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ImmunoMicro 2 > Stiner > Flashcards

Stiner Flashcards

1
Q

T1H (Type 1 Hypersensitivity) referred to as

A

allergy, atopy, or immediate hypersens.

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2
Q

How long after RE-exposure does T1H occur

A

minutes

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3
Q

Ex of T1H

A

hives, hay fever, food allergies, bronchial asthma, anaphylaxis

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4
Q

T1H sequence of events

A

1) Initial exposure to antigen causes IgE antibody production
2) IgE binds to Fc receptor on mast cell
3) Reexposure causes cross linking of bound IgE
4) Release of mast cell mediators
5) Immediate response-vasodilation and permeability, smooth m contraction
6) Late response-inflam

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5
Q

What mediates immediate response to mast cell degranulation?

A 
Vasoactive amines (serotonin and histamine)
Lipid mediators (prostaglandins and leukotrienes)
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6
Q

Prostaglandins

A
  • Vasoconstriction in lungs
  • Vasodilation in smooth m
  • constriction or dilation of bronchioles
  • aggregation or disaggregation of platelets
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7
Q

Leukotrienes

A
  • Bronchoconstriction
  • increased vascular permeability
  • increased mucus
  • referred to as slow reacting substance of anaphylaxis (SRS-A)
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8
Q

What mediates late response to mast cell degranulation?

A
  • Cytokines and chemokines

- Infiltration of eosinophils, monocytes, and neutrophils (release ROS)

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9
Q

How is asthma treated?

A
  • Inhaled corticosteroids
  • Leukotriene modifiers
  • Inhaled long acting beta2 agonists
  • Cromolyn
  • Theophylline
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10
Q

Most severe form of immediate hypersens.

A

anaphylaxis

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11
Q

What is anaphylaxis? Symptoms? Treatment?

A
  • Response driven by systemic release of vasoactive amines and lipid mediators from mast cells
  • Causes life threatening drop in BP and severe bronchoconstriction
  • Treated w/ epinehprine and antihistamine
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12
Q

What happens with T2H

A
  • Ab bind to foreign or self Ag
  • Primarily IgG or IgM
  • Activate complement cascade–>MAC
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13
Q

T2H diseases

A 
Hemolytic disease of Newborn
Hemolytic anemia
Blood transfusion rxns
Graves disease
Myasthenia gravis
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14
Q

Hemolytic disease of newborn and treatment

A

1st child has Rh
Mother makes anti-Rh antibody
2nd child has Rh and its RBCs are attacked
*Treated w/ rhogam

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15
Q

Hemolytic anemia and treatment

A

Auto antibodies produced against self Ag on RBC. Destruction of RBC–>anemia
*Prednisone or blood trans

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16
Q

Graves disease and treatment

A

TSH receptor stimulated by Ab. Overproduction of thyroid hormone
*radioactive iodine, anti-thyroid drugs, thyroid removal

17
Q

Myasthenia gravis and treatment

A

ACh receptor blocked by Ab

*cholinesterase inhibitors and corticosteroids

18
Q

What happens with T3H

A

Ab and Ag bind forming immune complexes that deposit in blood vessels or tissues causing inflam.
Can be caused by exogenous or endogenous Ag

19
Q

How do small immune complexes affect WBCs?

A

Ligate Fc receptors, causing activation and tissue damage

20
Q

Examples of T3H

A

SLE, Arthus rxn, serum sickness, lupus nephritis, rheumatoid arthritis

21
Q

How long after exposure does T3H occur?

A

3-10 hrs

22
Q

What mechanisms do immune complexes use to trigger inflam?

A

1)Mast cell activation
2)Macrophages release TNF-alpha and IL-1 (induce inflam. cascase
C3a,4a,5a-stim mast cells to release more vasoactive amines, and chemotatic factors.
Fc receptors for IgG may be crucial for antibody complex mediated hypersens.

23
Q

Arthus rxn mechanism and cause

A
  • Triggered in skin by IgG and immune complexes form
  • Complexes bind Fc receptors on mast cells and leukocytes
    • Local inflam rxn w/ vascular perm.
    • C5a activates leukocytes
  • Occurs in vessel walls, pleura, pericardium, synovium, or glomeruli
  • Repeated subQ injections of tetanus or diptheria vaccines
  • If high levels of IgG immune complex and subsequent exposure of that Ag occurs
24
Q

Arthus reaction symptoms and treatment

A
  • Swelling, induration, pain, edema, hemorrhage, necrosis

- Anti-inflamm agents

25
Q

Serum sickness mechanism and cause

A
  • Caused by foreign protein injection that leads to antibody response
    • Antivenin
    • Anti-lymphocyte globulin
    • antibiotics
    • Streptokinase
  • Immune complexes form, deposit in vessels, and activate complement and phagocytes
  • Although this is T3H, symptoms occur days or weeks after injection of serum
26
Q

serum sickness symptoms and treament

A
  • Chills, fever, rash, nephritis, lymphadenopathy, and arthritis
    • Rash from mast cell degran due to ligation of FcRy
  • Self limiting due to secondary Ab response
  • Antihistamines, corticosteroids
27
Q

SLE

A
  • IgG Ab against self Ag in all nucleated cells
  • Complexes deposit in blood vessels, kidney, joints and other tissues
  • Phagocytes activated by Fc receptors
  • Autoreactive T cells produce more Ab and destroy tissues
  • NSAIDs, corticosteroids, immunosuppressive agents
28
Q

Immune complexes directed against DNA and histones are deposited in ________

A

skin, joints, kidney, and choroid plexus

29
Q

What happens with T4H?

A

Ag specific T cells induce macrophage infiltration in sensitized individual
Activated CD8 T cells destroy target cells
Generally activated by haptens
AKA DTH

30
Q

How long after exposure does T4H occur

A

2-3 days

31
Q

DTH ex

A 
Tuberculin (TH1)
Contact dermatitis (TH1 or CTLs)
Chronic asthma (TH2)
Gluten sens (TH1 and TH2)
Graft rejection (TH2)
32
Q

TB test and therapy

A

Tuberculin injected
TH1 mediated response if individuals have been exposed in past
*self limiting

33
Q

Contact dermatitis

A
  • Haptens complexed w/ skin become internalized (think poison ivy)
  • Elicited by CD4 or CD8
  • Two phases: sensitization and elicitation
  • corticosteroids, antihistamines
34
Q

Sensitization

A 
First exposure to antigen
10-14 days to develop
Langerhans cells in skin
APC present Ag to T cell
CD4 Memory cells form
35
Q

Elicitation

A 
Reexposure
24-48 hrs
LC Ag presentation to memory T cells at site of Ag entry
T cells release IFN gamma and cytokines
Leads to inflam and recruitment
36
Q

Chronic asthma

A

DTH
Mast cell degranulation leads to TH2 and eosinophil influx
Eosinophils degranulate->damage tissue and recruit
Chronic inflammation can cause irreversible damage and death
*corticosteroids, bronchodilators, cromolyn

37
Q

Crohn’s disease

A

Thought to be due to unresolved DTH
Initial presentation may be in oral cavity
Chronic inflam of bowel mucosa
*corticosteroids, immunosppresants

ImmunoMicro 2 (7 decks)

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