Metabolic & Rheumatic Disorders Flashcards
(57 cards)
1
Q
What is osteopenia?
A
X-ray evidence of decreased bone mineral density (BMD)
2
Q
What causes osteopenia?
A
- Osteoporosis
- Osteomalacia
- Malignancies (multiple myeloma)
- Endocrine disorders
3
Q
What is osteoporosis?
A
- Decreased bone density & bone strength
- Matrix is weakened
- Mineralization is decreased
4
Q
What causes osteoporosis?
A
- UKE (unknown etiology)
- Bone resorption exceeds bone formation
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
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 **
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
8
Q
What is the relationship between fractures and osteoporosis?
A
- Loss of trabeculae from cancellous bone
- Thinning of cortex
9
Q
What is postmenopausal osteoporosis?
A
- Increased osteoclastic activity results in loss of trabeculae
- Microfractures occur, bone compresses
10
Q
What is senile/age-related osteoporosis?
A
Haversian system [osteons, functional bone unit] widens d/t loss of trabeculae
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
12
Q
What is osteomalacia?
A
- Softening of bones d/t inadequate mineralization
- Adult condition
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
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)
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
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)
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
18
Q
What is Paget’s disease?
A
- Abnormal bone remodelling
- Excessive osteoclast-mediated bone resorption followed by disorganized osteoblast-mediated bone repair
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
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
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
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
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
Define: Articular
Relating to joints
26
What are the articular manifestations of RA?
- 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
What are extra-articular manifestations of RA?
- 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
How do we diagnose RA?
- 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
What is Systemic Lupus Erythematosis? (SLE) What are some risk factors?
- 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
What is a type 3 hypersensitivity response?
Formation of autoantibodies and immune complexes which result in immune response
31
What are the triggers for SLE?
- Ultraviolet light
- Chemicals
- Foods
- Infectious agents
32
What are common complaints of patients with SLE?
- Arthralgia
- Myalgia
- Fever
- Malaise/fatigue
- Temporary loss of cognitive abilities
33
What are manifestations of SLE?
- 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
What are the integument manifestations of SLE?
- Butterfly rash on nose/cheeks
- Fingertip lesions
- Hair loss
- Mucous membrane lesions
- Sunlight sensitivity
35
What are the renal manifestations of SLE?
- Glomerulonephritis
| - Interstitial nephritis
36
What are the pulmonary manifestations of SLE?
- Pleural effusion
| - Pleuritis
37
What are the cardiac manifestations of SLE?
- Pericarditis
- Heart block
- Hypertension
- Ischemic heart disease
38
What are the CNS manifestations of SLE?
- Photosensitivity
- Hemorrhage/stroke
- Thrombus
- Seizures
- Psychotic S&S: depression, euphoria, confusion, etc.
39
What is Systemic Sclerosis?
- 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
What are the manifestations of Limited Systemic Sclerosis?
- 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
What is Diffuse Scleroderma?
Widespread, rapidly progressive fibrosis of skin with early movement to organs (kidneys, esophagus, heart, lungs)
42
What are the manifestations of Diffuse Scleroderma?
- Stone face
- Hair loss
- Telangiestasis on face, chest, hands
- Reynaud phenomenon
- Arthralgia, myalgia
- Malabsorption
- Pulmonary fibrosis
- Malignant hypertension
- Pericarditis, heart blocks, myocardial fibrosis
43
What is Ankylosing Spondylitis?
- Chronic systemic inflammatory disease of joints
| - Late adolescence/early adulthood
44
What is the etiology of Ankylosing Spondylitis?
- Genetic
- Immune response that destroys joints and fuses adjacent bones
- Begins in sacroiliac joint, moves to spine and up
45
What are the manifestations of AS?
- 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
What is reactive arthritis?
- Joint inflammation post GI or GU/STI/HIV infection
- Usually 1-4 weeks after
- Achilles tendon & plantar fascia are common sites
47
What is Reiter syndrome triad?
- Arthritis
- Nongonococcal urethritis or cervicitis (inflammation of urethra)
- Conjunctivitis
48
What are the manifestations of reactive arthritis?
- Asymmetric, lower extremity
- Enthesitis is common (warm, swollen, tender joint)
- Fever, weight loss
49
What is Osteoarthritis?
- 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
What are the risk factors for OA?
- Genetic
| - Environmental
51
Whta is the difference between primary and secondary OA?
PRIMARY: idiopathic
SECONDARY: genetic or acquired joint disease
52
What are the manifestations of OA?
- Insidious
- Joint pain, stiffness, motion limitations
- Crepitus/grinding
- Instability and deformity
53
What is Gout syndrome?
- Gout arthritis
- Gout nephropathy
- Uric acid kidney stones
54
What is the etiology of Gout syndrome?
- Elevated serum uric acid
| - Primary (unknown cause) vs. Secondary (nucleic acid breakdown, CKD)
55
What is the pathophysiology of Gout?
- 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
What are triggers for gout?
- Excessive exercise
- Medications
- Foods/Dieting
- Alcohol
57
What are the manifestations of gout?
- Abrupt pain onset that can last days/weeks, with periods of remission
- Redness/swelling
- Tophi (uric acid build-up in big toe)
