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Patho > Immunity > Flashcards

Immunity Flashcards

1
Q

Differences in T and B cell immunity

A

B- B cells fright of bacteria and create antibodies

T cells fight off bacteria, Protozoa, fungal infections

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2
Q

What are the first lines of defense in innate immunity?

A
  1. Skin
  2. Mucous membranes & secretions
  3. Normal flora
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3
Q

What are 2nd line natural immunity?

A
  1. Innate immune cells
  2. Inflammation
  3. Compliment system
  4. Antimicrobial substances
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4
Q

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

A

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

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5
Q

What are the differences between primary and secondary immunodeficiency states?

A

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

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

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6
Q

What are some examples of secondary immunodeficiency?

A

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

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7
Q

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

A

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

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8
Q

How do B cells normal help neutralize infection?

A
  1. Stimulate macrophage for phagocytosis

2. Make specific antibodies

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9
Q

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

A

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

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

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10
Q

Why are Cell mediated T cell immunodeficiencies the most severe?

A

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

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11
Q

What is an example of severe combined immunodefiency?

A

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

“Boy in the bubble”

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12
Q

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

A

Decreased or absent chemotaxis
Impaired opsonization
Decreased phagocytosis of invasive pathogens

  • more susceptible to infectious diseases
  • leading cause of autoimmune disease
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13
Q

What deficiencies can lead to disorders of phagocytosis?

A
  1. Dec. Leukocyte adhesion
  2. Microbial production and activity
  3. Cellular degranulation
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14
Q

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

A
  • bacterial and fungal infections including candid

- lung disorders

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15
Q

What is immunological mechanism behind allergic response?

A

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
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16
Q

What is the main chemical mediator in type 1 reaction?

A

Histamine.

17
Q

What is the difference between anaphylactic and atopic reactions

A

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
Q

What is Patho of type one res once?

A

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
Q

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

A

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

20
Q

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

A 
-antibiotic allergies
Food allergies
Hay fever
Urticaria (hives)
Allergic conjunctivitis
21
Q

What are symptoms of anaphylaxis?

A

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
Q

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

A
  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
Q

What are clinical manifestations of a type 2 hypersensitivity reaction?

A

If platlets: Heparin induce thrombocytopenia

RBCs: hemolytic anemia, penicillin-induced drug run

Muscle: myasthenia Travis

Thyroid: Graves’ disease

24
Q

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

A

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
Q

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

A
  1. Alterations in blood flow
  2. Increased vascular permeability
  3. Destructive action of inflammatory cells
26
Q

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

A

Vasculitis
Organ damage

Ex: glomerulonephritis
Serum sickness
Local immune complex diseases
Systemic lupus
Reactive arthritis
27
Q

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

A

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
Q

How long does type 4 hypersensitivity take?

A

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

29
Q

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

A

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
Q

Summary of 4 types

A
  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
Q

What are the 3 types of transplant rejection?

A

-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
Q

Explain graft vs host disease

A

Donor T cells on the graft attack recipients tissues

-presents with diarrhea, rash and jaundice

33
Q

How do automminue disease lead to damage?

A

Body loses immunologic self tolerance

—> response against host tissues —> affects any cell type, tissue, or organ —> damage

34
Q

What is the difference between central and peripheral tolerance?

A

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
Q

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

A

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

36
Q

Explain superantigens that lead to failure of self tolerance

A

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
Q

What are mechanisms of autoimmune disease?

A

-Heredity
Susceptibility genes

-Failure of self-tolerance
Breakdown of T-Cell anergy
Release of sequestered antigens
Molecular mimicry 
Superantigens
38
Q

What are 3 criteria for determining an autoimmune disorder?

A
  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

Patho (2 decks)

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