Ch. 10 Clinical Notes Flashcards
tetanus
- Clostridium tetani release toxin into CNS
- Supresses mechanism that inhibits motor neuron actvity
- Sustained, powerful contraction of skeletal muscles
2 week incubation, widespread muscle spasms within 2-3 days of initial symptoms
rigor mortis
- Muscles deprived of nutrients & oxygen (2-7 hours after death)
- ATP runs out => cross-bridges cannot detach
- sarcoplasm cannot pump out Ca2 ;
Ca2+ leaks into sarcoplasm from ExC fluid or SR
=> Sustained contraction - Lasts until enzymes break down Z lines & titin filaments (1-6 days after death)
Delayed-Onset Muscle Soreness
DOMS
- Highest = eccentric contractions
- Lower = concentric or isometric
- Elevated CK & myoglobin in blood = damage to muscle plasma membranes; does not correspond to contraction type or level of soreness
Proposed mechanisms:
- small tears and loss of enzymes stimulates pain receptors
- pain from muscle spasms
- Pain from tears in connective tissue
botulism
A severe, potentially fatal paralysis of skeletal muscle from the consumption of a bacterial toxin
Duchenne muscular dystrophy (DMD)
One of the most common and best understood of muscular dystrophies
a recessive X-linked form of muscular dystrophy, affecting around 1 in 3,600 boys, which results in muscle degeneration and eventual death. Muscle wasting replaced by fat and fibrotic tissue
fibromyalgia
a chronic disorder characterized by widespread musculoskeletal pain, fatigue, and localized tenderness
Its exact cause is unknown but is believed to involve psychological, genetic, neurobiological and environmental factors
described as a “central sensitization syndrome” caused by neurobiological abnormalities which act to produce physiological pain and cognitive impairments as well as neuro-psychological symptomatolog
muscular dystrophies
a varied collection of inherited diseases that produce progessive muscle weakness and deterioration
myasthenia gravis
a general muscular weakness resulting from a reduction in the number of ACh receptors on the motor end plate
myopathy
disease of muscle tissue
- Clostridium tetani release toxin into CNS
- Supresses mechanism that inhibits motor neuron actvity
- Sustained, powerful contraction of skeletal muscles
2 week incubation, widespread muscle spasms within 2-3 days of initial symptoms
tetanus
- Muscles deprived of nutrients & oxygen (2-7 hours after death)
- ATP runs out => cross-bridges cannot detach
- sarcoplasm cannot pump out Ca2 ;
Ca2+ leaks into sarcoplasm from ExC fluid or SR
=> Sustained contraction - Lasts until enzymes break down Z lines & titin filaments (1-6 days after death)
rigor mortis
- Highest = eccentric contractions
- Lower = concentric or isometric
- Elevated CK & myoglobin in blood = damage to muscle plasma membranes; does not correspond to contraction type or level of soreness
Proposed mechanisms:
- small tears and loss of enzymes stimulates pain receptors
- pain from muscle spasms
- Pain from tears in connective tissue
Delayed-Onset Muscle Soreness
DOMS
A severe, potentially fatal paralysis of skeletal muscle from the consumption of a bacterial toxin
botulism
One of the most common and best understood of muscular dystrophies
a recessive X-linked form of muscular dystrophy, affecting around 1 in 3,600 boys, which results in muscle degeneration and eventual death. Muscle wasting replaced by fat and fibrotic tissue
Duchenne muscular dystrophy (DMD)
a chronic disorder characterized by widespread musculoskeletal pain, fatigue, and localized tenderness
Its exact cause is unknown but is believed to involve psychological, genetic, neurobiological and environmental factors
described as a “central sensitization syndrome” caused by neurobiological abnormalities which act to produce physiological pain and cognitive impairments as well as neuro-psychological symptomatolog
fibromyalgia
a general muscular weakness resulting from a reduction in the number of ACh receptors on the motor end plate
myasthenia gravis
