Pbdi Rheumatic Disorders

Front 1

Rheumatology is the study of ______ and allied conditions including connective tissue disease and other inflammatory, degenerative and metabolic disorders of the ________ system.

Back 1

Arthritis

Musculoskeletal

Front 2

Is arthritis a disease?

Back 2

Inflammation of the joint

Front 3

What are the 3 types of joints?

Place where ____ meet.

Back 3

1. Synarthroidal or fibrous
2. Cartilaginous or amphiarthrosis
3. Synovial or diarthroidal

Bones

Front 4

Synarthroidial joints have little or ___ movement.
Ex: ____ bones

____ a joint cavity

Back 4

No

Skull

Lack

Front 5

Cartilaginous bones are joined by ______.
Ex: ______ ____

Back 5

Cartilage

Intervertebral disc

Front 6

Synovial joints are a ____ moving joint.

Most frequently affected by _____ diseases.

Back 6

Freely

Rheumatoid

Front 7

Joint capsule lined by _____ tissue.

Back 7

Synovial (synovium)

Front 8

Synovium does not cover ____ cartilage.

____ blood supply to the synovium.
Innervated by ______ fibers to vessels - no ___ fibers.

Back 8

Articulating

Good
Autonomic
Pain

Front 9

What two layers make up the synovium?

Back 9

Subitimal

Intimal

Front 10

Subitimal are _____ and composed of what?

Back 10

Vascular

Fibrous material, mast cells, macrophages, etc.

Front 11

Intimal cells are made of what 2 types of cells?

Back 11

A and B cells

Front 12

A cells _____ bacteria.

B cell secrete _______ ____

Back 12

Remove

Hyaluronic acid

Front 13

Synovial fluid is superfiltrated ____ from blood vessels of synovial membrane.

Back 13

Plasma

Front 14

What are the chracteristics of synovial fluid?

Back 14

Clear, straw colored
Thick - viscosity 50-200X water
Lubricated joint
Source of nutrient for articulating cartilage
WBC <200 cells/mm3

Front 15

In a mucin clot test, _____ acid is added to synovial fluid.

______ clot formed with more inflammation since hyaluronic acid is _____ by lysosomal action.

Fluid color becomes ____ with increased inflammation.

Back 15

Acetic

Poor
Reduced

Cloudier

Front 16

Articulating cartilage protects and covers the surface of _____.

Cartilage is not ____, undergoes turnover that is maintained by the ______.

Back 16

Bone

Static
Chondrocytes

Front 17

Articulating cartilage reduces ____ in joint and distributes forces.

Very _____.

Back 17

Friction

Resilient

Front 18

What is articulating cartilage composed of?

Back 18

Chondrocytes, collagen, protein, proteoglycans, polysaccharides and water

Front 19

T/F
Cartilage may wear down as there is no blood supply in adults.

Back 19

True

Front 20

Joint inflammation can occur due to a(n) _____ in synovial fluid.

Vascular phase of inflammation take place in synovium - _____ arthritis.

Back 20

Increase

Rheumatoid

Front 21

What disease is caused by a precipitation of urate crystals?

Back 21

Gout

Front 22

Systemic Lupus erythematosus (SLE) is when there is damage in the connective tissues of what 3 things?

Back 22

Lungs, kidneys, blood vessels

Front 23

Pathogenesis of joint inflammation involved immune system components, ____ factors and other small molecular mediators.

Back 23

Plasma

Front 24

In pathogenesis of joint inflammation, exudative _____ predominates followed by _______. Can get extensive formation of granulation tissue that may become fibrous and limit movement.

Back 24

Inflammation

Degeneration

Front 25

The American Rheumatoid Association recognizes 13 groups of joint disease. These disorders can be placed into what 2 categories?

Back 25

Inflammatory and non-inflammatory

Front 26

Non-inflammatory joint disease:
Reduced or absent ______ membrane inflammation.

____ of systemic signs and symptoms.

Near _____ synovial fluid.

Back 26

Synovial

Lack

Normal

Front 27

What is the most prevalent non-inflammatory joint disesase?

Back 27

Degenerative joint disease - Osteoarthritis

Front 28

In DJD, main pathological features include _____ and loss of _____ cartilage in synovial joints.

Back 28

Degeneration

Articulating

Front 29

What 2 factors increase the prevalence of DJD?

Back 29

Age and weight

Front 30

Primary DJD is ______ - not associated with known risk factors.

Most common type and ____ is the most important associated factor.

Back 30

Idiopathic

Aging

Front 31

Secondary DJD is associated with what 2 risk factors?

Back 31

Joint stress and trauma

Front 32

T/F
Secondary DJD involves all joints in the body

Back 32

False

Involves only joints subjected to a particular risk factor

Front 33

Pathophysiology of DJD:
Articulating cartilage becomes _____.

There is a change in both mechanical properties and ____ of the cartilage.

Back 33

Yellowish-grey

Composition

Front 34

Pathophysiology of DJD:
Get more water, less _____.

In the early stage, cartilage loses _____ appearance.

Back 34

Proteoglycans

Glistening

Front 35

Pathophysiology of DJD:
_____ in synthesis and increase in breakdown of ______.

Back 35

Decrease

Collagen

Front 36

Pathophysiology of DJD:
Eventually the bone becomes _______ (dense and hard)

_______ (bone spur) can grow out of margins of the joint.

Back 36

Sclerotic

Osteophytes

Front 37

Pathophysiology of DJD:
Articulating cartilage probably lost through _____ breakdown - cytokines such as IL-1 and ____, which produce/release _____ (enzymes) that are destructive.

Back 37

Enzymatic

TNF

Proteases

Front 38

Pathophysiology of DJD:
______ are less able to produce proteoglycans and new collagen.

Back 38

Chondrocytes

Front 39

What is the hallmark of the osteoarthritic process?

Back 39

The loss of proteoglycans from articulating cartilage

Front 40

Pathophysiology of DJD:
1. Erosion of ______ ______
2. Sclerosis of ____ underneath cartilage
3. Formation of _____

Back 40

1. Articulating cartilage
2. Bone
3. Osteophytes

Front 41

DJD:
Stiffness usually lasts _____ min and lessens with use.

Diagnosis through x-ray may show ____ bone changes, osteophytes, sclerosis.

Back 41

15-30

Cystic

Front 42

T/F
In DJD, typically synovial fluid shows no sign of joint inflammation - no systemic symptoms.

Back 42

True

Front 43

Inflammatory joint disease is commonly termed ____.

Characterized by inflammatory damage or destruction of _____ membrane, articulating cartilage and by ____ signs of inflammation.

Back 43

Arthritis

Synovial
Systemic

Front 44

Rheumatoid arthritis is the ____ most common form of arthritis.

Back 44

Second

Front 45

IJD (RA) is a ____ systemic progressive _______ disease.

Back 45

Chronic
Autoimmune

Front 46

RA is a ______ group of disorders in which inflammation of _____ joints is a major manifestation.

Back 46

Heterogeneous

Multiple

Front 47

T/F
In RA, many patients have no systemic manifestations with the most common manifestation joint involvement.

Back 47

False

They do have systemic manifestations

Front 48

RA:
Have fibrinoid ____ of collagen.

Characterized by joint ____ and disabilities.

Back 48

Necrosis

Deformities

Front 49

T/F
RA occurs more frequently in women than men during the childbearing years.

Back 49

True

Front 50

RA occasionally goes into ______ spontaneously. Indicates that one can restore some type of balance with intervention.

Back 50

Remission

Front 51

RA etiology has no single agent responsible. Combination of _____ and environment.

Back 51

Genetics

Front 52

RA appears to be an immune response initiated by an ______.

Back 52

Antigen

Front 53

What are 3 possible sources of RA?

Back 53

Epstein-Barr Virus
Parvovirus Infection
Bacteria and mycoplasms

Front 54

In RA, eventually normal antibodies somehow become _____. These are terms ____ _____ (RFs) - antibodies against IgG, IgMs, occasionally IgA and form immune complexes.

Back 54

Autoantibodies

Rheumatoid Factors

Front 55

RFs bind with their target self antigens in blood and form _____ in blood and synovial membranes.

Type of injury?

Back 55

Complexes

Type III

Front 56

RA has _____ production of antigenic material to stimulate the immune response.

Back 56

Continued

Front 57

Anti-_____ antibodies have been demonstrated in synovial fluid in patients with RA.

Back 57

Collagen

Front 58

In synovitis, can distinguish 2 aspects of synovial inflammation:
Synovial _____ and Synovial _____

Back 58

Fluid - bathes articulated cartilage

Membrane - outlines joint area

Front 59

Synovial fluid phase comprised predominantly of _____. They phagocytize immune complexes and release many ______.

Back 59

PMNs

Mediators

Front 60

RF is in _____ supply, unlike other microorganisms.

Back 60

Constant

Front 61

Synovial membrane - perivascular infiltration with _______ cells and a striking accumulation of new blood vessels (__________).

Back 61

Mononuclear

Angiogenesis

Front 62

Synovial Membrane:
Ultimately transforms to a granulation tissue (______) that covers the articulating cartilage.

Back 62

Pannus

Front 63

This tissue is rich in inflammatory cells that secrete _____ and various mediators of inflammation to destroy cartilage and bone.

Eventually can lead to joint ______ and muscle _______.

Back 63

Enzymes

Deformity
Atrophy

Front 64

In the destruction of articular structures:
Monocytes/macrophages and fibroblasts release _____ to resorb bone and connective tissue.

Back 64

Proteases

Front 65

In the destruction of articular structures:
_____ from diminished blood flow (loss of functional synovial membrane vascularity decreases as granulation tissue and fibrosis develops) causes ______, which stimulates release of hydrolytic enzymes leading to even more damage.

Back 65

Hypoxia

Acidosis

Front 66

Immune complexes - contain RF - play a major role in _______ of the immune response.

Lead to proliferative synovitis - serves as a ______ force.

Back 66

Amplification

Chemotactic

Front 67

Heparin can be released from _____ cells and play a role in bone ______.

Back 67

Mast

Resorption

Front 68

PMNs are also a major source of amplification of inflammatory condition - lead to aggregation, degranulation and ________ anion generation.

Back 68

Superoxide

Front 69

RA Consitutional symptoms (systemic disease) include?

Back 69

Fatigue, anorexia, fever, weight loss, etc.

Front 70

What are 5 broad spectrum clinical manifestations of RA?

Back 70

1. Constitutional symptoms
2. Symmetrical polyarthritis
3. Morning stiffness
4. Deformity
5. Extra-articular disease

Front 71

In symmetrical polyarthritis, one has pain at rest and with _____.

Occurs from swelling early and later from ______.

Back 71

Motion

Sclerosis

Front 72

RA patients have morning stiffness for more than ____ minutes.

Back 72

30

Front 73

In RA, deformity can result. Joints may become _______.

Loss of mobility first from the ____ and then later from ____/____.

Back 73

Ankylosed

Swelling
Fibrosis/sclerosis

Front 74

T/F
With disuse of joint, one can develop muscular atrophy with RA.

Back 74

True

Front 75

In extra-articular disease, 5-15% of patients have subcutaneous rheumatoid ______ (granulomas).

Back 75

Nodules

Front 76

In general, extra-articular disease is correlated with persistent joint inflammation and ____ titers of RF.

Back 76

High

Front 77

T/F
Amyloidosis (deposition of eosinophilic hyaline in soft tissues) is never fatal.

Back 77

False

Front 78

In RA, lab findings show that 70-__% of patients have circulating immune complexes and _______ in serum.

____ 100% diagnostic - will use to differentiate from other forms of arthritis.

Back 78

85

Autoantibodies

Not

Front 79

Presence of ____ factor is helpful in testing, but not ______.

Seen in ___-30% of people over 60.

Back 79

RF

Positive

20

Front 80

What are laboratory findings found in RA patients?

Need ___ of 7 diagnostic criteria for diagnosis.

Back 80

-Immune complexes and autoantibodies in serum
-RF factor
-Anemia
-Elevated ESR
-Synovial fluid viscosity
-Radiological features

4

Front 81

RA:
Anemia from the altered ___ function.

Synovial fluid viscosity ___ since many more leukocytes.

Back 81

Bone

Less

Front 82

Gout is the ____ most frequent form of arthritis.

Found predominantly in _____.

Back 82

3rd

Men

Front 83

Classical picture of the acute severe arthritis of gout is directly associated with ______ - eventual uric acid deposits.

Back 83

Hyeruricemia

Front 84

What are some sources of uric acid?

Back 84

-Food containing purines
-Synthesis of purine nucleotides
-Breakdown of nucleic acids (cell turnover)

Front 85

How is uric eliminated?
Kidney and ____.
Freely filtered
_____ in proximal tube.
Secreted in _____ tubule.

Back 85

GI

Reabsorbed

Distal

Front 86

Gout classified as _____ (due to overproduction of uric acid) or _____ process.

Back 86

Primary

Secondary

Front 87

Primary Gout (95%):
Inherent defect in _____ metabolism.

Diagnosed mainly in _____.

Back 87

Purine

Men

Front 88

Secondary Gout (5%):
Develop as consequence of an acquired or associate disorder or the use of ____.

Occurs in both men and women but increase in women after _____. This is because estrogen promotes uric acid _____.

Back 88

Drugs

Menopause
Excretion

Front 89

What are the causes of hyperuricemia?

Back 89

-Probably not due to abnormal purine absorption alone
-Increased production of uric acid
-And/or decreased renal clearance of uric acid
-Major error of purine metabolism

Front 90

There are 3 major enzymatic defects in purine metabolism. One is:
Patients that lack enzyme HGPRT - men with Lesch-Nyhan Syndrome (recessive x-linked).
_____production of uric acid.
Patients may also have ______ manifestations.

Back 90

Over

Neurological

Front 91

There are 3 major enzymatic defects in purine metabolism. One is:
Increased activity of PRPP synthetase.
____ disorder.
Overproduction of ____ pathway and hence uric acid.

Back 91

X linked

Purine

Front 92

There are 3 major enzymatic defects in purine metabolism. One is:
Deficiency in glucose-6-phosphatase.
Autosomal ____ disorder.
____ uric acid clearance.
_____production and under excretion.

Back 92

Recessive

Decreased

Over

Front 93

There are 3 major enzymatic defects in purine metabolism. What enzymes are affected?

Back 93

1. HGPRT
2. PRPP synthetase
3. Glucose-6-phosphatase

Front 94

Decreased uric acid clearance may contribute to hyperuricemia in __ to __% of patients with gout.

Back 94

75 - 85%

Front 95

Hyperuricemia:
Have an increase in uric acid in plasma and body fluid.
>__ mg% in men
>__ mg% in women

Can see 9-__ mg in gout

Back 95

7

6

10

Front 96

What is normal uric acid levels?

Back 96

Men: 5 +/- 1mg%

Women: 4 +/- 1mg%

Front 97

Only __% of hyperuricemia patients develop gout (genetics/environment).

Back 97

5

Front 98

Supersaturation results in uric acid _____ out.

Lower ____ and ___ of synovial fluid

Back 98

Precipitates

pH and temperature

Front 99

Uric acid crystals activate _____ factor.

This actually causes ____ damage.

Back 99

Hagemen

More

Front 100

What are the 4 stages of gout?

Back 100

1. Asymptomatic hyperuricemia
2. Acute gouty arthritis
3. Intracritical gout
4. Chronic tophaceous gout

Front 101

T/F
Those with asymptomatic hyperuricemia are considered a gout patient.

Back 101

False

Front 102

Asymptomatic hyperuricemia:
Levels 9-__% - no overt symptoms.

Back 102

10

Front 103

Acute gouty arthritis:
_____ arthritis.
Attacks last from several ____ to weeks (if untreated).

90% of initial attack involve a ____ joint.

Back 103

Monarticular

Hours

Single

Front 104

Acute gouty arthritis:
May be precipitated by trauma, ____ and/or alcohol.

Often pain usually occurs at ____.

Back 104

Drugs

Night

Front 105

Acute gouty arthritis:
Attacks usually _____, last 10-14 days and when over have complete resolution.

Back 105

Self-limiting

Front 106

T/F
Gout is more common in men than women.

Back 106

True

90% men

Front 107

Acute gouty arthritis:
Systemic signs of inflammation may occur, more likely to occur with ______ attacks.

Back 107

Polyarticular

Front 108

Intracritical Gout:
Clinical cause of this phase is _____.

Back 108

Variable

Front 109

T/F
Some patients with intracritical gout never have a second attack.

Back 109

True

Front 110

Intracritical gout:
If untreated, attack may ____ in frequency and severity and more associated with _____ symptoms.

Back 110

Increase

Systemic

Front 111

Chronic tophaceous gout:
Average time from acute to chronic is ____ years.
Have chronic ____ and aching of affected joints - persistent stiffness.

Back 111

11.6

Soreness

Front 112

Chronic tophaceous gout:
Eventually leads to grotesque ______.

Chronic inflammation results from the presences of _____ crystals.

Back 112

Deformities

Urate

Front 113

Chronic tophaceous gout:
Have the formation of granulomas - ____. These are deposits of urate crystals surrounded by granuloma (_____ and giant cells) - direct function of degree and duration of hyperuricemia.

Back 113

Tophi

Macrophages

Front 114

Urate ____ soluble at lower temperatures.

Back 114

Less

Front 115

How can you distinguish tophi from rheumatoid nodules?

Back 115

Biopsy

Front 116

Second to arthritis, most common clinical manifestation of gout is _____ involvement - get urate or uric acid ______.

Back 116

Renal

Nephropathy

Front 117

_____ nephropathy is a result of deposition of the urate salt crystals in renal interstitium and resulting inflammation. ______ common in these individuals.

Back 117

Urate

Hypertension

Front 118

Uric acid nephropathy results from deposition of uric acid crystals (renal stones) in collecting tubules. Can result in ____ ______ ______.

Back 118

Acute renal failure

Front 119

Renal failure accounts for ____% of deaths in patients with gout.

Back 119

10

Front 120

Associated condition and contributing factors of gout include?

Back 120

-Obesity
-Medical disorders
-Alcohol use
-Diet high in purines

Front 121

What medical disorders may contribute to gout?

Back 121

Hematological disorders, lead poisoning, starvation, hypertension, diabetes
Drugs that block uric acid excretion: diuretics, nicotinic acid, levodopa, aspirin

Front 122

Alcohol use ____ renal excretion of urate. Increases catabolism of purine nucleotides. Moonshine causes _____ damage. Beer contains large quantities of ____ which is catabolized to uric acid.

Back 122

Decreases

Tubular

Guanosine

Front 123

What foods are high in purines?

Back 123

Organ meats - liver, brains, etc.
Sardines, anchovies

Front 124

Gout can be diagnosed in patients who fulfill ___ of the three criteria diagnostic criteria.

Back 124

One

Front 125

Gout Diagnosis:
Presence of monosodium urate crystals in _____ found in the synovial fluid obtained from inflamed joint (found in 85% of patients).

Urate crystals found in blood of _____ patients only suggestive.

Back 125

Leukocytes

Asymptomatic

Front 126

Gout diagnosis:
Urate crystals in biopsy or aspirate of _____.

Back 126

Tophi

Front 127

Gout diagnosis:
A combination of following three findings:
1. Presence of ______.
2. Response of synovitis following ____ administration.
3. History of ____ arthritis followed by period free of symptoms.

Back 127

1. Hyperuricemia
2. Colchicine
3. Monarticulate

Front 128

Gout Treatment:
___ commitment of therapy usually required.

Back 128

Lifetime

Front 129

T/F
Drugs for acute attack (pain) of gout are different from those drugs used to normalize serum uric acid.

Back 129

True

Front 130

Gout treatment:
_____ is very important.
Compliance is very ____.
Disease can be controlled.
Patient needs to make ____ changes.

Back 130

Education

Low

Lifestyle