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Robbins' Basic Pathology > Robbins: Hypersensitivity > Flashcards

Robbins: Hypersensitivity Flashcards

1
Q

What are the 3 causes of hypersensitivity reactions?

A
  1. rxns against self (autoimmunity)
  2. excessive rxns against microbes (immune complex diseases)
  3. rxns against environmental Ags
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2
Q

What type of hypersensitivity results from activation of Th2 by environmental Ags, leading to the production of IgE Abs?

A

type I

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3
Q

Describe the sequence of events in immediate hypersensitivity rxn.

A

Ag bind BCR–>Th2 activates BC and induces IgE class switching (w/ IL-4)–> Mast cell binds IgE via FcERI –> repeat exposure to Ag –> mast cell degranulation/release of mediators –>response

*note: Th2 also secretes IL-5 (–> eosinophil recruitment and activation) and IL-13 (–> stimulates mucus secretion from epithelial cells)

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4
Q

What do mast cells release when they degranulate?

A
  1. vasoactive amines: histamine, adenosine, chemotactic factors, and neutral proteases
  2. Lipid Mediators: PGD2, LTB4, LTC4, and LTD4
  3. Cytokines: IL-4, IL-5, TNF, chemokines, and IL-13
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5
Q

When mast cells degranulate, they release histmamine. What does this mediator do?

A
  • vasodilate and inc vascular perm
  • smooth muscle contraction
  • inc mucous secretion
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6
Q

When mast cells degranulate, they release adenosine. What does this mediator do?

A
  • bronchoconstriction

- inhibit platelet aggregation

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7
Q

When mast cells degranulate, they release chemotactic factors. What does these molecules do?

A

recruit neutrophils and eosinophils

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8
Q

When mast cells degranulate, they release neutral proteases. What does these molecules do?

A
  • damage tissue
  • generate kinins
  • cleave complement
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9
Q

When mast cells degranulate, they release PGD2. What does this mediator do?

A
  • bronchospasm
  • inc mucous secretion
  • vasodilation and inc vascular perm
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10
Q

When mast cells degranulate, they release LTB4. What does this mediator do?

A

chemotactic for neutrophils, eosinophils, and monocytes

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11
Q

When mast cells degranulate, they release LTC4. What does this mediator do?

A
  • vasodilate and inc vascular permeability

- smooth muscle contraction (*1000xs more potent than histamine)

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12
Q

When mast cells degranulate, they release LTD4. What does this mediator do?

A
  • vasodilate and inc vascular permeability

- smooth muscle contraction (*1000xs more potent than histamine)

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13
Q

When mast cells degranulate, they release IL-4. What does this mediator do?

A

amplify Th2 response

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14
Q

When mast cells degranulate, they release IL-5. What does this mediator do?

A

amplify Th2 response

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15
Q

When mast cells degranulate, they release TNF. What does this mediator do?

A

leukocyte recruitment and activation

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16
Q

When mast cells degranulate, they release chemokines. What do these mediators do?

A

leukocyte recruitment and activation

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17
Q

When mast cells degranulate, they release IL-13. What does this mediator do?

A

epithelial cell mucous secretion

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18
Q

An IgE triggered hypersensitivity has 2 phases. What are they and what are the defining characteristics of each?

A

Immediate response:

  • vasodilation, inc vascular perm, smooth muscle spasm
  • 5-30 mins after exposure
  • subsides in 60 mins
  • mast cell mediated

Late Response:

  • inflammation
  • tissue destruction (mucosal epithelium)
  • 2-8 hrs after exposure
  • subsides after several days
  • neutrophil, eosinophil and Th2 mediated
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19
Q

What is the role of eosinophils in late response of an IgE triggered reaction?

A

to make…

  • eosinophil cation protein–>toxic to epithelial cells
  • LTC4 and PAF –> promote inflammation
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20
Q

T or F: an immediate hypersensitivity reaction may occur as a systemic disorder or as a local reaction.

A

true

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21
Q

What is atopy?

A

familial predisposition to localized type I HS reaction (i.e. hay fever and some forms of asthma)

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22
Q

Type II HS reactions are caused by …

A

Abs directed against host Ags (found on the surface of cells or other tissue components)

23
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Autoimmune hemolytic anemia

A
  1. Red cell membrane proteins (Rh blood group antigens, I antigen)
  2. Opsonization and phagocytosis of erythrocytes
  3. Hemolysis, anemia Bleeding
24
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Autoimmune throbocytopenia purpura

A
  1. Platelet membrane proteins (GpIIb/IIIa integrin)
  2. Opsonization and phagocytosis of platelets
  3. Skin vesicles (bullae)
25
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Pemphigus Vulgaris

A
  1. Proteins in intercellular junctions of epidermal cells (epidermal desmoglein)
  2. Antibody-mediated activation of proteases, disruption of intercellular adhesions
  3. Vasculitis
26
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Vasculitis caused by ANCA

A
  1. Neutrophil granule proteins, presumably released from activated neutrophils
  2. Neutrophil degranulation and inflammation
  3. vasculitis
27
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Goodpasture syndrome

A
  1. Noncollagenous protein (NC1) in basement membranes of kidney glomeruli and lung alveoli
  2. Complement- and Fc receptor– mediated inflammation
  3. nephritis, lung hemorrhage
28
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Acute Rheumatic Fever

A
  1. Streptococcal cell wall antigen; antibody cross-reacts with myocardial antigen
  2. Inflammation, macrophage activation
  3. Myocarditis
29
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Graves disease

A
  1. TSH receptor
  2. Antibody stimulates/agonist for TSH receptors
  3. Hyperthyroidism
30
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Insulin-resistant diabetes

A
  1. Insulin receptor
  2. inhibits binding of insulin to receptor
  3. Hyperglycemia, ketoacidosis
31
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Pernicious anemia

A
  1. Intrinsic factor of gastric parietal cells
  2. neutralization of intrinsic factor, decreased abs of vit B12
  3. Abnormal myelopoiesis, anemia
32
Q

Where are opsonized cells are usually eliminated? (organ)

A

spleen

33
Q

T or F: Abs directed against cell surface receptors always causes cell injury or inflammation.

A

F: it can impair or dysregulate cellular function (i.e. myasthenia gravis and grave’s disease)

34
Q

T or F: Immune complex diseases are always directed against endogenous Ags

A

F: can be both endogenous or exogenous

35
Q

Immune complex-mediated injury can be systemic when ________ or they may be localized when ______

A

systemic when formed in circulation and are deposited in several organs

localized when they are formed and deposited in a specific site

36
Q

Approximately ___ days after foreign protein in injected, specific Abs are produced

A

5 days

37
Q

What variables determine whether an immune complex will deposit into tissues and cause diseease?

A
  1. size of complex: large ones are rapidly removed by macrophages in spleen and liver –> SMALL/INTERMEDIATE sized ones are “more dangerous”
  2. must have inc vascular perm to have the complexes deposited within or outside the wall of a vessel (usually can occur when complexes bind mast cells and leukocytes to degranulate and release vasoactive molecules)
  3. charge of comples
  4. valency of Ag
  5. avidity of Ab
  6. hemodynamics of vascular bed
38
Q

What are the favorite sites of immune complex deposition?

A

kidneys, joints, and small blood vessels

39
Q

When does the inflammatory phase begin during the immune complex disease process?

What clinical features are often seen at this time?

A

10 days after Ag exposure/administration

fever, urticaria (itchy, red welts), arthralgias, lymph node enlargement, and proteinuria

40
Q

Describe what is causing tissue damage during the inflammatory reaction of an immune complex disease.

A
  • complexes activate complement system –> C5a inc vascular perm and recruit neutrophils and monocytes
  • complexes bind Fc-gamma-R on neutrophils and monocytes –> they become activated
  • attempted phagocytosis releases pro-inflamm substances and ROS
  • complexes also cause platelet aggregation and active Hageman factor –> initiate formation of micro-thrombi –> LOCAL ISCHEMIA
41
Q

Describe the morphology associated with immune complex disease. (microscopically)

A
  • necrotizing vasculitis, micro-thrombi –> acute inflammation
  • Vessel wall becomes eosinophillic –> fibrinoid necrosis
42
Q

What is the Arthus reaction? (experimentally)

A

Injection of Ag into skin of previously immunized animal –> acute immune complex vasculitis (due to excess Ab against Ag) –> area of tissue necrosis (ulceration)

43
Q

What are the 2 types of T cell reactions that are capable of causing tissue injury and disease (type IV HS)?

A
  1. cytokine mediate inflammation via Th1 and Th17

2. cytotoxicity/cytolysis via CTLs

44
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

Rheumatoid Arthritis

A
  1. collagen or citrullinated self proteins
  2. Th17
  3. chronic arthritis with inflamm and destruction of joints
45
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

Multiple Sclerosis

A
  1. myelin basic protein
  2. inflamm via Th1 and TH17 –> myelin destruction my macrophages
  3. demyelination in CNS with perivascular inflammation; paralysis and ocular lesions
46
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

Type I diabetes mellitus

A
  1. Ags of pancreatic islet Beta cells (insulin, glutamic acid decarboxylase, and others)
  2. CTLs
  3. Beta cell destruction –> Diabetus
47
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

Inflammatory Bowel Syndrome

A
  1. enteric bacteris (maybe self Ags)
  2. Th17
  3. chronic intestinal inflammation; ulceration; obstruction
48
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

Hashimoto thyroiditis

A
  1. thyroglobulin and other thyroid proteins
  2. CTL
  3. hypothyroidism
49
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

Autoimmune Myocarditis

A
  1. myosin heavy chain
  2. CTLs and Th1
  3. cardiomyopathy
50
Q

For the following T cell mediated disease, identify…

  1. What the T cells recognize
  2. Which T cells mediate it
  3. Clinical manifestation

contact sensitivity

A
  1. various environmental chemicals (poison oak)
  2. Th1
  3. epidermal necrosis, dermal inflammation with skin rash and blisters
51
Q

Upon activation of CD4 T cell by Ag presented on APC, what must occur for that CD4 T cell to differentiate into a Th1 cell? Th17 cell? (i.e. what molecules must be present for them to differentiate into these 2 subtypes)

What do these subtypes produce once they are activated and what is the consequence of this?

A

Th1 develop in the presence IL-12
Th17 develop in the presence IL-1, 6, or 23

once active…
Th1 make INF-gamma to recruit macrophages
Th17 makes IL-17 to recruit neutrophils
BOTH ultimately cause INFLAMMATION

52
Q

Describe a delayed-type hypersensitivity.

A

(type of T cell mediated reaction)

  • Requires that the individual be previously sensitized to Ag.
  • Once re-exposed, 12-48 hrs later (time it takes oft T cells to be recruited to site and be activated to release cytokines) there is inflammation and tissue injury
  • cytokines from Th1 and Th17 cause inc vascular perm –> edema and fibrin deposition
  • if Ag persistes long enough granulomas can form (Th1 replaced by macrophages after 2-3 weeks)
53
Q

T or F: INF-gamma activates macrophages to produce substances that cause tissue damage and promotes fibrosis .

A

true

54
Q

For the following disease, what is

  1. the target Ag
  2. the mechanism of the disease
  3. The clinical manifestation

Myasthenia Gravis

A
  1. Acetylcholine receptor
  2. Ab inhibits/antagonizes Ach binding –> down modulates Ach receptors
  3. muscle weakness, paralysis

Robbins' Basic Pathology (5 decks)

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