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All the things continued > 2.4 Autoimmune Disorders Part 2 > Flashcards

2.4 Autoimmune Disorders Part 2 Flashcards

1
Q

What are the components of the RASH OR PAIN mnemonic for SLE?

A
  • Rash (malar)
  • Arthritis
  • Soft tissue/ serositis
  • Heme DO
  • Oral/ nasopharyngeal ulcers
  • Renal dz
  • Photosensitivity
  • ANA
  • Immunosuppressants
  • Neurological DO
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2
Q

Who is the classic SLE patient?

A

Middle aged AA /hispanic female

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3
Q

Is the female:male ratio with SLE more or less pronounced at extremes of age?

A

Less

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4
Q

What is the general pathophysiology of SLE?

A

Antibodies directed against host nuclear material, leading to the activation of C3, C4, and CH50 complement

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5
Q

Which three components of complement are classically depleted with SLE?

A

CH50
C3
C4

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6
Q

What type of hypersensitivity rxn is SLE?

A

III

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7
Q

What is CH50?

A

Test that measures complement C1-C9 levels and ability for complement to lyse RBCs

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8
Q

What are the three classic antibodies that are seen in SLE?

A

ANA
Anti-smith (snRNP)
Anti-dsDNA

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9
Q

What is the classic antibody that is elevated with drug induced SLE?

A

Anti-histone

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10
Q

What is the pathophysiology behind ANA?

A

As cells are damaged, nuclear material is released, exposing B cells to nuclear material, and activating the adaptive immune system.
-Ag/ab complexes are then phagocytosed by APCs, and further activate the immune system

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11
Q

Patients with what deficiency have an increased risk of developing SLE?

A

C1q, C2, C4 deficiency

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12
Q

What are the components of C3 convertase?

A

C1, C4, C2

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13
Q

What is the major function of C3b?

A

Removal of ag/ab complex

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14
Q

What is the function of Cr1 on RBCs?

A

Binds C3b, and takes the bound ag/ab complex to the spleen for removal

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15
Q

A deficiency in what complement components predisposes patients to SLE?

A

C1q
C2
C4

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16
Q

When in particular are malar butterfly rashes present?

A

Upon exposure to sunlight

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17
Q

What are the characteristics of the discoid rash with SLE?

A

Circular rash with erythema and plaques

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18
Q

What are the different forms of serositis that can occur with SLE patients?

A

Pericarditis

Pleuritis

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19
Q

What are the neurological s/sx of SLE?

A

Psychosis or Seizures

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20
Q

What is the most severe form of kidney damage that can occur with SLE?

A

Diffuse proliferative glomerulonephritis

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21
Q

What are some of the hematological disorders that can occur with SLE? (3) What type of hypersensitivity reaction does this represent?

A

Anemia
Thrombocytopenia
Leukopenia

Type II

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22
Q

What is the specific heart abnormality that can occur with SLE? What is this?

A

Libman-Sacks endocarditis

-Wart-like vegetations on both side of a valve

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23
Q

What is the role of anti-dsDNA in the prognosis of SLE?

A

Follows with the course of disease, and is used to predict renal involvement

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24
Q

What, generally, are antiphospholipid antibodies?

A

Autoantibodies against proteins bound to phospholipids

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25
What are the three major antiphospholipid antibodies?
- Anticardiolipin - Lupus anticoagulant - Anti-beta2-glycoprotein I
26
Which antibody commonly found in SLE will produce a false positive VDRL and RPR test? Why?
Anticardiolipin | -lyses of cells 2/2 treponema pallidum infx releases cardiolipin
27
Which antibody commonly found in SLE will produce a falsely elevated PTT?
Lupus anticoagulant
28
What is the antiphospholipid antibody syndrome associated with SLE?
- Antiphospholipid antibody + a hypercoagulable state | - Leads to DVTs, hepatic vein, placental and cerebral thromboses
29
What is the treatment for APA syndrome?
Lifelong anticoagulation
30
What happens to PTT with APA syndrome? What is odd about this?
Falsely elevated, despite being a hypercoagulable state
31
What are the top three causes of death in SLE (not in order)?
- CV dz - Infx - Renal dz
32
What are the three major drugs that cause SLE?
Hydralazine Procainamide Isoniazid
33
What is the anti-arrhythmic drug that classically causes SLE?
Procainamide
34
What is the anti-TB drug that classically causes SLE?
Isoniazid
35
What organs are rarely involved with drug induced SLE, as compared to normal SLE?
CNS | Renal
36
True or false: removal of the drug that causes SLE usually results in remission
True
37
What is the treatment for SLE?
- Avoid sunlight - Glucocorticoids - NSAIDs - Hydroxychloroquine
38
What are the nephrotic and nephrotic syndromes most commonly encounters with SLE?
Nephritic = diffuse proliferative glomerulonephritis Nephrotic = Membranous nephropathy
39
What, generally, is Sjogren's syndrome?
Autoimmune destruction of lacrimal and salivary glands
40
What type of hypersensitivity reaction is Sjogren's syndrome?
IV (lymphocyte mediated with fibrosis)
41
What is the classical presentation of Sjogren's syndrome?
- Xerophthalmia - Xerostomia - Bilateral parotid enlargement
42
What are the antibodies that are found with Sjogren's syndrome? What are these against?
SS-A (Ro) SS-B (La) Against ribonuclear proteins
43
Can't chew a cracker, or dirt in eyes = ?
Sjogren's
44
What is the most common autoimmune disease associated with Sjogren's?
RA
45
True or false: rheumatoid factor can be elevated in Sjogren's syndrome, regardless if the patient actually has RA or not
True
46
What is the major issue associated with Anti-SSA and SS-B?
Can cross the placenta and cause congenital complete heart block
47
What is the lymphocytic sialadenitis that is found with Sjogren's syndrome?
Lymphocytes attacking the salivary glands of the mouth / lip / parotid
48
What are the three major criteria that are used to diagnose Sjogren's syndrome?
- Xerophthalmia - ANA, SSA/SS-B/ RF + - Lymphocytic sialadenitis
49
What hematological malignancy are pts with Sjogren's syndrome more susceptible to? How does this usually present?
- B cell lymphoma | - Enlargement of the parotid gland late in the disease course
50
Pt with Sjogren's syndrome + unilateral parotid gland enlargement = ?
B cell lymphoma
51
Who is usually affected with systemic sclerosis?
Middle aged females
52
What, generally, is systemic sclerosis?
Sclerosis of the skin and visceral organs
53
What is the pathophysiology behind systemic sclerosis?
Fibroblast activation leads to deposition of collagen
54
What is the theory behind the development of systemic sclerosis?
Endothelial damage leads to an immune reaction against collagen, causing release of TGF-beta and PDGF, leading to sclerosis and continued inflammation
55
What are the two major cytokines that activate fibroblasts?
TGF-beta | PDGF
56
What are the components of limited sclerosis? (Formerly known as CREST syndrome)?
- Calcinosis - Raynaud's phenomenon - Esophageal dysmotility - Sclerodactyly - Telangiectasias
57
True or false: there is early visceral involvement with CREST syndrome?
False--late involvement
58
What is the antibody that is found in CREST syndrome?
Anti-centromere antibody
59
What are the associated symptoms from esophageal involvement of CREST?
GERD and decreased peristalsis
60
Is visceral involvement with diffuse systemic sclerosis early or late in onset?
Early
61
What are the GI sequelae of diffuse systemic sclerosis?
GERD Esophageal dysmotility Malabsorption
62
What are the pulmonary sequelae of diffuse systemic sclerosis?
Interstitial fibrosis and pHTN
63
What are the renal sequelae of diffuse systemic sclerosis? What is the treatment for this?
Scleroderma renal crises--acute onset of renal failure and HTN ACEIs
64
What are the cardiac sequelae of diffuse systemic sclerosis?
HTN | Pericarditis
65
What is the antibody that if found with systemic sclerosis?
Anti-DNA topoisomerase I abs
66
What are the features of mixed CT disease?
Mixed features of SLE, systemic sclerosis, and polymyositis
67
What are the antibodies found in MCTD?
- ANA | - Anti-U1-RNP

All the things continued (28 decks)

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