Ch.16 Innate Immunity Part 2 Flashcards

1
Q

what are some inflammation responses?

A

Redness
pain
heat
swelling
may or may not have a loss of function

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2
Q

what are some inflammation responses functions?

A

(a) destroy/remove agent;

(b) confine agent to local area;

(c) repair/replace damaged tissue

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3
Q

what happens during early stage of inflammation ?

A

Cytokine release – TNF-tumor necrosis factor –> induces formation of
acute-phase proteins

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4
Q

what are the stages of inflammation?

A

vasodilation

phagocyte migration

phagocytosis

repair

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5
Q

what does vasodilation do?

A

increases blood flow in the area (redness & heat)

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6
Q

what is vasodilation triggered by?

A

chemicals

histamine

kinins

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7
Q

what does increased permeability do?

A

permits entry of blood cells into the site (edema, swelling)

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8
Q

what is increased permeability permits entry of blood cells into the site (edema, swelling) due to?

A

kinins

leukotrienes (mast cells)

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9
Q

steps to the inflammatory response

A
  1. chemicals such as histamine kinins, prostaglandin leukotrienes, and cytokines are released by damaged cells
  2. Blood clot forms
  3. Abcess starts to form
  4. margination- phagocytes
    stick to blood vessel walls
  5. Diapedisis-phagocytes squeeze between cells. exiting blood vessel
  6. Phagocytosis of invading bacteria occurs
  7. phagocytosis removes microbes, and damaged tissue; pus formation
  8. tissue repair; replacements of dead, damaged tissues
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10
Q

in response to cytokines, what does it cause?

A

cause phagocytes to stick to blood vessel walls margination

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11
Q

what happens during diapedesis?

A

phagocytes squeeze between cells. exiting blood vessel

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12
Q

what does the hypothalamus do?

A

body’s thermostat

regulates body temp

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13
Q

what causes fevers?

A

pyrogens

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14
Q

what are exogenous pyrogens?

A

outside the body (bacteria viruses, others)

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15
Q

what are endogenous pyrogens (interleukin-1)?

A

act on the hypothalamus raising the temperature set point

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16
Q

what does elevated temperature cause?

A

slow pathogen growth

increases T cell activity

lowers the concentration of available iron

17
Q

what does the complement cascade rely on?

A

on soluble protein factors in the blood to attack bacterial pathogens

18
Q

define classical pathway

A

C3 is activated by contact between complement and pathogen via antibodies

19
Q

define alternate pathway

A

C3 is activated by contact between complement & pathogen via surface glycolipid complexes

20
Q

define lectin pathway

A

C3 is activated by contact between lectin & pathogen via surface-specific carbohydrates

ex: mannose

21
Q

what are the effects of complement?

A

opsonization

inflammation

cytolysis

22
Q

how does complement affect opsonization?

A

activated C3b proteins bind microbe;

phagocyte binds to C3b-> enhances phagocytosis

23
Q

how does complement affect inflammation?

A

C3a & C5a bind mast cells causing the release of histamine, kinins

C5a also acts as a chemoattractant for phagocytes

24
Q

how does complement affect cytolysis?

A

C3b proteins split C5 -> C5a + C5b

C5b promotes the formation of a complete protein complex that inserts into the plasma

form membrane attack complex MAC

channels form in the microbe causing lysis

25
Q

what interferons?

A

cytokines that interfere with viral replication

26
Q

how are interferons produced?

A

in response to infection

27
Q

what kind of action is interferons?

A

is host specific

28
Q

what are type 1 interferons?

A

high antiviral potency

bind receptors on uninfected host cell

renders them resistant to viral infection

29
Q

what are type 2 interferons?

A

activates neutrophils and macrophages;

increases MHC antigen on their surface

30
Q

describe interferons

A

not very long-acting

not very stable

toxic in high doses

effective in acute viral infection

cannot help virus-infected cells

31
Q

what binds free irons in the human body?

A

transferrins

lactoferrins

ferritin

hemoglobin

32
Q

what are antimicrobial substances?

A

iron-binding proteins

compete with pathogens for iron

required as a cofactor for many enzymes

33
Q

what do pathogens produce to bind iron?

A

pathogens produce siderophores to bind

34
Q

what is AMPS synthesis triggered by?

A

proteins

carbohydrate molecules on microbial cell surface

35
Q

what does AMP act against?

A

bacteria
viruses
fungi
eukaryotic parasites

36
Q

how does AMP kill?

A

by lysing cells

inhibiting cell wall synthesis

hydrolyzing DNA, RNA

37
Q

what does AMP attract?

A

dendritic & mast cells