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Pathophysiology 210 > Metabolic & Rheumatic Disorders > Flashcards

Metabolic & Rheumatic Disorders Flashcards

1
Q

Describe osteopenia and its causes

A 
X-ray evidence of decreased bone mineral density (BMD)
Causes
Osteoporosis
Osteomalacia
Malignancies (multiple myeloma)
Endocrine disorders
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2
Q

Describe osteoporosis and its causes

A 
Decreased bone density & bone strength
Matrix is weakened
Mineralization is decreased
Cause
UKE
Bone resorption exceeds bone formation
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3
Q

Osteoporosis is associated with…

A
  • Gender
  • Postmenopausal osteoporosis
  • Male hormone declination
  • Genetics, Race
  • Activity level
  • Nutrition
  • Body size
  • Age-related changes
  • Decreased osteoblast activity
  • Decreased physical activity levels
  • Postmenopausal
  • Nutrition
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4
Q

Causes of secondary osteoporosis

A 
> Endocrine Disorders
- Hyper/hypothyroidism 
- Hyperparathyroidism
- Cushing syndrome
- Diabetes Mellitus
> Malabsorption Issues
> Malignancies
- Multiple myeloma
> Alcoholism
> Medications
- Corticosteroids
> Premature Infants
> Cystic Fibrosis
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5
Q

Female athlete triad

A 
Emphasis of leanness and low body weight:
Eating disorders (i.e. dietary restrictions) combined with excess exercise result in weight fluctuations
= affects gonadotropic hormones
= decreased LH, FSH
= decreased estrogen
   resulting in…
- Amennorhea 
- Osteoporosis/Osteopenia
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6
Q

Osteoporosis cont’d: fractures, postmenopausal, senile

A

> Fractures d/t
- Loss of trabeculae from cancellous bone
- Thining of cortex
Postmenopausal Osteoporosis
- Increased osteoclastic activity results in loss of trabeculae
- Microfractures occur, bone compresses
Senile/age-related osteoporosis
- Haversian system widens dT loss of trabeculae

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7
Q

Osteoporosis Manifestations

A

> Silent disorder
Sudden onset fracture (hip, pelvis, humerous, etc.)

> Wedging/collapse of vertebrae (loss of height and kyphosis/dowager hump)
- No bone pain unless fracture.

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8
Q

Osteomalacia and manifestations

A

> Softening of bones d/t inadequate mineralization
Adult condition

> Manifestations
Bone pain, tenderness
Muscle weakness an early sign
Fractures of radius, femur
But not a significant cause of hip fractures
Delayed healing of fractures = deformities
Hyperparathyroidism d/t low calcium levels

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9
Q

Causes of osteomalacia

A

> Insufficient Ca+2 absorption from intestines d/t

  • Lack of intake
  • Vitamin D deficiency
> Phosphate deficiency d/t
- Renal losses
- Poor absorption in GI tract
> Anticonvulsant use (long term)
 Renal rickets 
Vitamin D resistant rickets
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10
Q

Rickets (childhood disease)

A

> Inadequate calcium absorption from diet
Lack of Vitamin D
Failure/delayed calcification of cartilaginous growth plate = overgrowth
Metaphyseal regions widen/deform as unmineralized.

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11
Q

Rickets Causes

A
  • Nutritional deficits
  • Kidney failure
  • Malabsorption syndromes, GI loss
  • Medications (anticonvulsants, aluminum antacids)
    Genetic
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12
Q

Risks and Manifestations of Rickets

A 
> Risks:
- Breast fed only (need a Vitamin D supplement)
- Dark-skinned
- Limited sunlight
> Manifestations:
- Enlarged skull
- Oversized joints
- Delayed fontanel closure
- Slow tooth growth
- Abnormal shaped thorax
-Bowed legs
- Difficult ambulation
- Stunted growth
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13
Q

Paget disease and risks

A

> Abnormal bone remodelling as a result of
- Focal areas of excessive osteoclast-mediated bone resorption followed by
- Disorganized osteoblast-mediated bone repair
Unclear pathophysiology
Genetic, environmental, ? viral triggers
Risks:
Mid adulthood, progression
Men = women
Northern European heritage

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14
Q

Paget disease manifestations

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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15
Q

Rheumatoid Arthritis

A

> Autoimmune systemic disease
Polyarticular

> Etiology
Uncertain
Genetic predisposition
Women > men
Peak incidence 40-50 years of age
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16
Q

RA pathophysiology

A

> T-cell mediated response to trigger

  • Inflammatory mediators released in response to a microbial agent
  • Antibodies form against auto-antigens

> Rheumatoid factor (RF)
- Which is an antibody- occurs in 70-80% of patients
Synovial inflammation and joint destruction result

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17
Q

Con’t…

A

> Fluid accumulates (inflammatory process)
Neovascularization in synovial membrane

> Pannus: vascular granulation
Tissue is formed that is destructive to joint (specific to RA).
- Inflammatory erosion of cartilage/bone.

18
Q

RA articular manifestations

A

Symmetrical
Polyarticular
Diarthrodial/synovial

  • Joint pain
  • Joint swelling
    > Limited joint movement
  • Wrists, finger joints common
  • Pain when turning doorknob, opening jars, buttoning shirts, etc.
    > Feet
  • Pain on ball of foot when rising in the morning.
  • Widening of forefoot d/t inflammation
19
Q

Con’t…

A
  • Ankles, knees, elbows, shoulders, spine
    > Subluxation
    > Joint instability
    > Swelling and thickening of synovium stretches joint capsule and ligaments
  • Deformities
  • Muscle imbalances
  • Swan neck deformities of hand
20
Q

RA extra-articular manifestations

A

> Fatigue, weakness, anorexia, weight loss
Elevated ESR & C-reactive protein (CRP)
Rheumatoid nodules
- Granulomatous lesions with central necrotic core
- Tender, or not
- Moveable, or immovable
- Small or large

> Numerous other but they are more rare

21
Q

RA diagnosis

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
22
Q

Systemic Lupus Erythematosis (SLE)

A 
Chronic inflammatory disease affecting entire body!
Unknown cause
Young women (15-40)
African, Hispanic, Asian descent
Familial
Genetic

Type III hypersensitivity response
- Formation of autoantibodies and immune complexes which result in immune response.

23
Q

SLE common complaints

A
  1. Arthralgia
  2. Myalgia
  3. Fever
  4. Malaise, fatigue
  5. Temporary loss of cognitive abilities
24
Q

SLE Triggers

A
  1. Ultraviolet light
  2. Chemicals
  3. Foods
  4. Infectious agents
25
Q

SLE manifestations: skeletal

A

Acute or insidious
Exacerbations & remissions

Skeletal
Arthralgias/arthritis common early symptom
Most often hands, wrists, knees
- ligaments/tendons/joint capsule
No articular destruction like other arthritis’
Avascular necrosis (usually femoral head)
Contractures, tendon rupture, subluxation

26
Q

Con’t…Integument

A 
Integument 
Butterfly rash on nose/cheeks
Fingertip lesions
Hair loss
Mucous membrane lesions
Sunlight sensitivity
27
Q

Con’t…Renal, Pulmonary, Cardiac

A

Renal

  • Glomerulonephritis
  • Intersitial nephritis

Pulmonary

  • Pleural effusion
  • Pleuritis

Cardiac

  • Pericarditis
  • Heart block
  • Hypertension
  • Ischemic heart disease (with chronic SLE)
28
Q

Con’t…CNS

A 
CNS
Photosensitivity- headache (migraine)
Hemorrhage – stroke
Thrombus
Seizures
- More frequent with renal disease

> Psychotic symptoms
Depression
Euphoria
Confusion, etc…

29
Q

Systemic Sclerosis/Scleroderma and manifestations

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

Manifestations
Limited (most common)
Diffuse

30
Q

Limited scleroderma

A

> Fingers, forearms, face

> CREST syndrome is not uncommon

  • Calcium deposits on the skin and soft tissue
  • Reynaud phenomenon
  • Esophageal dysmotility
  • Sclerodactyly (curling of fingers)
  • Telangiestasias (spider veins)

Pulmonary arterial hypertension is also common

31
Q

Diffuse Scleroderma

A

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

  • Stone face
  • Hair loss
  • Telangiestasis on face, chest, hands
  • Reynaud phenomenon is common
  • Arthralgia, myalgia
  • Malabsorption
  • Pulmonary fibrosis
  • Malignant hypertension
  • Pericarditis, heart blocks, myocardial fibrosis
32
Q

Ankylosing Spondylitis

A

Chronic systemic inflammatory disease of joints
Late adolescence/early adulthood
Men > women
Etiology is unclear
Genetic
Immune response that destroys joints and fuses adjacent bones.
Begins in sacroiliac joint, moves to spine and up

33
Q

Ankylosing Spondylitis manifestations

A 
Pain
Peristent or intermittent
Can imitate sciatica pain
Worse when immobile
Enthesitis
- Juncture of tendon/ligament to bone
34
Q

Con’t…

A

Progressive stiffening/osteoporosis of spine
Loss of lumbar lordosis
Kyphosis 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 and lung are constricted d/t to forward bend
Uveitis (30%)
Weight loss, fatigue
Fever

35
Q

Reactive arthritis and manifestations

A 
> Joint inflammation post GI or GU/STI/HIV infection
- Usually 1-4 weeks after
- Achilles tendon & plantar fascia are common sites
> Reiter syndrome triad
- Arthritis
- Nongonococcal urethritis or cervicitis
- Conjunctivitis 
> Manifestations of reactive arthritis
- Asymmetric, lower extremity 
- Enthesitis is common
- Warm, swollen, tender joint
- Fever, weight loss
36
Q

Osteoarthritis and risk factors

A

> Degenerative changes to articular cartilage of joints
- Loss of cartilage
- Thickening of subchondral bone
- Osteophyte bone outgrowths at joint margins
- Mild synovial inflammation
Any synovial joint in the body

> Risk Factors

  • Genetic
  • Environmental
37
Q

OA primary, secondary and manifestations

A

> Primary: idiopathic

> Secondary
Genetic or acquired joint disease

> Manifestations
Insidious
Joint pain, stiffness, motion limitations
Crepitus, grinding
Instability and deformity can occur
38
Q

Gout Syndrome

A
  • Gout arthritis
  • Gout nephropathy
  • Uric acid kidney stones
    > Etiology
    Elevated serum uric acid (primary diagnostic)
    Primary: unknown cause
    Increased production, decreased elimination, or both.
    Secondary
    Nucleic acid breakdown (e.g. tumor cell lysis)
    Chronic kidney disease
39
Q

Con’t…

A

Precipitation of uric acid crystals in joint causes inflammation

Peripheral joints common (they are cooler)

Nodules form in synovial lining & cartilage of joint

Enzymes are released and cause cell damage, inflammation
- Cartilage and subchondral bone is destroyed.

40
Q

Gout Triggers

A 
Excessive exercise
Medications
Foods
Alcohol
Dieting
41
Q

Gout manifestations

A 
Abrupt pain onset
Redness, swelling
Lasts days to weeks
Remission can last months to years
Tophi (uric acid buildup)

Pathophysiology 210 (4 decks)

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