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Sem 2: Immuno > Hypersensitivity - Toka > Flashcards

Hypersensitivity - Toka Flashcards

1
Q

What is Type I hypersensitivity mediated by?

A

IgE

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2
Q

What is Type II hypersensitivity mediated by?

A

IgG and IgM

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3
Q

What is Type III hypersensitivity mediated by?

A

Ab-Ag complexes

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4
Q

What is Type IV hypersensitivity mediated by?

A

T-lymphocytes

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5
Q

What is atopy?

A

Excessive production of IgE

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6
Q

What is phase 1 of hypersensitivity Type I? How does it work?

A

Phase 1: Sensitization

APCs present to CD4+ T cells

CD4+ T cells differentiate into Th2 cells

Th2 cells promote humoral response of B cells by secreting IL-4 and IL-13

B cells make alot of IgE

IgE then binds to BASOPHILS and MAST CELLS in tissues where Ag first entered

Then Mast cell makes more IL-4 following degranulation which stimulates Th2 cells

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7
Q

How does IgE bind to mast cells?

A

Through Fc receptor - FcERI (most commonly)

Or by IgG using FcYRI

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8
Q

How does FcERI help with hypersensitivity Type I?

A

high affinity for IgE - binding is irreversible

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9
Q

IgG4

A

plays a role in atopic dermatitis in dogs

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10
Q

What is phase 2 of hypersensitivity Type I? How does it work?

A

Phase 2: Hypersensitivity rxn

** inflamm. occurs rapidly

Re-encounters Ag (allergen)

Binds to 2 IgE molecules (cross linking)

This leads to degranulation of mast cells and release of inflamm. mediators

= acute inflammation

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11
Q

What is the result of Phase 2, Type 1 hypersensitivity?

A

acute inflamm, results in URTICARIA, LACRIMATION, or SNEEZING

Edema, pruritis and hyperemia occur within 6-12 hours

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12
Q

What happens to mast cells after Type 1 Hypersensitivity?

A

They dont die

They regenerate contents of cytoplasmic granules

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13
Q

What is the clinical presentation of Type I Hypersensitivity?

A

Depends on:

  1. Dose of Ag
  2. Route of Admin of Ag
  3. # and location of mast cells
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14
Q

How does anaphylaxis occur?

A

When large doses of Ag are admin rapidly (intravenously)

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15
Q

What are symptoms of anaphylaxis?

A
  1. Difficulty breathing and talking
  2. Loss of consciousness
  3. Wheezing/ coughing
  4. Swelling of throat and tounge
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16
Q

Anaphylaxis in Horses

A

Shock organ: Resp tract + intestines

Symptoms: Cough, dyspnea

Pathology: Emphysema

Mediators: Histamine + Serotonin

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17
Q

Anaphylaxis in Dogs

A

Shock organ: HEPATIC VEIN

Symptoms: Collapse, dyspnea, diarrhea, vomiting

Pathology: Hemmorhage

Mediators: Histamine, Leukotrienes, Prostaglandins

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18
Q

Anaphylaxis in Swine

A

Shock organ: Resp tract + intestines

Symptoms: Cyanosis, pruritis

Pathology: Hypotension

Mediators: Histamine

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19
Q

Anaphylaxis in Ruminants

A

Shock organ: Resp Tract

Symptoms: cough, dyspnea, collapse

Pathology: lung edema, hemorrhage

Mediators: Serotonin, Leukotrienes, Kinins, Dopamine

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20
Q

Anaphylaxis in Cats

A

Shock organ: Resp tract

Symptoms: Dyspnea, vomiting, diarrhea, pluritis

Pathology: lung edema, intestinal hemorrhage

Mediators: Histamine, leukotrienes

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21
Q

Anaphylaxis in chickens

A

Shock organ: Resp. Tract

Symptoms: Dyspnea, convulsions

Pathology: lung edema

Mediators: Histamine, Serotonin, Leukotrienes

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22
Q

What are the routes of entry of an allergy?

A
  1. Inhalation
  2. Eyes
  3. Ingestion
  4. Intradermal
  5. Intravenous
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23
Q

What symptoms could you see from an allergen that entered the body through INHALATION?

A

Rxn in the resp tract

Sneezing, coughing, asthma

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24
Q

What symptoms could you see from an allergen that entered the body through the eyes?

A

Lacrimation, conjunctivitis

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25
Q

What symptoms could you see from an allergen that entered the body through INGESTION?

A

Colic, diarrhea, hemorrhage

26
Q

What symptoms could you see from an allergen that entered the body INTRADERMALLY?

A

Urticaria, pruritus, hyperemia, dermatitis

27
Q

What symptoms could you see from an allergen that entered the body INTRAVENOUSLY?

A

Systemic rxns

28
Q

A dog got stung by wasps, what is the route of entry and what symptoms would you see?

A

Entered intradermally through bee sting, causes urticaria (hives)

29
Q

What is an example of Type I Hypersensitivity in dairy cows?

A

Allergy to their own milk - common in dairy cows

Caused by lack of milking @ appropriate times

Allergic to A-casein in milk

These milk proteins are absorbed into blood and leads to allergic rxn causing skin lesions, anaphylaxis and death

Avoid by milking regularly

30
Q

Food allergy is an example of Type _____ hypersensitivity rxn

A

Type I

Ag can reach the skin and bind to IgE on mast cells causing skin lesions and diarrhea

30% of skin problems are from food allergies in dogs

31
Q

Food intolerance

A

Does NOT involve IR

results from toxic metabolites in food

Ex: Grapes, Chocolate

32
Q

Atopic dermatitis is an example of Type ____ hypersensitivity

A

Type I

Through Ag (allergens) ingested, inhaled, or penetrated through skin

33
Q

Penicillin

A

can lead to allergic or anaphylactic rxn (Type I Hypersensitivity)

metabolized to haptens which binds to host proteins and becomes immunogenic

34
Q

Flea allergy dermatitis is an example of Type ___ Hypersensitivity?

A

Type I

35
Q

How can you diagnose Type I Hypersensitivity?

A
  1. Direct skin test - inject dilute solutions of suspect allergens INTRADERMALLY, look for rxn

** not used in cats
** dogs cant be on steroids during testing

  1. Serology - Western Blot, ELISA
    ** neg result EXCLUDES atopy
36
Q

How to manage Type I Hypersensitivity?

A
  1. Avoid allergen
  2. Corticosteroids - inhibits prostaglandin, leukotrienes - immunosupression
  3. Cyclosporines - treats symptoms of atopic dermatitis but does not solve it
  4. Histamine inhibitors - Benadryl
37
Q

Desensitization of Type I Hypersensitivity

A

by reintroducing allergens to host

Giving IV injections of increasing amounts of allergen (Allergy shots)

Leads to decrease in IgE and increase in IgG

Activates T regs to secrete IL-10 and block IgE and mast cell degranulation

Reverses IR from Th2 to Th1

38
Q

Type II Hypersensitivity is mediated by

A

IgG or IgM

39
Q

How does Type II Hypersensitivity start?

A

By destruction of a target cell, leading to release of Antigens that sensitive the host

Leads to production of IgG and IgM Ab

40
Q

What are the 3 pathways of Type II Hypersensitivity?

A
  1. Ab-Ag complex - complement binds + leads to tissue damage via Classical pathway
  2. Ab-Ag complex on cell surface - NK cells with Fc receptors bind and activate ADCC pathway
  3. Ab on cell surface act as OPSONINS which allows phagocytosis through Fc Receptors
41
Q

Hemolytic Disease of Newborns (HDN) is an example of ____________

A

Type II Hypersensitivity

42
Q

How does Hemolytic Disease of the Newborn (HDN) occur?

A
  1. Ag of fetus RBCs are introduced to moms blood
  2. Mom makes Ab against fetus RBCs + concentrates them in colostrum
  3. Mom transfers Ab to newborn through colostrum
  4. Baby has an anti-RBC rxn leading to haemolysis of RBCs

occurs if: mom is sensitized to fetus Ag, if mom has repeated placental bleeding, if mom breeds with the same sire, and if the newborn drinks the colostrum from mom who has anti-RBC AB

43
Q

Type II hypersensitivity due to medications

A
  1. Drugs may bind to RBCs (Ex: penicillin) - RBCs recognized as non-self and get killed
  2. Drugs may modify RBC membranes and expose self Ag to which AB bind and opsonize for phagocytosis
  3. Drug + Ab activates complement and kill RBCs
44
Q

Antigens from infectious agents cause Type II Hypersensitivity by

A

Modifying RBC membranes and making them look foreign so they are removed by complement or macrophages

45
Q

Hypersensitivity Type III

A

Mediated by too many Ab-Ag complexes

Deposited in tissues leading to damage by neutrophils

46
Q

What are examples of Type III Hypersensitivity?

A
  1. Glomerulonephritis
  2. Rheumatoid arthritis
  3. Serum sickness
  4. Arthus Rxn
  5. Malaria
47
Q

What are the 2 forms of Type III Hypersensitivity?

A
  1. Localized
  2. Generalized
48
Q

Localized Type III Hypersensitivity

A

Ag-Ab complexes deposited in tissues -

ANTIBODY EXCESS

Ex: Arthus rxn

49
Q

Generalized Type III Hypersensitivity

A

Ag-Ab complexes formed in BLOOD during IV Ag administration.

Ag-Ab complexes deposited in glomerulus (kidney)

ANTIGEN EXCESS

Ex: Serum sickness - Ex Anti venom serum

50
Q

What conditions lead to Arthus reaction?

A
  • occurs in host who has alot of precipitating antibodies
  • occurs when large amount of antibodies are administered to host who already has antigens
  • occurs when already formed complexes with excess antibody are administered
51
Q

Blue eye is an example of

A

Type III Hypersensitivity

52
Q

How does blue eye occur?

A

In dogs following adenovirus infection or vaccination of live vaccine against adenovirus

Causes edema and opacity of cornea

53
Q

What is serum sickness?

A

A disease that happens after IV admin of large amounts of ANTIGEN

Reacts by making Ab against serum

Causes GLOMERULONEPHRITIS

54
Q

Type I Serum Sickness

A

Ag-Ab complexes deposited in endothelium of glomerulus

leads to production of TGF beta which stimulates production of collagen, fibronectin, and proteoglycan

these cause thickening of the glomerulus BM

55
Q

Type II Serum sickness

A

proliferation of vascular endothelium and mesangial cells

56
Q

Type III serum sickness

A

Deposition of Ag-Ab complexes on both sides of glomerular BM

results in kidney failure

57
Q

IgA nephropathy

A

Deposition of Ag-Ab complexes in the kidneys

in dogs 4-7 yrs old

causes renal failure

58
Q

Purpura hemorrhagica

A

in horses

after streptococcus equi infection

causes edema, hemorrhage on limbs and mucosa

A TYPE III Hypersensitivity

59
Q

Type IV Hypersensitivity is mediated by?

A

T-cells

60
Q

How long does it take for Type IV Hypersensitivity to occur?

A

72 hours

61
Q

What is the difference between Type I-III hypersensitivity vs Type IV?

A

Type I-III mediated by Ab-Ag complexes

Type IV mediated by T cells

62
Q

The tuberculin reaction is an example of _______

A

Type IV hypersensitivity

Sem 2: Immuno (17 decks)

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