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Pathophysiology > Exam #5- Musculoskeletal Pathophysiology > Flashcards

Exam #5- Musculoskeletal Pathophysiology Flashcards

1
Q

complete fracture

A

bone is broken all the way through

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2
Q

incomplete fracture

A

bone is damaged, but still in 1 piece

closed/simple- skin is intact

open/compound- skin is broken

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3
Q

comminuted fracture

A

bone breaks into more than 2 fragments

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4
Q

linear fracture

A

fracture runs parallel to long axis of bone

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5
Q

oblique fracture

A

fracture of shaft of bone is slanted

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6
Q

spiral fracture

A

encircles bone

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7
Q

transverse fracture

A

straight across bone

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8
Q

greenstick fracture

A

perforates 1 cortex and SPLINTERS spongy bone

common in children

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9
Q

torus fracture

A

cortex buckles BUT does NOT break

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10
Q

bowing fracture

A

longitudinal force is applied to bone

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11
Q

pathologic fracture

A

break happens at site of PRE-EXISTING abnormality

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12
Q

stress fracture

A

fatigue/insufficiency

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13
Q

a NP is reading a report of a humerus x/ray and reads that there is a communited transverse fracture of the distal humerus. what does this mean in regards to the characteristics of the fractures?

A

the bone is fractured in more than 2 pieces, and the break is straight across the bone

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14
Q

inflammatory phase of bone fracture

A

3-4 days

bone tissue destruction

triggers inflammatory response

hematoma forms

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15
Q

repair phase of bone fracture

A

several days

capillary ingrowth, mononuclear cells, fibroblasts form which leads to hematoma which leads to granulation tissue.

osteoblasts w/in procallus make collagen and matrix which form callus

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16
Q

remodeling phase of bone fracture

A

months to eyars

callus is reabsorbed (no longer necessary)

trabeculae are formed

now bone can withstand normal stress

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17
Q

what is the first thing that happens when a bone fractures to begin the healing process?

A

hematoma forms

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18
Q

what is the correct term used when a fracture heals in a nonanatomic position?

A

malunion

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19
Q

pathophysiology of support structure injuries

A

inflammatory exudate forms between torn ends

granulation tissue grows inward

collagen forms 3-4 days after injury

vascular fibrous tissues fuse new and surrounding tissues into 1 mass

healing tendon/ligament doesn’t have strength to withstand strong pull for 4-5 weeks after injury

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20
Q

dislocation

A

temporary displacement of bone FROM joint

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21
Q

subluxation

A

PARTIALLY LOST contract between bones in the joint

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22
Q

strain

A

tear/injury to TENDON (attaches MUSCLE to bone)

sTrain=Tendon

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23
Q

sprain

A

tear/injury to LIGAMENT (attaches BONE to bone)

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24
Q

avulsion

A

COMPLETE separation of TENDON or LIGAMENT

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25
Q

epicondylitis

A

inflammation of tendon where it attaches to bone

ex: tennis elbow (lateral) or golfer’s elbow (medial)

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26
Q

tendinitis

A

inflammation of tendon

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27
Q

tendinosis

A

painful wearing down of collagen fibers

tiny tears

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28
Q

bursitis

A

bursa inflammation (synovial fluid sacs) d/t repeated trauma

septic bursitis is d/t a wound infection

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29
Q

a patient presents with soreness of the lateral hip. the NP suspects inflammation of the greater trachanteric bursa. what would the NP document as the diagnosis in the chart?

A

bursitis

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30
Q

tennis elbow

A

lateral epicondylitis

causes pain on the outside of the albow

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31
Q

golfer’s elbow

A

also called medial epicondylitis

causes pain on the inside of the elbow

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32
Q

pathophysiology of myositis ossificans (heterotopic ossification)

A

complicated local muscle injury

inflammation of muscle tissue

calcification and ossification of muscle

calcification=think HARDENING

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33
Q

exampels of myositis ossificans (hetertopic ossification)

A

“rider’s bone” in equestrians

“drill bone” in infantry soldiers

thigh muscles in football players

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34
Q

what is it called when the muscle becomes hard like bone?

A

myositis ossificans

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35
Q

rhabdomyolosis pathophysiology

A

severe muscle trauma (compartment syndrome, crush syndrome)

QUICK breakdown of muscle

releases intracellular contents (MYOGLOBIN) into bloodstream

muscle cell loss (life-threatening)

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36
Q

s/s of rhabdomyolysis

A

muscle pain, weakness, and DARK URINE from MYOGLOBIN

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37
Q

compartment syndrome can lead to what?

A

rhabdomyolosis

38
Q

pathophysiology of compartment syndrome

A

complication of fracture

increases venous pressure

decreased arterial flow

not enough blood flow to affected area

ischemia and edema

39
Q

s/s of compartment syndrome

A

(5P’s)

pain (much more than initial injury should have caused)

paresthesia

pallor

pulselessness

paralysis (late)

40
Q

a patient presents to the provider with no pulse in their hand, pallor, and weakness/paralysis of their thumb after experiencing an ulnar fracture. the provider would document which diagnosis in the chart?

A

compartment syndrome

41
Q

osteoporosis “porous bone”

A

decreased bone mass/density

imbalance of bone resorption and formation

42
Q

**RANKL

A

ligand that’s released by osteoblast

activates receptor-RANK (on the osteclast)

RANKL SUPPRESSES apoptosis

osteoclasts survive longer=more bone BREAKING than bone MAKING

RANKL is BLOCKED by OPG

43
Q

causes/patho of osteoporosis

A

decreased estrogen/testosterone, decreased activity levels, decreased vitamin D, calcium, magnesium

alteration in osteoprotogen (OPG), receptor activator of nuclear factor kappa K (kB), ligand (RANKL), and receptor of nuclear factor kB (RANK): OPG/RANKL/RANK system

post menopause; glucocorticoids (increase RANKL, inhibits OPG production which decreases bone density)

44
Q

s/s of osteoporosis

A

pain, bone deformity, fracture, kyphosis, decreased height

treatment=denosumab

45
Q

what is RANK?

A

receptor on osteoclasts

KNOW THIS!!!!

46
Q

on of the theories behind the pathophysiology of osteoporosis is that there is an alteration of the RANK/RANKL/OPG’s normal system. how does estrogen play an important role with this system and in the development of osteoporosis in the post menopausal female?

A

decreased estrogen decreases OPG secretion from osteoblasts

47
Q

osteomalacia

A

soft bones

48
Q

pathophysiology of osteomalacia

A

decreased vitamin D

decreased absorption of calcium from intestines

slow/inadequate mineralization osteoid formation BUT calcification doesn’t happen

SOFT BONES

49
Q

s/s of osteomalacia

A

pain, bone fracture, vertebral collapse, bone malformation, waddling gait

50
Q

cause of osteomyelitis

A

STAPH INFECTION

infection spreads under periosteum and along bone shaft or into bone marrow

51
Q

s/s of osteomyelitis

A

acute/chronic inflammation, fever, pain, necrotis bone (SEQUESTRUM)

52
Q

pathophysiology of paget disease (osteitis deformans)

A

state of increased metabolic activity in bone

TOO MUCH bone resorption/formation of large/soft bones (usually axial skeleton)

53
Q

s/s of paget disease

A

brain compression, impaired motor function, deaf, optic nerve atrophy

advanced: enlarged head, headache, deafness due to compression of nerve in bony meatus, increased cardiac output due to great bone vascularity, kyphosis, bone pain, most commonly in back of hips, bowing of limbs, increased warmth and tenderness over bones, increased limb volume

54
Q

noninflammatory joint disease

A

NO synovial membrane inflammation, NO systemic s/s, NORMAL synovial fluid

OA

55
Q

inflammatory joint disease

A

inflammatory damage/destruction in synovial membrane or articular cartilage

does have systemic s/s (fever, increased WBC, malaise, anorexia, hyperfibrinogenemia)

can be infectious or noninfectious

RA

56
Q

what is one of the things that differentiates inflammatory joint disease from non-inflammatory joint disease?

A

inflammatory joint disease has prodromal symptoms

57
Q

prodromal symptoms

A

early symptoms that signals onset of disease/illness (so in inflammatory there are symptoms that signify a flare up is coming)

58
Q

osteoarthritis (DJD)

A

NONINFLAMMATORY

59
Q

pathophysiology of osteoarthritis

A

loss of articular cartilage, sclerosis (hardening) of underlying bone, new bone spurs (osteophytes)

60
Q

s/s of osteoarthritis

A

local areas of damage and loss of articular cartilage, new bone forms of joint margins, joint capsule thickens

pain, stiffness, joint gets bigger, deformed, swelling

61
Q

rheumatoid arthritis

A

INFLAMMATORY

62
Q

pathophysiology of RA

A

systemic AUTOIMMUNE destruction of synovial membrane and joints

synovial membrane is destroyed 1st

articular cartilage, joint capsule, and surrounding ligaments/tendons

63
Q

s/s of RA

A

RA or RF test- will have antibodies IgG and IgM

systemic s/s, symmetric joint swelling/deformities, stiffness 1 hour after rising, rheumatoid nodules in organs

caplan syndrome= pulmonary nodules and pneumoconiosis

64
Q

basics of bone tumors

A

may originate from bone cells, cartilage, fibrous tissue, marrow, or vascular tissue

all tumors have s/s of pain and swelling

65
Q

osteosarcoma

A

contain masses of osteoids

common in young people

usually occurs around the knees

66
Q

chrondrosarcoma

A

makes cartilage/chondroid

common in middle-age/elderly

usually in spongy bone of long bones

causes erosion of soft tissues

67
Q

fibrosarcoma

A

firm, fibrous masses of collagen

usually affects femur/tibia

lung mets is common

this mass you can actually feel

(picture of guy with tumor in calf)

68
Q

myelogenic tumors

A

develop from bone

Marrow cells. giant cell tumor leads to mass bone resorption. found in femur, tibia, radius, or humerus. slow and relentless growth rate. limited movement

Myelogenic=Marrow

69
Q

from which cells do collagenic tumors arise?

A

fibroblast

70
Q

pathophysiology of ankylosing spondylitis

A

chronic inflammatory joint disease of spine/sacroiliac joints

inflammatory cells infiltrate and erode fibrocartilage

repair w/ scar tissue that ossifies and calcifies

stiffening and fusion of joints

there is uncontrolled bone formation

71
Q

what gene is associated with ankylosing spondylitis

A

gene HLA-B27

72
Q

s/s of ankylosing spondylitis

A

low back pain, stiffness, pain, restricted motion, “bamboo” spine, kyphosis

73
Q

which disease process is characterized by the infiltration of inflammatory cells into the fibrocartilage and eventually erodes it, which leads to fusion of the bones?

A

ankylosing spondylitis

74
Q

pathophysiology of gout

A

r/t purine metabolism

metabolic disorder that disrupts body’s control of uric acid production/excretion

HIGH uric acid levels

crystallized uric acid

deposit in connective tissue b/c purine synthesis/breakdown is increased or uric acid is poorly secreted by kidneys

75
Q

stages of gout

A

asymptomatic hyperuricemia- URATE level is HIGH, but NO s/s

acute gouty arthritis- attacks are here

tophaceous gout- TOPHI appear in cartilage, synovial membranes, tendons, and soft tissues

76
Q

s/s of gout

A

pain in great toe (worse QHS), hyperuricemia, recurrent attacks of monoarticular arthritis, renal stones

TOPHI: small, white visible nodules

77
Q

physiologic contracture

A

muscle fiber shortens WITHOUT an AP

TEMPORARY

78
Q

cause of physiologic contracture

A

failure of SR (calcium pump) even though ATP is available

79
Q

pathologic contracture

A

muscle fiber shortens d/t muscle spasm/weakness

PERMANENT

drop foot (inability to lift the front part of the foot off the ground)- related to peroneal nerve

80
Q

cause of pathologic contracture

A

lots of ATOP

contracture occurs even though there’s a normal AP

81
Q

pathophysiology of chronic fatigue syndrome (myalgic encephalomyelitis)

A

profound fatigue, neuro energy production, immune impairments

can be caused by CNS dysregulation, heart/immune problems, chronic proinflammatory cytokines, cellular energy metabolism problems, ion transport problems

82
Q

s/s of chronic fatigue syndrome

A

unrestful sleep

debilitating fatigue made worse by physical/mental exercise

muscle pain, noninflammatory joint pain, HA, flu-like s/s, memory/concentration problems

83
Q

pathophysiology of disuse atrophy

A

prolonged inactivity

decreased muscle cell size

84
Q

causes of disuse atrophy

A

BR, trauma, casting, nerve damage

oxidative stress

decreased protein synthesis and increased proteolysis

85
Q

which disease process is the result of a mutation in the SCN4A gene?

A

periodic paralysis

86
Q

pathophysiology of fibromyalgia

A

chronic, widespread joint and muscle pain, fatigue, and tender points

CNS dysfunction amplified pain transmission and interpretation

may be d/t the flu, chronic fatigue syndrome, HIV, lyme disease, meds, physical/emotional trauma

87
Q

s/s of fibromyalgia

A

vague increased sensitivity to touch, no inflammation, fatigue, sleep problems

diffuse, chronic pain

must have tenderness in 11 of the 9 pairs (18 totel) of tender points

88
Q

9 areas of tender points for fibromyalgia

A

occiput

trapezius

supraspinatus

gluteal

greater trochanter

low cervical

second rib

lateral epicondyle

knee

89
Q

pathophysiology of poly/dermatomyositis

A

autoimmune inflammation of connective tissue and muscle fibers

90
Q

poly/dermatomyositis

A

symmetric proximal muscle (pelvic and shoulder girdle) weakness and myalgia that develops over weeks to months

91
Q

polymyositis

A

generalized muscle inflammation

mediated by T CELLS

92
Q

dermatomyositis

A

polymyositis PLUS skin rash

B CELL mediated

Pathophysiology (5 decks)

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