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24 Cards in this Set
- Front
- Back
describe Myoglobinuria/rhabdomyolysis
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myoglobinuria, also called fhabdo, is a result of severe muscle trauma
-excess of myoglobin, an intracellular muscle protein, in the urine secondary to muscle camage. -myoglobin crosses glomerular bowmans capsule (mol wt is 17,000)\ |
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• Causes:
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o Immobilization: move pts because muscles will atrophy (disuse atrophy) will start to activate processes that lead to cell damage, release of myoglobin
o Viral infection o Strychnine poisoning o Tetanus infection o Heat stroke o Fracture bonetears muscle group o Epilepsyseizure really intense muscle contraction for many minutes, creates heat causes muscles to begin to breakdown o Malignant hyperthermia o Muscle compression o Anesthetics |
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what does book say of causes
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severe form is crush syndrome, less severe forms are called compartment syndromw which can lead to volkman ischemic contracture in teh forearm or leg.
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myoglobinuria is seen when(book)
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viral infection, adm of anesthetics,strychnine poison, tetanus, heat stroke, electrolyte disturbance, fractures. escessive muscular activity in athletes, electrical shock, ect
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describe effects of MH
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severe muscle spasm and rhabdomyolysis can occur and lead to renal failure. other complications include rigidity, tachy, card dysryth, metabolic and resp acidosis, and rapid rise of temp (1 degree every 5 min). cerebral edema, cardiogenic and hypovolemic shock occcur and DIC.
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Name two types of contractures which are (Secondary muscle dysfunctions
• Not the primary disorder, there is something else wrong, and these occur secondarily.) |
physiologic
pathologic |
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describe physiologic contractures
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o Physiologic
No Action Potential Mucho ATP Failure of Ca pump Seen in McArdle’s disease (McArdle’s in primary disease; contracture is the secondary dysfunction that they will have) Pain can be eased Muscles are supposed to generate action potentials-these do not. They do have ATP, if something changes the permeability like an ion, depolarization happens IF calcium stays bound to TnC, and not reupd into the SR, you have permanent cross bridges=failure of the CA pump will eventually separate-so is a Can be relieved |
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descrribe pathologic contractures
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o Pathologic
Permanent shortening Muscle spasms Weakness Lots ATP & normal action potential (*not a Ca pump issue) Areas of body where you could see these contractures or abnormalities in which they could happen: Achilles tendon Muscular dystrophy CNS damage (you have to stimulate a muscle w/ a neuron. If you have problem w/ your neurons, your muscle won’t stimulate.) Scar tissue could lead to contractures (d/t scarring of the muscle) |
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describe two types of membrane abnormalities
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1) hyperexcitablemembranes (myotonic disorders
2) Periodic paralysis: intermittent unresponsive membranes (a specific type of hyperexcitable membrane: myotonic disorder) |
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describe
Periodic paralysis: intermittent unresponsive membranes (a specific type of hyperexcitable membrane: myotonic disorder) |
• Membrane is unresponsive to neural stimuli. The muscle simply responds to the membrane properties itself. Its Vm is not what it is supposed to be.
• Vm from -90 to -45 mV (REM: the resting membrane potential is -70mV usually. There are muscle groups in you that have a much lower membrane potential -90.) Have to stimulate the muscle to its “all or none” threshold so that the muscle can actually depolarize. Can get to threshold quickly from -45 compared to -70. Muscle is very susceptible to firing. • ; ions leak, depolarize cells, makes them unable to move; caused by cold/heat/stress/high carbs/bad diet/hyper-hypokalemia • |
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Muscle Metabolic Disorders
describe 2 classifications: |
endocrine or metabolic problem
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describe endocrine problem associated with muscle metabolic disorder
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Endocrine – ex: hypothyroidism is a metabolic problem to the musclelack of protein
• Thyroid hormone regulates protein synthesis • Without protein synthesis, your muscle cannot be as strong (muscles are made of proteins) • Lowers muscle strength o Thyroid gland releases thyroid hormone. It is metabolic b/c it affects your entire body metabolism then your muscle metabolism |
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describe muscle disorders associated with a metabolic problem
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Metabolic – energy source (all about deficiencies of enzymes)
• McArdle’s disease: person lacks the enzyme myophosphorylase, which is supposed to lead to glycogen breakdownso can’t breakdown to glucosemitochondria36 ATPfailure of Ca pump. Risk of secondary muscle dysfunction = physiologic contractures. so cant produce glucose therefore cannot undergoe any kind of aerobic respiraton. This is not supposed to accumulate, it is supposed to be broken down. (GLYCOGEN accumulating disorder) they can do ok with this but they cannot excersize • Acid Maltase (enzyme) Deficiency patient accumulates glycogen excessively in muscle (deficiency of lysosomal metabolism) draws water muscle is destroyed. Glycogen is excessively synthesized; not broken down. myozyme to treat, shit load of cash 300,000 a year for the drug • Myoadenylate Deaminase (MD) enzyme deficiency: lack MD. MD assists in the formation of phosphocreatine and ATP during exercise. Phosphocreatine transfers the phosphate group to allow you to do little bursts of exercise. These patients have NO exercise tolerance. Normally MD Breaks AMP adenosine mono phosphate to IMP (taking an ammonia group off), Buildup of AMP which you lose. If you don’t deaminate that you get a build up of AMP, transfer it to your blood, it is cleaned by the kidney, so you whiz it out. You take parts of the AMP and recycle it to ATP normally, if it is gone, you loose adenosine. You will also have an issue with the ammonia molecule. |
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Describe secondary muscle dysfunction according to book
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muscular symptoms arise from causes unrelated to muscle itself.
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Name three examples of secondary muscular phenomena
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1) contracture
2) stress related muscle tension 3) immobility |
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describe contractures
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CAN BE PATHOLOGIC OR PHYSIOLOGIC
PATHOLOGIC=permanent muscle shortening caused by muscle spasm or weakness PHYSIOLOGIC=occurs in the absence of a muscle action potential in the sarcolemma. |
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Expand on Physiologic muscle contracture
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Muscle shortening is explained on the basis of failure of the calcium pump in the preesence of plentiful ATP
=an example is that is McArdle disease and Malignant hyperthermia =usually temporary if paho reveresed |
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Expand on Pathologic muscle contracture
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ie. Hell cord (achilles tendon) contracutes.
=associated with plentiful ATP and occur despite normal action potential. Most common is seen in MD and CNS injury. also in burned tissues in the ac. |
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describe secondary muscular dysfunction called stress induced muscle tension
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na
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Describe the secondary muscular dysfunction called disuse atrophy
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muscular deconditioning associated with lack of physical activity apparent in a matter of daysbedrest p. loses muscle strength from baseline at 3% per day.
=pathologic reduction in normal size of muscle fibers after prolonged inactivity from bed rest, trauma etc. |
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Describe the notion of Muscle membrane abnormalities
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two defects of the muscle membrane (plasma membrane of the muscle fiber) have been linked to clinical syndromes:
1)hyperexcitable membrane seen in the myotonic disorders, 2) intermittently unresponsive membrane seen in periodic paralyses. |
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describe energy metabolism disease called mcardles
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first myopathy in whih a single enzyme defect was identified.
=lack muscle phosphorylase, which is responsible for the breakdown of glycogen in muscle. symptoms=exercise intolerance, fatigue, painful muscle cramps. why? cannot brak down glycogen or procuce lactic acid |
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Describe acid maltace deficiency
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glycogen storage disease associated with accumulation of glycogen in teh lysosomes of muscle cells and teh cells of other tissues.
abscence of encyme acid maltase resp for the abnormal glycogen metabolism autosomal recessive |
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describe myoadenylate deaminase deficiency
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produces changes in skeletal musclle assoc with excersice intol.
=lack of enzyme so have poor cap for sustained enerby production |