4th Exam: Bone & Joint Disease Flashcards Preview

Pathology > 4th Exam: Bone & Joint Disease > Flashcards

Flashcards in 4th Exam: Bone & Joint Disease Deck (107)
1

Shaft of bone:

diaphesis

2

Center of long bone:

spicules of bone, aka cancellous bone

3

Outer shell of long bone:

compact bone, cortex

4

Smoothest part of long bone:

articulating ends

5

Bone building molecules, etc.:

Vit D, Ca2+, Calcitonin, PTH

6

What is the bone covered by:

periosteum

7

Are there blood vessels in the periosteum?

yes

8

Osteoblast progenitors give rise to:

-blasts, -cytes, -oclasts

9

Mineralized osteoblast:

Osteocyte

10

These make osteoid:

osteoblasts

11

Osteoblasts have ____ receptors, secrete osteoclasts stimulating factor, bone break down.

PTH

12

Histology of -blasts:

blue stain: calcified bone, red stain: in bw osteoblast, mineralization front

13

Where is the inorganic material found?

ECM

14

What inorganic material is found in the ECM?

Hydroxyapatite crystals (calcium phosphate)

15

Organic material found in matrix:

collagen, proteoglycan, glycoprotein

16

What stimulates glycoprotein synthesis?

Vit D

17

How many days after matrix deposition does mineralization occur?

12-15d

18

Where is the mineralization front?

At osteoid-mineralization bone interface

19

What controls the mineralization front?

under osteoblast/osteocyte influence

20

When does mineralization occur?

if Ca2+ and PO4 adequate (need to crystalize), they displace H2 → Ca-OH apatite crystals

21

Lamellar:

mature, strong bone, parallel lines

22

Woven bone:

weaker than lamellar, fibers don’t look parallel

23

The osteon is part of what type of bone?

compact bone

24

Cancellous bone viewed thru polarized light:

bone breaks into spicules, not as dense, bone marrow in space

25

Osteoclasts:

multinucleated, form from macs
-

26

How do -clasts break up bone?

Burrow into calcified bone (blue), liberate calcium, demineralization

27

How do -Blasts signal -clasts:

RANK-RANK ligand receptors. Receptor on -clast precursor, -blast binds -clast receptor to tell it to break bone down, PTH: stimulates -blasts via its receptors, calcitonin: turns off -clasts

28

PTH, turns on or off -clasts?

turns off, stimulates -blasts via its receptors, calcitonin:

29

-clasts are derived from:

monocyte/mac system

30

-clasts secrete:

carbonic anhydrase → carbonic acid

31

TF? Exercise can stimulate new bone formation

T.

32

Types of fractures:

simple, displaced, comminuted, open (compound), compression, pathologic

33

Simple fracture:

unsially transvers, bone still aligned

34

Displaced fracture:

bone not aligned

35

Comminuted fracutre:

splintered, multiple pieces, crushing injury, longer to heal, bring pieces together surgically

36

Open fracture:

through skin

37

Compression fracture:

ex: mainly vertebra, and pt looses height- osteoporosis

38

Pathologic fracture:

pre-existing disease- bone wouldn’t fracture otherwise

39

Fracture complications

Infection, delayed union and nonunion, avascular necrosis

40

Fracture type most prone to infection:

compound

41

Most common cause of delayed healing:

Infection

42

What causes avascular necrosis?

loss of blood supply

43

What typically causes kyphosis?

spine disease: osteoporosis, disc disease, osteoarthritis

44

Metabolic bone diseases:

osteogenesis imperfect, osteoporosis, osteomalacia, Paget’s disease, Rickets

45

primary osteoporosis:

classic disease, post-menopausal or senile

46

secondary osteoporosis:

can cause or complicate primary osteoporosis

47

Cause and tx for secondary osteoporosis:

iatrogenic, corticosteroid therapy

48

Most cases found in this population:

post-menopausal elderly women

49

First signs of osteoporosis after possibly remaining silent for yrs:

bone pain, gradual loss in heigh

50

Most common fracture site due to osteoporosis:

hip

51

Who are more affected by osteoporosis, white or black women?

white, 1:2, vs 1:5

52

osteoprosis fractures are due to:

peak bone mass

53

Osteoporotic hip fractures mortality:

25%, high

54

Gross appearance of osteoporosis fracture:

a depression, dec bone density

55

Osteoporosis risk factors:

Female, age, asian, white, early menopaus, low peak bone mass, inadequate Ca2+ intake, lack of exercise, alcohol, smoking, steroids

56

There is low ___ activity and high ___ activity in osteoporosis:

blast, clast

57

Which types of bone are thin in osteoporosis?

cortical and trabecular

58

Common fracture sites:

Femoral neck, Colles’ fractures (distal radius) in the hand in the wrist

59

At what age do women meet their peak bone mass?

35yo, demineralization thereafter

60

Consequences of osteoporosis in the spine:

pain, compression fractures (fxs), loss of height, stooped posture, kyphosis

61

Therapy for osteoporosis:

Regular exercise, diet, Ca2+, vit D, Limit alcohol, smoking, estrogen supplements, bisphosphonates inhibit -clast activity

62

Cause of osteonecrosis of jaw:

bisphosphonate therapy, fewer -clasts interfere w bone remodellin

63

Osteonecrosis could easily be misdiagnosed as:

neuralgia inducing cavitating osetonecrosis (NICO_

64

NICO:

Due to avascular (ischemic) osteonecrosis (NOT bisphosphonate therapy), in any bone, more susceptible to fracture

65

Case: 60yo white man, head enlarging for past 2 years, bowing of tibias, X-ray: thickening of skull

Paget's Disease

66

Paget’s Disease:

White, euro descent, < age 40, ocalized or generalized (85%), etiology – myxovirus particles in -clasts, cycles of bone resorption and reformation (Woven instead of lamellar bone formed), X-rays: lytic (more dense) & sclerotic (less dense) lesions, bones look thick, imbalance of breaking and creating bone

67

osteolytic phase of Paget's Disease:

high lesion, less bone, bone breaking

68

Osteosclerotic phase of Paget's diseases:

less lesions, more bone, looks thick, bone creation

69

Paget's diseases happens here:

Tibia, ilium, femur, vertebra, skull

70

Symptoms of Paget's disease:

Cranial nerve compression → VIII cranial nerve – deafness

71

Bone thickening in Paget's disease happens here:

from OUTER cortex, so bone is not compressing brain

72

pattern of new bone

mosaic (woven)

73

How to see new, mosaic, woven bone best:

under polarized light

74

TF? lamellar bone is formed around mosaic bone:

F. not formed here

75

mosaic bone:

• Weak, woven, prone to fracture

76

Saber shin:

bowing of the tibia, the bone is soft

77

Calvarium:

osteosclerosis of the skull

78

Osteoarthritis:

Common in elderly, 90% > 60yo, morning stiffness, pain w use, improves w rest, related to physical stress, often weight bearing joints, exception is DIP (distal interphalangeal?) joints

79

Degeneration of articular cartilage:

Superficial layer flaking, fissuring of cartilage, then loss of cartilage. Resulting bone on bone, loss of articular surface, “Naked” bone against “naked” bone, abnormal bone growth → Osteophytes: bony outgrowth due to new stress on different part of bone, bone grows sideways), bone spurs, Heberden’s nodes

80

Diarthrodial joints involves:

synovial fluid

81

osteoarthritis histo:

Flaking at surface → fissures in the cartilage → loss of cartilage → bone on bone, he result is throwing the joint out of alignment → different forces on different parts of the bone → new bone formation, creating outgrowths (osteophytes)

82

Gray section of the gross view of a surface of a joint:

erosion of the articular cartilage, partial or total

83

Locations of arthritis:

Hip, distal joints of fingers

84

Arthridial knobs of fingers:

Heberden's nodes

85

Heberden's nodes, more common in men or women?

women

86

Case: 41 year old man in good health, awakes from sleep with pain in great toe, severe, pain, sudden onset, can’t tolerate bed covers on toe, on PE next day, MP joint very tender to touch, joint swollen, red

Gout-Acute Arthritis

87

Gout of the great toe

Podagra

88

Gout risk factors:

Middle age or older, male, obesity and “rich diet”, alcohol consumption, superior intelligence

89

Why does alcohol consumption lead to gout?

alcohol interferes with excretion of urates, purine metabolism issue

90

Hyperuricemia:

Excessive intake of purine – containing foods (beer, organ meats (liver), beans), Low renal urate excretion (24h urinary acid < 1000 gm (apparently don’t memorize this number)), Alcohol and other agents which retard excretion, makes disease worse

91

Uric acid, solubility level:

marginally soluble even at normal levels

92

Normal serum uric acid:

~ 7 mg/dl

93

Serum uric acid:

Tends to rise w age, rises at earlier age and faster in males

94

What causes gout, crystal formation or inflammatory reaction?

inflammatory reaction

95

Elevated serum acid:
o

Crystal form in joint fluid (especially at low temp), engulfed by polys → release lysosomal enzymes, synovitis and ultimate destruction of articular cartilage due to release of cytokines, crystals deposit in surrounding tissues → tendinitis, tophus formation (nodule, in soft tissue)

96

TF? Gout is an untreatable disease.

F.

97

How are urate crystals in joint fluid aspirate seen?

under polarized light

98

Histo of crystal-induced arthritis:

white deposits of urates below the articular cartilage

99

Histo of gouty arthritis:

White gout precipitating on destroyed articular cartilage

100

Histo of Tophi in soft tissue:

Common in the ear and adjacent to the involved joint, like in the toe

101

Second most common cause of facial pain:

TMJ

102

Causes of TMJ:

The joint, muscles, osteoarthritis, bruxism

103

Symptoms of TMJ:

Pain in muscles of mastication, headache

104

Benign bone tumor:

osteoma

105

Malignant bone tumor:

primary, metastatic

106

Osteoma:
-

Benign, slow growing, common locations sinuses, jaw, skull, mean age 35, often asymptomatic

107

Histology of osteoma:

Looks like normal bone, seems to arise from bone surface