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Exam 1 immuno > Hyper sensitivities > Flashcards

Hyper sensitivities Flashcards

1
Q

what are Hypersensitivity reactions

A

Immune responses that cause tissue injury

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2
Q

Hypersensitivity reactions arise from?

A

uncontrolled or Abnormal responses to foreign Ags

or Autoimmune responses against self Ags

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3
Q

General characteristics of: Type 1 hypersensitivity

A

mediated by IgE and results from actions of mediators secreted by mast cells

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4
Q

General characteristics of: Type II hypersensitivity

A

Mediated by Abs that bind tissue Ags and cause complement dependent tissue injury

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5
Q

General characteristics of: Type III hypersensitivity

A

Circulating Ag-Ab complexes that deposit in vessels and cause complement-dependent injury in the vessel wall (vasculitis)

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6
Q

General characteristics of: Type IV hypersensitivity

A

Mediated by T cells and results form inflammation caused by cytokines produced by CD4 Th1 and Th17 cells, macrophages, or killing of host cells via CD8 CTLs

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7
Q

What triggers Type 1 Hypersensitivity

A

Enviromental Ags whitch activate mast cells in an IgE manner

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8
Q

Atopy

A

genetic tendency to develop allergic diseases and are said to be atopic

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9
Q

Mediators of Type 1 Hypersensitivity

A

Mast cell: responsible for the acute reactions and inflammation

Histamine: dilation of small vessels and increase permeabillity

Proteases: local tissue damage

Prostaglandins: vascular dilation

Leuokotrienes: stimulate smooth muscle contraction

Cytokines: induce local inflammation (late phase reaction)

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10
Q

Initial Allergen encounter

A

Th2 cells and IL-4 create adaptive immune response by B cells that mature into plasma cells to make IgE to allergen

IgE bind to FcRe (CD23) on mast cells

Patient is now sensitized

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11
Q

Subsequent Allergen Encounter

A

Allergen cross-liking binds IgE on Mast Cells and cause degranulation of all type 1 mediators

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12
Q

Immediate Phase Type I Hypersensitivity

A

vascular and smooth muscle reactions within minutes

Vasodilation, congestion, and Edema

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13
Q

Late Phase Reaction Type I Hypersensitivity

A

2-24 hours later

inflammatory infiltrate rich in eosinophils, neutrophils, and T cells

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14
Q

Asthma

A

Airway obstruction via release of inflammatory mediators via the allergen

increased capillary permeabillity and spasmodic contraction of smooth muscle around bronchi

decrease size of bronchial lumen and shortness of breath

can happen via cold and exercise

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15
Q

Anaphylaxis

A

ecposure to food allergen cause massive release of Vasoactive Amines and cytokines

contraction of smooth muscle and Vasodilation of capillary endothelium

Blood pressure drops that results in vascular shock

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16
Q

Allergen testing

A

Type 1 Hypersensitivity and is performed on Arm or back if babies

injected in Dermis and wait 30 minutes to see the results

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17
Q

Allergen Specific Immunotherapy (SIT)

A

single curative approach by administration of increasing doses of Allergen

  • Induce peripheral T cell tolerance
  • Increase thresholds of mast cell and basophil activation
  • Decrease IgE mediated Histamine release (increased IgG and IgG)

Generation of induced regulatory Treg cells is the key mechanism

fix the Th1/Th2 ratio

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18
Q

Activation of Type II Hypersensitivities

A

via IgG and IgM activates Complement resulting in production of C3a and C5a to induce inflammation and recruiting

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19
Q

What are the 2 mechanisms of Type II Hypersensitivity

A

Complement mediated Cytotoxicity

Ab-dependent Cellular Cytotoxicity (CDCC)

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20
Q

Graves Disease Type II hypersensitivity

A

Ab stimulates the activity of the thyroid stimulating hormone receptors causing Hyperthyroidism

21
Q

Myasthenia Gravis: Type II hypersensitivity

A

Abs may inhibit binding of Acetylcholine neurotransmitter to ACh receptor

22
Q

ABO blood Transfusion Reaction

A

Type II hypersensitivity

have Antigen A means you produce Antibody B

23
Q

Hemolytic disease of Newborn: Type II hypersensitivity

A

if Mother is Rh- and kid is Rh + then the Antibodies of Mom will attack the fetus in the subsequent pregnancy

24
Q

Drug Induced Hemolytic Anemia Type II hypersensitivity: Hapten Model

A

Penicillin

Drug binds directly to the erythrocyte surface and induces an anti-drug antibody

25
Q

Drug Induced Hemolytic Anemia Type II hypersensitivity: Immune complex formation

A

quinidine

Autoantibodies from immune complexes with the drug

erythrocytes bind Immune complexes through CR1 and cause killing of the erythrocyte by complement

26
Q

Drug Induced Hemolytic Anemia Type II hypersensitivity: Auto immune model

A

Methyldopa-induced anemias

drug induces an antidrug antibody that cross reacts with an Rh antigen

27
Q

Type II Hypersensitivity Diseases: Autoimmune Hemolytic anemia

A

Opsonization and phagocytosis of erythrocytes due to Rh blood group

28
Q

Type II Hypersensitivity Diseases: Autoimmune idiopathic thrombocytopenic purpura

A

Platelet membrane proteins that cause opsonization and phagocytosis of platelets

29
Q

Type II Hypersensitivity Diseases: Goodpastures syndrome

A

non-collagenous protein in basement membranes of kidney glomeruli and lung alveoli cause complement activation and Fc receptor mediated inflammation

30
Q

Type II Hypersensitivity Diseases: Pemphigus Vulgaris

A

proteins in intercellular junctions of epidermal cells cause antibody mediated activation of proteases

31
Q

Type II Hypersensitivity Diseases: Rheumatic fever

A

Steptococcal cell wall antigen creates and antibody cross reaction with mycardial tissue.

32
Q

Major mechanism of triggering tissue damage in Hypersensitivity III

A

Ab-Ag complexes formed in the Blood in circulation deposit and recruit CP of complement and recruitment of leukocytes

33
Q

Type III Hypersensitivity Diseases: SLE

A

antibody binds on DNA, nucleo proteins and others and causes nephritis, vasculitis, and arthiritis

34
Q

Type III Hypersensitivity Diseases: Polyarteritis nodosa

A

antibody binds microbial antigens causes vasculitis

35
Q

Type III Hypersensitivity Diseases: Post-streptococcal glomerulonephritis

A

antibody binds on Streptococcal cell wall antigens and causes nephritis

36
Q

Type III Hypersensitivity Diseases: Serum sickness

A

systematic reaction and usually involves a toxin

37
Q

Type III Hypersensitivity Diseases: Arthus Reaction

A

involves a subcutaneous administration of a protein Ag to a previously immunized animal and is a local vasculitis usually at site of injection

38
Q

Major Triggers of Type IV Hypersensitivity

A

Autoimmunity, exaggerated response to environmental Ags or microbial Ags (TB)

39
Q

Delayed Hyper Hypersensitivity (DTH)

A

Type IV Hypersensitivity, mediated by T cells

40
Q

Type IV Hypersensitivity inflammation caused by:

A

Th1 and Th17 secret the cytokines that recruit the macrophage and neutrophils

41
Q

Type IV Hypersensitivity injury caused by:

A

Macrophages, neutrophils, and the lysosomal enzymes, reactive oxygen species, nitric oxide and pro-inflammatory cytokines

42
Q

Type IV Hypersensitivity diseases: Multiple Sclerosis

A

Attacking of the Mylein proteins

43
Q

Type IV Hypersensitivity diseases: Rheumatoid arthritis

A

Attacking of the antigens in the joints

44
Q

Type IV Hypersensitivity diseases: Type 1 diabetes

A

attacking of the Pancreatic islet antigens

45
Q

Type IV Hypersensitivity diseases: Crohns disease

A

Attacking of the intestine microflora which have an autoimmune component

46
Q

Type IV Hypersensitivity diseases: Contact sensitivity

A

DTH reaction on skin can be from metals or poison Ivy

47
Q

Type IV Hypersensitivity diseases: Chronic infections

A

Microbial proteins including TB

48
Q

Common metals to respond with Allergic Contact dermatitis

A

costume jewlery increases sensitization to nickel and cobalt

and leather sensitization of chromium

Exam 1 immuno (6 decks)

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