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General Pathology > Exam #3: Immuopathology II > Flashcards

Exam #3: Immuopathology II Flashcards

1
Q

What is conditioning regime?

A

Irradiation therapy to destroy the immune system and create a graft bed

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2
Q

What is timeline for acute GVHD?

A

Days to weeks post engraftment

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3
Q

What is the mechanism of acute GVHD?

A

Immunocomptent T-cells in the donor bone marrow recognize recipient HLA antigens as foreign & react to them

  • CTL response= direct destruction
  • CD4+= cytokines production and inflammation
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4
Q

What are the manifestations of acute GVHD? Why?

A

Mainly the immune system and the epithelial of the skin, liver, and intestines are effected

  • Skin= dequamating rash
  • Liver= small bile duct destruction leading to jaundice
  • Intestines= mucosal destruction leading to bloody diarrhea

**Profound IMMUNOSUPPRESSION

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5
Q

What is chronic GVHD?

A

Follows resolution of acute CVHD or may evolve insidiously

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6
Q

What is the mechanism of chronic GVHD?

A

Autoreactive T-cells deried from donor stem cells that cannot be clonally deleted due to immune compromise of recipient

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7
Q

What are the manifestations of chronic GVHD?

A

Generally, this is a worsening of acute GVHD that mimics systemic sclerosis

  • Destruction of skin appendages and fibrosis of the dermis
  • Chronic liver damage leading to jaundice
  • GI damage leading to esophageal stricture

**Patients also experience recurrent life-threatening infections

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8
Q

What is bronchiolitis oboliteratans?

A

Obstructive lung disease that results from chronic GVHD

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9
Q

Generally, what are autoimmune diseases?

A

Immune reactions against self-antigens

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10
Q

What are systemic autoimmune diseases?

A

Connective tissue or collagen-vascular diseases that target widely distributed intracellular molecules

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11
Q

Generally, what are the criteria for the diagnosis of an autoimmune disease?

A

1) Immune reaction for a self-antigen or self-tissue
2) Reaction is NOT secondary to tissue breakdown but is PRIMARY
3) Absence of other well-defined cause of disease

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12
Q

What are the two general mechanisms of self-tolerance?

A

1) Central tolerance

2) Peripheral tolerance

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13
Q

What is central tolerance?

A

Process by which self-reactive B & T-cells are killed during their maturation process in the central lymphoid organs i.e. bone marrow & thymus

  • Negative selection= T-cells, random rearrangement of somatic genes generates indiscriminate lymphocytes; these cells are presented with self antigens & those that react, die by apoptosis
  • Receptor editing= auto-reactive B-cells in the bone marrow get another shot at gene rearrangement to be non-self reactive
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14
Q

What is peripheral tolerance?

A

Process by which auto-reactive B & T-cells are silenced in peripheral lymphoid organs i.e. lymph nodes

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15
Q

What are the mechanisms of peripheral tolerance?

A

Anergy=

  • T-cells–normal tissues do NOT express the costimulatory molecules needed for activation–T-cells that react to self-antigen undergo a silencing reaction
  • B-cells–need helpter T-cells for activation, without, also undergo silencing reaction

Suppression by regulatory T-cells

Deletion by activation induced cell death= CD4+ T-cells that recognize self-antigens recieve signals that promote their apoptosis

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16
Q

What locus is associated with autoimmunity?

A

Expression of certain MHC alleles (D locus) confers higher susceptibility to loss of self tolerance

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17
Q

What is the genetic polymorphism is most commonly associated autoimmunity & RA?

A

PTPN-22 gene

- Encodes a tyrosine phosphatase

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18
Q

How do microbes precipitate autoimmunity?

A

Antigenic mimicry

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19
Q

Which gender is associated with higher incidence of autoimmunity? Why?

A

Female, which potentially suggests a role of sex hormones in autoimmunity

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20
Q

Generally, what balance is interrupted to cause autoimmunity?

A

Genetic background + enviornmental factors= autoimmunity

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21
Q

What is SLE?

A

Systemic Lupus Erythematous: prototypical multisystem autoimmune disorder

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22
Q

What gender is SLE more common in? What race?

A

African american females

23
Q

What are the ACR diagnostic criteria for SLE?

A

1) Malar/ butterfly rash on face
2) Discoid rash–erythematous raised patches with adherent keratotic scaling & follicular plugging
3) Photosensitivity
4) Oral ulcers (painless)
5) Arthritis
6) Serositis–pleuritis or pericarditis documented by ST elevation in all leads (except aVR)
7) Renal disorder i.e. proteinuria/ casts
8) Neurologic disorder i.e. seizures or psychosis
9) Hematologic disorder i.e. hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia
10) Immunologic disorder
11) Antinuclear antibodies

24
Q

Outline the pathogenesis of SLE.

A
  • UV irradiation or other environmental insult results in apoptosis
  • Inadequate clearance of these cells= high burden of nuclear antigens
  • Underlying genetic defect e.g. HLA-DQ= defective self-tolerance
  • Self-reactive lymphocytes remain active
  • Activation of helper T-cells & B-cells that produce autoantibodies to nuclear antigens
25
Q

What are the most common symptoms of SLE?

A

Chronic remitting & relapsing febrile illness, characterized by injury to the

  • skin
  • joints
  • kidney
  • serosal membranes

**Note that 100% of SLE patients have hematologic conditions at some point

26
Q

What are the hallmark autoantibodies associated with SLE?

A

Anti-nuclear antibodies; specifically, antibodies to DSDNA, or “SMITH ANTIGEN (SM)”

27
Q

What is ANA testing?

A

Flourescent testing of antinuclear antibodies (ANA) i.e.

1) Antibodies to DNA
2) Anditbodies to histones
3) Antibodies to nonhistone proteins bound to RNA
4) Antibodies to nucleolar antigens

28
Q

What is peripheral rim staining on fluorescent ANA testing indicative of?

A

Antibodies to dsDNA associated with active SLE

29
Q

What is homogenous staining on fluorescent ANA testing associated with?

A

Indicates antihistone antibodies associated with:

  • RA
  • Drug induced SLE
30
Q

What is speckled staining on fluorescent ANA testing associated with?

A

Indicates antibodies to non-DNA nuclear constituents & is the least specific ANA pattern. Associated with:

  • SLE
  • Sjogren’s Syndrome
  • Systemic scleroisis
31
Q

What is nucleolar staining on fluorescent ANA testing associated with?

A

Indicates antibodies to RNA, which is assocaited with:

  • SLE
  • Systemic Sclerosis
  • CREST
32
Q

What is the centromere staining pattern on fluorescent ANA testing associated with?

A

Indicates antibodies to centromeres.

**This is NOT associated with SLE, rather, systemic sclerosis & CREST

33
Q

List the specific Lupus ANAs.

A
  • Anti-dsDNA
  • Anti-ribonucleoprotein i.e. anti- Smith
  • Antibodies to blood cells
  • Antibodies complexed to phospholipids
34
Q

What Hypersensitivity mechanisms underlie the symptoms of SLE?

A
  • Type II is directed against blood cells & results in the frequent hematologic effects
  • Type III mechanism causes visceral lesions
35
Q

What percentage of SLE patients have arthralgia or arthritis? Why?

A
  • 80-90% if patients have joint symptoms

**Caused by immune complex (Type III) deposition in the synovium

36
Q

What does the malar/ butterfly rash spare?

A

Nasolablial fold

37
Q

What causes the malar rash associated with SLE?

A

Destruction of the epidermal/ dermal junction

38
Q

What are the acute & chronic vascular changes associated with SLE?

A

Acute= vasculitis with fibrinoid necrosis of arteries & arterioles in any tissue

Chronic= layered fibrous thickening

**Note that these are caused by circulating immune complexes to ANAs that deposit in vascular beds & initiate a Type III reaction

39
Q

What is “onion-skinning” ? What causes the “onion-skinning” associated with SLE?

A

“onion-skinning”= pathognomonic appearance of vascular lesions in SLE

  • Smooth muscle cell proliferation
  • Increased intercellular collagen
40
Q

What is the major cause of morbidity & mortality of lupus?

A

Kidney failure from “lupus nephritis”

41
Q

What is lupus nephritis?

A

This was the prototype immune complex glomerulonephritis

42
Q

What is serositis?

A

Serosal effusions principally involving the pleura & pericardium

43
Q

What cardiac complications are associated with SLE?

A
  • Pericarditis
  • Myocarditis
  • Nonbacterial endocarditis
  • Accelerated coronary artery disease
44
Q

What are Libman Sacks disease?

A

Nonbacterial endocaritis affecting any valve, both sides of the valve, & usually the AV valves

45
Q

How does lupus endocarditis compare to other forms of endocarditis?

A

RHD= Small, warty vegetations along lines of closure of valve leaflets

IE= Large, irregular destructive masses on valve cusps that extend into the chordae

NBTE= small bland vegetatons at the line of closure

LSE (SLE)= Small/ medium sized vegetations on either/ both sides of the valve leaflet

46
Q

What happens to the lungs with SLE?

A

Pleuritis w/ effusion

47
Q

Describe the pathology seen in the lungs of SLE patients with acute involvement.

A

Pneumonitis with alveolar damage, edema, & hemorrhage

48
Q

Describe the pathology seen in the lungs of SLE patients with chronic involvement.

A

Interstitial & vascular fibrosis leading to pulmonary fibrosis & pulmonary HTN

49
Q

What are the neurologic manifestations of SLE?

A
  • Focal deficit
  • Seizures
  • Neuropsychiatric symptoms
50
Q

What is the clinical course of SLE associated with?

A

Titers of autoantibodies

*****Note that the course of SLE is highly variable

51
Q

What is discord lupus?

A

Skin only without systemic features

52
Q

What is subacute cutaneous LE?

A

An intermediate between discord & SLE

53
Q

What drugs can cause drug-induced lupus?

A
  • D-penicillamine
  • Procaianamide
  • Hydralazine
  • Isoniazid
54
Q

What symptoms differentiate drug induced & SLE?

A

NO renal or CNS pathology

General Pathology (33 decks)

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