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Musculoskeletal + skin > Autoimmune diseases > Flashcards

Autoimmune diseases Flashcards

1
Q

Libman-Sacks endocarditis

A

Sterile platelet vegetations occuring on mitral valve, leading to valve thickening + regurgitation sx; vegetations can be on either surface of valve (mainly undersurface)

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2
Q

Renal involvement in scleroderma and which type it’s more often associated w/

A

Scleroderma renal crisis (SRC)- characterized by sudden onset of malignant HTN, which causes acute renal failure

  • Occurs mostly in diffuse scleroderma
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3
Q

Pattern of Raynauds

A

Pallor (white) –> cyanosis (blue) –> hyperemia (red)

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4
Q

Manometry of scleroderma and why

A

All the waves are flattened- smooth muscle of esophagus is replaced by collagen, resulting in decreased peristalsis

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5
Q

Presentation of antiphospholipid syndrome

A

Hypercoagulable state results in arterial and venous thrombosis (DVT, hepatic vein, placental, cerebral strokes)

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6
Q

Important player in scleroderma

A

In response to inciting endothelail injury, CD4+ T cells respond by releasing cytokines and other inflammatory cells/ fibroblasts, which results in widespread small blood vessel damage –> progressive fibrosis –> intimal thickening –> occlusion of organ supply –> fibrosis of organ/ skin

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7
Q

What is used to detect early scleroderma?

A

Distorted nailfold capillary loops - indicates vascular damage that’s happening all over the body

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8
Q

Types of lung involvement in scleroderma and which one is associated w/ which type (limited vs. diffuse)

A

1) Interstitial fibrosis- seen in diffuse scleroderma
2) Pulmonary arterial HTN- seen in limited scleroderma

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9
Q

Etiology of Sjogren

A

Primary- sicca syndrome

Secondary- associated w/ other autoimmune disorders (esp. RA)

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10
Q

Lupus anticoagulant’s effects on bleeding tmie

A

In vitro, causes elevated PTT; however, in vivo, produces hypercoagulable state

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11
Q

Difference in epidemiology between SLE and drug-induced lupus (2)

A

In drug induced lupus, older individuals are affected (e.g. 50-70), and there is no gender preference

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12
Q

Autoantibodies found in SLE and how they can be used for diagnosis

A

1) ANA: sensitive but not specific for lupus
2) Anti-dsDNA: specific for lupus; titers fluctuate w/ disease activty so levels can be used to manage pts; however, this level can be low when disease is quiescent
3) Anti-Sm: antibody against nuclear non-histone proteins; specific for lupus; titers are elevated regardless of disease activity

*Presence of Anti-dsDNA + Anti-Sm is virtually diagnostic for SLE

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13
Q

Epidemiology of Sjogren syndrome

A

Affects 40-60 year olds

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14
Q

Lab complement levels in SLE

A

Decreased C4, C5, CH50 due to immune complex deposition + activation of complement

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15
Q

Autoantibodies associated w/ scleroderma

A

1) ANA- sensitive but not specific
2) Anti-centromere antibodies- limited SSc
3) Anti-DNA topoisomerase I antibodies (Anti-Scl70) - diffuse SSc
4) Anti-RNA polyermase III antibody- diffuse SSc; increased risk for SR

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16
Q

Presentation of drug-induced lupus

A

Similar to SLE but CNS and renal sx are rare

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17
Q

Autoantibody asscociated w/ diffuse scleroderma

A

Autoantibody against DNA topoisomerase I (Anti-Scl70)

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18
Q

Autoantibodies found in drug-induced lupus

A

ANA, Anti-histone antibodies

Anti-ds DNA is rare

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19
Q

Autoantibodies associated w/ scleroderma renal crisis (SRC)

A

Autoantibodies to RNA polymerase III

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20
Q

Mechanisms of injury in SLE

A

1) Type III HSR- immune complex deposition in variety of tissues
2) Type II HSR- autoantibodies specific for RBC, WBC, platelets opsonize these cells
3) Antiphopsholipid autoantibodies- hypercoagulable state

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21
Q

Autoantibodies present in Sjogren

A

1) ANA - sensitive but not specific
2) Anti-ribonucleoprotein antibodies (Anti-SSA/Ro, Anti-SSB/La)
3) RF- can be present w/o RA

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22
Q

Histology of SRC

A

Onion skinning appearance of arterioles (malignant HTN)

23
Q

Unexplained spontaneous abortions, premature birth, pre-eclampsia

A

Antiphospholipid syndrome- due to placental thromboses

24
Q

Types of antiphospholipid antibodies (3)

A

1) Anticardiolipin
2) Anti-beta2 glycoprotien 1
3) Lupus anticoagulant

25
Q

Most specific antibodies for Sjogrens

A

Anti-ribonucleoprotein antibodies (anti-SSa/Ro and anti-SSB/La)

26
Q

GI sx of scleroderma

A

1) Difficulty swallowing- Low esophageal peristalsis
2) Constipation alternating w/ diarrhea- small + large intestine smooth muscle affectd
3) GERD- decreased LES resting tone

27
Q

Common drugs that cause drug-induced lupus

A

Hydralazine, isoniazid, procainamide

28
Q

Presentation of pulmonary arterial HTN

A

dyspnea on exertion

prominent P2 component of S2

right ventricular heave

hepatosplenomegaly + lower extremity edema

29
Q

Biopsy of Sjogren- where to look and findings

A

Look at labial salivary gland (minor salivary glands)- shows lymphocytic infiltration of minor salivary glands (sialadenitis)- assume that other glands are being attacked

30
Q

Type of CA associated w/ Sjogren and presentation

A

Risk of B-cell lymphoma (MALT)- present as unilateral enlargement of parotid gland (both should normally be enlarged due to extra-glandular manifestations)

31
Q

Why pregnant SLE patients should be screened for Sjogrens

A

If they have Anti-SSA antibody, they can be at risk for giving birth to babies w/ neonatal lupus/ congenital heart block

32
Q

How do skin changes present in scleroderma

A

Insiduous swelling of distal extremities (puffiness) which leads to gradual thickening of skin of fingers –> atrophy of skin –> may cause digital ischemic ulcers

33
Q

How is Primary Raynaud phenomenon (raynaud disease) different frmo Raynaud phenomenon due to scleroderma (raynaud syndrome)?

A

In primary Raynaud, it’s painless and symmetric w/ no evidence of microvascular disease.

In scleroderma pts, Raynaud can be painful, leading to digital ulcerations, gangrene, or even amputation.

34
Q

Presentation of limited scleroderma

A

CREST

C: Calcinosis/ anti-centromere antibodies

R: Raynaud phenomenon (earliest sign)

E: Esophageal dysmotility –> dysphagia

S: Sclerodactyly- tightening, swelling, thickening of fingers

T: Telangiectasias

35
Q

Pattern of skin involvement in diffuse scleroderma

A

Diffuse skin involvement

36
Q

Pitted areas on distal finger w/ loss of digital pad

A

Scleroderma

37
Q

Antiphospholipid antibody that gives false positive VDRL/RPR readings

A

Anticardiolipin

38
Q

Presentation of Sjogren

A

1) Keratoconjunctivis sicca (dry eyes)- gritty sensation in eyes, blurred vision)
2) Dry mouth (xerostomia)- difficulty speaking, recurrent dental carries, oral candidiasis
3) Extraglandular manifestaiotns- bilateral parotid enlargement, neuorpathy, arthritis, renal damage, et.c

39
Q

Autoimmune destruction of exocrine glands (lacrimal + salivary) by lymphocytic infiltrates

A

Sjogren syndrome

40
Q

Why does Raynaud phenomenon occur?

A

Due to reduced blood flow to the skin from arteriolar (small vessel) vasospasm, occuring in response to stress or cold

41
Q

Presentation of SLE

A

RASH OR PAIN

1+2) R: Malar/ discoid rash

3) Arthritis (non-erosive)
4) Serositis- inflammation of serosal surfaces (pleuritis, pericaditis, pericardial effusion)
5) Hematologic disroders- anemia, thrombocytopenia, leukopenia (Type II HSR)
6) Oral/nasopharyngeal ulcers

7 ) Renal disease (diffuse proliferative glomerulonephritis, membranous glomerulonephritis)

8) Photosensitivity- rashes get worse after exposure to sun
9) ANA
9) Immunologic disorders (Anti-ds DNA, anti-Sm, antiphospholipid)
10) Neurologic disorders (seizures, psychosis)

Libman-sacks endocarditis

Nonspecific sx: fever, fatigue, Raynauds

42
Q

Main causes of mortality in SLE

A

1) Cardiovasculr disease (accelerated coronary atherosclerosis due to chronic inflammation)
2) Infections (immunosuppressants, pancytopenia)
3) Renal disease

43
Q

Why is SLE associated w/ inherited deficiencies of early complement proteins? Which proteins?

A

Becuase lack of complement may impair removal of circulating immune complexes, which favors tisseu deposition.

Complement components deficient: C1q, C4, C2

44
Q

Association between Anti-SSA and pregnant women

A

Pregnant women w/ anti-SSA are at risk of delivering babies w/ neonatal lupus + congenital heart block

45
Q

Pattern of clinical involvement in limited scleroderma

A

Benign clinical course w/ late visceral involvement

46
Q

Skin involvement pattern distribution in limited scleroderma

A

Confined to extremities distal to elbow + knees

Also the face

47
Q

SLE arthritis vs. RA

A

Main problem w/ SLE arthritis is tendon sheath inflammation, leading to joint laxity w/ NO EROSION OF BONES; patients have deformities that are reducible

in RA, problem is synovitis

48
Q

Anti-histone antibodies

A

Drug-induced lupus

49
Q

Pattern of clinical involvement in diffuse scleroderma

A

Early visceral involvement

50
Q

Antibodies to U1 RNP

A

Mixed CT disease

51
Q

HSR related to Sjogren

A

Type IV HSR

52
Q

Arthritic presentation of scleroderma

A

Non-erosive arthritis affecting small joints (loss of joint mobility can result due to skiin thickening/ fibrosis, not due to inflammation)

53
Q

Most common form of renal disease in SLE pts

A

Diffuse proliferative glomerulonephritis

54
Q

Autantibody associated w/ limited scleroderma

A

Anti-centromere antibodies

Musculoskeletal + skin (12 decks)

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