Ketchum BSC Flashcards

1
Q

what is the term describing the general effect this injury would have on sensation of the patients hand

he has a deep laceration and completely severs the ulnar nerve where it is most superficial at the elbow joint?

A

anesthesia

total or partial loss of sensation especially tactile

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2
Q

what is synesthesia

A

one type of sensation evokes a sensation of another

feel a color

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3
Q

what is paraesthesia

A

skin sensation, burning, prickling, itching, or tingling with no apparent physical cause

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4
Q

what is kinesthesia

A

detection of bodily position, weight or movement of the muscles, tendons and joints

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5
Q

hypersensitivity to cold?

A

cryesthesia

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6
Q

what is the term describing the general effect this injury would have on motor funciton of the patients hand?

A

paralysis
nerve paralysis
myoparalysis
motor paralysis

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7
Q

what effect would loss of innervation have on the muscle cell?

A

atrophy- shrinking

muscle cells get smaller
actin and myosin are the cytoskeletal elements that are lost in muscle cells

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8
Q

apoptosis and necrosis difference?

A

apoptosis is planned

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9
Q

denervation causes

A

no myonecrosis
no rhabdomyelosis b/c cells aren’t dying

loss and disarry of myofilaments inside the muscle cell

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10
Q

what is dystrophy

A

form of atrophy that specifically results from wasting process that is disease related

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11
Q

what is myopathy

A

muscular disease in which muscle fibers do not function

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12
Q

what is the primary cause of myofilament degradation in denvervation atrophy?

A

Increased proteosome activity

NOT suppresion of protein synthesis (some but not main cause)
NOT enhanced lysosomal enzyme activity
b/c lysosomes degrade…
NOT expanded metalloproteinase activity b/c these function mainly in the ECM
NOT increased activity in caspase b/c these play a role in apoptosis and necrosis

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13
Q

what is the ubiquitin proteosome system

A

primary means of degrading muscle cells

involves target protein is polyubiquitinated
then 26S proteasome recognizes ubiquitin and degrades substrate

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14
Q
case two lady with fatigue when she chews (progressively weaker as she uses her muscles)
diplopia (double vision) 
facial muscles weak
she is a gymnast
ptosis (droopy eye lids)
sneering when smiling

is this a neuropathy or myopathy

A

myopathy

EMG shows progressive weakness
contraction amplitude is decreasing –> this tells us that muscles aren’t able to recapture their functionality as quick as they should be able to

myesthenia gravis

see a smoothing of the membrane in the cleft

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15
Q

symptoms and EMG reversed after IV administration of an acetylcholinesterase inhibitor what does this mean?

also she has anti-AChR antibodies

A

myesthenia gravis

NOT amyetrophic lateral sclerosis (b/c this is damage to spinal cord which will cause muscle atrophy and weakness due to abnormal nerves!) NOT Immune so wouldn’t have antibodies, wouldn’t have normal nerve condction test

NOT MS b/c
the antibodies seen in this would not be antiAChR antibodies, wold not have normal NCV test (it would be slow)

NOT WNV polio-like syndrome- neurotoxic, death of central motor neurons, not autoimmune, wouldn’t have normal nerve conduction test

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16
Q

myesthenia gravis and the eyes??

A

acetylcholine release is binding up small available ACh receptors

as it continues to be released there are fewer receptors for it to bind to

as this happens the ACh that are bound, open and allow ions to chanell through, but then it takes them a while to recover

so channels tend to stay open and you get progressive fatigue

ACh receptors in the eyes muscles are reduced compared to the rest of the body***

17
Q

why does she have diplopia

A

b/c their musculature isn’t working in her eyes in myesthenia gravis

2 major clinical forms of myesthenia gravis
occular MG- ocular symptoms
-85 percent of ocular MG patients progress to general MG within two years

general MG- generalized weakness

18
Q

case with 5 year old boy
no progression in speech
CK level of >10, 000 (normal is under 200)
walked funny (trendelenburg gait and gower’s maneuver to stand up)

diagnosis

A

most likely diagnosis is primary myopathy

(not denervation- no wound)
not MS- age of onset is usually greater
not nutritional deficiency (no evidence to support this)
NOT rhabdomyolysis ( no mention of kidney failure)

19
Q

trendelenburg gait

A

lost abductors at the hip

gluteus minimus and medius

20
Q

what is gower’s maneuver

A

don’t have enough hip strength to rise from sitting position

so he straightens legs, puts hands out in front of him and then tries to stand up

21
Q

Duchenne muscular dystrophy

A

Primary myopathy

costamere (ties filaments to the cell membrane)
this compex tranverses the cell membrane, containes the protein dystrophin

dystrophin is mutated - becomes a nonfunctional protein and don’t get transmission of force out of the cell and into the connective tissue, tendons transmitted to the muscle

cells atrophy and are replaced by fat

x-linked recessive genetic disease