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Clin Med I > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Entire muscle surrounded by

A

Epimysium

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2
Q

Fascicle surrounded by

A

Perimysium

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3
Q

Muscle fibers surrounded by

A

Endomysium

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4
Q

Smallest functional unit of SkM

A

Sarcomere (made up of myofilaments - actin and myosin)

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5
Q

Calsequestrin

A

Protein in SR that regulates Ca

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6
Q

Tropomyosin function

A

Blocks myosin binding site on actin at rest
One Tm runs 7 G-actin (1 F actin)
Lies within actin groove

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7
Q

Troponin function

A

Regulates tropomyosin

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8
Q

Troponin subunit Tc

A

Binds Ca

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9
Q

Troponin subunit Ti

A

Inhibits tropomyosin movement off of myosin binding site

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10
Q

Troponin subunit Tt

A

Binds troponin to tropomyosin

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11
Q

Proteins that anchor myosin

A

Titin and M-line proteins

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12
Q

Proteins that anchor actin

A

Alpha actinin and Dystrophin

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13
Q

“power stroke”

A

Repetitive crossbridges –> continued force generation

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14
Q

Relaxation of SkM (3 steps)

A

ATPase pumps pump Ca back into SR
Tc no longer bound to Ca, Tropomyosin slides over myosin binding site
Ti becomes active again

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15
Q

Serial/Vertical orientation of sarcomeres

A

Facilitate velocity of contraction (greater shortening)

E.g. hamstring

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16
Q

Parallel/ Pennate orientation of sarcomeres

A

Facilitate force generation (packing of more sarcomeres)

E.g. quads, gastrocnemius

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17
Q

Torque- velocity relationship

A

Takes eccentric phase into account

Force generation ability: E>I>C

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18
Q

Why do eccentric contractions generate the most force?

A
  • Myosin heads ripping

- CT resists lengthening

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19
Q

Which type of activation do we maintain best with age?

A

Eccentric

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20
Q

Size of motor unit defined as

A

Number of fibers innervated by one nerve

Smaller = greater control

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21
Q

Structural changes of muscle with aging

A

Fast twitch motor units die, fibers are rescued by slow twitch motor units
–> Fewer, slower, larger motor units overall
Increased tensile ability in CT
Fewer muscle fibers
Possibly more precipitous in females

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22
Q

Alpha motor neuron

A

Efferent neuron to SkM (from muscle spindle reflex)

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23
Q

Gamma motor neuron

A

Efferent neuron to muscle spindle

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24
Q

Muscle spindle afferent neurons (1a and II endings)

A

Sense passive elongation of muscle

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25
Q

Golgi Tendon Organs

A

Lie within tendon, respond to increases in tension.
Muscles with increased tension inhibited
Input is conscious level?

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26
Q

Afferent neurons in golgi tendon reflex sense

A

Tension in golgi and in extrafusal fibers

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27
Q

Smooth muscle differences from skeletal

A

3rd filament (intermediate) –> No striation
Dense bodies instead of sarcomeres (actin approximates dense bodies) - analogous to z line approximation
Muscle shortens and widens (nonlinear contractions)
Wider length-tension relationship

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28
Q

Multiunit Smooth Muscle contractions

A

“Neurogenic” - innervated by ANS

e.g. blood vessels

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29
Q

Single Unit Smooth Muscle contractions

A

“Myogenic” - activated by stretch

e.g. visceral organs

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30
Q

Atrial muscle

A

Bilayer - deep fibers specific to one atrium

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31
Q

Ventricular muscle

A

Coil-like fibers

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32
Q

Hierarchical structure of muscle

A

Muscle, fascicles, fibers (cell), myofibrils (organelles), myofilaments

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33
Q

Sarcopenia

A

Age related muscle loss - greatest decline occurs with inactivity

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34
Q

Bone density peaks ____, remains stable for____

A

After 3rd decade; 20 years

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35
Q

Preclinical disability

A

Progressive and detectable, but unrecognized decline in physical function (65+ y.o.)
Pt says they can still do everything they want, but objective measures show that their function has declined
–> Increased risk for severe disability. Early intervention important (EXERCISE- both strength and endurance)

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36
Q

Which type of bone is osteoporosis more common in?

A

Trabecular (vertebrae, epiphysis) - common in hips

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37
Q

Which type of bone is osteoporosis more common in?

A

Trabecular (vertebrae, epiphysis) - common in hips

Pain is severe and localized

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38
Q

Osteoporosis Treatment

A

Try to stop progression of disease:
Promote weight bearing
Meds, supplemental Ca

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39
Q

Paget’s disease

A

High bone turnover, but new bone is weakened (fibrous tissue)
Osteoclasts gone wild

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40
Q

Paget’s disease Sxs

A

Bowing of legs, bone pain, fx, OA

*slow progression, often not caught early

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41
Q

Paget’s disease Tx goal:

A

Normalize bone activity

Note: Avoid high impact exercise

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42
Q

Osteomyelitis

A

Inflammation of bone due to infection - usually Staph

Becoming more common due to bacterial resistance and prosthetic implants

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43
Q

Acute vs. chronic osteomyelitis

A

Acute: Children, spreads through bloodstream from other infection site
Chronic: Adults, esp. immunosupressed

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44
Q

Osteomyelitis sxs

A

Fever, pain, erythema (children)
Vague sxs, back pain (adults)
Pain with weight bearing
Sausage toe

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45
Q

Dx of Osteomyletis

A
  • Systemic signs (fever, WBC increase)
  • Only 50-80% have positive bacterial culture
  • MRI, bone scans (X-rays only effective after 10 days)
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46
Q

Osteomyelitis treatment

A

IV Antibiotics for 3-4 weeks

Acute: good prognosis. Chronic: Poor

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47
Q

Infectious (Septic) Arthritis

A

Infection in joint
Happens at any age
Either due to direct infection (bacterial, viral, fungal) or reactive from infection elsewhere in body.

48
Q

Infectious (Septic) Arthritis Treatment

A

Medical emergency - IV antibiotics

49
Q

Muscular dystrophy

A

X-linked recessive error in dystrophin

50
Q

Spinal Muscular Atrophy

A

Autosomal recessive reduced number of anterior horn cells

Marked hypotonia and weakness

51
Q

Spinal Muscular Atrophy diagnosis

A

EMG studies to check nerve conduction

52
Q

Plagiocephaly

A

Mishapen head, can be side effect of torticollis

53
Q

Callous formation stage of bone healing

A

Cartilage replaced with bone

54
Q

Strongest predictor of mortality in older adults with surgery to repair hip fx

A

Inability to stand up, sit down, walk after 2 weeks

55
Q

Most common intervertebral discs for DDD

A

L4-L5

56
Q

Greatest risk factor for DDD

A

Family history

age, overweight, underweight also risk factors

57
Q

3 stages of age-related disc degeneration

A
  1. Dysfunction (tear in annulus, hypermobility of facter jts)
  2. Instability (degeneration of facet jts, subluxation)
  3. Stabilization (spinal stenosis)
58
Q

DDD symptoms

A

LBP - but many cases asymptomatic
Slow progression of pain
Worse with activity and prolonged static position, better with rest
Disc herniation common

59
Q

DDD diagnosis and treatment

A

Xray and MRI findings poorly coordinate with symptoms
Conservative vs. surgery: = outcomes
NSAIDs, PT, weight loss

60
Q

Signs of disc herniation

A

Ankle dorsiflexion, great toe extensor weakness

Impaired ankle reflexes, loss of sensation in foot

61
Q

Osgood- Schlatter

A

Mechanical problem related to extensor mechanism of knee - fibers of patellar tendon pull immature bone from tibia
Occurs before complete fusion of epiphysis

62
Q

Osgood-schlatter treatment

A

Rest from painful activities until sxs abate - no immobilization
NSAIDs and ice
Address inefficient extensor mechanism, stretch and strengthen
-90% respond well to above treatment

63
Q

Arthrogryposis Multiplex Congenita

A

Non-progressive disease characterized by severe muscle contractures, weakness, fibrosis at birth. (Sometimes have muscles missing).

64
Q

Osteogenesis Imperfecta

A

Non progressive, diffuse osteoporosis (both types of bone)
Autosomal dominant
Bowing of long bones, extremities appear small compared to trunk

65
Q

Osteogenesis Imperfecta pathology

A

Defect in collagen synthesis (dysplasia) –> Bone, ligament, muscle weakness

66
Q

Differentiating child abuse from osteogenesis imperfecta

A

Epiphyseal fractures common in abuse, rare in OI

67
Q

Developmental Hip Dysplasia

A

Congenital abnormal growth, dislocation, or sublaxation of hip (shallow acetabulum)

68
Q

To develop normally, hip needs:

A

Muscle balance
Bony congruence
Weight bearing forces through joint
^ Wolfe’s Law

69
Q

Developmental Hip Dysplasia clinical presentations

A

Decreased hip ROM, especially ABD

Asymmetrical gait, posture, muscle bulk

70
Q

Developmental Hip dysplasia, diagnosis needed before

A

18-36 months

71
Q

Legg-Calve-Perthes Disease

A

Avascular necrosis of femoral head (medial femoral circumflex artery)
Predictable, self limiting course

72
Q

4 Stages of Perthes disease

A

Takes 1-3 years

73
Q

Incidence of Perthes disease

A

4-8 year old thin, active boy
Caucasian
20% bilateral
Often associated with learning disability

74
Q

Clinical presentation of Perthes disease

A 
Limp, Trendelenburg gait
Limited ABD and ER
Pain: Groin, knee, anterior medial thigh
Buttock and thigh atrophy
No history of obvious injury
75
Q

Steps to take if you find a case of Perthes

A

Refer to a surgeon (not and emergency)

76
Q

Slipped Capital Femoral Epiphysis Incidence

A

African american males around puberty
75% obese
25-33% bilateral

77
Q

Slipped Capital Femoral Epiphysis clinical presentation

A

Antalgic limp
Held in ER
Decreased ABD, flex, and IR
Pain: Groin, knee, anteromedial thigh

78
Q

What to do if you suspect a SCFE

A

Medical emergency - send to surgeon

79
Q

SCFE vs. Perthes

A

SCFE: Overweight, puberty, african american, held in ER, limited ABD, flex, IR
Perthes: Thin, active, 4-8 y.o., cuacasian, limited ABD and ER
Both have increased risk of degenerative arthritis as adults

80
Q

Club foot clinical presentation

A

Forefoot adduction
Hindfoot varus, small calcaneus
Hypoplastic muscles
Ankle equinus - unable to DF

81
Q

Club foot treatment

A

Medical emergency
Serial casting immediately
Surgery, PT, taping, manipulation

82
Q

Kyphosis –>

A

SC compression

83
Q

Scoliosis –>

A

Spinal nerve compression

84
Q

Fetal age when terratogens –> Limb deficiencies

A

3-8 weeks

85
Q

Complications of Myelography

A

HA, meningitis, allergic reaction to dye

What is myelography?

86
Q

DEXA t scores and z scores

A

T-score: Compared to healthy young adults (peak BMD)

Z-score: Compared to age-matched controls

87
Q

Complications of Arthrocentesis

A

Infection, hemorrage

88
Q

Contraindications of arthrography

A

Active arthritis, joint infection

89
Q

Complications of arthroscopy

A

Infection, hemarthrosis, swelling, synovial rupture

90
Q

Contraindications for EMG

A

Anticoagulant meds, skin infection

91
Q

Inner layer of periosteum

A

Cambrium - precursor cels to osteoblasts

92
Q

Osteocytes

A

Mature osteoblasts surrounded by the collagen matrix they secrete

93
Q

Increase in bone thickness

A

Osteoblast activity - add new bone to cambrium

94
Q

Increase in bone length

A

Chondrocyte activity -
Chondrocytes near epiphysis multiply
Chondrocytes on epiphyseal side of line multiply
Older chondrocytes near diaphysis hypertrophy and are ossified

95
Q

Growth hormone

A

Promotes growth in both length and thickness of bone

96
Q

Bones most susceptible to effects of DID

A

Weight bearing bones of lower extremity, pelvis, lumbar spine
-Demineralization occurs in trabecular bone - not externally apparent

97
Q

What type of cartilage forms growth plate?

A

Hyaline

98
Q

Proteoglycans

A

Protein + GAG, syrupy substance that hold cartilage cells together.
e.g. hyaluronic acid, chondroitin and keratan sulphate

99
Q

Superficial layer of cartilage

A

Fibers horizontal, easily compressed, resist friction

100
Q

Middle layer of cartilage

A

Increases tensile strength and compression resistance

Fibers oblique to superficial layer

101
Q

Deep layer of cartilage

A

Greatest resistance

More proteoglycans, less water

102
Q

Calcified layer of cartilage

A

Anchors cartilage to bone

103
Q

2 classes of ligaments

A

Capsular and non capsular (non capsular can be internal and external)

104
Q

Most common IV General anesthetic

A

Propofol

105
Q

Most common inhaled general anesthetic

A

Nitrous oxide

106
Q

Types of neuromuscular junction blockers

A 
Non depolarizing (iums) - block ACh receptors
Depolarizing (succinyl-choline) -  Prevent re-polarization
107
Q

General anesthetics mechanism of action

A
  1. Stimulate GABA receptors - hyperpolarize cell

2. Inhibit ACh receptors

108
Q

Local anesthetic mechanism of action

A

Bind Na chanels in membrane of afferent neuron –> blocks depolarization, no pain sensation sent to brain

109
Q

Typical level of epidural or spinal block

A

L3-4 or 4-5, to avoid spinal chord

110
Q

Order of anesthesia

A

Small, unmyelinated nerves first, then larger, myelinated ones.
Pain, temp, pressure, proprio, motor

111
Q

Drugs that treat spasm

A

Polysynaptic inhibitors

Receptor specific drugs

112
Q

Polysnaptic inhibitors

A

Decrease excitatory input at alpha motor neuron to block pain - spasm - pain cycle
(Smooth muscle affected too - constipation)
Tolerance and dependence possible.
Meprobomate - antianxiety

113
Q

Drugs to treat spasticity

A 
Diazepam (valium)
Baclofen
Tizanidine/ Clonidine
Gabapentin (neuronin)
Dantrolene Na
114
Q

Ascending mechanism of opioids

A

Block release of pain neurotransmitters; hyperpolarize post-synaptic terminal

115
Q

Descending mechanism of opioids

A

Bind opioid receptors in brain, activating pain inhibitory pathways

116
Q

Proteins responsible for pain, fever, inflammation, etc.

A

Prostoglandins (produced via cyclooxygenase pathway)

*COX 2 is the pathway with the negative products

117
Q

S/s of ASA overdose:

A

Hearing loss, tinnitus, confusion, HA

Clin Med I (5 decks)

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