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Patho II > EXAM 2: Immune disorders > Flashcards

EXAM 2: Immune disorders Flashcards

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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

Study These Flashcards
A

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

25
second lupus chain component
T helpers-> help further stimulate B cell production of IgG
26
third component of lupus chain
macrophages recruited to further attach cells of vessel walls-> further destruction
27
fourth component of lupus chain
igG also attacks RBC's because it sees them as foreign as well (leads to anemia)
28
fifth component of lupus chain
T suppressor cells are not effective in slowing down process (should have regulated/slowed destruction but didn't)
29
clinical mani of lupus
1. arthritis of peripheral jts 2. vasculitis/photosensitivity 3. renal disease 4. anemia 5. CV disease- pericarditis
30
why does renal diseases happen with lupus
-damage of vascular wall over time as well as lysed RBC's not getting through
31
rheumatoid arthritis
Autoimmune, inflammatory jt disease characterized by destruction of the synovial membrane
32
RA patho chain
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
early RA clinical mani
1. synovitis (inflammation of synovial membrane) | 2. systemic manifestations of inflammation (minor, low grade fever, fatigue)
34
what type hypersensitivity is RA
both type III and type IV | -normal antibodies become "autoantibodies (RF) (IgM, IgG) and attack "antigens" on cell mems
35
which jts are effected first with RA
usually peripheral jts (wrists and fingers)
36
later clinical mani of RA
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
immune dificiencies
-impaired function of the immune response
38
congenital (primary) immune deficiencies
Genetic (immune cells are improperly developed)
39
acquired (secondary) immune dificiencies
associated with conditions (PG, infancy, elderly, chronic illness, malnutrition)
40
iatrogenic deficiencies
(an acquired immune D) - iatrogenic (from medical treatment_ - Trauma (burns) - stress
41
HIV1
a retrovirus viral disease- carries it genetic coding in its RNA
42
how does HIV 1 infect
- 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
step one HIV infection
- HIV-surface glycoprotein (gp120) attaches to CD-4 receptor and enters cell
44
step two HIV infection
chemokine (a co-receptor) aids in the binding of gp120
45
step three HIV infection
Viral RNA converted into DNA (with help from 3 enzymes, reverse transcriptase, integrase, and protease)
46
step four HIV infection
the DNA is inserted and integrated into the T helper cell DNA and takes over the cell
47
what are the three way HIV spreads to other cells
1. Remain latent (no spread) 2. New HIV particles but out 3. Lysis of cell with release of particles
48
lab values in HIV
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
what are the four possible conditions with HIV
1. serologically negative 1. serologically positive 3. early stages of HIV disease 4. AIDS
50
serologically negative
but they can have virus without an AB produced or detected YET
51
serologically positive
-asymptomatic -detectable AB, but no real symptoms (this stage is the goal)
52
early stages of HIV disease
symptoms but not AIDS
53
AIDS
- serious clinical symptoms and or malignancies | - often t helper less than 200
54
what is the HIV time line
1. enter body 2. no AB production 3. AB production 4. Early stages and AIDS of HIV disease
55
clinical mani of serologically negative
ASYMPTOMATIC - high risk groups - ability to unknowingly transmit the virus
56
clinical mani of serologically positive
ASYMPTOMATIC | -some experience a seroconversion illness resembling mono or flu
57
clinical mani of early stages HIV disease
- chronic lymphadenopathy - night sweats - recurrent fevers - flu-like, fatigue - anorexia, wt. loss, diarrhea
58
clinical mani of AIDS
- opportunistic infections | - malignancies

Patho II (23 decks)

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