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Pathophys > Alterations in Immune Response > Flashcards

Alterations in Immune Response Flashcards

1
Q

What are the four types of Hypersensitivity rxns?

A

IgE-Mediated Immediate
IgE Mediated Cytotoxic
Immune complex mediated
Cell-mediated

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2
Q

What are the two phases of Type 1 Immediate Hypersensitivity? What characterizes this phase?

A

Sensitization of mast cells and Degranulation of mast cell

Anaphylaxis

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3
Q

What occurs during the sensitization of mast cell hypersensitivity Type 1 phase?

A

antigen leading to IgE antibodies attaching to the mast cells; on next exposure, the antigen now binds to IgE AB
(IL-4 from CD4 cell stimulates B cell, which becomes plasma cell that secretes IgE = IgE binds to mast cell)

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4
Q

What occurs during the degranulation of the mast hypersensitivity type 1 phase? What are the two phases?

A

Initial response mediators- mast cells degranulate and preformed mediators like histamine are released; leads to vasodilation, inc permeability, smooth muscle contraction, and bronchial constriction
Late response- 2-8 hours later; same effects but last several days (prostaglandins, leukotrienes, cytokines)
NSAIDs block prostaglandin metabolism

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5
Q

What two cells are most important in Type 1 hypersensitivity rxns?

A

Type 2 helper T cells and mast cells

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6
Q

What is primary and secondary treatment for a Type 1 hypersensitivity rxn?

A

Primary: Epinephrine (beta 2 is bronchodilator and Alpha 1 is vasoconstrictor), stabilize airway, vascular access
Secondary: zantac, Benadryl, solumedrol
Discharge= prescribe epipen

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7
Q

What two ABs mediate Type 2 Hypersensitivity rxns? what happens during this type of hypersensitivity?
What are the three types

A

IgM or IgG
ABs are formed against target antigens on surface of self cell or tissue
1). Complement and AB mediated cell destruction
2). Complement and AB mediated inflammation
3). AB mediated Cellular dysfunction

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8
Q

Define complement and AB mediated cell destruction (type 2 hypersensitivity). What is example

A

deletion of cells targets by AB; can occur by complement system or ADCC
ex: mismatched blood transfusion; hemolytic disease of newborn

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9
Q

Define complement and AB mediated inflammation (type 2 HS rxn). Give example

A

AB deposited in cell matrix, complement is activated, injury occurs from inflammation
ex: vascular rejection of organ grafts

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10
Q

Define AB mediated cellular dysfunction (type 2 HS rxn) and give example

A

AB binds to specific target cell receptor which changes cell function
ex: Grave’s disease (activates thyroid cell and increases hormone production)

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11
Q

What is type 3 HS rxn?

A

Mediated by AB-antigen complex, complement fixation, and localized inflammation
unphagocytosed complexes settle into tissues and excessively activate complement (activates neutrophils and ends in chronic inflammation)

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12
Q

What’s the difference between Systemic and local immune complex disorders for type 3 HS rxns?

A

Systemic: serum sickness (IgM, IgG, sometimes IgA)
Local: arthus rxn (local inflammation and tissue necrosis from vasculitis)

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13
Q

What is Type 4 cell mediated hypersensitivity?

A

Cell MEDIATED not AB

Mechanism of response to variety of microorganisms; can lead to cell death and injury in response to chemicals

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14
Q

What is direct cell mediated cytotoxicity under Type $ HS rxn?

A

CD8 cytotoxic T lymphocytes destroy APCs

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15
Q

What does the delayed type hypersensitivity disorder under Type 4 HS rxn occur under?
how long does it take? give examples

A

occurs in response to antigens and APCs (macrophages/CD4 helper T ONE cells)
T one helper cells release cytokines- activates macrophages or CD8
takes about 48-72 hrs before T helper system forms effector cell to target antigen
TB test- recognized by T memory cells and rxn occurs
Allergic contact dermatitis- poison ivy takes 12-24 hrs after exposure for rxn
Hypersensitivity pneumonitis: activation of lung cytotoxic t cells in response to inhaled dust (farmer’s lung from chronic exposure)
Graft rejection
Autoimmune disorders

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16
Q

What is self tolerance?

A

the ability to tolerate your own antigens

Human leukocyte antigens coded by MHC genes serve as recognition markers of self (on most nucleated cells)

17
Q

What body part deletes problematic T cells? How about B cells?

A

Thymus
Bone marrow
spleen or lymph nodes (peripheral mechanisms in place for problematic T cells that get missed)

18
Q

Why do we get autoimmune diseases?

A

No definite reason

  • know in women, estrogen stimulates the immune system
  • could be inheritance of susceptible genes that contributes to maintenance of self tolerance (certain LHA genotypes occur more frequently in ppl with AI disorders)
  • could be environmental factors (infections)
19
Q

What 4 environmental factors can influence autoimmune disease? Describe what each is

A

1) . Breakdown of T cell anergy (when lymphocyte is functional inactivated following an antigen encounter)
2) . release of sequestered antigens-release of self-antigen after being hidden in development will be regarded as foreign
3) . Molecular mimicry: microbe shares immunologic epitope with host (ex pericarditis usually develops after renal strep infection; epitopes on pericardial sac are similar to strep antigen)
4) . superantigens: staph and strep exotoxins that short circuit the normal events in an immune response

20
Q

How do you diagnosis an autoimmune disorder? (suggested criteria vs clinical findings/testing)

A

suggested criteria: evidence of autoimmune rxn, immunologic findings aren’t secondary to another disorder, lack of other identifiable cause
Clinical findings/testing: demonstration of ABs against tissue antigens or cell components

21
Q

What is the treatment for an autoimmune disease based on? What are the first two meds usually administered?

A

based on tissue or organ involved, effector mechanism involved, magnitude and chronicity of effector process
Corticosteroids and immunosuppressive drugs administered first and then plasma exchange therapy

22
Q

What is happening during transplant rejection and what are the specific antigens that make the determination?

A

Recipients immune system recognizes the graft as foreign and attacks it
HLA recognizes graft as foreign

23
Q

What are autologous, syngeneic, and allogeneic grafts?

A

autologous: donor and recipient are the same (ex: skin graft from yourself)
Syngeneic: donor and recipient are identical twins
Allogeneic: donor and recipient are related or unrelated but share HLA types

24
Q

What type of immunity does transplant rejection involve?

A

Cell-mediated immunity and circulating ABs

T cells IMPORTANT

25
Q

What are the two pathways by which T lymphocytes recognize allogenic antigens? Describe what happens during them

A

Direct Pathway- T cells of recipient recognize allogenic MHC on surface of APCs in the graft; CD4 and CD8 involved and kill graft cells

Indirect Pathway- recipient CD4 cells recognize donor MHC molecule after they’ve already been processed on recipient’s APCs; activates DTH pathway (type IV hypersensitivity rxn) so ABs are produced against graft

26
Q

What are the three transplant rejection reactions?

A

Hyperacute, acute, and chronic

27
Q

What is the hyperacute rxn during transplant rejection?

A 
occurs immediately (hrs or days)
most common in kidney transplants
existing recipient AB attack graft antigens and initiate type III hypersensitivity rxn in graft BVs
28
Q

What is the acute rxn during transplant rejection

A

Occurs in first few months

activated T cells cause direct lysis of graft cells and recruit/activate inflammatory cells that injure graft

29
Q

What is the chronic rxn during transplant rejection

A

occurs over prolonged period (years)
can see dense intimal fibrosis of BVs in transplant graft
mechanism is unclear (may be cytokines)

30
Q

What is graft versus host disease? (GVHD) When is it most common? what cells are attacking and what type of rxn does this provoke?

A

immune competent cells are transplanted into recipients who have a compromised immune system
Most common after BM or liver transplant
Donor CD4 and CD8 T cells are activated and attack recipient (type IV hypersensitivity rxn)

31
Q

What is acute vs chronic GVHD?

A

Acute- epithelial cells of skin, liver, GI tract (skin is most affected); creates rash on palms and soles
Chronic- develop skin lesions resembling systemic sclerosis or other AI disorder symptoms

32
Q

What two types of cells can have problems in them that lead to immunodeficiency disorders?

A

B lymphocytes- humoral immunity

T lymphocytes and cytokines- cell mediated immunity

33
Q

What is primary vs secondary immunodeficiency disorders?

A

primary- congenital or inherited; usually recessive traits on X chromosome
Secondary- acquired (like AIDS)

34
Q

What are the three phases of HIV and CD4 count numbers?

A

Primary acute HIV infection- >500 (29%)
latency- 200-499 (12-28%)
overt AIDS- <200 (<14%)

35
Q

What characterizes AIDS?

A

low CD4 counts
profound immunosuppression with signs of opportunistic infections
malignancies, wasting, CNS degeneration

36
Q

What are the three types of opportunistic infections of AIDS?

A

Respiratory- bacterial pneumo (P jiroveci), pulm TB in HIV, CMV (cytomegalyvirus)
GI-herpes simplex, diarrhea and gastroenteritis, esophageal candidiasis
NS- cognitive disorders (HANDs), Toxoplasmosis

37
Q

What is wasting syndrome in AIDS? What is it treated with?

A

involuntary weight loss of 10% of baseline body weight, diarrhea more than 2 stools/day, chronic weakness & fever
Oral supplements or parenteral nutrition

38
Q

How do we currently treat HIV/AIDS?

A 
combination therapy (at least three antiretroviral drugs)
Nucleoside/tide reverse transcriptase inhibits, NonNRTIs, protease inhibitors, entry inhibitors, and integrase inhibitors
39
Q

How do we reduce maternal transmission of AIDS?

A

maternal antivirals (zidovudine); reduce by 2/3rds

Pathophys (13 decks)

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