation, Anti-Thrombin III Def, Prothrombin mutation, anti-phospholipid syndrome, OTC use), PCV, CNS

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4
Q

Which two systems can a TIA affect? How do they present?

A

1) CAROTID - Temporary hemiparesis, clumsiness of one limb, dysarthria
2) VERTEBROBASILAR SYSTEM - Decreased perfusion of the posterior fossa (medulla and pons - dysarthria, horseness, dysphagia, numbness of ipsilateral face, projectile vomiting, double vision, vertigo, headaches, drop attacks

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5
Q

What is AMAUROSIS FUGAX? How do they classically present?

A

Example of TIA that presents with TRANSIENT, CURTAIN-like loss of eyesight in IPSILATERAL EYE due to MICROEMBOLI to retina

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6
Q

What is the first imaging study that should be obtained in the evaluation of an acute stroke? Why?

A

CT Head WITHOUT CONTRAST - To distinguish between ischemic and hemorrhagic infarct

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7
Q

How do you tell the difference between ISCHEMIC and HEMORRHAGIC stroke on CT scan without contrast?

A 
ISCHEMIC = DARK 
HEMORRHAGIC = WHITE
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8
Q

Why might you miss an ISCHEMIC STROKE on CT head w/o contrast? (2 reasons)

A
  1. Timespan - Ischemic strokes usually take 24-48hrs to visualize the infarct on CT
  2. Small size - <1cm may be missed
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9
Q

What is the MOST SENSITIVE imaging test for stroke eval? Why is this one not preferred in an emergency setting?

A

MRI - Identifies ALL infarcts + detects earlier than CT (95% infarcts detected within 24hrs)

NOT preferred in emergency because it takes LONGER to perform + Not suitable for potentially UNSTABLE pts

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10
Q

What is the MOST DEFINITIVE test for identifying etiology of stroke?

A

MRA - Magnetic resonance arteriogram
Identifies stenotic vessels of the head and neck
Evaluates carotids, vertebrobasilar circulation, circle of willis, anterior, middle, and posterior cerebral arteries

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11
Q

If pt has carotid bruit, peripheral vascular disease, and CAD, what SCREENING TEST should be ordered?

A

CAROTID DUPLEX US - Estimates degree of carotid stenosis

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12
Q

If a pt is young (<50) and presents with stroke, what states should you look out for? (3)

A
  1. CNS VASCULITIS
  2. HYPERCOAGULABLE STATES
  3. THROMBOPHILIA
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13
Q

What tests should be ordered in a young pt (<50) presenting with stroke?

A
  1. Test hypercoagulable states - PROTEIN C, PROTEIN S, anti-phospholipid Abs, Factor V Leiden mutation
  2. Test autoimmune conditions - ANA, ESR, RF
  3. Test infectious causes - VDRL/RPR, Lyme serology
  4. Test cardiac embolic sources - TEE
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14
Q

Which type of stroke classically presents in a SLOWLY PROGRESSIVE in which pt AWAKES from sleep with neuro deficits?

A

THROMBOTIC STROKE

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15
Q

Which type of stroke classically presents with MAX DEFICITS AT ONSET (VERY RAPID WIHTIN SEC)?

A

EMBOLIC STROKE

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16
Q

What are the 3 possible complications of a stroke?

A
  1. CEREBRAL EDEMA - Occurs within 1-2 days -> Cause MASS EFFECTS for up to 10days
  2. HEMORRHAGE INTO INFARCTION Rare
  3. SEIZURES <5%
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17
Q

What is the TREATMENT for CEREBRAL EDEMA-RELATED MASS EFFECT as a complication of stroke?

A

HYPERVENTILATION + MANNITOL(osmotic diuretic) - to lower ICP

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18
Q

What are the 3 categories of STROKE TREATMENT?

A
  1. ACUTE Treatment
  2. BP Control
  3. Prevention Recurrence
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19
Q

ACUTE TREATMENT: What must be secured most initially?

A

ABC - Airway, Breathing, Circulation (O2, IVF)

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20
Q

ACUTE TREATMENT: What is the window of tPA?

A

3hours - Improves clinical outcome in 3mo

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21
Q

ACUTE TREATMENT: What are the exclusion criteria of tPA due to increased risk of HEMORRHAGIC TRANSFORMATION?

A
  1. UNCONTROLLED HTN (BP>185/110)
  2. WARFARIN USE with INR>1.7
  3. HEP USE with PTT>15
  4. PLT<100K
  5. Disorders that INCREASE risk of bleeding (AVM, ANEURYSM, NEOPLASM)
  6. <3mo of INTRACRANIAL or INTRASPINAL SURGERY
  7. <3wks of ACTIVE INTERNAL BLEEDING
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22
Q

ACUTE TREATMENT: If tPA is given, what must you NOT give for the first 24hrs?

A

ASA - due to 3% risk of intrancranial hemorrhage

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23
Q

ACUTE TREATMENT: If tPA window is past (>3hrs since stroke onset), which medication can be given to pt?

A

1) ASA
2) If pt cannot take ASA, give CLOPIDOGREL
3) If pt cannot take ASA or PLAVIX, then TICLOPIDINE

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24
Q

ACUTE TREATMENT: What is the efficacy of ANTICOAGULANT USAGE in stroke?

A

HEP or WARFARIN - NOT Shown to have efficacy in acute stroke
Generally NOT given in acute setting

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25
Q

ACUTE TREATMENT: What are the measures of preventing aspiration?

A

1) HEAD OF BED ELEVATION 30deg

2) Assess pt’s ability to protect his/her airway -> NPO

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26
Q

BP CONTROL: Do NOT give anti-hypertensives unless which conditions?

A

1) VERY HIGH BP - Systolic >220, Diastolic >120, MAP >139
2) Significant medical indication for anti-hypertensive - MI, aortic dissection, HF, HTN encephalopathy
3) RECEIVED TPA - aggressive BP control necessary to reduce bleeding likelihood

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27
Q

PREVENTION: What are the recommended preventative measures of LARGE VESSEL ATHEROSCLEROSIS-mediated STROKE?

A

1) Control RISK FACTORS - HTN, DM, HL, HL, OBESITY
2) ASA
3) SURGERY - carotid endarterectomy

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28
Q

PREVENTION: What is the indication of CAROTID ENDARTERECTOMY?

A 
LARGE VESSEL (>70% carotid artery stenosis) in SYMPTOMATIC pts with ACUTE THROMBOTIC STROKE 
**NASCET TRIAL
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29
Q

PREVENTION: What is the recommended preventative measure for ASYMPTOMATIC LARGE VESSEL ACUTE THROMBOTIC STROKE?

A

REDUCTION of atherosclerotic factors and ASA only
NO CAROTID ENDARTERECTOMY

**4 major studies - 3 showed no benefit of CE, 1 (ACAS) showed very small benefit with Asx CA stenosis >60^% pts

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30
Q

PREVENTION: What are the recommended preventative measures of ACUTE STROKE of EMBOLIC etiology?

A

1) ANTI-COAG (ASA)

2) Reduce risk factors - HTN, HL, DM, Smoking, obesity

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31
Q

PREVENTION: What are the recommended preventative measures of ACUTE THROMBOTIC LACUNAR STROKE?

A

1) Control HTN!!

32
Q

What is the MOST COMMON cause of INTRA-CEREBRAL HEMORRHAGIC STROKE?

A

HTN

33
Q

What are some other less common causes of INTRA-CEREBRAL HEMORRHAGIC STROKE other than HTN?

A

1) ISCHEMIC STROKE conversion to hemorrhagic stroke
2) CEREBRAL AMYLOID ANGIOPATHY - Complication of Alzheimer’s
3) Hypo-coagulable state - Liver disease, anti-coag/anti-thrombolytic use
4) Neoplasm
5) AVM
6) Drugs - Cocaine
7) Trauma

34
Q

What is the classic presentation of a INTRA-CEREBRAL HEMORRHAGIC STROKE?

A

Sudden onset of focal neuro deficits that worsen steadily over 30-90min -> INCREASED ICP (Headache, vomiting, bradycardia, decreased alertness/consciousness/stupor/coma)

35
Q

What types of stroke are associated with COCAINE USE?

A

1) ISCHEMIC - Vasospasm
2) HEMORRHAGIC - INTRACEREBRAL (ICH)
3) SAH
ALL TYPES OF STROKE

36
Q

Which physical exam finding is particularly useful in localizing the lesion of the ICH?

A

PUPILLARY FINDINGS

37
Q

Pupillary finding of ICH in PONS? in THALAMUS? in PUTAMEN?

A

1) PONS = PINPOINT PUPILS (Lesion of SYMPATHETIC fibers = Unopposed PARASYMPATHETIC-mediated constriction)
2) THALAMUS = POORLY REACTIVE PUPIL
3) PUTAMEN = DILATED PUPILS

38
Q

What are the possible complications of ICH?

A

1-3) INCREASED ICP, REBLEEDING, HYDROCEPHALUS
4-5) SEIZURES, VASOSPASM
6) SIADH

39
Q

What are the 3 steps of Treatment of HEMORRHAGIC STROKE? (Same as ISCHEMIC)

A

1) ACUTE TREATMENT - Secure ABC, MICU admission
2) BP CONTROL
3) PREVENTION of recurrence

40
Q

ACUTE TREATMENT: Why is airway management particularly important in HEMORRHAGIC STROKE pts?

A

Altered mental status + Decreased respiratory drive -> Often require INTUBATION

41
Q

BP CONTROL: Why must BP reduction be GRADUAL?

A
  • ELEVATED BP -> INCREASES ICP -> Causes FURTHER RE-BLEEDING
  • HYPOTENSION -> Lowers cerebral blood flow -> WORSENS neuro deficits

RESULT - BP Control must be gradual so as to NOT induce HYPOTENSION

42
Q

BP CONTROL: What are the measures for treating HTN in ICH?

A

SBP>160-180

DBP>105

43
Q

What is often the TREATMENT of choice for lowering BP in a HEMORRHAGIC STROKE PT?

A

NITROPRUSSIDE

44
Q

HEMORRHAGIC STROKE: Which other treatment scan be given to reduce ICP? Can this be given PPX?

A

MANNITOL (Osmotic agent) + DIURETICS

NO, DO NOT give them prophylactically

45
Q

HEMORRHAGIC STROKE: Is the use of steroids recommended?

A

NO - actually harmful

46
Q

HEMORRHAGIC STROKE: Rapid surgical evaluation of ___ HEMATOMAS can be lifesaving particularly if hemorrhage >3cm

A

CEREBELLAR HEMATOMA evacuation (SURGICAL DECOMPRESSION) can be lifesaving

Often times, surgical intervention is NOT helpful in most ICH cases

47
Q

What is the most common cause of SAH?

A

Ruptured saccular (berry) aneurysm at BIFURCATIONS OF ARTERIES of CIRCLE OF WILLIS -

1) Anterior communicating Artery w/ ACA
2) PCommArtery w/ ICA
3) MCA Bifurcation

48
Q

What are other causes of SAH?

A

TRAUMA
AVM
VENOUS INFARCT

49
Q

What is the classic description of a SAH?

A

1) WORST HEADACHE of my life in the ABSENCE of focal neuro deficits
2) Sudden transient LOC
3) Vomiting
4) Meningeal signs - Nuchal rigidity + Photophobia (Takes several hrs to develop)
5) Retinal hemorrhages - 30% pts

50
Q

Which pathologies are associated with BERRY ANEURYSMS?

A

1) POLYCYSTIC KIDNEY DISEASE
2) AORTA COARCATION
3) MARFAN DISEASE

51
Q

Which exam is absolutely mandatory for SAH candidate? Why?

A

OPTHALMOLOGIC EXAM! - R/o papilledema

If + Papilledema - Do NOT perform LP (May cause herniation)

52
Q

If papilledema is present in a SAH candidate, what test do you NOT perform? What diagnostic test do you do instead?

A

Do NOT do an LP - possible herniation

INSTEAD do CT scan

53
Q

What is the initial SCREENING test for SAH?

A

CT Scan WITHOUT CONTRAST - Identifies 90% of SAHs

54
Q

What is the DIAGNOSTIC TEST for SAH?

A

LP - Perform this if CT is unremarkable or negative + high clinical suspicious

BLOOD in CSF (not from traumatic spinal tap) = XANTHOCHROMIA (YELLOW CSF) from RBC lysis

Yellow indicates that the blood has been in CSF for several hours

55
Q

After diagnosis of SAH is made, what is the DEFINITIVE study for detecting site of bleeding?

A

CEREBRAL ANGIOGRAM - Detect site of bleeding for surgical clipping

56
Q

What are possible complications (5) of an SAH? Hint: Think vascular (2), too much blood (2), endocrine

A

1-2) Vascular - RERUPTURE + VASOSPASM (More often with ANEURYSMAL SAH) resulting in ISCHEMIA/INFARCTION -> ISCHEMIC STROKE
3-4) Too much blood - COMMUNICATING HYDROCEPHALUS 2/2 blood within subarahcnoid space hindering normal CSF flow + SEIZURE (blood acts as irritant)
5) SIADH

57
Q

What are two possible avenues of treatment of an SAH?

A

1) SURGICAL - Consult neurosurg: Surgically treat berry aneurysms (ANEURYSM CLIPPING)
2) MEDICAL

58
Q

MEDICAL TX SAH: What are the main goals of medical treatment for SAH?

A

Prevent risk of REBLEEDING + VASOSPASM

  1. Rebleeding - STOOL SOFTENERS -> Avoid straining/sex (which would INCREASE ICP -> Risk of re-rupture)
  2. Vasospasm - Ca CHANNEL BLOCKER (NIFEDIPINE/NIMODIPINE) generally peaks 7-10d

OTHER

  1. BP Control - Lower BP gradually bec ELEVATED BP could be COMPENSATION for decrease in cerebral perfusion pressure 2/2 INCREASED ICP OR CEREBRAL ARTERY STENOSIS
  2. Headache control - ACETAMINOPHEN
  3. Hydration - IVF
  4. BED REST in quite, dark room
59
Q

What is the most common cause of ICH (LOBAR) in elderly pts (>70yo) without HTN + MULTIPLE CORTICAL HEMORRHAGES (often seen on gradient Echo MRI) +/- dementia?

A

CAA - CEREBRAL AMYLOID ANGIOPATHY

60
Q

What type of lesions can be clarified with NERVE CONDUCTION STUDIES?

A

PERIPHERAL NERVOUS SYSTEM

61
Q

What does it mean when a lesion appears largely the same on UNENHANCED + ENHANCED CT scans?

A

Means that it is a HEMATOMA

62
Q

What is the most common cause of a SAH? What is this pathology most likely 2/2?

A

Ruptured SACCULAR BERRY, MYCOTIC ANEURYSM - 2/2 Gm+ or Gm- infections (relatively low virulence) that form over cerebral convexities with SUBACUTE BACTERIAL ENDOCARDITIS -> Bleed directed into subarachnoid space

63
Q

What is the most appropriate choice of therapy for FOCAL SEIZURE as a complication of ICH?

A

LEVETIRACETAM (KEPPRA)

64
Q

Why is LAMOTRIGINE (LAMICTAL) generally NOT given for a FOCAL SEIZURE as a complicaiton of ICH?

A

Bec LAMOTRIGINE needs to be SLOWLY TITRATED over many weeks when first started due to risk of SEVERE RASH

65
Q

What is the most common AE of LAMOTRIGINE?

A

SEVERE RASH

66
Q

FOCAL WEAKNESS lasting for 24hrs AFTER MOTOR SEIZURE is evidence of __? What diagnostic test must be ordered to r/o something more serious?

A

POSTICTAL PARALYSIS - TODD PARALYSIS

CT imaging - necessary to r/o bleeding or new areas of cerebrocrotical damage

67
Q

What is the pathophysiology of TODD PARALYSIS?

A

TODD PARALYSIS = Post-ictal paralysis - Neuronal exhaustion (Epileptic focus neuronal Glc depletion) after frequent repetitive discharges

68
Q

FACIAL CUTANEOUS ANGIOMAS (Port-wine nevus) + INTRACRANIAL LEPTOMENINGEAL ANGIOMAS + MENTAL RETARDATION = __?

A

STURGE-WEBER SYNDROME (ENCEPHALOFACIAL ANGIOMATAOSIS)

69
Q

For STURGE-WEBER SYNDROME pts, what motor deficits are generally seen?

A

HEMIPARESIS/ HEMIATROPHY on side CONTRALATERAL to port-wine nevus

70
Q

Where is the nevus associated with STURGE-WEBER SYNDROME generally located?

A

SENSORY DISTRIBUTION of first division of trigeminal nerve (usually on ONE SIDE of face) + ANGIOMA of the CHOROID OF EYE

Intracranial angioma UNLIKELY if UPPER FACE is not involved

71
Q

What are associations of HEMANGIOBLASTOMAS? (Hint: VHL SYNDROME)

A

CEREBELLAR HEMANGIOBLASTOMAS + RENAL CELL CARCINOMA + PHEOCHROMOCYTOMA + POLYCYSTIC KIDNEY DISEASE + RETINAL TELANGIECTASIAS

72
Q

Where is the most common site for hematoma formation 2/2 CHARCOT-BOUCHARD MICROANEURYSMS (Due to chronic HTN-mediated hyaline arteriosclerosis of the arteries)?

A

PUTAMEN

73
Q

What is the difference between CHARCOT-BOUCHARD and FUSIFORM aneurysms?

A

CHARCOT BOUCHARD - SMALL aneurysms 2/2 chronic HTN, most commonly appears in PERFORATING ARTERIES

FUSIFORM - DIFFUSELY WIDENED aneurysms 2/2 atherosclerotic damage to arterial wall + Evaginations along walls (BERRY-SHAPED/SACCULAR structures WITHOUT stalks)

74
Q

What are some example CLASSICAL Sx of EXTRACRANIAL INTERNAL CAROTID ARTERY DISEASE?

What diagnostic test should be done to confirm this?

A

IPSILATERAL TRANSIENT MONOCULAR CLINDNESS (AMAOUROSIS FUGAX) + CONTRALATERAL ischemic attacks consisting of motor weakness

CAROTID DOPPLER OR MRI/MRA

75
Q

What type of infarct is generally mostly associated with MIXED TRANSCORTICAL APHASIA (-F,-C,-R)?

A

WATERSHED INFARCTS - 2/2 protracted hypotension and limits of supply of principal cerebral arteries is LIMITED/ HYPOPERFUSED -> Isolated infarcts in speech areas of FRONTAL (broca) and TEMPORAL (wernicke) areas

76
Q

What type of infarct is generally mostly associated with ANOMIC APHASIA (+F,+C,+R)?

A

DIFFUSE BRAIN DYSFN - isolated word finding deficit

77
Q

What are the typical features of CEREBELLAR INTRAPARENCHYMAL HEMORRHAGE?

A

OCCIPITAL HEADACHE (radiates to neck/shoulders) + NECK STIFFNESS (blood extends into 4th ventricle) + N/V over long duration of hours + NYSTAGMUS + IPSILATERAL HEMIATAXIA of trunk (vermis) and/or limbs (cerebellar hemispheres)

STEP 5: NEURO SHELF (9 decks)

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