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Anatomy and Phyisology > BIOL: intrinsic and innate immunity > Flashcards

BIOL: intrinsic and innate immunity Flashcards

1
Q

classic inflammation response (latin version)

A

calor, tumor, rubor, and dolar

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2
Q

calor

A

refers to heat

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3
Q

tumor

A

refers to swelling

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4
Q

rubor

A

refers to redness

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5
Q

dolar

A

refers to pain and loss of function

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6
Q

acronym for inflammation symptoms

A

PRISH; pain, redness, immobility, swelling, and heat

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7
Q

adjuvants

A

inflammatory molecules that are added to vaccines are help non-infectious agents replicate and initiate a host immune response

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8
Q

inflammation

A

is a nonspecific response to tissue damage and is part of the innate response of the immune system to help heal and attack the injectious agent

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9
Q

how might tissue damage occur?

A

excess heat or cold, chemical damage, UV damage, cuts, pathogens, etc .

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10
Q

acute inflammation

A

develops quickly and is beneficial because it eliminates causes; is usually quite localized

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11
Q

chronic inflammation

A

is long-lasting, damages tissues, and causes diseases; is a result of the immune system overreacting

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12
Q

ex. of a chronic inflammation

A

rheumatoid arthritis or Crohn’s disease

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13
Q

what is the first response in inflammation?

A

vasodilation and increased blood vessel permeability

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14
Q

what is the result of vasodilation and increased permeability?

A

allows for cells to migrate from the bloodstream into the ISF; this is what causes redness and temperature in the inflammatory response

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15
Q

what does blood clotting trigger the release of?

A

this initial source of injury activates bradykinin and histamine, and these are mediators that cause vasodilation

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16
Q

what causes vasodilation of the vessels?

A

histamine and bradykinins

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17
Q

what causes increased permeability of the blood vessels?

A

prostaglandins and leukotrienes which are activated by the wound

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18
Q

diapedesis

A

the process of WBCs migrating from the blood circulation to specific sites of injury due to increased permeability of the vessels

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19
Q

how long does it take for phagocytosis to begin after inflammation?

A

1 hour

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20
Q

what are neutrophils attracted to?

A

kinins, prostaglandins, and complement

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21
Q

what are prostaglandins released from?

A

damaged cells

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22
Q

what is a fever?

A

an abnormally high body temperature caused by the reset of the hypothalamic thermostat

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23
Q

why does the heat of a fever do?

A

intensifies the effect of inferons, inhibits the growth of microorganisms, and speeds up the body reactions that aid in repair

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24
Q

another name for blood clotting

A

hemostasis

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25
Q

3 stages in hemostasis

A

vascular spasm, platelet plug formation, and blood coagulation

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26
Q

vascular spasm

A

first stage of hemostasis; vessels constrict to limit blood flow to the area (tunica media smooth muscle), inhibiting blood loss

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27
Q

three steps of the platelet plug formation

A

platelet adhesion, platelet release reaction, and platelet aggregation

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28
Q

platelet adhesion

A

the exposed collagen in the break of the vessel attracts platelets to the endothelium

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29
Q

platelet release reaction

A

changes the shape and appearance of platelets, allowing them to attach to each other around the wound, while also releasing their products from their vesicles

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30
Q

what materials do platelets release?

A

liberated ADP, thromboxane A2, and serotonin

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31
Q

what released platelet factors activate nearby platelets?

A

ADP and thromboxane A2

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32
Q

what released platelet factors maintain contraction of the vessels?

A

serotonin and thromboxane A2

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33
Q

platelet aggregation

A

as a result of activated platelets that release chemicals, a platelet plug is formed to block the wound (a group of many platelets that form a ‘plug’)

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34
Q

fibrin

A

is activated to make blood clots after the platelet plug is formed

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35
Q

what clotting factors begins the blood clot formation?

A

tissue factor which is part of the extrinsic pathway

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36
Q

what ion is essential for blood clot formation

A

calcium

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37
Q

what does the extrinsic pathway activate?

A

factor X

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38
Q

what is the result of factor X?

A

prothrombinase (an enzyme), which converts prothrombin to thrombin

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39
Q

what is thrombin?

A

converts fibrinogen to fibrin

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40
Q

fibrinogen

A

converted to fibrin by thrombin; it is an inactive protein that circulates in the blood

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41
Q

intrinsic pathway

A

can be activated by thrombin and this is a positive feedback mechanism that triggers more production of prothrombinase to eventually produce more fibrin

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42
Q

three jobs of thrombin

A

convert fibrinogen to fibrin, reinforce the strength of the threads, and via a positive feedback mechanism triggers the production of prothrombinase via the intrinsic pathway

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43
Q

how many clotting factors are there?

A

12

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44
Q

clot retraction

A

is the tightening of the fibrin clot; as it tightens, the edges of the wound are brought closer together and fibroblasts can start doing their job

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45
Q

role of fibroblasts in clot formation

A

they make underlying CT to repair the gap in the vessel

46
Q

vitamin K significance

A

vitamin K is significant for being a precursor for a numerous amount of clotting factors (4/12)

47
Q

how is vitamin K created?

A

as a waste product of E coli in the large intestine

48
Q

vitamin K deficiency

A

can be dangerous for abnormal blood clotting

49
Q

why can blood clotting be dangerous?

A

it can create blood clots that can create obstructions

50
Q

fibrinolytic system

A

is a complicated pathway that interacts with the clotting pathway; plasminogen is converted to plasmin, which inactivates fibrin to dissolve the clot

51
Q

plasminogen

A

is an inactive enzyme that gets incorporated into the clot; is later converted to plasmin

52
Q

plasmin

A

created from plasminogen and inactives fibrin to dissolve the clot

53
Q

what converts plasminogen to plasmin

A

chemicals in the blood and healthy body tissues

54
Q

two anti-blood clotting drugs

A

heparin and warfarin (coumarin)

55
Q

heparin

A

is given via injection to prevent or delay blood clots from forming via blocking clotting factors

56
Q

what does heparin interact with in the blood

A

antithrombin III, enhancing its ability to inhibit blood clotting factors

57
Q

APTT

A

activated partial thromboplastin time; this isolates blood plasma and adds calcium and some downstream effect like a phospholipid, then the intrinsic pathway is activated and clotting time is measured

58
Q

warfarin

A

this blocks the reactions in the liver to make vitamin K, thus inhibiting the formation of clotting factors (specifically it inhibits 4); longer effects

59
Q

prothrombin time

A

measures the extrinsic pathway by adding tissue factor, then calcium, which then activates the intrinsic pathway

60
Q

APPT and PT

A

PT < APTT

61
Q

intrinsic immunity

A

is the non-specific first line of defence that is the skin and the mucus membrane

62
Q

what is part of the skin and mucus membranes?

A

epidermis (sweat, sebum, dead cells), mucus membranes (cilia and mucus), lacrimal apparatus (lysozyme), saliva (contains antibacterial chemicals), urine (flow cleanses the urethra), defecation/vomiting, and gastric juice (low pH)

63
Q

lysozyme

A

an enzyme that targets bacterial cell walls to create osmotic forces and is found in tears to protect the conjunctiva

64
Q

innate immunity

A

second line of defence that is non-specific and include interferons, the complement system, and phagocytosis

65
Q

complement system

A

a defence system that consists of over 30 proteins that are constantly circulating in the bloodstream waiting to be activated

66
Q

3 results of activated complement system

A

phagocytosis, inflammation responses, and cytolysis

67
Q

cytolysis

A

a combination of proteins insert themselves into the membrane of a microorganisms, breaking down concentration gradients which cause them to die

68
Q

3 complement activating pathways

A

classical, alternative, and lectin

69
Q

classical pathway

A

occurs when an antigen binds to an antibody triggering the complement pathway

70
Q

alternative pathway

A

activates the complement system by microbe specific lipid carbohydrate complexes on the surface of microorganisms that are specific to them

71
Q

lectin pathway

A

is produced when a macrophage releases certain chemicals after they have phagocytosed a new invade; this produces lectin which activates the liver to produce lectin, activating complement

72
Q

iron binding proteins

A

iron need bacteria to live so free circulating iron in the body needs to be protected

73
Q

key iron proteins

A

transferrin, ferritin, lactoferrin, hemoglobin, and myoglobin

74
Q

where is transferrin found?

A

plasma and ISF

75
Q

where is ferritin found?

A

the liver

76
Q

where is lactoferrin found?

A

milk, saliva, and mucus

77
Q

where is hemoglobin found?

A

RBCs

78
Q

where is myoglobin found?

A

muscle cells

79
Q

4 antimicrobial proteins

A

dermcidin, defensins, cathelicidins, and thrombocid

80
Q

dermcidin

A

produced in sweat glands and function to create osmotic forces to kill bacteria

81
Q

defensins

A

are naturally released by macrophages, neutrophils, and epithelia

82
Q

cathelicidins

A

are released by macrophages, neutrophils, and epithelia

83
Q

thromdocidin

A

released by platelets

84
Q

what are functions of antimicrobial proteins?

A

they kill the microorganism in question and attract dendritic cells (phagocytes) and mast cells (histamine) to the scene

85
Q

natural killer cell

A

is a lymphocyte that kill foreign material by directly attaching to to its receptors and releasing destructive proteins

86
Q

where are natural killer cells found?

A

the spleen, red bone marrow, lymph nodes, and blood

87
Q

destructive proteins released by natural killer cells

A

perforin and granzyme

88
Q

perforin

A

released by natural killer cells and put a hole in the membrane, creating osmotic forces

89
Q

granzyme

A

released by natural killer cells and make the target cell undergo apoptosis

90
Q

apoptosis

A

programmed cell death

91
Q

what are the first responders to an injury site or infection?

A

neutrophils and macrophages (large phagocytes)

92
Q

2 types of macrophages

A

fixed or wandering

93
Q

wandering macrophages

A

actively undergoing phagocytosis

94
Q

fixed macrophages

A

defensive cells for important tissues; ex. kupfer cells or microglial cells

95
Q

first stage of phagocytosis

A

chemotaxis

96
Q

what does hemostasis prevent?

A

hemorrhages

97
Q

where are complement proteins created?

A

in the liver

98
Q

how is phagocytosis complement activated?

A

the complement system tags proteins onto the microorganism, making them attracted to a phagocytic cell

99
Q

opsonization

A

the addition of proteins to a microorganism to enhance the phagocytosis process

100
Q

most commonly used antimicrobial proteins

A

decisions and defensins

101
Q

why does redness occur for inflammation?

A

vasodilation

102
Q

what causes heat for inflammation?

A

vasodilation

103
Q

why does swelling occur in inflammation?

A

excess ISF due to increased permeability of the vessel

104
Q

why does pain occur in inflammation?

A

increased ISF puts pressure on nerves

105
Q

extrinsic pathway

A

damage to a vessel releases tissue factor and this is spreads into the bloodstream, and through a series of steps, activates factor X, resulting in prothrombinase

106
Q

extrinsic/intrinsic activation times

A

extrinsic occurs fast but doesn’t last long, whereas intrinsic takes longer to occur but has permanent effects

107
Q

another name for warfarin

A

coumarin

108
Q

components of the innate system

A

antimicrobial proteins, macrophages, complement proteins, interferons, iron binding proteins, and natural killer cells

109
Q

what does plasmin inactivate?

A

prothrombin and fibrinogen

110
Q

heparin vs coumarin

A

coumarin takes longer for results but is more long lasting than heparin; coumarin also is taken orally, whereas heparin is given via injection

Anatomy and Phyisology (94 decks)

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