Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Sem 2: Immuno > Hypersensitivity - Toka > Flashcards

Hypersensitivity - Toka Flashcards

1
Q

What is Type I hypersensitivity mediated by?

A

IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Type II hypersensitivity mediated by?

A

IgG and IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Type III hypersensitivity mediated by?

A

Ab-Ag complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Type IV hypersensitivity mediated by?

A

T-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is atopy?

A

Excessive production of IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does IgE bind to mast cells?

A

Through Fc receptor - FcERI (most commonly)

Or by IgG using FcYRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does FcERI help with hypersensitivity Type I?

A

high affinity for IgE - binding is irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IgG4

A

plays a role in atopic dermatitis in dogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens to mast cells after Type 1 Hypersensitivity?

A

They dont die

They regenerate contents of cytoplasmic granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does anaphylaxis occur?

A

When large doses of Ag are admin rapidly (intravenously)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Anaphylaxis in Horses

A

Shock organ: Resp tract + intestines

Symptoms: Cough, dyspnea

Pathology: Emphysema

Mediators: Histamine + Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Anaphylaxis in Dogs

A

Shock organ: HEPATIC VEIN

Symptoms: Collapse, dyspnea, diarrhea, vomiting

Pathology: Hemmorhage

Mediators: Histamine, Leukotrienes, Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Anaphylaxis in Swine

A

Shock organ: Resp tract + intestines

Symptoms: Cyanosis, pruritis

Pathology: Hypotension

Mediators: Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Anaphylaxis in Ruminants

A

Shock organ: Resp Tract

Symptoms: cough, dyspnea, collapse

Pathology: lung edema, hemorrhage

Mediators: Serotonin, Leukotrienes, Kinins, Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Anaphylaxis in Cats

A

Shock organ: Resp tract

Symptoms: Dyspnea, vomiting, diarrhea, pluritis

Pathology: lung edema, intestinal hemorrhage

Mediators: Histamine, leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Anaphylaxis in chickens

A

Shock organ: Resp. Tract

Symptoms: Dyspnea, convulsions

Pathology: lung edema

Mediators: Histamine, Serotonin, Leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the routes of entry of an allergy?

A
  1. Inhalation
  2. Eyes
  3. Ingestion
  4. Intradermal
  5. Intravenous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

Lacrimation, conjunctivitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What symptoms could you see from an allergen that entered the body through INGESTION?
Colic, diarrhea, hemorrhage
26
What symptoms could you see from an allergen that entered the body INTRADERMALLY?
Urticaria, pruritus, hyperemia, dermatitis
27
What symptoms could you see from an allergen that entered the body INTRAVENOUSLY?
Systemic rxns
28
A dog got stung by wasps, what is the route of entry and what symptoms would you see?
Entered intradermally through bee sting, causes urticaria (hives)
29
What is an example of Type I Hypersensitivity in dairy cows?
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
Food allergy is an example of Type _____ hypersensitivity rxn
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
Food intolerance
Does NOT involve IR results from toxic metabolites in food Ex: Grapes, Chocolate
32
Atopic dermatitis is an example of Type ____ hypersensitivity
Type I Through Ag (allergens) ingested, inhaled, or penetrated through skin
33
Penicillin
can lead to allergic or anaphylactic rxn (Type I Hypersensitivity) metabolized to haptens which binds to host proteins and becomes immunogenic
34
Flea allergy dermatitis is an example of Type ___ Hypersensitivity?
Type I
35
How can you diagnose Type I Hypersensitivity?
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 2. Serology - Western Blot, ELISA ** neg result EXCLUDES atopy
36
How to manage Type I Hypersensitivity?
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
Desensitization of Type I Hypersensitivity
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
Type II Hypersensitivity is mediated by
IgG or IgM
39
How does Type II Hypersensitivity start?
By destruction of a target cell, leading to release of Antigens that sensitive the host Leads to production of IgG and IgM Ab
40
What are the 3 pathways of Type II Hypersensitivity?
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
Hemolytic Disease of Newborns (HDN) is an example of ____________
Type II Hypersensitivity
42
How does Hemolytic Disease of the Newborn (HDN) occur?
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
Type II hypersensitivity due to medications
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
Antigens from infectious agents cause Type II Hypersensitivity by
Modifying RBC membranes and making them look foreign so they are removed by complement or macrophages
45
Hypersensitivity Type III
Mediated by too many Ab-Ag complexes Deposited in tissues leading to damage by neutrophils
46
What are examples of Type III Hypersensitivity?
1. Glomerulonephritis 2. Rheumatoid arthritis 3. Serum sickness 4. Arthus Rxn 5. Malaria
47
What are the 2 forms of Type III Hypersensitivity?
1. Localized 2. Generalized
48
Localized Type III Hypersensitivity
Ag-Ab complexes deposited in tissues - ANTIBODY EXCESS Ex: Arthus rxn
49
Generalized Type III Hypersensitivity
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
What conditions lead to Arthus reaction?
- 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
Blue eye is an example of
Type III Hypersensitivity
52
How does blue eye occur?
In dogs following adenovirus infection or vaccination of live vaccine against adenovirus Causes edema and opacity of cornea
53
What is serum sickness?
A disease that happens after IV admin of large amounts of ANTIGEN Reacts by making Ab against serum Causes GLOMERULONEPHRITIS
54
Type I Serum Sickness
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
Type II Serum sickness
proliferation of vascular endothelium and mesangial cells
56
Type III serum sickness
Deposition of Ag-Ab complexes on both sides of glomerular BM results in kidney failure
57
IgA nephropathy
Deposition of Ag-Ab complexes in the kidneys in dogs 4-7 yrs old causes renal failure
58
Purpura hemorrhagica
in horses after streptococcus equi infection causes edema, hemorrhage on limbs and mucosa A TYPE III Hypersensitivity
59
Type IV Hypersensitivity is mediated by?
T-cells
60
How long does it take for Type IV Hypersensitivity to occur?
72 hours
61
What is the difference between Type I-III hypersensitivity vs Type IV?
Type I-III mediated by Ab-Ag complexes Type IV mediated by T cells
62
The tuberculin reaction is an example of _______
Type IV hypersensitivity

Sem 2: Immuno (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions