Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Foundations > Immunology II > Flashcards

Immunology II Flashcards

1
Q

Define: hypersensitivity rxn

A
  • Exaggerated, inappropriate immunologic rxn that is harmful to the host
  • Subsequent exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define: sensitivity

A

1st exposure to antigen w/ immune response (antibody)

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

Type I action

A
  • 1st exposure to antigen –> IgE formation
  • IgE binds to mast cells & basophils
  • Subsequent exposure – > antigen binds to IgE
  • Degranulation of mast cells
  • Release of mediators (histamine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type I result

A
  • Increased vascular permeability
  • Edema
  • SM contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type I timing

A

Minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type I manifestations

A
  • Edema
  • Erythema
  • Itching
  • Urticaria
  • Eczema
  • Rhinitis
  • Conjunctivitis
  • Asthma
  • Systemic anaphylaxis
  • Food/drug allergies
  • Hay fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Allergic response

A
  • During sensitization, APC presents allergen presents to Th2 cell, which helps B cell become a plasma cell.
  • Plasma cells produce IgE, which binds to mast cells.
  • When allergen returns, mast cells release histamine
  • Th2 cells release chemicals that attract inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Allergic response results in what?

A

Allergy sx

  • Sneezing
  • Mucus, runny nose
  • Swelling
  • Itching
  • Coughing, wheezing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the effect of histamine?

A
  • Vasodilation
  • Increased capillary permeability
  • SM contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the emergency concern of anaphylaxis?

A
  • Airway
  • Hypotension
  • Shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the emergency tx for anaphylaxis?

A
  • Epinephrine
  • Antihistamine
  • Steroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Anaphylaxis prevention

A
  • Antihistamine
  • H2 blocker
  • Avoid allergen
  • Immunosuppression therapy w/ allergy shots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the rationale of desensitization?

A

Tiny amount of antigen over long period of time to blunt rxn

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

What infections may exacerbate asthma?

A
  • Flu

- PNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common food allergies (90%)

A
  • Milk
  • Egg
  • Fish (bass, flounder, cod)
  • Shellfish (crab, lobster, shrimp)
  • Tree nuts (almonds, pecans, walnuts)
  • Wheat
  • Peanuts
  • Soybeans

*Also consider fruits, preservatives, dyes.

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

Type I hypersensitivity common presentation

A
  • Facial edema
  • Systemic histamine release in anaphylaxis:
    ˚ Hypotension
    ˚ Nausea
    ˚ Hives
    ˚ Swollen hands/feet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Type II (cytotoxic) hypersensitivity rxn

A
  • Antibody mediated cytotoxic rxn

- Antigens on cells or in ECM (endogenous or exogenously absorbed)

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

Type II action

A

Antigens on cell surface combine w/ IgG antibodies –> complement-mediated lysis of cells

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

Type II time of onset

A

Hours to days

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

Type II manifestations

A
  • Hemolytic anemia
  • Neutropenia
  • Thrombocytopenia
  • ABO transfusion rxns
  • Rh incompatibility (erythroblastosis fetalis, hemolytic disease of the newborn)
  • Rheumatic fever
  • Goodpasture’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hemolytic anemia (Type II)

A
  • Antibody attaches to antigen on RBC
  • Complement mediated lysis via MAC
  • Complement attracts phagocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Type III (Immune complex) hypersensitivity

A
  • Antigen–antibody immune complexes are deposited in tissues –> inflammatory response
  • Complement is activated & PMN cells are attracted to the site –> release of lysosomal enzymes –> tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Type III time of onset

A

2-3 wks

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

Type III manifestations

A
  • SLE
  • RA
  • Poststreptococcal glomerulonephritis
  • IgA nephropathy
  • Serum sickness
  • Hypersensitivity pneumonitis (farmer’s lung)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
SLE (Type III)
- Antibodies formed to DNA & nucleus - Antibodies form immune complexes that activate complement --> production of C5a --> attracts neutrophils --> release enzymes --> damage tissue
26
RA (Type III)
- Serum & synovial fluid contain “rheumatoid factor” (IgM & IgG antibodies that bind to the Fc fragment IgG) - Deposits of immune complexes (containing the normal IgG & Rh) on synovial membranes & in blood vessels - Activate complement & attract PMN cells --> inflammation. - Pts have high titers of Rh & low titers of complement in serum (esp. during periods when disease is most active) 
27
Type IV: Delayed (Cell-mediated) hypersensitivity
- T lymphocytes, activated/sensitized by an antigen, release lymphokines upon 2nd contact w/ same antigen - Lymphokines induce inflammation & activate macrophages --> release of inflammatory mediators.
28
Type IV time of onset
2-3 days
29
Type IV manifestations
- Contact dermatitis - Poison oak/ivy - TB skin test rxn - Drug rash - Stevens-Johnson syndrome - Toxic epidermal necrolysis - Erythema multiforme
30
Type IV continued
- Macrophage ingests antigen, processes it, & presents an epitope on its surface in association w/ class II MHC - Helper T (Th-1) cell is activated & produces gamma interferon --> activates macrophages * These 2 cells mediate delayed hypersensitivity
31
Hereditary angioedema
- Congenital immunodeficiency (deficiency of C1 protease inhibitor, autosomal dominant) - Excess C3a, C4a, C5a
32
Hereditary angioedema result
Capillary permeability & edema
33
Hereditary angioedema dx
- Family hx - Lack of pruritis & urticarial lesions - Recurrent abdominal colic &/or laryngeal edema - Labs: decreased C1 inhibitor levels (or decreased fxn, or mutation in C1 inhibitor gene altering synthesis/fxn)
34
Fxn of immune system
Provide a protective response against infective organisms & foreign cells, while avoiding damage to self
35
Markers of self
- Distinctive surface proteins that identify “self” - Able to coexist w/ immune system - Unique markers on human cells are the MHC proteins (type I = all cells, type II = specialized cells)
36
Markers of non-self
- Non-self substance (antigen) can trigger the immune system - Epitope: area on the antigen that triggers a response - Ex: transplanted tissues are recognized as foreign & attract antibodies
37
Self-antigens
Mechanisms for avoiding damage to self - Sequestration - Tolerance of relevant T or B cells - Regulatory cells
38
What is an autoimmune disease?
A trigger interferes w/ normal mechanisms protecting antigens against immune response --> tissue injury
39
Types of autoimmune triggers
- Exogenous - Endogenous - Molecular mimicry (pathogen derived antigen)
40
Autoimmunity criteria
- Autoantibodies - Self-reactive T lymphocytes - Imbalance btwn T & B cell & regulatory factors
41
Etiologies of autoimmune disease
- Genetic susceptibility - Environmental immune stimulants - Infectious agents - Loss of T regulatory cells - Decreased clearance of apoptotic material - Antibodies that react w/ apoptotic material
42
Graves disease - Environmental & genetic factors
- Stress - Smoking (minor risk, but major risk for opthalmopathy) - Sudden increased iodine intake - Post-partum
43
Graves disease
- Autoantibody stimulation of TSH receptor (TSI) | - Thyroid associated ophthalmopathy (T cells activate cytokine infiltration)
44
Rheumatic fever
- Autoimmune rxn to infection w/ group A streptococcus | - Molecular mimicry
45
Rheumatic fever susceptibility
- Inherited - Human leukocyte antigen class II alleles – some associated w/ susceptibility & some are protective - Cardiac valve damage = rheumatic heart disease
46
Myasthenia Gravis
- Autoantibody blocking/inactivation of alpha-chain of nicotinic acetylcholine receptor at neuromuscular junctions
47
Abnormalities of the thymus (Myasthenia Gravis)
- Hyperplastic - Tumors - Muscle-like cells within thymus (have AChRs on surface - may be source of auto antigen triggering)
48
Myasthenia Gravis antibodies
Anti-AChR - Increases receptor turnover - Damage to postsynaptic muscle membrane by antibody & complement - Blockage of AChR active site that normally binds Ach
49
SLE
- Type III - Immune complex formation targeting DNA - Genetic susceptibility & environmental factors --> abnormal immune response - Immune cell activation --> sustained autoantibody & immune complex production, activation of complement, release of chemical mediators
50
SLE antibodies
Anti-dsDNA, anti-Smith
51
SLE chronic inflammation
Leads to irreversible tissue damage
52
Type I DM genetic susceptibility
Genes that code for MHC class II molecules
53
Type I DM environmental factors
- Perinatal - Viruses - Dietary
54
Type I DM autoantibodies
- Insulin | - Islet cell
55
Type I DM destruction of pancreatic cells
Caused by T cell cytokine production and cytotoxicity
56
Rheumatoid arthritis
- Type III - Genetic factors - Pro-inflammatory cytokines
57
RA environmental factors
- Tobacco smoke exposure | - Exposure to silicone dust & mineral oil
58
RA autoantibodies
- Rheumatoid factor | - Anti-CCP antibodies
59
Multiple sclerosis
- Genetic susceptibility | - Pro-inflammatory autoimmune response --> destruction of CNS myelin (both T & B cell involvement)
60
Immunizations
Exploit adaptive immune response - Uninfected individuals given controlled infection or exposed to antigen that elicits an immune response - When exposed to pathogen in environment, memory T & B cells mount immune response before pathogen can spread
61
Passive immunity
Antibody transferred from immune individual to nonimmune individual
62
Advantage & disadvantage of passive immunity
- Advantage: immediate availability | - Disadvantage: short duration (months)
63
Active immunity
- Artificial antigens administered to elicit controlled immune response - Mediators: Antibody and T cells
64
Active immunity: Advantage & disadvantage
- Advantage: long duration | - Disadvantage: Slow onset
65
Live attenuated vaccines
- Weakened form of virus - Antigens stimulate immune response - Must be refrigerated - Possible to become virulent again if mutates in host (rare) - Not for immune compromised or pregnancy
66
Examples of live attenuated vaccines
``` Measles Mumps Rubella Varicella Rotavirus Influenza ```
67
Inactivated vaccines
- Pathogens killed – isolates antigenic material - Freeze-dried, don’t require refrigeration - Induce weaker immune response - Need multiple doses to sustain immunity
68
Examples of inactivated vaccines
Poliovirus Hep A Japanese encephalitis
69
Subunit vaccine
- Use component of the pathogen as vaccine antigen to mimic exposure - Weaker immune response than live attenuated
70
Recombinant subunit vaccine
Antigens manufactured via recombinant DNA technology
71
Polysaccharide subunit vaccine
Utilize polysaccharide antigens
72
Surface protein subunit
Utilize purified proteins from the pathogen
73
Toxoids
Inactivated or killed toxins used to elicit immune response --> antibodies that can neutralize toxins (Diphtheria)
74
Conjugate subunit vaccine
- Technology binds polysaccharide from bacterial capsule to a carrier protein - This antigen combo induces long-term protection
75
Conjugate subunit vaccine examples
Hib, Pneumococcal (PCV), meningococcal

Foundations (9 decks)

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