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Pathology block 2 > immunopathology > Flashcards

immunopathology Flashcards

1
Q

Describe the 2 types of Type I hypersensitivity

A

Immediate (type I) hypersensitivity is a rapid immunological reaction within minutes after the combination of an antigen with antibody bound to mast cells in individuals previously sensitized to the antigen.

Anaphylaxis is a systemic form of type I hypersensitivity characterized by shock, edema, and respiratory compromise (due to upper airway edema)

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2
Q

Define Type II hypersensitivity

A

Antibody-mediated (type II) hypersensitivity is an immunological reaction caused by antibodies against cell surface or extracellular matrix antigens.

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3
Q

Define type III hypersensitivity

A

Immune complex-mediated (type III) hypersensitivity is a damaging inflammatory reaction to antigen-antibody complexes, especially in blood vessels or glomeruli.

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4
Q

Define type IV hypersensitivity

A

Cell-mediated [delayed] (type IV) hypersensitivity is an immunological reaction caused by sensitized CD4 T-lymphocytes, sometimes producing aggregates of activated macrophages working together (granulomas).

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5
Q

Anti-cyclic citrullinated peptide (anti-CCP) test=>

A

Rheumatoid arthritis

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6
Q

Anti-centromere test =>

A

CREST syndrome
(limited systemic sclerosis)

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7
Q

Anti-Jo-1 (one type of anti-synthetase) =>

A

Polymyositis / dermatomyositis

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8
Q

Anti-Scl70 (= anti-DNA topoisomerase)

A
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9
Q

Anti-RNA polymerase (anti-U3 RNP)

A

Systemic sclerosis

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10
Q

Anti-U1 RNP (anti-RNP not otherwise specified)

A

Mixed connective tissue disease

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11
Q

Anti-Smith (anti-Sm)

A
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12
Q

Anti-double-stranded DNA (anti-dsDNA)

A

Lupus

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13
Q

Anti-nuclear (ANA)

A

Lupus and many other rheumatic diseases

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14
Q

Anti-SSA (= anti-Ro)

A

Sjogren syndrome,

neonatal lupus,

subcutaneous lupus

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15
Q

Anti-SSB (= anti-La)

A

Sjogren syndrome,

neonatal lupus,

subcutaneous lupus

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16
Q

Anti-myeloperoxidase
(= perinuclear anti-neutrophil cytoplasmic, P-ANCA)

A

Microscopic polyangiitis,

eosinophilic granulomatosis with polyangiitis (Churg
Strauss)

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17
Q

Anti-proteinase-3 (= diffuse cytoplasmic
anti-neutrophil cytoplasmic, C-ANCA)

A

Granulomatosis with polyangiitis (Wegener’s)

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18
Q

What are 2 drugs that are used for immunosuppressive therapy as well as cancer therapy?

A

methotrexate

cyclophosphamide.

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19
Q

What is a drug that helps autoimmune diseases and inflammatory diseases?

A

Corticosteroids

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20
Q

What drugs are given to transplant patients to prevent or treat transplant rejection? Why?

A
  • cyclosporine
  • tacrolimus

they block promotion of T cell activation and block secretion of TNF, IFN, IL-2 and IL-4

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21
Q

What allows cyclosporine and tacrolimus to have their speciifc action?

A

they are calcineurin inhibitors

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22
Q

What are calcineurins?

A

calcineurin dephosphorylates intracytoplasic nuclear regulatory proteins in lymphocytes which are translocated into the nucleus and activated

this promotes T lymphoctye activations and secretion of TNF, IFN, IL-2 and IL-4

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23
Q

How do cyclosporine and tacrolimus inhibit calcineurins?

A

by binding to intracytoplasmic receptor proteins called immunophilins which form complexes then bind to and inhibit a calcineurin

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24
Q

How much calcineurin activity is blocked by cyclosporine and tacroliumus?

A

half the activity at therapeutic levels

must be monitored to determine if levels are therapeutic

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25
Q

What is Mycophenolate mofetil (trade name CellCept)?

A

reversible inhibitor of inosine monophosphate dehydrogenase in purine biosynthesis (specifically guanine synthesis) that inhibits DNA replication, which inhibits lymphocyte proliferation.

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26
Q

Why would you administer mycophenolate?

A

treating autoimmune diseases, particularly systemic lupus erythematosus,

preventing and treating transplant rejection.

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27
Q

A patient comes into your clinic and is taking Azathioprine. What is the reason she is taking the medication? How does it work?

A

has an autoimmune disease or treating systemic lupus erythematosus and/or rheumatoid arthritisa

it is a purine analogue that messes up DNA replication;

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28
Q

A patient comes to your office after suffering from malaria and taking hydroxychloroquine as an antibiotic. The patient notices feeling much better and does not have as much pain in her hands and joints. Why is this?

A

anti-inflammatory activity

used in treating systemic lupus erythematosus and rheumatoid arthritis.

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29
Q

What drugs would you prescribe someone suffering from an acute phase inflammation reaction? why?

A
  • infliximab,
  • etanercept
  • adalimumab

block TNF-a

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30
Q

What is Belimumab (trade name Benlysta)?

A

an antibody to B-cell activating factor.

31
Q

What would be affected by giving Belimumab?

A

would not allow the first signal of B cell activation to be given by the

too much BAFF causes abnormally high antibody production causing SLE, RA

32
Q

A paitent presents with a B cell lymphoma. What drug should you give and why?

A

Rituximab

an antibody to CD20 on B lymphocytes

33
Q

A patient presents to your clinic with increased acute inflammation. What drug would you give and why?

A

Tocilizumab is a new antibody that blocks IL-6 receptors.

34
Q

Where is CD52 expressed?

A

high levels by both normal and malignant B and T lymphocytes, with lower levels found on monocytes, macrophages and eosinophils.

35
Q

Why must a patient who takes a dose of Alemtuzumab be relatively healthy?

A

powerful immunosuppressant that gives permanent effect likened to AIDS

36
Q

Define SLE

A

multisystem autoimmune disease

connective tissue disease that mainly affects the blood, joints, skin and kidneys

37
Q

What are the 2 major factors in SLE? what do they cause?

A

genetic => increased risk in family members, genetic links on chromosome 6

environmental=> medications, UV light, estrogen, infections, extreme stress

these lead to destruction of cells leading to Ab directed against nuclear antigens

38
Q

What are the immunologic factors of SLE?

A

activaiton of Th cells and B cells, IgG autoantibody production, immune complexes

39
Q

When will you see pericarditis in SLE?

A

commonly polyserositis

acute, subacute, chronic

40
Q

What is the most common gross pathology in SLE?

A

non-erosive synovitis

41
Q

What is Libman-Sacks associated with SLE?

A

1-3 mm verrucous vegetations on either side of valve

42
Q

What are the 3 most common microscopic pathologic findings in SLE?

A
  1. acute necrotizing vasculitis of small arteries and arterioles (with fibrinoid deposits)
  2. glomerulonephritis in 50% of patients
  3. cerebritis in 50%
43
Q

What are the 5 patterns of glomerulonephritis?

A
  1. minimal
  2. mesangial
  3. focal proliferative
  4. diffuse proliferative
  5. membranous
44
Q

A patient with SLE presents that is in active form in the disease, what would you expect to find?

A

glomerular granular deposits of IgG and complement

subendothelial dense deposits causing wire loop lesions

diffuse proliferative and indicative of active disease

45
Q

What are the syptoms of SLE?

A
  • joint pain (90%)
  • fever (83%)
  • fatigue (81%)
  • weight loss (63%)

pleuritic chest pain, photosensitivity, nephrotic syndrome, angina, alopecia, myalgias

46
Q

What are the signs of SLE?

A

malar distribution (butterfly rash) causing erythematous skin rash over bridge of nose and cheeks=> 50%

edema occurs in the feet first

blood in the urine

neuropsychiatric

oral ulcers

interarticular skin rash on fingers

peri-ungual erythema around fingernails

alopecia

47
Q

What are the steps that you would use to diagnose a patient with SLE?

A

ANA (100% in autoimmune)

anti-ds DNA or anti-Sm antibodies (specific)

48
Q

What are the hematologic findings in SLE?

A
  • anemia
  • thrombocytopenia

are present in 100%

also leukopenia

49
Q

Other than ANA and hematologic abnormalities, how is the diagnosis of SLE done?

A
  • proteinuria
  • urinary red cell casts
  • kidney biopsy
  • small joint inflammation
  • splenomegaly
50
Q

What is common in pregnancies in SLE?

A

recurrent spontaneous abortions caused by antiphospholipid Abs

51
Q

How should you treat SLE?

A

corticosteroids and immunosuppressive medications

52
Q

What is the prognosis of SLE?

A

90% for a 5 year survival rate

80% for a 10 year survival rate

53
Q

Define sjogren syndrome

A

autoimmune chronic inflammatory disease of lacrimal glands and salivary glands causing dry eyes and mouth

54
Q

Describe the primary form of Sjogren syndrome

A

primary => limited to eyes and mouth => sicca syndrome

  • eye involvement called kerato-conjunctivitis sicca
  • oral involvement called xerostomia
55
Q

Describe the Sjogren syndrome in the secondary form

A

associated with autoimmune diseases

rheumatoid arthritis, lupus, polymyositis, systemic sclerosis, vasculitis, thyroidits

56
Q

Does Sjogren syndrome only involve the glands?

A

No

extraglandular involvement of kidneys, joints, skin, muscle, peripheral nerves and brain

57
Q

What is the common age of a person with Sjogren syndrome?

A

90% are 35-45 years old

58
Q

What is the pathogenesis of Sjogren syndrome?

A

T lymphocyte-mediated immunological attack of some self antigen in ductal epithelial cells of these glands or an antigen in cells in these glands infected by some virus that has a tropism for the epithelial cells of these specific glands.

59
Q

Why would you think your patient has an increased risk of Sjorgen syndrome?

A

dry eyes and mouth

enlarged salivary and lacrimal glands

ulcers

60
Q

Name the micropscopic pathology of Sjorgen’s syndrome

A
  1. intense infiltration of CD4 T cells
  2. destruction of gland architecture with a change in plasma cells, germinal centers

Renal cells can have interstitial nephritis rather than glomerulonephritis

61
Q

What test would you use to diagnose Sjorgen’s syndrome?

A

Anti-SSA (Ro)

anti-SSB (La)

62
Q

What is the best treatment for the primary form of Sjorgen’s syndrome?

A

topical therapy of dry eyes, dry mouth

systemic cholingergic agents to stimulate secretions

63
Q

What would you use to treat secondary Sjorgen’s syndrome?

A

Hydroxychloroquine or rituximab for extraglandular disease

64
Q

What is the prognosis for Sjorgen’s syndrome?

A

not a bad prognosis

increase risk for developing lymphoma

65
Q

Define systemic sclerosis

A

chronic disease characterized by abnormal accumulation of fibrous tissue in skin and other organs

66
Q

What is the difference between diffuse and limited sclerosis?

A

diffuse is widespread skina and early visceral involvement

Limited=> skin of fingers/forearms/face and late visceral involvement

Limited systemic sclerosis is often within the context of CREST syndrome

67
Q

Who is most likely to get this disease?

A

highest incidence in 50-60 year old in African american women

68
Q

What is CREST syndrome?

A

Calcification, centromere Ab

Raynaud’s phenomenon

Esophageal dysmotility

Sclerodactyly

Telangiectasias

69
Q

What is the general pathogenesis of sytemic sclerosis? specific?

A

abnormal immune response + vascular damage = increased growth factors for fibrosis

CD4 T cells respond to unidentified antigen release cytokine stimulate fibroblasts to produce collagen

70
Q

What are the microvascular portions of systemic sclerosis?

A

intimal proliferation,

capillary dilatation

endothelial injury (increased vWF) and platelet activation leads to fibrosis

71
Q

Where will you initially see systemic sclerosis?

A

begins in face and fingers then progresses proximally

72
Q

What are the most common places systemic sclerosis is present?

A

skin (100%)

GI (90%)

73
Q

Why and what type of metaplasia is seen in systemic sclerosis?

A

Barrett metaplasia => lower esophageal sphincter dysfunction and decreased peristalsis cause gastroesophageal reflux

Fibrous replacement of muscular wall usually in esophagus

74
Q
A

Pathology block 2 (6 decks)

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