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Advanced Pathophysiology > Chapter 2-Immunity > Flashcards

Chapter 2-Immunity Flashcards

1
Q

how does the stress response happen?

A

sympathetic nervous system. Signals from the brain go to the adrenal gland (on top of kidneys) to release hormones in order to increase energy stores (glucose), increases metabolism, HR, RR, and blood sugar

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2
Q

why is chronic stress bad?

A

constant release of hormones= prolonged elevation of HR, RR, blood sugar. Once you blow through stored blood sugar we use it from structural parts of the body which breaks down tissue

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3
Q

what are manifestations of stress? (7)

A
  1. Increased HR/RR
  2. diaphoresis
  3. increased blood flow to muscles/increased muscle strength
  4. increased alertness
  5. increased fat/protein metabolism
  6. increased glucose availability
  7. decreased inflammation
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4
Q

what perpetuates the stress hormone response

A

cortisol release/glucocorticoids

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5
Q

what causes autoimmune disorders?

A

the immune system doesn’t recognize tissues as their own

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6
Q

what are the 2 kinds of response systems for infections?

A

Innate and adaptive (aquired) response

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7
Q

what is the innate response? what is 1 example?

A
  • what you were born with.
  • general, immediate, nonspecific protection from all invaders
  • 1 example=skin
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8
Q

what is adaptive (aquired) response?

A

slower- takes 7-10 days. specific response to specific antigen->antibodies formed to fight antigens

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9
Q

What part of defense are mucous membranes part of?what is included?

A

innate defense. Line entrie GI tract from mouth to anus. strong response to protect from external agents

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10
Q

what is included in additional bloodborne innate defense? (4)

A
  1. inflammatory response
  2. pyrogens (induce fever)
  3. interferons (inhibits virus replications)
  4. complement proteins
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11
Q

What cells trigger an inflammatory response?

A

Mast cells

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12
Q

what do mast cells release during an inflammatory response?

A

histamine–vasodilator to increase WBC to that area

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13
Q

what do phagocytes do?

A

eat microbes to keep them from entering the body

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14
Q

what do lymph vessels do?

A

help remove poisonus substaces, they go to the lymph nodes

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15
Q

what is a pyrogen? what produces pyrogens?

A

it is a fever producing molecule produced by macrophages

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16
Q

how do pyrogens work?

A

cause the temp to rise, increases metabolism to increase healing and increase phagocytosis

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17
Q

What fever is severe-life threatening in adults?

A

> 105

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18
Q

what are interferons? how do they work?

A

proteins released from virus-infected cells.

they bind to uninfected cells, the uninfected cells release an enzyme that prevents viral replication

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19
Q

what are compliment proteins? how are they activated?

A

plasma proteins that enhance antibodies and are activated by antigens

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20
Q

what are the 3 functions of compliment proteins?

A
  1. attack bacteria itself
  2. vasodilation to the infected areass
  3. chemotaxis to draw WBC to the area
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21
Q

what are 5 unique characteristic of adaptive (aquired) immunity?

A
  1. specific
  2. develop over time
  3. use memory
  4. distinguish self from non-self AND between pathogens
  5. include lymphocytes (T/B cells)
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22
Q

what is the function of a T cell?

A

it destroys cells directly or stimulates B cells

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23
Q

What do B cells do?

A

they provide humoral immunity i.e. release antibodies into the tissue of the body

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24
Q

what is the immature form of T cells and B cells?

A

lymphocytes

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25
Q

Where are T cells produced/where do they mature?

A

produced in bone marrow and mature in thymus

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26
Q

What do T helper cells do?

A

activate B cells to produce antibodies

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27
Q

What to T suppressor cells do?

A

turn off antibody production

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28
Q

what do killer cells (cytotoxic cells) do?

A

destroy infected cells by destroying cell walls. (poke holes in bacteria cell walls which induces apoptosis–> cell takes in too much fluid/electrolyte/breaks down

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29
Q

how is Cellular immunity mediated?

A

mediated by T cells on RECOGNITION of antigen

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30
Q

how is humoral immunity mediated?

A

mediated by B cells on ENCOUNTERING antigens

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31
Q

Cellular immunity uses which kind of cells? what about humoral immunity?

A 
cellular= T cells
humoral= B cells
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32
Q

Where are B cells made/ where do they mature?

A

Bone marrow for both. also found in lymph/spleen

33
Q

what is humor

A

where you find the antibodies that B cells create

34
Q

what to memory cells do? what part of immunity are the part of?

A

take the memory of an antigen to fight quicker in the future. Part of humoral immunity

35
Q

what are immunoglobulin-secretiong cells (plasma cells or effector cells)?
What kind of immunity are they part of?

A

type of B cell that we create in bone marrow that create immunoglobulin (fancy name for antibodies)

humoral immunity

36
Q

what is Immunoglobulin G (IgG)?

A

it is a type of antibody, the main defense against bacteria

37
Q

what is immunoglobulin E (IgE)?

A

it is a type of antibody, triggered during allergic reactions

38
Q

With aquired immunity comes 2 types. what are they?

A

Active Immunity: aquired by having the disease. Long lasting but takes time to become effective
Passive Immunity: Receiving antibodies from external sources i.e. maternal-fetal transfer or breastfeeding. these are short lasting.

39
Q

what are seeker cells?

A

go “try out” or learn various tissues so the body knows which tissues are their own.

40
Q

what is a hypersensitivity?

A

an exaggerated immune response to a foreign substance

41
Q

what is an autoimmune alteration?

A

Mistakes self for non-self

42
Q

what is immunodeficiency?

A

inadequate immune reaction

43
Q

what is type 1 (IgE) mediated hypersensitvity? What gets activated?

A

Allergic response. Allergen activates T-helper cells that stimulate B cells to produce IgE. Can be local or systemic.

44
Q

what happens on a cellular level with IgE hypersensitivity? What happens with next exposure?

A

Allergen activates T helper cells–>stimulate B cells to produce IgE. IgE coats mast cells and basophils, sensitizing them to the allergen. These cells release histamine causing the allergic reaction
Next exposure the antigen binds with the surface IgE, releasing mediators and triggering the compliment system.

45
Q

What are 3 examples of IgE mediated hypersensitivity?

A
  1. hay fever
  2. food allergies
  3. anaphylaxis
46
Q

what is Type II hypersensitivity ?

A

cytotoxic hypersensitivity

47
Q

what happens with Type II hypersensitivity (cytotoxic) on a cellular level?

A

IgG or IgM antibodies bind to antigen on individual’s own cells. Macrophage recognize these cells and trigger antibody production. Lysis of cells occurs b.c of the activation of compliment and by phagocytosis…usually an immediate response

48
Q

what is an example of type II hypersensitivity (cytotoxic)?

A

blood transfusion reactions and erythroblastosis fetalis (RH compatability)

49
Q

what is type III hypersensititivity?

A

immune complex-mediated hypersensitvity reaction

50
Q

what happens on a cellular level with Type III hypersensitivity (immune complex-mediated)?

A

circulating antigen-antibody compolexes accumulate and are deposited in the tissue—–usually kidneys, joints, skin, and blood vessel

51
Q

what is an example of type III hypersensitivity?

A

autoimmune conditions. i.e. systemic lupus

52
Q

What is Type IV hypersensitivity reaction?

A

delayed sensitivity reaction

53
Q

what happens on a cellular level with type IV (delayed) hypersensitivity reaction?

A
  1. its cell mediated, not antibody mediated..involves T cells
  2. antigen presentation results a delayed response of macrophages and T cells causing severe tissue injury and fibrosis
54
Q

what is an example of type IV (delayed) hypersensitivity reaction?

A

tuberculin testing, transplant reactions, contact dermatitis

55
Q

what is an allogenic transplant?

A

donor and recipient are related or unrelated but share a similar tissue type

56
Q

what is syngenic transplant?

A

donor and recipient are identical twins

57
Q

what is an autologous transplant?

A

donor and recipient are teh same person—most successful. ex: using your own stored blood

58
Q

what is xenogenic transplant?

A

use of tissue from another species (pig heart valve)

59
Q

what is the onset of hyper-acute tissue rejection?

A

onset immediate or 3 days after transplant.

compliment system kicks in–signals B cells

60
Q

what happens on a cellular level with hyper-acute tissue rejection?

A

due to compliment system–compliment system kicks in, sends signals to B cells, B cells create antibodies, antibodies for antibody antigen complexes (try to destroy antigens (i.e. the new tissue). New tissue hasn’t had time to develop and becomes necrotic

61
Q

what is the onset of acute tissue rejection? what is good about it?

A

4 days-3 months. most common and its treatable.

62
Q

what happens on a cellular level with acute tissue rejection?

A

cell mediated. T cells come in directly and cause a response, they try to attack the tissue. Tissue has viable blood supply but there will be systemic effects: fever, redness, swelling, tenderness, impairment of that organ

63
Q

what is the onset of chronic tissue rejection?

A

> 4 months

64
Q

What happens in chronic tissue rejection?

A

antibody mediated response. antibodies in the compliment cells deposit in the vessels of the transplanted tissue causing a decrease to blood supply of that tissue

65
Q

what is the significance of human leukocyte antigen (HLA) or major histocompatability complex? what gets triggered in this response?

A

genes code for porteins on cell surfaces (many alleles or variations)—many variations of these proteins makes it hard to find 2 people with the same or similar tissue types
if tissue is not well matched, receptors on macrophages will signal T cells to alert them of foreign bodies & ingest them

66
Q

what happens in host vs graft disease?

A

host fights graft. recipients immune system attempts to eliminate donor cells

67
Q

what happens in graft vs host disease? where is it most commonly seen? how is it treated?

A

occurs when immunocompetent fatal cells recognize host tissue as foreig and mount a CELL-MEDIATED immune response. Seen in bone marrow transplant

68
Q

what factors play a role in autoimmune disorders

A
  1. stress= increased risk or increased flare up
  2. more common in females
  3. genetics do play a role
69
Q

What happens on a cellular level with lupus erythematosus Wolf?

A

B cells are activated to produce autoantibodies and autoantigens that combine to form immune complexes that attack the body’s own tissue
hyperactive T helper cells continue to trigger B cells and repressed T suppressor cells don’t tell them to stop—>Triple threat!

70
Q 
Systemic Lupus Erythematosus
S
O
A
P
B
R
I
A
N

M
D

A

S: serotosis (serous membranes of internal organs [lungs, heart, abdomen] get inflammed)
O: Oral Ulcers
A: arthritis
P: photosensitivity

B: blood disorders (decreased count)
R: renal involvement (autoantibody autoantigen
complexes deposit in kidney, decrease fx
I:immunological phenonema
A: antinuclear antibody (intermittently positive)
N: neurologic disorders (seizures/psychosis)

M: malar rash (butterfly rash)
D: discoid rash (patchy redness that can cause scarring)

71
Q

why is plasmapheresis useful with lupus?

A

gets rid of antibody antigen complexes

72
Q

What is HIV? How does it replicate?

A

parasitic retrovirus that infects CD4 and macrophages
(CD4 is the protein on T helper Cell surfaces)
retrovirus goes back trough RNA to DNA, permanently changing DNA

73
Q

describe the asymptomatic phase of HIV

A
  1. virus is reproducing–>usually for several years
  2. then acute retroviral syndrome–>flu like symptoms
  3. infections begin as the viral # increases, destroying CD4 cells —> symptom onset swollen nodes, diarrhea, weight loss, fever, cough
74
Q

what three forms of progression does AIDs take?

A
  1. immunodeficiency (opportunistic)
  2. autoimmunity (arthritis, pneumonitis)
  3. neurological dysfunction (AIDS dementia)
75
Q

What are category 1, 2, and 3 for AIDS classification system?

A
  1. > 500 cells/mL
  2. 200-49 cells/mL
  3. < 200 cells/mL
76
Q

What is category A, B, and C for AIDS classification system?

A

A: asymptomatic
B: some less serious manifesations of immune deficiency
C: AIDS-defining illness present

77
Q

who is at risk for immune dysfunction? (10)

A
  1. Very young/very old
  2. poor nutrition
  3. impaired skin integrity
  4. circulatory issues
  5. alterations in normal flora from ABX
  6. chronic disease (DM)
  7. corticosteroid therapy
  8. chemo
  9. smoking/alcohol
  10. immunodeficiency
78
Q

What are some immune-building strategies? (7)

A
  1. increase fluid intake
  2. well balanced diet
  3. increased antioxident/protein
  4. adequate sleep
  5. avoid refined sugar/caffeine
  6. spend time outside
  7. reduce stress

Advanced Pathophysiology (4 decks)

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