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Applied Biochemistry > Overview of Hemostatic Systems > Flashcards

Overview of Hemostatic Systems Flashcards

1
Q

hemostatic system

A

ancestral system designed to keep an individual from bleeding

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2
Q

what other systems within the body does the hemostatic system include? (7)

A 
vascular system
coagulation system
fibrinolytic system 
platelets 
kinin system
serine protease inhibitors 
complement system
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3
Q

3 main stages of the hemostatic system

A
  1. vasoconstriction of blood vessels
  2. formation of a platelet plug
  3. blood clotting which reinforces the platelet plug with a fibrin mesh
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4
Q

what does a balance between procoagulant and anticoagulant forces maintain?

A

blood in a fluid state and flowing through the vasculature to deliver oxygen to tissues systemically and remove carbon dioxide and toxic waste products

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5
Q

where does the term hemostasis come from

A

greek words
heme=blood + states
halt= halt from blood

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6
Q

why do you pinch a cut?

A

to prevent blood flow

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7
Q

decreased blood pressure can lead to which 2 mechanisms?

A

endocrine mechanism

neural mechanism

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8
Q

endocrine mechanism

A

ASH, angiotensin 2, aldosterone, EPO released
increase in blood volume
homeostasis restored

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9
Q

neural mechanism

A

baroreceptors, chemoreceptors stimulated
cardiovascular centers stimulated
general sympathetic activation, release norepinephrine, epinephrine

increase cardiac output
peripheral vasoconstriction, increase blood pressure, decrease venous reserve

homeostasis restored

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10
Q

vasoconstriction

A

contraction of smooth muscle cells to vessel walls to restrict the loss/flow of blood at site of injury

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11
Q

what is the mechanism of vasoconstriction?

A

sympathetic nerves trigger reflexive contraction of vascular smooth muscle

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12
Q

what are the other regulatory substances which also affect vascular tone? (3)

A

serotonin
endothelia-1
histamine

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13
Q

serotonin is made and released by

A

platelets at neuromuscular junctions

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14
Q

what are the direct actions of serotonin?

A

vasoconstrictor where present at high concentrations at sites of injury

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15
Q

what are the indirect actions of serotonin?

A

can act as a vasodilator when stimulates nitric oxide release by endothelial cells

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16
Q

serotonin is also synthesized by serotonergic neurons of the CNS, where it regulates (3)

A

mood
appetite
sleep

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17
Q

endothelin-1 is made and released by

A

damaged endothelial cells

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18
Q

endothelin-1 is normally kept in balance by other mechanisms, but when over expressed can contribute to (3)

A

hypertension
heart disease
other vascular diseases of the heart, lung, kidney, and brain

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19
Q

histamine bind to

A

one of four different histamine GPCR on GI, uterus, lung, and vascular smooth muscle cells

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20
Q

histamine is produced and released from (2) during

A

basophils (circulation) and mast cells (connective tissue) during local immune responses

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21
Q

prostacyclin (PGI2) is a

A

vasodilator

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22
Q

thromboxane A2 is a

A

vasoconstrictor

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23
Q

PGI2

A

prostaglandin or eicosanoid

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24
Q

what does PGI2 inhibit?

A

platelet activation and is also an effective vasodilator (acts to counteract actions of TXA2)

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25
Q

prostacyclin (PGI2) mechanism

A

Mechanistically, PGI2 binds to the PGI2 receptor which is a Gs protein coupled receptor which signals via adenylyl cyclase to produce cAMP. cAMP activates protein kinase A which promotes the phosphorylation and inhibition of myosin light chain kinase which leads to vascular smooth muscle relaxation and vasodilation.

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26
Q

PGI2 half life

A

42 seconds and is broken down to a weaker chemical form

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27
Q

where is TXA2 made and released?

A

by activated platelets and endothelial cells

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28
Q

TXA2 is a

A

prostaglandin

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29
Q

TXA2 stimulates

A

activation of new platelets as well as increases platelet aggregation by increasing expression of glycoprotein complex GP2b/3a (fibrinogen receptor) on platelet membranes

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30
Q

TXA2 half life

A

30 seconds, limits action to near site of production

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31
Q

state of vascular tone

A

balance between constrictor and dilator influences

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32
Q

what are extrinsic factors? (2)

A

sympathetic nerves

circulating factors

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33
Q

what increases and what decreases vascular tone?

A

increase: constrictors
decrease: dilators

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34
Q

vasoconstrictor and vasodilator influences acting on arteries and veins determine their state of

A

vascular tone

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35
Q

what are intrinsic factors influencing vascular tone? (4)

A

myogenic
endothelial
local substances
metabolic byproducts or hypoxia

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36
Q

myogenic mechanisms arising from vascular smooth muscle

A

increase tone, constrict vessels

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37
Q

endothelial factors (2)

A 
nitric oxide (vasodilator) 
endothelin (increase tone, vasoconstriction)
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38
Q

local factors (3)

A 
arachidonic acid metabolites 
histamine 
bradykinin (vasodilator or vasoconstriction)
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39
Q

metabolic byproducts or hypoxia

A

generally decrease tone (vasodilation)

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40
Q

what are examples of extrinsic factors influencing vascular tone? (2)

A

angiotensin 2

circulating factors like atrial natriuretic peptide

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41
Q

angiotensin 2

A

increase vascular tone

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42
Q

circulating factors like atrial natriuretic peptide

A

decrease vascular tone, vasodilation

43
Q

what do cell stressors such as ischemia active?

A

phospholipase A2

44
Q

what does phospholipase A2 cleave?

A

arachidonic acid from membrane phospholipids and facilitates the formation of prostaglandins

45
Q

what are the principle postanoids we focus on? (3)

A

PGI2
TXA2
PGE2

46
Q

activated macrophage function (2)

A

phagocytosis and activation of bacterial mechanisms

antigen presentation

47
Q

where are macrophages present?

A

in almost all tissues

48
Q

macrophages are the mature form of

A

monocytes

49
Q

what do macrophages orchestrate?

A

immune responses and half induce inflammation

50
Q

what do macrophages secrete?

A

signaling proteins that activate other immune cells

51
Q

macrophages are the general — cells in the body

A

scavenger

52
Q

what is the activated function of neutrophils?

A

phagocytosis and activation of bactericidal mechanisms

53
Q

where are the primary neutrophil cells recruited?

A

to the site of acute inflammation (PNMs)

54
Q

what are the most numerous of the phagocytic cells and most important in innate immune responses?

A

neutrophils

55
Q

what is the activated function of mast cells?

A

release of granules containing histamine and active agents

56
Q

what is histamine a critical factor in initiating?

A

the immune response mechanisms to fight inflammation

57
Q

histamine causes

A

vasodilation

58
Q

histamine permits entry of cells and proteins into the site of the infection to

A

engage invading pathogens

59
Q

what is histamine a mediator of?

A

itching

60
Q

what are RBC produced from?

A

hemocytoblast (stem cell)

61
Q

do you genotype RBC or WBC?

A

WBC because RBC are enucleate

62
Q

platelets are released as

A

nuclear membrane limited bags filled with granules and vesicles from very large bone marrow cells called megakaryocytic

63
Q

do platelets gave true cells?

A

no

64
Q

platelets are cytoplasmic fragments with purple granules that contains chemicals for

A

blood clotting

65
Q

blood clotting chemicals include (5)

A 
enzymes 
serotonin
ca2+ ions 
ADP
PDGF
66
Q

platelets are usually keep in the — state, but

A

inactive

molecules secreted by endothelial cells of blood vessels

67
Q

when activated, what do platelets form?

A

a temporary plug that helps to seal breaks in blood vessels

68
Q

inflammation

A

the body process of fighting against things that harm it, such as infections, injuries, and toxins, in attempt to heal itself

69
Q

5 cardinal signs of inflammation

A 
pain
heat 
redness
swelling
loss of function
70
Q 
allergic reaction
chemical irritants 
infection
trauma injury 
burns 
laceration, cuts, wounds
frostbite
A

acute inflammation

71
Q 
cardiovascular disease 
neurological disease
autoimmune disease
rheumatoid arthritis 
cancer lupus
fibromyalgia 
chronic fatigue syndrom
A

chronic inflammation

72
Q

what are the 3 major components of acute inflammation?

A

vascular changes
cellular events
mediators

73
Q

vascular changes

A

increased blood flow (vasodilation), increased vascular permeability

74
Q

cellular events

A

migration of leukocytes (mainly neutrophils of PMNs) into the site of injury (cellular recruitment and activation)

75
Q

mediators

A

derived from plasma cells and proteins

76
Q

3 stages of the healing cascade

A

inflammation
proliferation
remodeling

77
Q

inflammation

A

early phase

  • neurtophil arrival
  • pinoeering

late phase
-monocyte-mnacrophage

78
Q

proliferation (3)

A

re-epithelialization
-keratinocyte migration

angiogenesis

  • spourting
  • endothelial migration

granulation tissue

  • fibroblast migration
  • fibrin-collagen GT
  • glycosaminoglycans proteoglycans
79
Q

remodeling

A
  • apoptosis
  • collagen 3-1
  • matrix-mellaproteinase activity
80
Q

exudate:

A

high protein (>1.02)

81
Q

transudate

A

low protein -alb. (<1.01)

82
Q

pus

A

enriched in neutrophils

83
Q

inflammation and hypersensitivity disease

A

type 1-4

84
Q

type 1

A

anaphylactic

85
Q

type 2

A

antibody dependent

86
Q

type 3

A

immune complex type

87
Q

type 4

A

cell mediated

88
Q

type 1 inflammation and hypersensitivity diseases (allergy and atrophy)

A
  • Hayfever
  • Bee sting
  • Allergic Asthma
  • Penicillin-prototype
  • Codeine•Morphine
  • Heat/Cold/UV
  • Allergen “skin prick tests”
  • Nasal Polyps
  • Aspirin
  • Parasites (schistosomes “nuked” by IgE armed leukocytes)
89
Q

type 2 is — dependent

A

antibody

90
Q

type 2 cell membrane antigens are altered to

A

non-self

91
Q

potential mechanisms of type 2 may be (3)

A
  • Complement mediated lysis of host cells (e.g., Rh incompatibility, blood transfusion, RX drug)
  • Antibody dependent cell mediated cytotoxicity (ADCC) without complement as in dealing with schistosomes
  • Direct binding by antibody to stimulate the cell
92
Q

Direct binding by antibody to stimulate the cell (2)

A
  • Blocking Ach receptor at NMJ (Myasthenia gravis)

* TSH receptor – Graves disease

93
Q

what does type 3 involve?

A

soluble immune complexes (IgM, IgG, IgA) of antibody and antigen

94
Q

type 3 only involves

A

complement binding antibodies

95
Q

type 3 complexes are spread to

A

joints/kidneys

96
Q

type 3 complexes precipitate and activate complement causing

A

tissue damage

97
Q

type 4 is an important mechanism to

A

protect against intracellular pathogens (AIDS patients often get TB)

98
Q

type 4 is mediated by

A

T cells rather than by antibody

99
Q

what is the most important mediator of type 4 reaction?

A

IFNy

100
Q

either — or — make cytokines after recognizing MHC2 of APCs

A

CD4 helper T cells

CD8 cytotoxicity T cells

101
Q

what is critical for this process?

A

IL-12

102
Q

examples of CD4 helper T cells (3)

A

Mantoux test for TB (tuberculin)
nickel
poison ivy

103
Q

examples of CD8 cytotoxicity T cells (3)

A

graft rejection
TB
leprosy

Applied Biochemistry (52 decks)

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