Overview of Hemostatic Systems Flashcards by sophie rosen

hemostatic system

ancestral system designed to keep an individual from bleeding

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

vascular system
coagulation system
fibrinolytic system 
platelets 
kinin system
serine protease inhibitors 
complement system

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3 main stages of the hemostatic system

vasoconstriction of blood vessels
formation of a platelet plug
blood clotting which reinforces the platelet plug with a fibrin mesh

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what does a balance between procoagulant and anticoagulant forces maintain?

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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where does the term hemostasis come from

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

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why do you pinch a cut?

to prevent blood flow

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decreased blood pressure can lead to which 2 mechanisms?

endocrine mechanism

neural mechanism

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endocrine mechanism

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

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neural mechanism

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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vasoconstriction

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

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what is the mechanism of vasoconstriction?

sympathetic nerves trigger reflexive contraction of vascular smooth muscle

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

serotonin
endothelia-1
histamine

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serotonin is made and released by

platelets at neuromuscular junctions

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what are the direct actions of serotonin?

vasoconstrictor where present at high concentrations at sites of injury

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what are the indirect actions of serotonin?

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

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

mood
appetite
sleep

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endothelin-1 is made and released by

damaged endothelial cells

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

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

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histamine bind to

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

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histamine is produced and released from (2) during

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

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prostacyclin (PGI2) is a

vasodilator

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thromboxane A2 is a

vasoconstrictor

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PGI2

prostaglandin or eicosanoid

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what does PGI2 inhibit?

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

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prostacyclin (PGI2) mechanism

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.

PGI2 half life

42 seconds and is broken down to a weaker chemical form

where is TXA2 made and released?

by activated platelets and endothelial cells

TXA2 is a

prostaglandin

TXA2 stimulates

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

TXA2 half life

30 seconds, limits action to near site of production

state of vascular tone

balance between constrictor and dilator influences

what are extrinsic factors? (2)

sympathetic nerves | circulating factors

what increases and what decreases vascular tone?

increase: constrictors decrease: dilators

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

vascular tone

what are intrinsic factors influencing vascular tone? (4)

myogenic endothelial local substances metabolic byproducts or hypoxia

myogenic mechanisms arising from vascular smooth muscle

increase tone, constrict vessels

endothelial factors (2)

``` nitric oxide (vasodilator) endothelin (increase tone, vasoconstriction) ```

local factors (3)

``` arachidonic acid metabolites histamine bradykinin (vasodilator or vasoconstriction) ```

metabolic byproducts or hypoxia

generally decrease tone (vasodilation)

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

angiotensin 2 | circulating factors like atrial natriuretic peptide

angiotensin 2

increase vascular tone

circulating factors like atrial natriuretic peptide

decrease vascular tone, vasodilation

what do cell stressors such as ischemia active?

phospholipase A2

what does phospholipase A2 cleave?

arachidonic acid from membrane phospholipids and facilitates the formation of prostaglandins

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

PGI2 TXA2 PGE2

activated macrophage function (2)

phagocytosis and activation of bacterial mechanisms | antigen presentation

where are macrophages present?

in almost all tissues

macrophages are the mature form of

monocytes

what do macrophages orchestrate?

immune responses and half induce inflammation

what do macrophages secrete?

signaling proteins that activate other immune cells

macrophages are the general --- cells in the body

scavenger

what is the activated function of neutrophils?

phagocytosis and activation of bactericidal mechanisms

where are the primary neutrophil cells recruited?

to the site of acute inflammation (PNMs)

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

neutrophils

what is the activated function of mast cells?

release of granules containing histamine and active agents

what is histamine a critical factor in initiating?

the immune response mechanisms to fight inflammation

histamine causes

vasodilation

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

engage invading pathogens

what is histamine a mediator of?

itching

what are RBC produced from?

hemocytoblast (stem cell)

do you genotype RBC or WBC?

WBC because RBC are enucleate

platelets are released as

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

do platelets gave true cells?

platelets are cytoplasmic fragments with purple granules that contains chemicals for

blood clotting

blood clotting chemicals include (5)

``` enzymes serotonin ca2+ ions ADP PDGF ```

platelets are usually keep in the --- state, but

inactive | molecules secreted by endothelial cells of blood vessels

when activated, what do platelets form?

a temporary plug that helps to seal breaks in blood vessels

inflammation

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

5 cardinal signs of inflammation

``` pain heat redness swelling loss of function ```

``` allergic reaction chemical irritants infection trauma injury burns laceration, cuts, wounds frostbite ```

acute inflammation

``` cardiovascular disease neurological disease autoimmune disease rheumatoid arthritis cancer lupus fibromyalgia chronic fatigue syndrom ```

chronic inflammation

what are the 3 major components of acute inflammation?

vascular changes cellular events mediators

vascular changes

increased blood flow (vasodilation), increased vascular permeability

cellular events

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

mediators

derived from plasma cells and proteins

3 stages of the healing cascade

inflammation proliferation remodeling

inflammation

early phase - neurtophil arrival - pinoeering late phase -monocyte-mnacrophage

proliferation (3)

re-epithelialization -keratinocyte migration angiogenesis - spourting - endothelial migration granulation tissue - fibroblast migration - fibrin-collagen GT - glycosaminoglycans proteoglycans

remodeling

- apoptosis - collagen 3-1 - matrix-mellaproteinase activity

exudate:

high protein (>1.02)

transudate

low protein -alb. (<1.01)

pus

enriched in neutrophils

inflammation and hypersensitivity disease

type 1-4

type 1

anaphylactic

type 2

antibody dependent

type 3

immune complex type

type 4

cell mediated

type 1 inflammation and hypersensitivity diseases (allergy and atrophy)

* 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)

type 2 is --- dependent

antibody

type 2 cell membrane antigens are altered to

non-self

potential mechanisms of type 2 may be (3)

* 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

Direct binding by antibody to stimulate the cell (2)

* Blocking Ach receptor at NMJ (Myasthenia gravis) | * TSH receptor – Graves disease

what does type 3 involve?

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

type 3 only involves

complement binding antibodies

type 3 complexes are spread to

joints/kidneys

type 3 complexes precipitate and activate complement causing

tissue damage

type 4 is an important mechanism to

protect against intracellular pathogens (AIDS patients often get TB)

type 4 is mediated by

T cells rather than by antibody

what is the most important mediator of type 4 reaction?

IFNy

either --- or --- make cytokines after recognizing MHC2 of APCs

CD4 helper T cells | CD8 cytotoxicity T cells

what is critical for this process?

IL-12

examples of CD4 helper T cells (3)

Mantoux test for TB (tuberculin) nickel poison ivy

examples of CD8 cytotoxicity T cells (3)

graft rejection TB leprosy