Weakness Flashcards

1
Q

the main difference between GBS and CIDP is

A

time course

CIDP lasts greater than 8 weeks
GBS peaks in severity at 8 weeks

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2
Q

Guillain-Barre causes […] paralysis

A

ascending

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3
Q

proximal and distal bilateral diffuse neuropathies are categorized as [2]

A

time course

GBS (acute)
CIDP (chronic)

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4
Q

[…] is the most common pathogen associated with GBS.

A

C. jejuni

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5
Q

most common demyelinating disease affecting the central nervous system

A

multiple sclerosis

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6
Q

what kind of deficit pattern does MS cause?

A

multifocal

discrete areas of transient inflammatory deyelination

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7
Q

signs and symptoms of MS are dependent on […] of the lesion

A

location

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8
Q

diagnostic criteria for MS

A

two or more lesion of the CNS separated in space and time without other explanation

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9
Q

free radicals damage cells via membrane lipid […]

A

peroxidation

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10
Q

what would you expect to see on biopsy 0-4 hrs post MI?

A

wavy fibers

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11
Q

what would you expect to see on biopsy 4-24 hrs post MI?

A

early coagulative necrosis: edema, lysed cells
reperfusion injury –> hypercontraction of myofibrils (dark eosinophilic stripes)

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12
Q

what would you expect to see on biopsy 1-3 days post MI?

A

extensive coagulative necrosis
surrounding tissue with acute inflammation and neutrophils
more edema

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13
Q

what would you expect to see on biopsy 3-14 days post MI?

A

macrophages
granulation tissue at margins

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14
Q

what would you expect to see on biopsy 2+ weeks post MI?

A

contracted scar tissue

(white is scar tissue)

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15
Q

Collagen is deposited by […] starting at around seven days post MI then continues in a linear pattern for months

A

fibroblasts

“graph this out from 7 days to 6 months” (not really sure what is meant by that)

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16
Q

activation of clopidogrel is dependent on […]

A

CYP enzymes

(Not effective in individuals with genetic polymorphisms of CYP enzymes or drug-induced inhibition of CYP enzymes)

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17
Q

MOA of clopidogrel

A

Inhibition of P2Y12 receptor on platelets (ADP receptor) → ↓ expression of Gp IIb/IIIa receptors on platelets → inhibition of platelet aggregation

18
Q

Name three complications that can be seen in the first two weeks after a myocardial infarction and explain why they occur

A

arrhythmia: due to myocardial death and scarring

papillary muscle rupture: more often posteromedial papillary muscle because it is only supplied by the PDA. The anterolateral has dual supply

interventricular septum rupture: macrophage mediated degradation causes VSD

pericarditis: neutrophilic infiltrate 1-3 days post MI can cause pericarditis

19
Q

MOA of nitroglycerin/isosorbide

A

Exogenous supply of nitric oxide (NO) through nitrate → activation of guanylyl cyclase → ↑ cyclic guanosine monophosphate (cGMP) → activation of protein kinase G

Increases SERCA activity → ↓ intracellular calcium → ↓ recruitment of contractile units → vasodilation

Increases myosin light chain phosphatase activity → ↓ phosphorylated myosin → smooth muscle relaxation → vasodilation

20
Q

how to prevent tolerance in people using nitrates

A

nitrate free intervals of at least 8 hrs

21
Q

pain/temperature loss in a cape-like distribution

A

syringomelia

22
Q

why is the anterior white commissure significant in syringomelia?

A

the 2nd order neuron of the spinothalamic tract decussates here
often the first structure compressed as the syrinx expands

23
Q

Look for progressive pain-sensation-loss, and temperature-sensation-loss in the […] as an initial complaint to differentiate syringomyelia from other common foils

24
Q

spinal cord lesion presenting with combined UMN and LMN degeneration
no sensory or bowel/bladder defects

25
spinal cord lesion presenting with UMN signs below the lesion and LMN signs at the level of the lesion and loss of pain/temperature below the lesion dorsal columns intact
anterior spinal artery occlusion
26
spinal cord lesion presenting with progressive sensory ataxia and absent DTRs
tabes dorsalis
27
spinal cord lesion presenting with ataxic gait, paresthesias, impaired proprioception, UMN signs
subacute combined degeneration loss of Spinocerebellar tracts Corticospinal tracts Dorsal columns
28
what would you expect to find on physical exam in Brown-Sequard syndrome?
at level of lesion: ipsilateral loss of all sensation ipsilateral LMN below level of lesion: ipsilateral UMN signs below level of lesion ipsilateral loss of proprioception, fine touch, vibration contralateral loss of pain temperature
29
[MG vs LE] fatigable weakness spared reflexes worsens with use
MG
30
[MG vs LE] proximal muscle weakness autonomic symptoms hyporeflexia improves with use
LE
31
[MG vs LE] associated with thymoma
MG
32
[MG vs LE] associated with SCLC
LE
33
[MG vs LE] antibodies to the postsynaptic ACh-R
MG
34
[MG vs LE] antibodies to the presynaptic Ca2+ channel
LE
35
humoral hypercalcemia of malignancy causes [...]calcemia and [...]phosphatemia
humoral hypercalcemia of malignancy causes [hyper]calcemia and [hypo]phosphatemia (hypercalcemia suppresses PTH --> low PTH)
36
Occlusion of which artery is most likely to cause papillary muscle rupture and acute mitral regurgitation?
posterior descending artery
37
Rupture of the left ventricular free wall will most likely result in [...]
cardiac tamponade (beck's triad: hypotension, muffled heart sounds, and jugular venous distention)
38
Infarction affecting the inferior heart is most likely to show changes in which ECG leads?
leads II, III, and aVF RCA
39
Abnormalities found in leads I, aVL, and V5-V6 suggest dysfunction of the [...] portion of the heart
lateral LCX
40
An infarction in the anterior heart would show abnormalities in leads [...]
V1-V4 LAD
41
An infarction affecting the [...] heart would show abnormalities in leads I, aVL, and leads V1-V6.
anterolateral (occlusion of left main, so would affect LCX and LAD)