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Immunosuppresive therapy > Hypersensitivities I-IV > Flashcards

Hypersensitivities I-IV Flashcards

1
Q

What is the mechanism for type II hypersensitivities?

A

Either IgG or IgM is made against normal self antigens or a foreign antigen resembling some molecule on the surface of host cells enters the body

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2
Q

What does the binding of antibodies to the surface of host cells lead to?

A

Opsonization of the host cells. Activation of the classical complement pathway.ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY (ADCC) destruction of the host cells

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3
Q

What are some examples of antibody-dependent cytotoxicity (type II hypersensitivities) diseases?

A

transfusion rxns, ITP, Hastiomoto’s thyroiditis, Grave’s, myasthenia gravis, goodpasture’s, MS

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4
Q

What is the most common adverse rxn to a blood transfusion?

A

febrile non-hemolytic transfusion rxn. fever and dyspnea

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5
Q

What are symptoms of an acute hemolytic transfusion rxn?

A

feeling of doom, chills, fever, and pain in the back and flanks

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6
Q

What is delayed hemolytic transfusion rxn?

A

donor RBCs are destroyed by the recipient’s antibodies, but the hemolysis is “delayed” because the antibodies are only present in low amounts initially.

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7
Q

Why is a delayed hemolytic transfusion rxn difficult to prevent?

A

by the time a cross match is done, the level of antibody in the recipient’s plasma is too low to cause agglutination

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8
Q

What do IgG antibodies bind to in immune thrombocytopenic purpura?

A

platelet membrane glycoproteins IIb-IIIa

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9
Q

What happens as a result of IgG coating of platelets in ITP?

A

renders them susceptible to opsonization and phagocytosis by splenic macrophages. also damage megakaryocytes

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10
Q

What is the stimulus for auto-antibody production in ITP?

A

abnormal T cell activity

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11
Q

What is Hashimoto’s thyroiditis?

A

chronic autoimmune thyroiditis that eventually leads to goiter and hypothyroidism

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12
Q

What does a patient have antibodies to in Hashimoto’s thyroiditis?

A

Thryoglobulin, thyroid peroxidase, TSH receptor

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13
Q

What happens to the thyroid at the cellular level if a patient has Hashimoto’s thyroidits?

A

diffuse lymphocytic infiltrate with thyroid-specific B & T cells and follicular destruction

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14
Q

What happens due to auto-Antibodies to TSHR (thyroid stimulating hormome receptor) seen in Grave’s disease?

A

Activation of the receptor stimulates thyroid hormone synthesis, secretion and leads to thyroid growth due to an overproduction and overactivation of T3 and T4

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15
Q

What are symptoms of Graves?

A

hyperthyroidism, goiter, bulging eyes, anxiety

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16
Q

What is the targeted antigen in myasthenia gravis?

A

Nicotinic Acetylcholine Receptor (AChR)

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17
Q

What happens as a result of myasthenia gravis?

A

AChR becomes blocked over time. muscle fatigues and can become paralyzed

18
Q

What is one of the first symptoms of myasthenia gravis?

A

eyelid droop

19
Q

Describe type III hypersensitivity rxns.

A

Antigen-antibody complexes form circulating immune complexes that are deposited in vessel walls or at extra-vascular sites & induce inflammation directly or by activating complement.

20
Q

Where do antigen-antibody complexes lodge in type III hypersensitivites?

A

between the endothelial cells and the basement membrane (glomeruli, joints, skin, heart, serosal surfaces & small blood vessels)

21
Q

What can glomerulonephritis occur secondary to?

A

Systemic infection (Hep B, malaria). Neoplasm (tumor antigens). Autoimmune. Systemic illness such as Lupus

22
Q

What do AB-AG complexes target in glomerulonephritis?

A

GBM, Bowman’s space, endothelium. Result is destruction of glomeruli and progression to renal compromise and renal failure

23
Q

Where do immune complexes get deposited in Rheumatoid arthritis?

A

in the synovial lining

24
Q

What are extra-articular diseases seen with RA?

A

cardiopulmary, renal, skin, vasculitis, ocular, Rheumatoid nodules

25
Q

What is systemic lupus erythmatosus (SLE)?

A

Presence of antinuclear-Antibodies involving multiple organ systems that’s more common in women

26
Q

What are environmental influences of SLE?

A

Sex hormones, Sun exposure, Medications, Dietary factors, Infections, Stress

27
Q

What auto-antibodies are involved with SLE?

A

Anti-ds-DNA, Anti-Smith, and AB Ribosomal P

28
Q

What are common examples of type III sensitivities?

A

SLE, RA, glomerulonephritis,

29
Q

Describe type IV hypersensitivity

A

Delayed hypersensitivity is cell-mediated and is initiated by antigen activated (sensitized) T lymphocytes

30
Q

What are the two types of type IV hypersensitivities?

A

Type 1 (mediated by CD4 T cells) and Type 2 (mediated by CD8 T cells)

31
Q

What happens as a result of type IV hypersensitivities?

A

lymphocyte infiltrates and granuloma formation

32
Q

What is contact dermatitis?

A

Perivascular infiltrates of lymphocytes & monocytes in upper dermis first, with edema in epidermis

33
Q

What is the pathophysiology of contact dermatitis?

A

induced the CD4+ T cells are activated and start releasing cytokines.

34
Q

What is the clinical presentation of contact dermatitis?

A

mild erythema to edematous papules, can be vesicular, itching is hallmark

35
Q

What are symtpoms of temporal arteritis?

A

unilateral Headache, visual disturbances, tender or enlarged temporal artery, elevated ESR; can cause blindness

36
Q

What is the pathophysiology of temporal arteritis?

A

lymphocyte infiltrate of vessel wall by CD4 T cells & CD8 T cells

37
Q

What is celiac sprue (gluten-sensitive enteropathy?

A

Hypersensitivity to cereal grain proteins–gluten or substance derived from gluten

38
Q

What happens as a result of celiac sprue?

A

villous atrophy of small intesine resulting in malabsorption, steatorrhea & weight loss.

39
Q

What are histologic changes associated with celiac sprue?

A

lymphocytic infiltrate in the lamina propria beneath the epithelial layer. no granulomas

40
Q

What are some examples of type IV hypersensitivities?

A

celiac sprue, temporal arteritis, contact dermatitis

Immunosuppresive therapy (5 decks)

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