Chapter 36 Flashcards
(29 cards)
What is hypotonia?
State of low muscle tone
- soft muscles on palpation
- diminished resistance and reflexes
What is hypertonia?
State of increased muscle tone
- hyper excitability causing rigidity and spasticity
What is clonus?
Involuntary rhythmic muscle contractions and relaxations
What is plegia?
stroke or paralysis
What is paralysis?
loss of movement
What is paresis?
weakness
What is mono?
One limb
What is Hemi?
Both limbs on one side
What is di- or para?
Both upper/ or both lower limbs
What is quadi- or tetra?
All 4 limbs
What is UMN (upper motor neuron) damage?
weakness or loss of voluntary motion
- spinal reflexes are intact but cannot be controlled by the brain
- increased muscle tone, hyperreflexia, spasticity
What is LMN (lower motor neurone) damage?
neurone directly supplying muscles are affected
- irritated neurons you get spontaneous muscle contractions (fasciculations= contracting and relaxing)
- Death of neurons leading to spinal reflex lost, flaccid paralysis, denervation atrophy of muscles
What is a cause of muscle disorders?
Muscle atrophy
What 2 things can muscle atrophy be broken down into?
disuse: not using muscle (decrease diameter/loss of protein filaments)
Denervation: deprived nerve supply
What is muscular dystrophy?
Contractile proteins don’t properly attach to cytoskeleton of muscle cells
- muscles can’t contract properly
Explain muscular dystrophy. What is the cause?
Genetic disorder (progressive degeneration and necrosis of skeletal muscle fibers and tissue
- Fat and connective tissue replace it ( incr. muscle size= weakness)
- Cause: mutation in the dystrophingene
What are the 2 types of muscular dystrophy?
- Duchene
- common and severe (females are asymptomatic or milder symptoms) - Becker
- slower and less severe
- later in childhood
What is the presentation of MD?
- boys asymptomatic at birth
- 2-3 abnormal posture, falls, contractors, scoliosis= wheelchair by teens
- hip/ shoulders are affected first
- calf muscle hypertrophy (broken down and replaced with fat/ tissue)
- incontinence
- weak cough= infection, cardiomyopathy
- GROWERS SIGN- can’t stand- use hands to push them selves up/ using knees)
What is the diagnosis for MD?
- family hx
- observation of movement
- elevated creatine kinase (leaks out of damaged muscles)
- muscle biopsy (shows fat/scar formation)
- Echo/ ECG (shows cardiac involvement)
What is the treatment of MD? (note: no known cure)
- maintain ambulation
- prevent deformities (stretching/ splinting)
- prevent respiratory infections
- death in young adults
What is acetylcholinesterase? What are 3 ways disorders of neuromuscular junctions can occur?
- enzyme that inactivates transmitters
1. decreased acetylcholine release
2. decreased acetylcholine effects on muscles d/t decreased receptors
3. decreased acetylcholinesterase activity (buildup at junction = interference with impulses)
What is myasthenia gravis?
Decreased motor response d/t loss of acetylcholine receptors
- Auto immune disorder
- Antibodies destroy receptors at neuromuscular junction
- receptor sites are blocked d/t antibodies
What are the risk factors of myasthenia gravis?
- early adulthood for women, 50 for men
- placental transfer of acetylcholine anti-bodies (spontaneous resolution)
- Thymus tumor or hyperplasia in 75 % of cases (T cells not working properly to prevent infection)
What is the manifestations of MG? (explain them in the 3 stages)
Initial: progressive throughout day, muscle weakness, ptosis/drooping, diplopia/ double vision, fatigue
Progression: resp. muscle weakness, diff. speaking, chewing, swallowing, weak limb
Myasthenia crisis: muscle weakness becomes severe and compromises ventilation d/t stress, infection, emotional upset, pregnancy, alcohol, surgery, cold
