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Pathophysiology > Metabolic & Rheumatic Disorders > Flashcards

Metabolic & Rheumatic Disorders Flashcards

1
Q

What is osteopenia?

A

X-ray evidence of decreased bone mineral density (BMD)

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2
Q

What causes osteopenia?

A
  • Osteoporosis
  • Osteomalacia
  • Malignancies (multiple myeloma)
  • Endocrine disorders
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3
Q

What is osteoporosis?

A
  • Decreased bone density & bone strength
  • Matrix is weakened
  • Mineralization is decreased
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4
Q

What causes osteoporosis?

A
  • UKE (unknown etiology)

- Bone resorption exceeds bone formation

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5
Q

What is osteoporosis associated with?

A
  • Gender
  • Postmenopausal osteoporosis
  • Male hormone declination
  • Genetics
  • Activity level
  • Nutrition
  • Body size
  • Race
  • Age-related changes
  • Decreased osteoblast production
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6
Q

What are some secondary causes of osteoporosis?

A
  • Endocrine disorders (ex. thyroid disorders, cushing’s, diabetes)
  • Malabsorption issues
  • Malignancies (ex. multiple myeloma)
  • Alcoholism
  • Medications (ex. corticosteroids, anticonvulsants)
  • Premature infancy
  • Cystic fibrosis
    • Al affect either osteoblast function and/or calcium absorption **
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7
Q

What is the Female Athlete Triad?

A
  • Eating disorders combined with excess exercise, resulting in weight fluctuations, causing:
  • Decreased gonadotropic hormone
  • Decreased LH, FSH
  • Decreased estrogen
  • Causes amenorrhea, osteoporosis/osteopenia
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8
Q

What is the relationship between fractures and osteoporosis?

A
  • Loss of trabeculae from cancellous bone

- Thinning of cortex

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9
Q

What is postmenopausal osteoporosis?

A
  • Increased osteoclastic activity results in loss of trabeculae
  • Microfractures occur, bone compresses
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10
Q

What is senile/age-related osteoporosis?

A

Haversian system [osteons, functional bone unit] widens d/t loss of trabeculae

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11
Q

What are the manifestations of osteoporosis?

A
  • Silent disorder
  • Sudden onset fracture (ex. Hip, pelvis, humerous)
  • Wedging/collapse of vertebrae (loss of height, kyphosis/dowager hump)
  • No bone pain unless fracture
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12
Q

What is osteomalacia?

A
  • Softening of bones d/t inadequate mineralization

- Adult condition

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13
Q

What are the manifestations of osteomalacia?

A
  • Bone pain and tenderness
  • Muscle weakness an early sign
  • Fractures of radius, femur
  • Delayed healing of fractures, deformities
  • Hyperparathyroidism d/t low calcium levels
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14
Q

What are the causes of osteomalacia?

A
  • Insufficient Ca+2 absorption from intestines (Lack of intake, Vitamin D deficiency)
  • Phosphate deficiency d/t renal losses & poor absorption in GI tract
  • Anticonvulsant use (long term)
  • Renal rickets (occurs with CKD, inability to activate vitamin D or excrete phosphate)
  • Vitamin D resistant rickets (renal tubular defect)
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15
Q

What is Rickets? (in childhood)

A
  • Inadequate calcium and Vitamin D
  • Failure/delayed calcification of cartilaginous growth plate
  • Metaphyseal regions of long bones widen/deform as unmineralized
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16
Q

What are the causes of rickets?

A
  • Nutritional deficits (Breast fed only with no Vit. D supplement)
  • Kidney failure
  • Malabsorption syndromes, GI loss
  • Medications (anticonvulsants, aluminum antacids)
  • Genetic (ex. dark-skinned)
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17
Q

What are the manifestations of rickets?

A
  • Enlarged skull
  • Oversized joints
  • Delayed fontanel closure
  • Slow tooth growh
  • Abnormal shaped thorax
  • Bowed legs
  • Difficulty ambulating
  • Stunted growth
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18
Q

What is Paget’s disease?

A
  • Abnormal bone remodelling

- Excessive osteoclast-mediated bone resorption followed by disorganized osteoblast-mediated bone repair

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19
Q

What are risk factors for Paget’s disease?

A
  • Unclear pathophysiolgy
  • Genetic, environmental or viral triggers?
  • Mid-adulthood
  • Men same as women
  • Northern European heritage
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20
Q

What are the manifestations of Paget’s disease?

A
  • Isolated lesions or widespread
  • Long-bone bowing and fractures
  • Large joint osteoarthritis
  • Skull, spine, pelvis, femur, tibia are common
  • “Cement lines” from new bone growth over old bone
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21
Q

What is Rheumatoid Arthritis? What is the etiology?

A
  • Autoimmune systemic disease
  • Uncertain
  • Genetic predisposition
  • Women > men
  • Peak incidence 40-50 years of age
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22
Q

What is the pathophysiology behind RA?

A
  • T-cell mediated response to trigger
  • Inflammatory mediators released
  • Antibodies form against auto-antigens
  • Rheumatoid factor (RF), an antibody, occurs in 70-80% of patients
  • Synovial inflammation and joint destruction result
  • Fluid accumulates (inflammatory process)
  • Neovascularization in synovial membrane
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23
Q

Define: Neovascularization

A

Formation of functional microvascular networks with red blood cell perfusion

24
Q

Define: Pannus

A
  • Vascular granulation tissue is formed that is destructive to joint (specific to RA)
  • Inflammatory erosion of cartilage/bone
25
Q

Define: Articular

A

Relating to joints

26
Q

What are the articular manifestations of RA?

A
  • Symmetrical
  • Polyarticular
  • Diarthodial/synovial
  • Joint pain/swelling
  • Limited joint movement
  • Wrist & finger joints common (pain turning doorknobs, opening jars, etc.)
  • Feet (pain on ball of foot when rising in morning, widening of forefoot d/t inflammation)
  • Subluxation
  • Joint instability
  • Swelling/thickening of synovium stretches joint capsule and ligaments, causing deformities, muscle imbalances, etc.
27
Q

What are extra-articular manifestations of RA?

A
  • Fatigue, weakness, anorexia, weight loss
  • Elevated ESR & C-reactive protein (CRP)
  • Rheumatoid nodules (ex. granulomatous lesions, tender or not, moveable/immovable, small/large)
  • Numerous other, but they are more rare
28
Q

How do we diagnose RA?

A
  • Four or more:
  • Morning stiffness of > 1 hour x 6 weeks
  • > 3 joint swelling x 6 weeks (simultaneous)
  • Swelling of wrist or finger joints x 6 weeks
  • Symmetric joint swelling x 6 weeks
  • Rheumatoid nodules
  • Serum RF
  • Radiographic evidence
29
Q

What is Systemic Lupus Erythematosis? (SLE) What are some risk factors?

A
  • Chronic inflammatory disease affecting entire body!
  • Type III hypersensitivity response
  • Unknown cause, but risk factors: Young women (15-40); African, Hispanic, Asian descent; Familial; Genetic
30
Q

What is a type 3 hypersensitivity response?

A

Formation of autoantibodies and immune complexes which result in immune response

31
Q

What are the triggers for SLE?

A
  • Ultraviolet light
  • Chemicals
  • Foods
  • Infectious agents
32
Q

What are common complaints of patients with SLE?

A
  • Arthralgia
  • Myalgia
  • Fever
  • Malaise/fatigue
  • Temporary loss of cognitive abilities
33
Q

What are manifestations of SLE?

A
  • Acute or insidious
  • Exacerbations and remissions
  • Arthralgies/arthritis common early symptom (most often hands, wrists, knees)
  • No articular destruction like other arthritis’
  • Avascular necrosis (usually femoral head)
  • Contractures, tendon rupture and subluxation
34
Q

What are the integument manifestations of SLE?

A
  • Butterfly rash on nose/cheeks
  • Fingertip lesions
  • Hair loss
  • Mucous membrane lesions
  • Sunlight sensitivity
35
Q

What are the renal manifestations of SLE?

A
  • Glomerulonephritis

- Interstitial nephritis

36
Q

What are the pulmonary manifestations of SLE?

A
  • Pleural effusion

- Pleuritis

37
Q

What are the cardiac manifestations of SLE?

A
  • Pericarditis
  • Heart block
  • Hypertension
  • Ischemic heart disease
38
Q

What are the CNS manifestations of SLE?

A
  • Photosensitivity
  • Hemorrhage/stroke
  • Thrombus
  • Seizures
  • Psychotic S&S: depression, euphoria, confusion, etc.
39
Q

What is Systemic Sclerosis?

A
  • Autoimmune disease of connective tissue
  • Widespread fibrosis (thickened skin, organ involvement)
  • Cause is poorly understood
  • More women than men, but men have more serious progression
40
Q

What are the manifestations of Limited Systemic Sclerosis?

A
  • Fingers, forearms, face;
  • CREST syndrome:
  • Calcium deposits on skin/soft tissue
  • Reynaud phenomenon
  • Esophageal dysmotility
  • Sclerodactyly (deformity/bending of fingers)
  • Telangiestasias (similar to spider veins, except large)
  • Pulmonary arterial hypretension is also common
41
Q

What is Diffuse Scleroderma?

A

Widespread, rapidly progressive fibrosis of skin with early movement to organs (kidneys, esophagus, heart, lungs)

42
Q

What are the manifestations of Diffuse Scleroderma?

A
  • Stone face
  • Hair loss
  • Telangiestasis on face, chest, hands
  • Reynaud phenomenon
  • Arthralgia, myalgia
  • Malabsorption
  • Pulmonary fibrosis
  • Malignant hypertension
  • Pericarditis, heart blocks, myocardial fibrosis
43
Q

What is Ankylosing Spondylitis?

A
  • Chronic systemic inflammatory disease of joints

- Late adolescence/early adulthood

44
Q

What is the etiology of Ankylosing Spondylitis?

A
  • Genetic
  • Immune response that destroys joints and fuses adjacent bones
  • Begins in sacroiliac joint, moves to spine and up
45
Q

What are the manifestations of AS?

A
  • Persistent or intermittent pain that can imitate sciatica pain ***
  • Worse when immobile **
  • Enthesitis: juncture of tendon/ligament to bone
  • Progressive stiffening/osteoporosis of spine
  • Loss of lumbar lordosis, kyhosis of thoracic spine and neck
  • Difficulty maintaining balance when walking (leaning forward)
  • Degeneration of hips & knees d/t altered center of gravity
  • Difficulty looking up and ahead
  • Heart & lung are constricted
  • Uveitis (30%)
  • Weight loss, fatigue and fever
46
Q

What is reactive arthritis?

A
  • Joint inflammation post GI or GU/STI/HIV infection
  • Usually 1-4 weeks after
  • Achilles tendon & plantar fascia are common sites
47
Q

What is Reiter syndrome triad?

A
  • Arthritis
  • Nongonococcal urethritis or cervicitis (inflammation of urethra)
  • Conjunctivitis
48
Q

What are the manifestations of reactive arthritis?

A
  • Asymmetric, lower extremity
  • Enthesitis is common (warm, swollen, tender joint)
  • Fever, weight loss
49
Q

What is Osteoarthritis?

A
  • Degenerative changes to articular cartilage of joints
  • Loss of cartilage
  • Thickening of subchondral bone
  • Osteophyte bone outgrowths at joint margins
  • Mild synovial inflammation
  • Can occur in any synovial joint in the body
50
Q

What are the risk factors for OA?

A
  • Genetic

- Environmental

51
Q

Whta is the difference between primary and secondary OA?

A

PRIMARY: idiopathic
SECONDARY: genetic or acquired joint disease

52
Q

What are the manifestations of OA?

A
  • Insidious
  • Joint pain, stiffness, motion limitations
  • Crepitus/grinding
  • Instability and deformity
53
Q

What is Gout syndrome?

A
  • Gout arthritis
  • Gout nephropathy
  • Uric acid kidney stones
54
Q

What is the etiology of Gout syndrome?

A
  • Elevated serum uric acid

- Primary (unknown cause) vs. Secondary (nucleic acid breakdown, CKD)

55
Q

What is the pathophysiology of Gout?

A
  • Precipitation of uric acid crystals in joint causes inflammation
  • Peripheral joints common
  • Nodules form in synovial lining & cartilage of joint
  • Enzymes are released and cause cell damage, inflammation (cartilage and subchondral destroyed)
56
Q

What are triggers for gout?

A
  • Excessive exercise
  • Medications
  • Foods/Dieting
  • Alcohol
57
Q

What are the manifestations of gout?

A
  • Abrupt pain onset that can last days/weeks, with periods of remission
  • Redness/swelling
  • Tophi (uric acid build-up in big toe)

Pathophysiology (4 decks)

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