Chapter 44 RHEUMATIC Flashcards

1
Q

Define osteopenia as it relates to osteoporosis and osteomalacia

A

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

OSTEOPOROSIS
-decreased bone density & strength

Fractures d/t

  • Loss of trabeculae from cancellous bone
  • Thinning of cortex

Postmenopausal Osteoporosis

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

Senile/age-related osteoporosis
-Haversian system widens d/t loss of trabeculae

MANIFESTATION
Silent disorder
Sudden onset fracture (hip, pelvis, humerous, etc.)**
Wedging/collapse of vertebrae (loss of height and kyphosis/dowager hump)
No pain unless fracture

OSTEOMALACIA

  • softening of bones d/t inadequate mineralization
  • adult condition

CAUSES

  • insufficient calcium absorption from intestines
  • phosphate deficiency d/t renal losses or decreased intestinal absorption
  • Anticonvulsant use

MANIFESTATION
Bone pain, tenderness
Muscle weakness an early sign
Fractures of radius, femur
Not a significant cause of hip fracture
Delated healing of fractures = deformities
Hyperparathyroidism d/t low calcium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the risk factors and factors that contribute to the development of osteoporosis and relate them to the prevention of the disorder

A
Gender
Postmenopausal osteoporosis
Male hormone declination
Genetics
Activity level
Nutrition
Body size
Race
Age-related changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the primary features of osteoporotic bone and resulting manifestations of this disease

A

Fractures d/t

  • Loss of trabeculae from cancellous bone
  • Thinning of cortex

Postmenopausal Osteoporosis

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

Senile/age-related osteoporosis
-Haversian system widens d/t loss of trabeculae

MANIFESTATION

  • Silent disorder
  • Sudden onset fracture (hip, pelvis, humerous, etc.)**
  • Wedging/collapse of vertebrae (loss of height and kyphosis/dowager hump)
  • No pain unless fracture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Compare the pathogenesis and manifestations of osteomalacia and rickets

A

RICKETS

Inadequate calcium absorption from diet
Lack of vitamin D

Failure/delayed calcification of cartilaginous growth plate =
Over growth
Metaphyseal regions of long bones widen/deform as unmineralized

CAUSES
Nutritional deficits
Kidney failure
Malabsorption syndromes, GI loss
Medications (anticonvulsants, aluminum antacids)
Genetic
MANIFESTATION
Enlarged skull
Oversized joints
Delayed fontanel closure
Slow tooth growth
Abnormal shaped thorax
Bowed legs
Difficult ambulation
Stunted growth

OSTEOMALACIA
Softening of bones d/t inadequate mineralization
Adult condition

MANIFESTATION
Bone pain, tenderness
Muscle weakness an early sign
Fractures of radius, femur
Not a significant cause of hip fracture
Delated healing of fractures = deformities
Hyperparathyroidism d/t low calcium levels

CAUSES 
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 chronic renal failure
d/t inability of kidney to activate
Vitamin D & excrete phosphate
Vitamin D resistant rickets
Familial renal tubular defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Characterize the risk factors, cause and manifestations of Paget disease

A

Abnormal bone remodelling as a result of
Focal areas of excessive osteoclast-mediated bone resorption followed by
Disorganized osteoblast-mediated bone repair
Unclear patho
Genetic, environmental, ? Virus trigger

RISKS
Mid adulthood, progression
Men = women
Northern European heritage

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Discuss the etiology, patho and general manifestations of rheumatoid arthritis

A

Autoimmune systemic disease
polyarticular
Can affect the organs

CAUSE
Uncertain
Genetic predisposition
Women > men
Peak incidence 40-50 years

PATHO

T-cell mediated response to trigger

  • Inflammatory mediator released
  • Antibodies form against autoantigens

Rheumatoid factor (RF) – which is an antibody – occurs in 70% to 80% of patients (Forms an immune complex)

Synovial inflammation and joint destruction result

Fluid accumulates (inflammatory process)
Neovascularization in synovial membrane
Pannus: vascular granulation tissue is formed is destructive to joint
-Inflammatory erosion of cartilage/bone

MANIFESTATION
Symmetrical
Polyarticular
Diarthodial/synovial
Joint pain
Joint swelling
Limited joint movement
Wrist, finger joints common
-Pain when turning doorknob, opening jars, buttoning shirts

Feet

  • Pain on ball of foot when rising in morning
  • Widening of forefoot d/t inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List the extraarticular manifestations of rheumatoid arthritis

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 immoveable
Small or large
Numerous other but they are more rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Discuss the parameters for diagnosing rheumatoid arthritis.

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Discuss the risk factors and typical triggers associated with systemic lupus erythematous

A
RISK
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 responses

TRIGGER
UV light
Chemicals
Foods
Infectious agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the immunologic process that occurs in systemic lupus erythematosus.

A
  • characterized by the formation of autoantibodies and immune complexes (type 3 hypersensitivity)
  • person with SLE have defective elimination of self-reactive B cells that results in an increase in production of antibodies that damages tissues
-Chronic inflammatory disease affecting entire body!
Unknown cause
Young women (15-40)
African, Hispanic, Asian descent
Familial
Genetic

Triggers

  • UV light
  • Chemicals
  • Foods
  • Infectious agents

Common complaints

  • Arthralgia
  • Myalgia
  • Fever
  • Malaise, fatigue
  • Temporary loss of cognitive abilities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Identify and discuss the major organ systems that may be involved in systemic lupus erythematosus.

A

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

INTEGUMENTARY
Butterfly rash on nose/cheeks
Fingertip lesions
Hair loss
Mucous membrane lesions
Sunlight sensitivity
RENAL
Glomerulonephritis
Interstitial nephritis
Pulmonary
Pleural effusion
Pleuritis
CARDIAC
Pericarditis
Heart block
Hypertension
Ischemic heart disease (chronic SLE)
CNS
Photosensitivity
Hemorrhage – stroke
Thrombus
Seizures
More frequent with renal disease
Psychotic symptoms
Depression
Euphoria
Confusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the etiology and manifestations of limited and diffuse 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

Fingers, forearms, face

CREST syndrome is not uncommon
Calcium deposits on skin/soft tissue
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiestasias 

Pulmonary arterial hypertension is also common

DIFFUSE
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 fibrosisa

Manifestations
Limited (most common)
Diffuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe ankylosing spondylitis in terms of cause, pathogenesis, and clinical manifestations.

A

ANKYLOSING SPONDYLITIS
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

MANIFESTATION
Pain
-Persistent or intermittent
-Can imitate sciatica pain
-Worse when immobile
Enthesitis
-Juncture of tendon/ligament to bone

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
Uveitis (30%) (inflammation of the middle layer of the eye)
Weight loss, fatigue
Fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Compare rheumatoid arthritis and osteoarthritis in terms of joint involvement, level of inflammation, and local and systemic manifestations

A

RHEUMATOID ARTHRITIS
-synovial inflammation and destruction of the joint
-inflammatory process progresses, synovial cells and subsynovial tissue undergoes hyperplasia
-Fluid accumulates (inflammatory process)
Neovascularization in synovial membrane
Pannus: vascular granulation tissue is formed is destructive to joint
Inflammatory erosion of cartilage/bone

MANIFESTATION
Symmetrical
Polyarticular
Diarthodial/synovial
Joint pain
Joint swelling
Limited joint movement
Wrist, finger joints common
Pain when turning doorknob, opening jars, buttoning shirts
Feet
Pain on ball of foot when rising in morning
Widening of forefoot d/t inflammation

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

EXTRA-ARTICULAR MANIFESTATION

Fatigue, weakness, anorexia, weight loss
Elevated ESR & C – reactive protein (CRP)
Rheumatoid nodules
-Granulomatous lesions with central necrotic core
-Tender, or not
-Moveable, or immoveable
-Small or large
Numerous other but they are more rare

OSTEOARTHRITIS
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

Manifestations
Insidious
Joint pain, stiffness, motion limitations
Crepitus, grinding
Instability and deformity can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the pathologic joint changes associated with 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
Any synovial joint in the body

Risk Factors
Genetic
Environmental

CAUSE
Primary: ideopathic
Seconary
Genetic or acquired joint disease

MANIFESTATION
Insidious
Joint pain, stiffness, motion limitations
Crepitus, grinding
Instability and deformity can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Relate the metabolism and elimination of uric acid to the pathogenesis of crystal-induced arthropathy (gout)

A
  • Crystal deposition in joints produces arthritis.
  • In gout, uric acid crystals are found in the joint cavity

-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 subcondral bone is destroyed

Etiology

  • Elevated serum uric acid (primary diagnostic)
  • Primary: unknown cause
  • Elevated production of uric acid, decrease elimination in kidney, or both
  • Secondary
  • Nucleic acid breakdown (tumor cell lysis)
  • Chronic kidney disease
17
Q

Describe the clinical manifestations of gouty arthritis.

A
Manifestations
Abrupt pain onset
Redness, swelling
Lasts days to weeks
Remission can last months to years
Tophi (large hard nodule found in the synovium of joint, takes 10 years)
Triggers
Excessive exercise
Medication
Foods
Alcohol
dieting
18
Q

reactive arthritis in terms of cause, pathogenesis, and clinical 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