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FNP Advanced Pathophysiology > Skeletal and Muscle Systems Part 3 > Flashcards

Skeletal and Muscle Systems Part 3 Flashcards

1
Q

Sprain V Strain

A

A sprain is a stretch and/or tear of a ligament (a band of fibrous tissue that connects two or more bones at a joint). One or more ligaments can be injured at the same time. The severity of the injury will depend on the extent of injury (whether a tear is partial or complete) and the number of ligaments involved.
A strain is an injury to either a muscle or a tendon (fibrous cords of tissue that connect muscle to bone). Depending on the severity of the injury, a strain may be a simple overstretch of the muscle or tendon, or it can result from a partial or complete tear.

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2
Q

Structure of Skeletal Muscle

A 
-CONNECTIVE TISSUE COVERINGS
Fascia
epimysium
perimysium (separate fibers into fascicles)
endomysium (individual muscle fibers)
-TENDONS
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3
Q

Skeletal Muscle Fibers

A

-single cell!!!!!!
-cell membrane = sarcolemma
-cytoplasm = sarcoplasm
-myofibrils (filament proteins)
1) actin
-2 proteins associated - troponin , tropomyosin
2) myosin
3) sarcomere-repeating units of actin/myosin
-organelles
sarcoplasmic reticulum (like ER)
Ca transport to sarcomere
transverse tubules

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4
Q

Motor Unit

A
  • Motor neuron in brain or spinal cord
  • Somatic Neuron (axon)
  • Synapse (NMJ)
  • Skeletal Muscle fibers that are innervated
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5
Q

Neuromuscular Junction (NMJ):

A

Synapse of the somatic neuron (axon) to Skeletal muscle fiber
neurotransmitter –Acetylcholine (Ach)
Action potential - motor end plate potential
ACh causes the muscle fiber to conduct an impulse over the surface of the fiber that reaches deep within the fiber by means of transverse tubules.

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6
Q

Alterations in Muscles

A

General Terms

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7
Q

Weakness

A
  • Loss of strength in one of more muscle groups

- primary or secondary

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8
Q

Cramps (Spasms):

A

-involuntary contractions
-skeletal
-idiopathic, disease motor, -metabolic, electrolytes
low glucose, K, Na, -dehydration

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9
Q

Injury

A

trauma to tissue

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10
Q

Twitches

A

Spontaneous discharge of motor units and single muscle fibers

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11
Q

Fasiculations:

A
  • spontaneous discharge of single motor unit
  • dimple or twitch of skin
  • rhythmic, start/stop
  • Hypersensitivity to Ach?
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12
Q

Fibrillations

A
  • involuntary contraction single muscle fibers
  • not visible
  • e.g.- cardiac
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13
Q

Tetany

A
  • spasmodic contraction

- hypocalcemia, hypomagnesemia

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14
Q

Myoclonus

A
  • sudden unexpected contraction of single muscle group limbs or trunk
  • e.g. night jerks, CNS disease
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15
Q

Myotonia

A

-sustained involuntary contraction of a group of muscles

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16
Q

Tics

A
  • sudden and behavior related repetitive motions

- e.g.- tourettes syndrome

17
Q

Hypertrophy v Atrophy

A
  • can you recall this from basic pathophysiology
18
Q

Atrophy

A

-non specific
-abnormally small muscle fibers
-causes:
neurogenic
disuse
glucocorticoids
Endogenous hypercortisolism (cushings disease)
myopathies

19
Q

Pathological Process of Skeletal Muscles

A

See below

20
Q

Skeletal Muscle Disorder Categories

A
  1. Neurogenic changes or myofiber atrophy
  2. Muscular Dystrophies
  3. Congenital, toxic, or infectious myopathies
  4. Neuromuscular junction
21
Q

Muscular Dystrophies

A
  • genetic
  • progressive degeneration of muscle fibers
  • progressive weakness of voluntary muscles
  • progressive wasting (muscle fiber atrophy)
  • Muscle fibers can be replaced by fibrofatty tissue
  • ——–Key distinction between dystrophies and myopathies
22
Q
  • 2 common forms that a X-linked (same gene in both)
A
  • Duchenne Muscular Dystrophy (DMD)
    most severe and most common
    -Becker Muscular Dystrophy
23
Q

Morphology of DMD and BMD:

A 
● variation muscle fiber size
● degenerative changes- splitting or necrosis
● regenerative changes
● Increased connective tissue
● Abnormal staining for dystrophin
● fat tissue
24
Q

Pathogenesis (note the term!) of DMD and BMD:

A

● abnormalities of dystrophin gene on short arm X chromosome (Xp21)
● What is the role of dystrophin?
Muscles, brain, peripheral nerves
Attaches portions of sarcomere to cell membrane
Maintains structure and function
Transfer force of contraction to connective tissue
● What is the dystrophin defect?
Missing in DMD!
Diminished in BMB

25
Q

Clinical Presentation of DMD:

A

●1 of 3500 live male births
●evident by 5 yrs
●wheelchair dependent by 10-12 yrs
●Death by early 20’s
● Initial clumsiness
● developmental motor skill delays
● Weakness in pelvic girdle then progress to shoulder girdle
● Pseudohypertropy of calf muscle (big, but weak)
● Heart (failure or arrhythmias)
● Cognitive impairment
● Death respiratory insufficiency, pulmonary infection, cardiac decompensation

26
Q

Clinical Presentation of BMD:

A

● onset later childhood or early adolescence
● slower and variable progression rate
● Normal life span possible

27
Q

Autosomal Muscular Dystrophies:

A

● Several types, some of which affect specific muscle groups
Limb girdle muscular dystrophies
● Muscle weakness
● Inherited on autosomal genes
● 4 types due to mutations of sarcolgycan complex of proteins
● other types due to mutations of cytoskeletal proteins
● other types due to mutations of caveolin

28
Q

Myotonic Dystrophy

A

● Inherited autosomal
● Extra CTG trinucleotide repeats on Chromosome 19 that affects the mRNA for the dystrophila myotonia-protein kinase. This leads to increase amount of protein.
● presents late in childhood
● Gait abnormalities due to weakness in foot dorsiflexors
● progress to weakness of intrinsic muscles of hands and wrist extensors
● atrophy of facial muscles with ptosis (droopy eyelids)

29
Q

Myopathy : Congenital myopathies

A

Congenital Myopathies
● Inherited mutations of ion channels (Channelopathies)
● Inborn errors of metabolism
● Mitochondrial myopathies

30
Q

Inherited mutations of ion channels (channelopathies):

A
  • Hyperkalemic periodic paralysis
    mutation in skeletal muscle sodium channel gene
    myotonia and/orrelapsing episodes of hypotonic paralysis
  • Malignant hyperthermia
    mutation in calcium channel gene
    Rare
    Dramatic hypermetabolic state triggered by anesthesia
    Tachycardia, tachypnea, muscle spasms, hyperpyrexia
31
Q

Inborn errors of metabolism

A

-disorders of glycogen -synthesis and degradation

disorders of lipid handling

32
Q

Mitochondrial Myopathies

A
  • mutations in mitochondrial or nuclear DNA that code for mitochondrial constituents
  • mito. ATP required for muscle contraction
  • Young adulthood
  • Proximal weakness
  • Some neurologic symptoms, lactic acidosis, cardiomyopathy
33
Q

Toxic Myopathies

A 
● Intrinsic
- Thyrotoxic myopathy
acute or chronic proximal muscle weakness
● Extrinsic
- Alcohol
- Drugs (e.g. Statins)
rhabdomylosis
pain, myocyte swelling, necrosis, myophagocytosis, regeneration
34
Q

Inflammatory Myopathies:

A
  • Polymyositis and Dermatomyositis
  • –autoimmune or viral
  • –rare inflammatory
35
Q

Disorders of NMJ:

A

See below

36
Q

Myasthenia Gravis

A 
Pathogenesis
-autoimmune
 -Antibodies to NMJ Ach receptors
loss of receptors
-block Ach binding
37
Q

Clinical features:

A
  • females more likely
  • Initial weakness extraocular muscles
    • ptosis
    • diplodia (double vision)-Generalized muscle weakness
    • fluctuations
    • variable- course of days, hours, minutes
  • electrophysiologic stimulation leads to weakness
  • Anticholinesterase drugs improve function
  • NO Sensory and autonomic dysfunction
  • Due to various treatments, 95% patients live
38
Q

Lambert-Eaton Myasthenic Syndrome:

A
  • Paraneoplastic syndrome such as with small-cell lung carcinoma
  • muscle weakness
  • Not improved by increasing Ach at NMJ
  • DOES affect autonomic function
  • electrophysiologic stimulation increases strength
  • Antibodies to presynaptic calcium channels
39
Q

Describe Rhabdomyolysis:

also called myoglobinuria

A
  • based on McCance pages 1547-1550

FNP Advanced Pathophysiology (6 decks)

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