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MOD > Mechanisms of Immune Injury > Flashcards

Mechanisms of Immune Injury Flashcards

1
Q

What antigens attract women to men?

A

HLA

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2
Q

Haptens

A

molecules that bind to bodily proteins and becomes attacked by immune system
- cause of small molecule allergies (nickel, poison ivy)

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3
Q

What does adaptive immunity consist of?

A

B/T-lymphocytes

-specific and diverse receptors for antigens

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4
Q

Function of B-Lymphocytes

A

neutralization of microbe, phagocytosis, complement activation

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5
Q

Function of Helper T-lymphocytes (CD4)

A

Activation of macrophages, inflammation, activation/profileration of T/B lymphocytes

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6
Q

Function of cytotoxic T lymphocytes (CD8)

A

killing infected cells

- acute cellular rejection

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7
Q

Function of Regulatory T-lymphocytes

A

suppression of immune system

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8
Q

Function of NK cells

A

killing infected cells

- cells with no MHC I expression

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9
Q

What cytokine lines the medulla of the lymph node?

A

Dendritic Macrophages

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10
Q

What cytokines process antigens in outer skin?

A

Dendritic cells

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11
Q

What cytokines are produced to by Th1? To defend against what?

A

IFN-gamma for intracellular microbes

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12
Q

What cytokines are produced to by Th2? To defend against what?

A

IL-4, IL-5, IL-13 for helminthic parasites

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13
Q

What cytokines are produced to by Th17? To defend against what?

A

IL-17, IL-22 for extracellular bacteria, fungi

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14
Q

Where doe B-cells undergo maturation?

A

germinal follicles of lymph nodes

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15
Q

Where are plasma cells generally found?

A

Produce antibodies in tissue rather than blood

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16
Q

Hypersensitivity

A

disease caused by the immune system causing harm to the body

- failure of control through feedback mechanisms

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17
Q

Type 1 Immune Injury

A

in response to allergies/anaphylaxis (hay-fever, asthma)

  • Th2 produces IgE and histamine from mast cells (high IL-5)
  • later reaction is mediated by leukotrienes, PGD2
  • symptoms: vascular dilation, sm. m. contraction, mucus production
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18
Q

What is a common cause for urticaria?

A

IgE/Type I immune injury

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19
Q

What is a common cause of eosinophilic gastroenteritis?

A

food allergy

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20
Q

Cause of anaphylaxis

A

massive IgE-mediated response

21
Q

Cause of atopic dermatitis

A

people with allergies

- look for FCeRI and dendritic macrophages

22
Q

What is chronic urticaria and it’s cause?

A

patches of skin that swell from local IgE/histamine

- from autoimmunity, food, “unknown”

23
Q

Cold urticaria

A

get hives from cold temperatures

- non-immune mediated

24
Q

Cholinergic urticaria

A

hives from wet heat (sweating, shower)

- non-immune mediated

25
Q

Dermatographism

A

skin gets inflamed where it is scratched

26
Q

Type II Immune Injury

A

antibody mediated

  • antibodies attack antigen (autoimmune hemolytic anemia, goodpasture syndrome)
  • IgG, IgM
27
Q

Coomb’s test

A

test for antibodies in patient’s blood

28
Q

Goodpasture’s disease

A

antibodies against basement membrane of lungs and kidney

29
Q

Why are men preferentially used as plasma donors?

A

Women can have antibodies in the plasma against HLA antigens from previous pregnancy

30
Q

What is the most common cause of hypothyroidism?

A

Autoimmunity (hashimoto’s thyroiditis)

- antibodies and T/B-cells

31
Q

Type II immune response in adrenal

A

Addison’s disease

- T-cell destruction

32
Q

Type II immune response in pancreas

A

Type I Diabetes Mellitus

- t-cells destroy islet of langerhans

33
Q

What clotting factor do hemophiliacs develop antibodies against?

A

Factor VIII

34
Q

What receptors do antibodies in Graves’ disease bind to?

A

TSH receptors causing hyperthyroidism

35
Q

Isaac’s antibodies

A

Ab against muscles

- keeps muscles firing and causes pain

36
Q

Type III immune injury

A

immune complex-mediated (vasculitis, arthritis, glomerulonephritis)

  • Ag + Ab + Complement
  • deposits into vascular intima (feel bad all over)
  • ends when antibody becomes more abundant and immune complexes leave
37
Q

What type of immune injury is associated with fibrinoid necrosis ?

A

Type III

38
Q

Arthus Reaction

A

sore muscles from injection of something that you already have Ab for

39
Q

What type of immune injury is associated with hyperacute rejection of donor kidney?

A

Type III

40
Q

Type IV immune injury

A

T-cell mediated (contact dermatitis, MS, rheumatoid arthritis, psoriasis)

  • inflammation –> cytolysis
  • Th1/Th17
41
Q

Anergy

A

no immune response to things you have already encountered
- dysfunction in T-helper cells
(sarcoidosis, lymphomas, cancers, HIV, measles)

42
Q

Halo nevus

A

T-cells destroy melanocytes around nevus

43
Q

What cells are responsible for granuloma formation?

A

Th1 (no Ab necessary)

- miliary TB

44
Q

What is responsible for acute humoral rejection?

A

antibodies

- intimal hyperplasia in arteries

45
Q

Hyperacute rejection

A

Type III response

  • IgG precipitates
  • fibrinoid in arterial walls (lymphocytes)
46
Q

What is responsible for acute cellular rejection?

A

CD8

  • destroy heart transplant
  • tubulitis, endotheliitis
47
Q

Chronic transplant rejection

A

vessels narrow or totalled

  • intima is thickened (concentric)
  • T-cells cause thickening of intima/media
48
Q

Signs of acute graft v host disease

A

days to weeks after transplant

  • attack by CD8, Type IV immune response
  • generalized rash, loss of epidermis (starts in palms)
  • jaundice from bile duct damage
  • ulcers along GI tract/orally
49
Q

Signs of chronic graft v. host disease

A

appears after ~100 days

  • more fibrosis, less necrosis
  • fibrosis of dermis with loss of skin
  • cholestatic jaundice from bile duct damage
  • GI damage
  • damage of host T-cells (immunocompromised)
  • cytomegalovirus pneumonitis infection

MOD (7 decks)

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