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Pathophysiology 210 > Chapter 44 > Flashcards

Chapter 44 Flashcards

1
Q

What is osteopenia?

A

Lower bone mineral density, common to all metabolic bone diseases (determined with X-ray)

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2
Q

What is osteopenia due to?

A

Decrease formation, deossification, and mineralization

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3
Q

What is osteoporosis?

A

Decreased bone density and strength (matrix is weakened and mineralization is decreased)

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4
Q

What are causes of osteoporosis?

A

UKE, but imbalance between breakdown and formation. (bone breakdown exceeds formation)

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5
Q

What is osteoporosis associated with?

A

Gender (post menopausal, male hormone decline)
Genetics
Activity level (strain on bones =strength)
Nutrition
Body size
Race
Age related changes (decreased osteoblast replication, change in activity)

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6
Q

There are many secondary causes of osteoporosis. Name a few and how they work.

A

Hyperparathyroidism: pth increases blood calcium
Alcoholism: stops osteoblasts
Antacids with aluminum: increases calcium excretion

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7
Q

Osteoporosis fractures are due to

A

loss of trabecular from cancellous bone and thinning of the cortex

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8
Q

What happens in post menopausal osteoporosis ?

A

Osteoclastic activity increases resulting in a loss of trabeculae

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9
Q

What happens in senile/age related osteoporosis?

A

Haversian widens because trabeculae is lost

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10
Q

What are manifestations of osteoporosis?

A

Silent disorder, sudden onset of a fracture, wedging or collapse of vertebrae (loss of height= kyphosis or dowager hump)

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11
Q

What is female athlete triad?

A

Eating disorder with excessive amount of exercise (decrease in calcium intake, decrease fat to muscle ratio)

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12
Q

In female athlete triad what does it lead to?

A

Decreased gonadotropic hormone (decreased amount of estrogen), Amenorrhea, and osteoporosis

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13
Q

What is osteomalacia?

A

Adult condition where there is softening of bones d/t inadequate mineralization

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14
Q

What are manifestations of osteomalacia?

A

Bone pain, tenderness, fractures, muscle weakness (early sign), delayed healing of fractures with deformities, hyperparathyroidism d/t low calcium levels

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15
Q

What are causes of osteomalacia?

A 
Insufficient Ca absorption (lack of intake, Vit D def) 
Phosphate defieciency (renal losses, poor absorption in GI tract) 
Anticonvulsant use (decreases the activation of Vit D)
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16
Q

A form of osteomalacia is renal rickets. What is this?

A

Occurs with chronic renal failure. The kidneys are unable to activate Vit D and excrete phosphate

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17
Q

A form of osteomalacia is Vit D resistant rickets. What is this?

A

Genetic renal tubular defect. Occurs in boys>girls

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18
Q

What is rickets?

A

Childhood disease
Failure/delayed calcification of growth plate= overgrowth
There is an inadequate calcium absorption and lack of Vit D
Metaphyseal regions of long bones widen/deform

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19
Q

What are the causes of rickets?

A

Nutritional deficits (decreased sunlight, Vit D, Ca, phosphate), kidney failure (decrease Vit D), malaborption, medications, genetics

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20
Q

What are 3 risks for getting rickets?

A

Breast fed only, dark skinned, decrease sunlight

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21
Q

Manifestations of rickets?

A

Enlarged skull, oversized joints, delayed fontanel closures, slow tooth growth, sharp thorax, bowed legs, stunted growth, difficult to walk

22
Q

What is pagets disease?

A

Abnormal bone remodelling- excessive osteoclast-bone activity followed by unorganized osteoblast bone repair

23
Q

What is the pathophysiology of pagets disease?

A

Unclear- genetics? environmental? viral?

24
Q

What are some risk factors for pagets disease?

A

Mild adulthood, northern european, men = women

25
Q

What are manifestations of pagets disease?

A

“cement lines”, bowing of long bones, can be isolated or widespread, large joint osteoarthritis

26
Q

What are SARDS disorders ?

A

Inflammation of connective tissue disorders

27
Q

What is rheumatoid arthritis?

A

Autoimmune systemic disorder that is polyarticular (numerous joints)

28
Q

What is the etiology of rheumatoid arthritis?

A

Peaks at 40-50 in woman >men, uncertain why but may be genetic

29
Q

What is the pathophysiology of RA?

Note: Pannus is vascular granulations tissue is formed that is destructive to joint/cartilage

A

T cell mediated response to trigger (inflam. mediators release, antibodies form against antigens, rheumatoid factor results in 70-80%)-> synovial inflammation and joint destruction-> fluid accumulation-> Neovascularization in synovial membrane (ingrowth of blood vessels)

30
Q

What are articular manifestations in RA?

A

Symmetrical, polyarticular, pain in joints, swelling, limited joint movement, in the foot there is pain on ball and widening of forefoot, subluxation (displacement), joint instability, swelling and thickening of synovium stretches joint capsule and ligaments (deformities, muscle imbalances, swan neck)

31
Q

What are extra articular manifestations in RA?

A

Fatigue, weakness, anorexia, weight loss, elevated ESR and C reactive protein b/c of inflammatory process, rheumatoid nodules (tender?, small or large, moveable or not, granulomatous with necrotic core)

32
Q

What is the diagnosis criteria for RA?

A

4 or more: morning stiffness, 3 or > joints swelling, swelling to wrist or fingers, symmetric joint swelling, rheumatoid nodules, serum rheumatoid factor, radiographic evidence

33
Q

What is systemic lupus erythematosis (SLE)?

A

Chronic inflammatory disease that affects the entire body, unknown cause, young woman 15-40, familial, genetic, type III hypersensitivity (formation of antibodies and immune complexes which result in immune response)

34
Q

What are common complaints and triggers of SLE (the great imitator)?

A

arthralgia, myalgia, fever, fatigue, , malaise, loss of cognition temp.

UV light, chemicals, foods, infectious agents

35
Q

Name SLE manifestations in each system

A

Skeletal
-arthralgias/arthritis
-often in hands, wrist, knees
-no articular destruction like other arthritis
-avascular necrosis (usually femoral head)
contractures, tendon rupture, subluxation
Integument
-butterfly rash on nose/cheek
-fingertip lesions
-hair loss, sunlight sensitivity
Renal: glomerulonephritis, nephritis
Pulmonary: pleuritis, pleural effusion
Cardiac: pericarditis, heart block, HT, ischemic heart block
CNS: photosensivity, stroke, thrombus, seizures, psychotic symptoms (euphoria, depression, confusion)

36
Q

What is sclerosis/scleroderma?

A

An autoimmune disease of connective tissue

Widespread thickening of the skin/organ involvement

37
Q

What are the manifestations of sclerosis/scleroderma?

A

limited(most common), diffuse

38
Q

What is CREST syndrome in relation to limited scleroderma?

A 
Calcium deposits on skin 
Reyna (lack of blood flow)
Esophageal dismotility 
Sclerodactyly (Ca deposits in fingers, thickness)
Telangiestasias (spider web venules)

fingers, forearms, face
HT is common

39
Q

What are manifestations of diffuse scleroderma?

A

widespread, rapid progressive fibrosis of skin with early movement to organs
-stone face, hair loss, telangiestasis, reynaud, arthragia, myalgia, malabsorption, pulmonary fibrosis, malignant HT, pericarditis, heart blocks, myocardial fibrosis

40
Q

What is ankylosing spondylitis?

A

Chronic inflammatory disease of joints- immune response that destroys joints and fuses adjacent bones
late adulthood/early adulthood
men>woman

41
Q

What are manifestations of ankylosing spondylitis?

A

Pain (worse when immobile, persistent or intermittent)
Enthesitis (inflammation of juncture of tendon
progressive stiffening of spine
loss of lumbar lordosis
kyphosis , difficulty looking up
altered centre of gravity, difficulty with balance
heart and lung constricted
uveitis (inflammation of uvea)
weight loss, fever, fatigue

42
Q

What is Reactive arthritis?

A

Joint inflammation secondary to post GI GU/HIV/STI infection (1-4 weeks after)
Achilles tendon and plantar fascia are common sites

43
Q

A form of reactive arthritis is reiter syndrome triad. What is this?

A

Arthritis, conjunctivitis, nongonococcal urethritis and cervicitis

44
Q

What are manifestations of reactive arthritis?

A

asymmetric, lower extremities, enthesitis is common (warm, swollen, tender joints), fever, weight loss

45
Q

What is osteoarthritis ?

A

Degenerative changes to articular cartilage of joints (loss of cartilage, thickening of subchondal bone, mild synovial inflammation), any synovial joint in the body

46
Q

What are osteoarthritis risk factors? Manifestations?

A

Genetic, environmental
Primary: UKE
Secondary: genetic or acquired joint disease

Insiduous, pain, stiffness, motion limitations, crepitus, instability and deformity can occur

47
Q

What is gout syndrome?

A

Elevated serum uric acid
Primary: UKE (increase production, decrease elimination or both)
Secondary: nucleic acid breakdown, chronic kidney disease

48
Q

What is gout..

A

precipitation of uric acid crystals in joints cause inflammation

  • peripheral joints are common
  • nodules form and enzymes are released and cause cell damage, inflammation, destroyed bone
49
Q

what are triggers of gout?

A

Excessive exercise, dieting, alcohol, medication, foods

50
Q

What are manifestations of gout?

A

Abrupt pain, redness, swelling, lasts days to weeks, remission can last months to years, tophi (collection of uric acid where crystals gel together)

Pathophysiology 210 (3 decks)

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