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Capstone Test 2 > Weakness > Flashcards

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

A

hands

24
Q

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

A

ALS

25
Q

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

A

anterior spinal artery occlusion

26
Q

spinal cord lesion presenting with progressive sensory ataxia and absent DTRs

A

tabes dorsalis

27
Q

spinal cord lesion presenting with ataxic gait, paresthesias, impaired proprioception, UMN signs

A

subacute combined degeneration

loss of
Spinocerebellar tracts
Corticospinal tracts
Dorsal columns

28
Q

what would you expect to find on physical exam in Brown-Sequard syndrome?

A

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
Q

[MG vs LE]
fatigable weakness
spared reflexes
worsens with use

A

MG

30
Q

[MG vs LE]
proximal muscle weakness
autonomic symptoms
hyporeflexia
improves with use

A

LE

31
Q

[MG vs LE]
associated with thymoma

A

MG

32
Q

[MG vs LE]
associated with SCLC

A

LE

33
Q

[MG vs LE]
antibodies to the postsynaptic ACh-R

A

MG

34
Q

[MG vs LE]
antibodies to the presynaptic Ca2+ channel

A

LE

35
Q

humoral hypercalcemia of malignancy causes […]calcemia and […]phosphatemia

A

humoral hypercalcemia of malignancy causes [hyper]calcemia and [hypo]phosphatemia

(hypercalcemia suppresses PTH –> low PTH)

36
Q

Occlusion of which artery is most likely to cause papillary muscle rupture and acute mitral regurgitation?

A

posterior descending artery

37
Q

Rupture of the left ventricular free wall will most likely result in […]

A

cardiac tamponade

(beck’s triad: hypotension, muffled heart sounds, and jugular venous distention)

38
Q

Infarction affecting the inferior heart is most likely to show changes in which ECG leads?

A

leads II, III, and aVF

RCA

39
Q

Abnormalities found in leads I, aVL, and V5-V6 suggest dysfunction of the […] portion of the heart

A

lateral

LCX

40
Q

An infarction in the anterior heart would show abnormalities in leads […]

A

V1-V4

LAD

41
Q

An infarction affecting the […] heart would show abnormalities in leads I, aVL, and leads V1-V6.

A

anterolateral

(occlusion of left main, so would affect LCX and LAD)

Capstone Test 2 (5 decks)

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