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clin med > rheumatic disease > Flashcards

rheumatic disease Flashcards

1
Q

rheumatic diseases

A

localized or systemic inflammation
- msk system damage, internal organ damage

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2
Q

endogenous vs exogenous in initiating forces of acute diseases

A

edo: crystal deposition, uric acid (gout)
exo: new medication of infection

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3
Q

general principels of rheumatic diseases

A

disease initiation, propagation, flares

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4
Q

chronic disease initiating force

A

remote and unrecognizable (no longer present with typical acute inflammation symptoms)
disease phenotype is fully established

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5
Q

propagation of rheumatic disease

A

autoimmune response- self-amplified cycle of damage, self-antigens, can elicit innate and adaptive immune response

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6
Q

self-limited

A

acute episodes of RD. removal of stimulus that causes the inflammation, re-exposure can cause flares

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7
Q

pathogenesis of inflammation 1) cytokines

A

upregulation of cytokines

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8
Q

2) endothelial activation

A

pro-inflammatory cytokines-> promote inflammation-> trigger adhesion-promoting receptors on blood vessel endothelium (Adhesion!)
contributes to atherosclerosis

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9
Q

3) complement pathway

A

augments, amplifies the inflammatory response.
or upregulation= abnormal response

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10
Q

4) immune complex formation

A

macrophages and neutrophil complexes- damage healthy tissue if released in large amounts- follows upregulation of complement pathway
might present as a rash

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11
Q

5a) cellular cytotoxicity upregulation

A

cell mediated: cytotoxic T lymphocytes - capable of destroying target cells

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12
Q

5b) cellular cytotoxicity upregulation

A

antibody-dependent cellular cytotoxicity: destruction of antibody-coated target cells by natural killer cells

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13
Q

6) host tissue differentiation

A

inflammatory mediators and t cells stimulate cells unrelated to immune response to change function. (think metaplasia)

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14
Q

gout clinical presentation

A

crystal-induced inflammation of synovial joints
male 3x more than female
monosodium urate crystals in joint space= sever acute joint pain and swelling
most common locations: great toe, midfoot, ankle and knee

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15
Q

gout flare ups

A

flares: one week, typically resolve spontaneously (self-limiting)
overtime flares can become more frequent and painful- results in chronic destructive condition (joint deformity)

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16
Q

underexcretion vs overproduction etiology in gout

A

under: 90% of patients, most often due to impaired renal function or diuretics
over: 10% of patiens diet, medication, defects in pathway leading to increased uric acid production

17
Q

immune system mechanisms involved in gout

A

triggers complement pathway- attracts neutrophils
vasodilators- pain and swelling
macrophage destruction of crytsals- increased adhesion molecules and localized endothelium response

18
Q

gout clinical manifestations

A

podagra: sever inflammatory arthritis at the first metatarsal joint- most frequent
d/dx episodic oligoarticular arthritis: most common type of juvenile arthritis
tophi formation: chronic gout most often occurs on tendon tissue on extensor side of hand
chronic erosive polyarthritis: over years, destruction of joints

19
Q

gout treatment

A

anti-inflammatory medication, activation of involved joints- AROM/PROM
prevention: decrease serum uric acid levels (diet)

20
Q

immune complex vasculitis clinical presentation

A

acute inflammatory disease of the small blood vessels, palpable purpura, arthritis, abdominal pain

21
Q

etiology of immune complex vasulitis

A

antigen from exogenous source- skin infection, virus, seasonal allergies
antigen from endogenous source- systemic lupus, vascular immunoglobins (proteins)
both result in intense inflammatory response

22
Q

pathophysiology of ICV

A

antigens elicit an ongoing humoral response due to abundant quantities- initiators
deposition of immune complexes in vessel endothelium- propagator
typically self limiting

23
Q

serum sickness

A

immune system reacts to medicines that contain proteins used to treat immune conditions

24
Q

clinical presentation of lupus

A

systemic autoimmune RD- chronic inflammation injury damage to multiple organs
females 9x more than men

25
Q

lupus etiology

A

complex- genetic susceptibility and poorly defines environmental factors
inefficient clearance of nonimmune apoptotic cells- upregulation inflammatory response

26
Q

initiation of lupus

A

hyperactive autoantibody response to self-antigens (comp pathway)
unique apoptotic cell death stimulates immune response

27
Q

propagation of lupus

A

combined result- continued immune response and tissue damage due to response derived from apoptotic cells and damaged cells
auto-amplification: hallmark of lupus

28
Q

clinical manifestation of lupus

A

multisystem autoimmune disease, characterized by periodic flares, symptoms are highly varied, universal feature: production of autoantibodies, skin rash, renal disease, hematologic disturbances, inflammation of serosal surfaces, neurologic syndromes.

29
Q

clincial presentation of rheumatoid arthritis

A

chronic systemic inflam disease
persistent symmetric inflammattion of multple peripheral joints
characterized by chronic inflam proliferation of synovial lining of diarthrodial joints- aggressive cartilage destruction adn bony erosion **

30
Q

epidemiology of rheumatoid arthritis

A

1% of pop
femal 3x more
onset in 60s

31
Q

etiology of RA

A

majority of destruction occurs in joint rynovium- lungs, skin and blood vessels can be affected
genetic and environmnetal factors can influence condition

32
Q

pathophysiology of RA

A

synovium significantly expansion of cellular lining composed of activated cells, high concentration of b cells, t cells, macrophahes= joint pannus
RA synovium can invade adjacent tissue such as cartlage and bone
decreased ROM

33
Q

initiaitino of RA

A

genetic factor
environmental factor: cigarette smoking
autoantibodies: hallmark featur- development of antigen-driven autoantibodies

34
Q

RA propogation

A

autoantigen interact with immune cells- amplify disease process

35
Q

RA clinical manifestation

A

persistent progressive disease, fatigue and joint inflammation, small and large joints (bilateral) joint deformities, cervical spine can be involved but not lower spine

36
Q

RA treatment

A

anti-inflammatories, immunomodulatory
all aim to slow progressive joint erosion

37
Q
A

clin med (10 decks)

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