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Block 3 Found Sci > 2-Hypersensitivity Reactions > Flashcards

2-Hypersensitivity Reactions Flashcards

1
Q

hypersensitivity reaction

definiton

A

host response to antigen that dev into deleterious effects like tissue damage and death

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2
Q

types

A

I = allergy, anaphylaxis
II = antibody mediated cytotoxicity
III = immune complex disease
IV = delayed type hypersensitivity, only one not cell mediated

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3
Q

type I

general

A

rapidly progressing immune rxn thru antigen bindning IgE coated basophils or mast cells

‘immediate hypersensitivity’

i.e. respiratory allergies, allergic asthma, hives, food, anaphylaxis

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4
Q

allergens

A

anaphylaxis induced by insect venom, penicillin, seafood, nuts

allergens go directly into blood stream or rapidly absorbed from gut so systemic mast cell activation

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5
Q

acute urticaria

A

aka wheal and flare

allergy testing, insect bites, animal hair

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6
Q

seasonal rhinoconjuctivitis

A

pollen (ragweed, grass, tree)

dust mite feces

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7
Q

asthma

A

dander, pollen, dust mite feces

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8
Q

food allergy

A

fish, shellfish, peanuts, tree nuts, milk, soy, eggs, wheat

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9
Q

atopy

A

inc tendency to dev allergies

atopic indivs make IgE to allergens instead of parasites so physiologic resp to parasites usually in skin, airways, gut same as allergic

Th2 resp so no inflamm

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10
Q

hygiene hypothesis

A

dec exposure to pathogens early in life > TH2 immunity and IgE instead of TH1 so allergy/asthma inc in developed countries

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11
Q

respiratory allergens

A

small moles carried on larger particles like pollen grains or mite feces
-soluble allergen elutes/diffuses into mucosa at very small doses
-transmucosal delivery in very low doses so effective elicit TH2 IgE resp

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12
Q

basophils

characteristics

A

part of peripheral blood WBC
-purple staining, granules present
-non phagocytic
-related to mast cells so prominent in allergies/anaphylaxis

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13
Q

dev of anaphylaxis

A
  1. first exposure = IgE antibodies made
  2. IgE binds Fc receptors on basophils and mast cells
  3. subsequent exposure to allergen binds surface bound IgE and release granule contents, memory resp
  4. granules have vasoactive compounds so edema and SM contraction, 2-30 min after exposure
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14
Q

mast cell granule contents

A
  1. histamine - bronchial SM contract + inc vascular permeability
  2. proteases- act matrix metalloproteinases to cleave tissue matric proteins = damage
  3. TNF alpha - promote inflamm
  4. eosinophils- acc of esoins locally or in blood will counteract effects of histamine
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15
Q

leukotrienes

A

LTC/D/E4
-most potent substance cause SM contraction and inc vascular permeability
-released more slowly and longer effect than histamine

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16
Q

eosinophils

A

acc in nasal and bronchial mucosa in resp allergies and in intestinal mucosa during worm infections

attach to worms and release granules with hydrolytic enzs

17
Q

late phase response

A

6-8 hours after immediate rxn thru secretion of prostaglandins, leukotrienes, chemokines, cytokines

-2nd phase of SM contraction
-sustained edema
-recruit eosins and TH2 cells
-remodel tissue i.e. SM hypertrophy and hyperplasia

18
Q

treatments for type I

A
  1. epinephrine- only one that reverses anaphylaxis, binds beta adrenergic receptors
  2. antihistamines-bind hista receptors
  3. cromolyn sodium- block degranulation
  4. theophylline- block degranulation
  5. repeated subq allergen infections so IgE dec and IgG inc
  6. humanized mouse anti-IgE antibody- binds IgE to prevent binding to receptors

beta = Gs so inc cAMP and relax SM, tighten juctions, stim heart

19
Q

type I general

A

antibody mediated cytotoxicity uses IgM, IgG antibodies vs cell surface or ECM antigens
-opsonize and phagocytosis of cells, complement and Fc receptor mediated inflamm, act leukocytes

20
Q

hemolytic disease of newborn

A

Mo makes IgG to Rh antigen expressed by RBCs of child
-assume Mo Rh neg and baby Rh pos
1. first Rh pos child stims immune resp but not affected
2. later Rh pos child - Mo IgG will cross placenta and destroy RBCs in spleen and liver of child = mild symptoms or still birth

use anti-Rh antibodies to prevent sensitization

21
Q

non-cytotoxic reactions

A
  1. graves disease- antibodies to TSH receptor = overprod of thyroid hormones > hyperthyroidism
  2. myasthenia gravis - antibodies to Ach receptor blocks nerve impulse transmission
22
Q

type III general

A

immune complex disease induced by
1. autoimmune diseaes like lupus, SLE
2. serum sickness
3. drug rxns - penicillin
4. infectious disease- subacute endocarditis, chronic viral hepatits, poststrep nephritis
5. inhaled allergens- mold spores, hay dust

system is overwhelmed

23
Q

pathogenesis

A

antibody + antigen = immune complex
-antigen must persist for long periods time for disease to dev
-medium size immune complexes cause problems bc lodge in tissue and act complement > C5a > neutrophil acc
-lysosomal enz damage tissue = fever, urticaria, arthritis, lymph node enlarge, proteinuria

24
Q

serum sickness

A

prototype immune complex disease
-as conseq of repeat injection of foreign serum
1. horse anti-tetanus
2. horse antirabies
3. antiserum to snake venoms
4. antilymphocyte globulin

25
Q

type IV general

A

delayed type hypersensitivity DTH
-24-72 hrs after exposure
-cell mediated immune resp so TH1 + memory resp so requires prior sensitization

i.e. tuberculin rxn, contact dermatitis, delayed graft rejection

26
Q

contact dermatitis

A

skin expo to nickel, chromium, cosmetics, hair dye, poison oak/ivy
-small moles complexed with skin proteins presented on APC to T helpers so CD4/CD8 secrete inflamm cytokines like IFN gamma

-poison ivy/pentadecacatechol is lipid soluble so modifies intracell proteins and xpr on class I MHC for CTLs

27
Q

tuberculin skin rxn

mechanism

A

PPD injected intradermally so vascular endo or macros present antigen to memory T cells
-endo cells upreg xpr of VCAM-1 to bind memory helper VLA-4 and T cells migrate into skin
-small portion of migrating T cells specific for PPD so interact with antigen xpr macros
-secrete IFN-gamma to inc macros for better presentation
-more T cells act > more IFN gamma > amplifiy rxn
-tissue damage - redness and pos PPD test

if neg PPD then antigen dose too small to stim primary immune resp

28
Q

granuloma formation

A

if antigen not eradicated then DTH > granuloma to wall off
-macros ingest org and surrounded by other macros
-CD4 lymphs surround macros to maintain macro activation and structural integrity
-AIDS pts lose CD4 so lead to systemic infect

Block 3 Found Sci (60 decks)

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