Ketchum BSC Flashcards
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?
anesthesia
total or partial loss of sensation especially tactile
what is synesthesia
one type of sensation evokes a sensation of another
feel a color
what is paraesthesia
skin sensation, burning, prickling, itching, or tingling with no apparent physical cause
what is kinesthesia
detection of bodily position, weight or movement of the muscles, tendons and joints
hypersensitivity to cold?
cryesthesia
what is the term describing the general effect this injury would have on motor funciton of the patients hand?
paralysis
nerve paralysis
myoparalysis
motor paralysis
what effect would loss of innervation have on the muscle cell?
atrophy- shrinking
muscle cells get smaller
actin and myosin are the cytoskeletal elements that are lost in muscle cells
apoptosis and necrosis difference?
apoptosis is planned
denervation causes
no myonecrosis
no rhabdomyelosis b/c cells aren’t dying
loss and disarry of myofilaments inside the muscle cell
what is dystrophy
form of atrophy that specifically results from wasting process that is disease related
what is myopathy
muscular disease in which muscle fibers do not function
what is the primary cause of myofilament degradation in denvervation atrophy?
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
what is the ubiquitin proteosome system
primary means of degrading muscle cells
involves target protein is polyubiquitinated
then 26S proteasome recognizes ubiquitin and degrades substrate
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
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
symptoms and EMG reversed after IV administration of an acetylcholinesterase inhibitor what does this mean?
also she has anti-AChR antibodies
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
myesthenia gravis and the eyes??
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***
why does she have diplopia
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
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
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)
trendelenburg gait
lost abductors at the hip
gluteus minimus and medius
what is gower’s maneuver
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
Duchenne muscular dystrophy
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
