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Rheum Boards Studying > Lupus > Flashcards

Lupus Flashcards

1
Q

ACR Lupus Criteria 1997

A 
Malar Rash
Discoid rash 
Photosensitivity 
Serositis
Hematological d/o
Neurological d/o
Arthritis 
Renal disease 
Autoantibodies
ANA 
Oral Ulcers

Need four of 11

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2
Q

Pathways involved in clearing apoptotic materials

A 
Complement and receptors 
PD1
BCL1
Fas/Fas ligand 
Immunoglobulin receptors
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3
Q

What are NETs rich in?

A
  • DNA
  • LL37
  • High mobility group protein B1 (HMGB1)
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4
Q

Adaptive Immunity pathology of lupus

A

IC are formed and activate pDC
pDC produce IFNa
Fc gammaR IIa on the pDC membrane delivers IC to TLR7 (if RNA) and TLR9 ( if DNA)
TLR induced production of IFNa leads to differentiation of monocyte to DCs and activation of immature myeloid DCs
myeloid DCs activate auto reactive T and B cells, leading to increased autoantibody production
mDCs also cause CD8T cells to differientate into cytotoxic T cells

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5
Q

Risk of a sibling of a patient with lupus having lupus

A

20 fold increased compared to general population

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6
Q

Which single gene mutations can cause lupus?

A 
homozygous c1q deficiency (90%)
C2 deficiency (1/3), higher association with Ro antibodies 
C4 (increased risk)
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7
Q

Name a disease in which hormones play a role in the development of lupus

A

Klinefelter syndrome has an increased risk of lupus but they generally have milder disease as compared to XY adult men with SLE (higher risk of nephritis)

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8
Q

Viruses implicated in lupus

A

EBV

CMV

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9
Q

Drugs implicated in DIL

A 
Hydralazine (HIGH) 
Procainamide (HIGH) 
Isoniazid
Methyldopa 
Quinidine (Moderate) 
Minocycline 
Chlorpromazine

In children-anti epileptics meds are commonly implicated

TNFi can cause signs suggestive of SLE (anti ds DNA, low complement etc)

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10
Q

Anti histone ab

A

Suggestive of DIL but not diagnostic

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11
Q

Pathogenesis of LN

A

Formation of ICs lead to activation of complement and FC gamma receptors

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12
Q

DNASE I

A

Major renal nuclease
Found to be down regulated in LN leading to impaired clearance of apoptotic cells leading to further exposure of chromatin fragments

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13
Q

What is a full house?

A

Deposition of IgA, IgM, IgG, C3, C1q, and kappa and lambda light chains

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14
Q

Acute nephritic syndrome

A

Microscopic hematuria (occ macro)
HTN
Proteinuria (mild to nephrotic)

*Commonly a manifestation of Class III or IV

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15
Q

What to consider if you notice gross hematuria in a lupus patient

A

Renal vein thrombosis
Thrombotic microangiopathy
Clotting factor deficiency (PT deficiency)

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16
Q

Nephrotic Syndrome

A

Nephrotic range proteinuria
Hyperlipidemia
hypoalbuminemia
Edema

*Commonly seen in class V

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17
Q

Complications associated with Class V

A

Thrombosis

CV events

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18
Q

Predictors of poor renal outcomes

A 
African American race 
low GFR (<60 mL/min/1.73m2 
Nephrotic range proteinuria at presentation
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19
Q

Recurrence of SLE after transplantation

A

20-30% though recurrence is generally mild and not associated with decreased patient survival

20
Q

Leading cause of death in pediatric LN patients before and after ESRD

A

Infection

Cardiovascular complications

21
Q

Which antibody triggers neutrophils to become apoptotic?

A

RNP

22
Q

Percentage of first degree relatives of patients with SLE who also have the disease

A

10%

23
Q

Percentage of children with a mother with lupus who have a positive ANA

A

27%

24
Q

Pathology of acute cutaneous lupus

A

Disruption of the dermal-epidermal junction, infiltration of T cells and fibrinoid degeneration

25
Q

Pathology of chronic cutaneous lesions

A

Thickening of the keratotic layer, epidermal atrophy, follicular plugging, and fibrosis of the elastic tissues

26
Q

Most common sign of neuropsychiatric disease in cSLE

A

Headache –> described as a migraine or unrelenting, severe headache requiring narcotic analgesia

27
Q

Most common cardiac manifestation of lupus

A

Pericarditis

  • Chest x ray may show an enlarged cardiac silhouette
  • EKG shows elevated ST segments and peaked t waves
  • Treatment if mild is usually steroids and NSAIDs
  • May require IV steroids pulse
28
Q

Signs of myocarditis

A
  • Elevation in CK mB and troponin
  • Enlarged silhouette
  • EKG shows nonspecific ST and T wave changes and arrythymias
  • Echo shows global hyperkinesis, reduced LV EF, regional wall motion abnormalities
29
Q

Most common valvular disease in lupus

A

Libman Sacks endocarditis

  • Sterile, small, verrucous value lesions typically on the mitral valve but also found on other valves, chordae tendineae and endocardium
  • most common in longer disease activity, with APLs, high disease activity
  • Usually asymptomatic
30
Q

Most common PFT finding in lupus

A

restrictive disease and or impaired diffusion.

31
Q

Bronchoscopy findings supportive of PAL

A

Frank blood in airways

serosangionous BAL fluid, hemosiderin laden macrophages, absence of purulent sputum, lack of infectious organisms

32
Q

Cause of Autoimmune hemolytic anemia

A

Warm agglutinins

33
Q

Signs of anemia of chronic disease

A

Low Hg, normocytic, normochromic, low iron, low relic count, high ferritin

34
Q

Signs of HUS

A

MAHA, thrombocytopenia, acute kidney injury

–look for schistocytes

35
Q

Signs of TTP

A

MAHA, thrombocytopenia, fever, AKI, neurological deficits

-look for schistocytes

36
Q

Leukocytoclastic vasculitis

A

Erythematous or violaceous punctate, non blanching less of the fingertips or palms

37
Q

Cause of thrombocytopenia associated with ITP

A

Antibodies against GP11B/IIa and thrombopoietin receptor TPOR

38
Q

Most common areas to clot with positive LAC

A

Legs
Cerebral veins
Pulmonary vasculature

39
Q

Anti Ro/SS-A

A

Strongly associated with neonatal lupus and subacute cutaneous lupus

40
Q

Anti- C1q

A

Good marker of LN activity and correlates with severity of nephritis and proteinuria
- also associated with angioedema symptoms

41
Q

What can be tested to find those at risk of AZA toxicity ?

A

Thiopurine methyltransferase (TPMT)

42
Q

Most often causes of death

A

Infection, renal failure, cardiopulmonary

43
Q

Findings suggestive of lupus in lymphoid tissue

A

Hematoxylin bodies

44
Q

What can be found in patients with transverse myelitis?

A
  • APls
45
Q

When do clinical manifestations of drug induced lupus resolve?

A
  • 6 months after the drug is removed
46
Q

When do ds DNA antibodies go away?

A
  • 12 to 24 months

Rheum Boards Studying (34 decks)

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