Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q 
ascending paralysis (rubbery legs) 
delayed DTRs (hypo, areflexia)
peripheral nerve involvement (tingling dyesthesia)
Bulbar weakness
myelin damage
A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Axon hillock is rich in

A

sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common cause of acute paralysis
Acute/Subacute
Symmetric limb weakness with absent or reduced DTR
Widespread inflamm demyelination 2 to hypersensitivity (autoimmune) reaction
Potentially reversible condition (90%)

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Age
Axonopathy
Autonomics

A

Poor prognosis in GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GBS pathophy

Immune response to nonself antigen misdirecting host nerve tissue through resemblance of epitope

A

Molecular mimicry
Ganglioside - myelin sheath attack
Antiganglioside antibody (GM1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GBS is related to antecedent infections:

A 
C jejuni infection GM1 antiganglioside
CMV
EBV
Mycoplasma 
Lymphoma
Rabies and swine vaccine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Classical form of GBS

A

Demyelinating
Acute Inflammatory Demy PN

Worldwide distrib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Axonal form

A

Acute motor axonal PN
Acute motor sensory PN

China, Japan, Mexico

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ataxia
Areflexia
Ophthalmoplegia

AntiGQ1b IgG antibody

A

Miller Fisher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

AIDP vs AMAN

A 
AMAN more of children, AIDP equal
AMAN also in C jejuni 80
Site of attack
AMAN: nodes of ranvier (mac demyelination and lympho infiltration)
AIDP: Schwann cell (axonal loss)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

GBS criteria for diagnosis

A 
Ascending symmetrical motor paralysis 
Max deficit in 4 weeks peaking at 2
Areflexia
EMG NCV abnormality
CSF - elevated CSF protein 100-1000 
CSF cell count less than 10
Cytoalbuminologic dissociation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Electrodiagnostic medicine finding earliest feature in AIDP

A

Prolonged F wave latency

Distal motor latency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

GBS mx

A

IV Ig
Plasma exchange
Supportive (pneumonia and DVT prophy)
Monoclonal antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

IVIg in GBS

A

shortens duration of course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common form of progressive motor neuron disease

Most devastating of neurodegen disorders

A

ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ALS rf

A

Pesticide, insecticide
Smoking
Service in military

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ALS hallmark

A

Death of LMN and UMN

Selective loss of fxn then both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ALS affects

A

Anterior horn cell

also polio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

If LMN predominantly:

A 
Bulbar palsy (brainstem)
SMA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Upper MN

A

Pseudobulbar palsy

Primary lateral sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

insidious developing asymmetric weakness
distal first
ms wasting
atrophy, twitching, fasciculation, small muscle groups
hyperactivity of reflex
dysarthria and exaggerated motor expression of emotion

A

ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ALS develops concurrently with

A

frontotemporal dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ALS pathogenesis

A

Superoxide dismutase 1 SOD1 mutation

AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Drug that lengthens survival of ALS

Diminishes glutamate release

A

Riluzole

Nausea, dizziness, weight loss and LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Leakage or rupture of congential aneurysm on circle of willis, angioma

Headache, stiffness, loss of consciousness

A

SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Most common cause of SAH is

A

head trauma

ruptured saccular aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Perimesencephalic cistern, benign

A

Idiopathic SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Annual risk of rupture in >/= 10 mm

A

0.5-1%

<10 0.1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Giant aneurysm >2.5cm risk of rupture

A

6% in 1st year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Most common locations of sacular aneurysm

A

Terminal ICA
MCA bifurcation
Top of basilar artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Distal to first bifurcation of major arteries in circle

due to bacterial endocarditis becoming septic degeneration

A

Mycotic aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

85% of ruptured aneurysms are at

A

anterior circulation

ACom, MCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

In aneurysm development, this disappears at base of neck

A

internal elastic lamina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Greatest risk of rupture

A

> 7mm diameter
Top of basilar
Origin of PCom (oculomotor palsy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

SAH is associated with severe headache with exertion in

A

45%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Four major causes of delayed neurologic deficit

A

1 rerupture
2 vasospasm
3 hydrocephalus
4 hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Major cause of delayed morbidity and death SAH

A

Vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

vasospasm tx

A

Nimodipine for 21 days

signs appear 4-14 days mean 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hunt and Hess grading 1

A

Mild headache
Normal mental status
No CN/Motor finding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Severe headache
Normal mental status
Cranial nerve deficit

A

H & H Type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Somnolent
Confused
Cranial nerve and mild motor deficit

A

H & H Grade III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Stupor
Moderate to severe motor def
Intermittent reflex posturing

A

H & H Grade IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Coma
Reflex
Flaccid

A

H & H Grade V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Fisher grade is

A

based on radiologic thickness of SAH on CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Indicated only if CT scan not available at time of suspicion

A

Lumbar puncture

46
Q

Yellowing of spinal fluid in SAH at

A

6-12 h peaking in intensity at 48h

Xanthochromia

47
Q

SAH dx

A

Four vessel angiography

CT angiogram (alternative)

48
Q

SAH hyponatremia may occur during

ECG may reveal:

A

1st two weeks

ST segment and T wave or prolonged QRS
changes similar to mi

49
Q

Eliminates risk of rebleeding

Assoc with neurologic morbidity

A

Clipping

50
Q

Endovascular SAH technique
platinum coil through femoral catheter
Thrombosis and walling off circulation

A

Coiling

51
Q

2nd leading cause of death worldwide

Abrupt onset of neurologic deficit that is attributable to a focal vascular cause

Clinical manif are variable:
Location
Blood vessel involved

A

Stroke

52
Q

Most of the time abrupt onset within minute (maximal symptom within minutes)

A

Cardioembolic

53
Q

Normal cerebral blood flow

A

50-55 ml/100g brain

54
Q

Core infarct

A

<12 ml/100g / min

55
Q

Electrically silent, structurally intact, potentially salvageable area of viability surrounding ischemic core

A

Penumbra

18 - 35 ml/100g / min

56
Q

Area between normal brain and penumbra

A

Benign oligemia

57
Q

Histologic effect are similar to hypoxia and anoxia

A

Hypoglycemia

58
Q

Zone of neurons most sensitive to hypoxia

A

CA-1 of hippocampus pyramidal cell

59
Q

Reduction in blood flow lasting longer than several seconds

Neuro symptoms manifest due to lack of glycogen

A

Cerebral ischemia

60
Q

Cessation of blood flow lasting more than a few minutes

Death of brain tissue

A

Cerebral infarct

61
Q

Causes of generalized/global infarction

A

Hypotension

Cardiac arrest

62
Q

Cause of focal infarction

A

Atherosclerosis
Arteriolosclerosis
Embolism
Vasculitis - CTD SLE, TB Meningitis

63
Q

Virchow’s triad

A

Bood flow stasis
Hypercoagulability
Endothelial dysfunction

64
Q

Hypotension resulting in generalized ischemia is felt especially in

A

Arterial border zone pattern
Watershed area
After a few days: Wedge shaped hemorrhagic infarct usually between MCA and ACA
Subject to reduction in blood flow
If patient dies immediately, no microscopic change

65
Q

Cardiac arrest leading to diffuse neuronal necrosis of the cerebral and cerebellar cortices
More severe within sulci than gyri
Inc in severity from frontal and temporal to occipital lobe

A

Laminar necrosis

Hippocampus
Purkinje of cerebellum

66
Q

Spectrum of change accompanying acute CNS hypoxia/ischemia
Earliest morphologic marker of neuronal death
Hallmark of acute neuronal injury

A

Red neuron

acute neuronal injury

67
Q

Red neurons are seen after irreversible hypoxic/ischemic insult:

A

12-24 hours

68
Q

Hyperacute CT findings

A 
Loss of grey-white matter interface
Obscuration of lentiform nucleus
Dense MCA sign (sludging of flow due to thrombus)
Insular ribbon size
Sulcal effacement
69
Q

CT scan should be carried out in suspected stroke within

A

30 mins

70
Q

Infarct ensues within

A

4-10 mins

71
Q

Blood flow restored to ischemic tissue before significant infarct develops

Not time bound

No neuroimaging evidence of infarct

ABCD2 scoring system

A

Transient ischemic attack

72
Q

Block of central retinal artery
or from blockage of internal carotid (ophthalmic)
leading to transient monocular blindness of ipsilateral eye

A

Amaurosis fugax

73
Q

Ischemic but reversibly dysfunctional tissue surrounding a core area of infarct
Saving this is goal of revasc therapy

A

Ischemic penumbra

74
Q

Infarct Pathogenesis

A 
Hypoxia/Anoxia
Altered Na/K ATPase pump (cellular swelling) 
Glutamate activation
Calcium influx 
Ischemic injury (red neuron, vacuolation cell death karyorrhexis >1d) 
Inflammation-edema (>3d) 
Macrophage (>5d) 
Liquefaction cavity (>1w) 
Glial proliferation (>1w)
75
Q

Nitric oxide synthase

Vasodilation
Angiogenesis
Neural development

A

Enzyme catalyzing production of nitric oxide from arginine

76
Q

Contralateral hemiparesis and hemisensory loss
Face and UE > LE
Aphasia (Wernicke, Broca, Conduction) if infarct involves dominant cerebral hemisphere left parietal and temporal
Homonymous hemianopsia
Paralysis of conjugate gaze to opposite side

A

MCA syndrome

77
Q

C/l hemiparesis and hemisensory
LE> UE
Urinary incontinence (medial frontal micturition center)
Contralateral grasp, sucking and Gegenhalten (paratonic rigidity)
Abulia, slowness, delay
Impairment of gaze and stance

A

ACA syndrome

78
Q 
C/l hemiparesis and hemisensory loss 
Homonymous hemianopsia, amnesia
Unformed visual hallucination
Pendular hallucinosis
Complex hallucination
A

Peripheral PCA syndrome

79
Q 
Thalamic pain syndrome Dejerine-Roussy 
Sensory loss
Spont pain and dysthesia
Claude syndrome
Weber syndrome
A

Central PCA syndrome

80
Q

Constellation of B long tract (motor and sensory)
Signs of cranial nerve dysfunction
Cerebellar dysfunction
Quadriparesis

A

Basilar Artery distribution

81
Q

Preserved consciousness
Quadriplegia
Only eyes are able to move

A

Locked in syndrome

82
Q

Lacunes
Little lakes
20% of strokes due to arteriolar sclerosis (lipohyalinosis)

A

Small vessel stroke
Multiple small 3mm to 2cm old cavitary infarct
Basal ganglia and thalamus

Rf: hypertension and age

83
Q

Pure motor hemiparesis (face-arm-leg)

A

Post limb of internal capsule or pons

84
Q

Pure sensory stroke

A

ventral thalamus

85
Q

Ataxic hemiparesis

A

Ventral pons and internal capsule

86
Q

Dysarthria and clumsy hand or arm

A

Ventral pons or genu of internal capsule

87
Q

Most significant cause of cardioembolic stroke

A

Nonvalvular non rheumatic atrial fib

88
Q

CHADSVASC Score

A

Risk of stroke for px with AF

89
Q

Cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy originates from

A

CADASIL

thrombus

90
Q

Stroke tx goal

A

Reverse brain injury

1 medical support
2 IV thrombolysis

91
Q

BP goal

reduce if

A

Permissive hypertension

BP >220/120
concomitant MI
BP > 185/110 and thrombolytic therapy anticipated

92
Q

Glucose goal

A

140-180 mg/dl

93
Q

IV thrombolysis

Cut off:

A

RTpA
Dose: 0.9mg/kg, maximum 90mg
0.6/kg in Japan and Asian countries

3 - 4.5h

94
Q

Alternative or adjunct tx for acute stroke ineligible for or with contraindications to thrombolytics

Failed vascular recanalization with IV

A

Endovascular revascularization

95
Q

Only antiplatelet for effective acute treatment of ischemic stroke
Prevents early recurrence <14d less death/disability at 6 mos

A

160mg at 4 weeks CAST
300 mg at 2 weeks IST

Risk of bleeding: 2/700

96
Q

Accounts for 10% of strokes
High in blacks and Asian

Caused by

A

Intracerebral hemorrhage

HTN most common
Coagulopathy
Sympathomimetic
Cerebral amyloid angiopathy (elderly)

97
Q

ICH dx
highly sensitive
highly specific
Determines bleeding location

Finding

A

Non contrast CT

hyperdensity

98
Q

Most common site of hypertensive hemorrhage

A 
Putamen
Globus pallidus
Thalamus
Cerebellar hemisphere
Pons
99
Q

Primary CA that metastasize in brain

A 
Lung
Breast
Skin/Melanoma
Kidney
GI
100
Q

Transformation of prior ischemic infarct

A

Basal ganglion
Subcortical region
Lobar

101
Q

Drugs causing ICH

A

Amphetamine

Cocaine

102
Q

Pathology of hypertensive ICH

A

Lipohyalinosis fibrinoid necrosis

Charcot Bouchard microaneurysm

103
Q

Sites of deep penetrating arteries

A 
Basal ganglia (lenticulostriate) putamen
Thalamus
104
Q

<10 secs

A

Microaneurysm
<6 h expansion. 38-40% expand in 24h most in 6 hr
<3 days early edema (cytotoxic, glutamate, thrombin, fibrin)

105
Q

Pontine stroke
Narcotic overdose
Optic overdose

A

Pinpoint pupil

106
Q

BP control in hypertensive ICH

A

130-150/160

107
Q

Target MAP for stroke

A

110-130 mmHg

108
Q

Lab value elevated in pseudoseizure

A

prolactin

not in true seizure

109
Q

Most common tumor in cerebellopontine angle in adult

A

Schwannoma

110
Q

Bilateral schwannoma

A

Neurofibromatosis type 2

Medicine (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions