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Patho II > EXAM 2: Immune disorders > Flashcards

EXAM 2: Immune disorders Flashcards

1
Q

exaggerated

A

against environmental antigens

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2
Q

misdirected against host’s own cells

A

autoimmunity

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3
Q

directed against beneficial foreign tissues

A

isoimmunity (like to transplants)

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4
Q

hypersensitivity

A
  • a pathologic immune response

- an exaggerated AND inappropriate immune response

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5
Q

Autoimmunity

A

-breakdown of that “code of recognition” and begins to recognize self as foreign

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6
Q

what causes the development of autoimmunity

A
  • genetics

- exposure to antigens (ie: drugs/infections)

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7
Q

why do genetics and exposure to antigens cause autoimmunity

A

-thought to alter membranes (and the expression of self DNA) and induce this autoimmunity

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8
Q

what are the two types of hypersensitivity

A
  • autoimmunity

- isoimmunity

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9
Q

isoimmunity

A

bodies IS reacts against tissues of usually other members of same species

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10
Q

type 1 hypersensitivity

A

IgE mediated allergic reactions

allergy/anaphylaxis

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11
Q

type 2 hypersensitivity

A

tissue-specific reaction

blood transfusion reaction

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12
Q

type 3 hypersensitivity

A

immune-complex mediated reactions

-AG-AB complexes from and deposit in tissues

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13
Q

type 4 hypersensitivity

A

cell-mediated reactions

-involve t-cells, macrophages

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14
Q

anaphylaxis

A

a rapid, immediate hypersensitivity reaction upon RE-EXPOSURE to antigen

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15
Q

allergy chain first time

A

allergen-> in contact with B cell-> produces IgE antibody specific to allergen-> IgE goes to receptors on mast cell-> mast cell for next time it comes in contact with allergen

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16
Q

allergy chain second time

A

IgE recognizes allergen-> induce mast cell degranulation-> release of histamine andleukotrienes-> S/S of allergy

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17
Q

which exposure causes mast cell degranulation

A

second exposure

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18
Q

localized clinical mani of allergies/anaphylaxis

A
  1. local inflammation
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19
Q

systemic clinical mani of allergies/anaphylaxis (5)

A
  1. bronchial constriction,
  2. skin is itchy and red
  3. increased secretions of mucous mems
  4. abdominal cramps, V/D
  5. increased vascular permeability and vasodilation
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20
Q

which systemic manis of allergies are life threatening

A
  1. bronchial constriction

2. vascular permeability and vasodilation

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21
Q

systemic lupus erythematosus

A

chronic, autoimmune, multisystem inflammatory disease

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22
Q

where is lupus common

A

-females
20-40 years of age
genetic predisposition

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23
Q

what type of hypersensitivity reaction is lupus

A

mostly type III

AG-AB complexes form and deposit in vessel walls

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24
Q

first lupus chain

A

B cell produces IgG immunoglobulin-> attacks cells of the vessel wall it views as foreign->antibody complexes deposit in vessel walls

25
Q

second lupus chain component

A

T helpers-> help further stimulate B cell production of IgG

26
Q

third component of lupus chain

A

macrophages recruited to further attach cells of vessel walls-> further destruction

27
Q

fourth component of lupus chain

A

igG also attacks RBC’s because it sees them as foreign as well (leads to anemia)

28
Q

fifth component of lupus chain

A

T suppressor cells are not effective in slowing down process (should have regulated/slowed destruction but didn’t)

29
Q

clinical mani of lupus

A
  1. arthritis of peripheral jts
  2. vasculitis/photosensitivity
  3. renal disease
  4. anemia
  5. CV disease- pericarditis
30
Q

why does renal diseases happen with lupus

A

-damage of vascular wall over time as well as lysed RBC’s not getting through

31
Q

rheumatoid arthritis

A

Autoimmune, inflammatory jt disease characterized by destruction of the synovial membrane

32
Q

RA patho chain

A

normal antibodies(IgM, IgG) are transformed into rheumatoid factor-> RF attacks cells of synovial mem->vasodialation/increased permeability->WBC enter synovial fluid->further attack synovial mem->fibrin, collagen and scar tissue is deposited in synovial jt fluid

33
Q

early RA clinical mani

A
  1. synovitis (inflammation of synovial membrane)

2. systemic manifestations of inflammation (minor, low grade fever, fatigue)

34
Q

what type hypersensitivity is RA

A

both type III and type IV

-normal antibodies become “autoantibodies (RF) (IgM, IgG) and attack “antigens” on cell mems

35
Q

which jts are effected first with RA

A

usually peripheral jts (wrists and fingers)

36
Q

later clinical mani of RA

A

Start to get tenderness, stiffness of jts (destruction has started)

  • pain, deformity, loss of function of the jts
  • rheumatoid nodules
  • Ulnar drift (hand drifts toward ulnar, pinkie side)
37
Q

immune dificiencies

A

-impaired function of the immune response

38
Q

congenital (primary) immune deficiencies

A

Genetic (immune cells are improperly developed)

39
Q

acquired (secondary) immune dificiencies

A

associated with conditions (PG, infancy, elderly, chronic illness, malnutrition)

40
Q

iatrogenic deficiencies

A

(an acquired immune D)

  • iatrogenic (from medical treatment_
  • Trauma (burns)
  • stress
41
Q

HIV1

A

a retrovirus viral disease- carries it genetic coding in its RNA

42
Q

how does HIV 1 infect

A
  • infects and depletes a portion of the IS (cells with CD-4 receptors) (t-helpers)
  • then starts to attack macrophages and cytotoxic t cells
43
Q

step one HIV infection

A
  • HIV-surface glycoprotein (gp120) attaches to CD-4 receptor and enters cell
44
Q

step two HIV infection

A

chemokine (a co-receptor) aids in the binding of gp120

45
Q

step three HIV infection

A

Viral RNA converted into DNA (with help from 3 enzymes, reverse transcriptase, integrase, and protease)

46
Q

step four HIV infection

A

the DNA is inserted and integrated into the T helper cell DNA and takes over the cell

47
Q

what are the three way HIV spreads to other cells

A
  1. Remain latent (no spread)
  2. New HIV particles but out
  3. Lysis of cell with release of particles
48
Q

lab values in HIV

A
  1. overall # of t helper cells (n800-1000)
  2. Ratio of T helpers to T suppressors (n2/1)
  3. Viral load (the lower the better)- amount of “active” virus in the blood stream
49
Q

what are the four possible conditions with HIV

A
  1. serologically negative
  2. serologically positive
  3. early stages of HIV disease
  4. AIDS
50
Q

serologically negative

A

but they can have virus without an AB produced or detected YET

51
Q

serologically positive

A

-asymptomatic
-detectable AB, but no real symptoms
(this stage is the goal)

52
Q

early stages of HIV disease

A

symptoms but not AIDS

53
Q

AIDS

A
  • serious clinical symptoms and or malignancies

- often t helper less than 200

54
Q

what is the HIV time line

A
  1. enter body
  2. no AB production
  3. AB production
  4. Early stages and AIDS of HIV disease
55
Q

clinical mani of serologically negative

A

ASYMPTOMATIC

  • high risk groups
  • ability to unknowingly transmit the virus
56
Q

clinical mani of serologically positive

A

ASYMPTOMATIC

-some experience a seroconversion illness resembling mono or flu

57
Q

clinical mani of early stages HIV disease

A
  • chronic lymphadenopathy
  • night sweats
  • recurrent fevers
  • flu-like, fatigue
  • anorexia, wt. loss, diarrhea
58
Q

clinical mani of AIDS

A
  • opportunistic infections

- malignancies

Patho II (23 decks)

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