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Flashcards in Immunity Deck (38):
1

Differences in T and B cell immunity

B- B cells fright of bacteria and create antibodies

T cells fight off bacteria, Protozoa, fungal infections

2

What are the first lines of defense in innate immunity?

1. Skin

2. Mucous membranes & secretions

3. Normal flora

3

What are 2nd line natural immunity?

1. Innate immune cells

2. Inflammation

3. Compliment system

4. Antimicrobial substances

4

What are 3rd Line of defense and considered Acquired immunity?

Specialized lymphocytes
B cells
T cells (helper T & Killer T)

5

What are the differences between primary and secondary immunodeficiency states?

Primary (congenital or inherited)—> defect present at birth

Secondary (acquired later in life in response to another diesease or entity/condition)

6

What are some examples of secondary immunodeficiency?

-malnutrition
Infections
Neoplasticism disease (lymphoma
Therapies that create high risk for infection (chemo, transplant rejection meds)

7

In humoral or B cell immunodeficiency, what is decreased and what is a patient at risk for?

Decreased Ig production

At risk for recurrent infections b/c lack of defense against bacterial invasion. (Viral response in unaffected)

B cells fight Bacteria and can be substituted with antiBiotics

8

How do B cells normal help neutralize infection?

1. Stimulate macrophage for phagocytosis

2. Make specific antibodies

9

What are the different functions of CD4+ T cells and CD8+ T cells?

CD4+helper T cells —> help immune system work more efficiently

CD8+ cytotoxic T cells —> focused on fugal, viral, intracellular infections —> “trouble fighting off viruses”

10

Why are Cell mediated T cell immunodeficiencies the most severe?

They impair the ability of the immune system to protect against viral, fungal, protozoan, and intracellular bacterial infections

11

What is an example of severe combined immunodefiency?

A person who has defects in both humoral and cell-mediated immune responses —> disruption in communication pathways —> severe deficiency

“Boy in the bubble”

12

What happens as a result of the loss of the compliment system?

Decreased or absent chemotaxis
Impaired opsonization
Decreased phagocytosis of invasive pathogens

*more susceptible to infectious diseases
*leading cause of autoimmune disease

13

What deficiencies can lead to disorders of phagocytosis?

1. Dec. Leukocyte adhesion

2. Microbial production and activity

3. Cellular degranulation

14

What is a person more suseptible to if they have disorders of phagocytosis?

-bacterial and fungal infections including candid

-lung disorders

15

What is immunological mechanism behind allergic response?

Hypersensitivity reaction (4 types)

1. IgE antibodies
2. Modification of cell surfaces
3. Accumulation of antibody-antigen complexes in different tissues
4. Entirely T cell mediated —> takes time

16

What is the main chemical mediator in type 1 reaction?

Histamine.

17

What is the difference between anaphylactic and atopic reactions

Anaphylactic- first causes vasodilation, smooth muscle contraction, bronchial dilation, and muscle spasms (5-30 min)—> intense inflammation, epithelial damage, mucosal edema, bronchi spasm (2-8hours)

Atopic- local, causes allergic rhinitis

18

What is Patho of type one res once?

Antigen/allergen —> IgE antibodies produced —> attach to mast cells and basophils —> release of mediators —> histamine —> inflammatory response —> edema and large amounts of mucus —> constriction of bronchioles

19

Why is 2nd exposure to allergen worse than 1st?

After sensitization —> IgE abs are already formed and stay in body, more quickly degranulate

20

What are some changes that occur in the body from type 1 hypersensitivity reactions?

-antibiotic allergies
Food allergies
Hay fever
Urticaria (hives)
Allergic conjunctivitis

21

What are symptoms of anaphylaxis?

*massive vasodilation*
Headache, sissy ness, parenthesis
Puritis, angioedem, erythema, urticaria
Hoarseness, coughing, narrow airway, wheezing, strider, resp. Arrest
Hypotension, dysrythmias, tachycardia, cardiac arrest
Cramping, n/v, diarrhea

22

Type 2 antibody mediated disorders/ cytotoxic hypersensitivity are mediated by IgG or IgM, what are different types?

1. Complement-activated cell destruction (phagocytosis or injury)—> Rh incompatibility

2. Antibody-mediated cell cytotoxicity (goodpasture disease)

3. Complement- and antibody-mediated inflammation (Graves’ disease, myasthenia Travis)

4. Antibody-dependent modulation of normal cell surface receptors

23

What are clinical manifestations of a type 2 hypersensitivity reaction?

If platlets: Heparin induce thrombocytopenia

RBCs: hemolytic anemia, penicillin-induced drug run

Muscle: myasthenia Travis

Thyroid: Graves’ disease

24

What is Patho behind type 3 immune complex-mediated disorders?

Formation of antigen–antibody complexes in the bloodstream that are deposited in the vascular epithelium or extravascular tissues. —> activate compliment system —> attraction of leukocytes —> massive inflammatory response —> vessel and tissue injury

25

What are 3 ways that type 3 rxns cause tissue damage?

1. Alterations in blood flow
2. Increased vascular permeability
3. Destructive action of inflammatory cells

26

What types of injury can occur from type 3 immune response?

Vasculitis
Organ damage

Ex: glomerulonephritis
Serum sickness
Local immune complex diseases
Systemic lupus
Reactive arthritis

27

What are differences in type 4 direct cell-mediated cytotoxicity and delayed type hypersensitivity?

Direct cell-mediated cytotoxicity (CD8+T cells)
Causes cell death and tissue injury in sensitized people
topically administered chemical antigens (contact dermatitis)
systemic antigen exposure
autoimmune process


Delayed-type hypersensitivity
Presensitized CD4+ T cells release cytokines – damaging cells

28

How long does type 4 hypersensitivity take?

Several days after exposure b/c T cell activation takes time

29

Type 1 and type 4 both target allergen molecules.. what is the difference?

Type 1 has IGE mediator, immediate
Type 4 is T cells, delayed reaction

Ex: latex allergy can be both type 1, IgE mediated from sensitization to latex protein, or
Type 4- delayed hypersensitivity to rubber additives causing contact dermatitis.

30

Summary of 4 types

1. Allergic response to allergen molecules with IgE
2. IgM and IgG respond to modified cell surfaces
3. IgG responds to antigen-antibody immune complexes
4. T cells respond to allergen molecules in a delayed reaction

31

What are the 3 types of transplant rejection?

-Hyperacute Reaction
Occurs almost immediately
Type II hypersensitivity response

-Acute Rejection
Occurs within weeks to months
May occur months or years after immunosuppression has been terminated
Type IV hypersensitivity response

-Chronic Rejection
Occurs month to years later
Manifests with dense intimal fibrosis of blood vessels of the transplanted organ
Type III & IV hypersensitivity reaction

32

Explain graft vs host disease

Donor T cells on the graft attack recipients tissues

-presents with diarrhea, rash and jaundice

33

How do automminue disease lead to damage?

Body loses immunologic self tolerance
—> response against host tissues —> affects any cell type, tissue, or organ —> damage

34

What is the difference between central and peripheral tolerance?

Central tolerance
-The elimination of self-reactive T cells and B cells in the central lymphoid organs (i.e., the thymus for T cells and the bone marrow for B cells)

Peripheral tolerance
-Derives from the deletion or inactivation of autoreactive T cells or B cells that escaped elimination in the central lymphoid organs (thymus)

35

Explain molecular mimicry as a failure of self tolerance leading to autoimmunity

Molecular mimicry: something happens so body thinks its foreign
-ex: heparin included thrombocytopenia
Body sees heparin complex of foreign —> kills platlets instead

36

Explain superantigens that lead to failure of self tolerance

Superantigens: tissue antigen
Ex: fat in liver —> body knows it shouldn’t be fatty —> gets attacked b/c body knows it isn’t right
-happens secondary to disease or disorder

37

What are mechanisms of autoimmune disease?

-Heredity
Susceptibility genes


-Failure of self-tolerance
Breakdown of T-Cell anergy
Release of sequestered antigens
Molecular mimicry
Superantigens

38

What are 3 criteria for determining an autoimmune disorder?

1. Evidence of an autoimmune reaction

2. Determination that the immunologic findings are not secondary to another condition

3. The lack of other identified causes for the disorder