Weakness Flashcards
the main difference between GBS and CIDP is
time course
CIDP lasts greater than 8 weeks
GBS peaks in severity at 8 weeks
Guillain-Barre causes […] paralysis
ascending
proximal and distal bilateral diffuse neuropathies are categorized as [2]
time course
GBS (acute)
CIDP (chronic)
[…] is the most common pathogen associated with GBS.
C. jejuni
most common demyelinating disease affecting the central nervous system
multiple sclerosis
what kind of deficit pattern does MS cause?
multifocal
discrete areas of transient inflammatory deyelination
signs and symptoms of MS are dependent on […] of the lesion
location
diagnostic criteria for MS
two or more lesion of the CNS separated in space and time without other explanation
free radicals damage cells via membrane lipid […]
peroxidation
what would you expect to see on biopsy 0-4 hrs post MI?
wavy fibers
what would you expect to see on biopsy 4-24 hrs post MI?
early coagulative necrosis: edema, lysed cells
reperfusion injury –> hypercontraction of myofibrils (dark eosinophilic stripes)
what would you expect to see on biopsy 1-3 days post MI?
extensive coagulative necrosis
surrounding tissue with acute inflammation and neutrophils
more edema
what would you expect to see on biopsy 3-14 days post MI?
macrophages
granulation tissue at margins
what would you expect to see on biopsy 2+ weeks post MI?
contracted scar tissue
(white is scar tissue)
Collagen is deposited by […] starting at around seven days post MI then continues in a linear pattern for months
fibroblasts
“graph this out from 7 days to 6 months” (not really sure what is meant by that)
activation of clopidogrel is dependent on […]
CYP enzymes
(Not effective in individuals with genetic polymorphisms of CYP enzymes or drug-induced inhibition of CYP enzymes)
MOA of clopidogrel
Inhibition of P2Y12 receptor on platelets (ADP receptor) → ↓ expression of Gp IIb/IIIa receptors on platelets → inhibition of platelet aggregation
Name three complications that can be seen in the first two weeks after a myocardial infarction and explain why they occur
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
MOA of nitroglycerin/isosorbide
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
how to prevent tolerance in people using nitrates
nitrate free intervals of at least 8 hrs
pain/temperature loss in a cape-like distribution
syringomelia
why is the anterior white commissure significant in syringomelia?
the 2nd order neuron of the spinothalamic tract decussates here
often the first structure compressed as the syrinx expands
Look for progressive pain-sensation-loss, and temperature-sensation-loss in the […] as an initial complaint to differentiate syringomyelia from other common foils
hands
spinal cord lesion presenting with combined UMN and LMN degeneration
no sensory or bowel/bladder defects
ALS
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
spinal cord lesion presenting with progressive sensory ataxia and absent DTRs
tabes dorsalis
spinal cord lesion presenting with ataxic gait, paresthesias, impaired proprioception, UMN signs
subacute combined degeneration
loss of
Spinocerebellar tracts
Corticospinal tracts
Dorsal columns
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
[MG vs LE]
fatigable weakness
spared reflexes
worsens with use
MG
[MG vs LE]
proximal muscle weakness
autonomic symptoms
hyporeflexia
improves with use
LE
[MG vs LE]
associated with thymoma
MG
[MG vs LE]
associated with SCLC
LE
[MG vs LE]
antibodies to the postsynaptic ACh-R
MG
[MG vs LE]
antibodies to the presynaptic Ca2+ channel
LE
humoral hypercalcemia of malignancy causes […]calcemia and […]phosphatemia
humoral hypercalcemia of malignancy causes [hyper]calcemia and [hypo]phosphatemia
(hypercalcemia suppresses PTH –> low PTH)
Occlusion of which artery is most likely to cause papillary muscle rupture and acute mitral regurgitation?
posterior descending artery
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)
Infarction affecting the inferior heart is most likely to show changes in which ECG leads?
leads II, III, and aVF
RCA
Abnormalities found in leads I, aVL, and V5-V6 suggest dysfunction of the […] portion of the heart
lateral
LCX
An infarction in the anterior heart would show abnormalities in leads […]
V1-V4
LAD
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)
