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coagulation Essay Example

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Published: May 15, 2018

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question

what is hemostasis?

answer

the balance between procoagulants and anticoagulants.

question

what happens when there is injury to a blood vessel?

answer

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question

vessel contraction, platelet aggregation and fibrin formation

what does von willebrand factor do?

answer

vWF binds to the edges of the perforation and to platelets, which stick together forming the primary hemostatic plug

question

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what is the difference between the primary and secondary hemostatic plugs?

answer

the platelets in the the secondary plug are more crammed together and the blood clot forms more tightly

question

what happens when platelets are activated?

answer

quiescent platelets are nondescript, but when activated they they throw out pseudopods and give off inflammation activators

question

where do platelets come from?

answer

megakaryocytes, have A LOT of DNA, found in the center of long bones

question

do platlets have

nuclei?

answer

question

what do platelets have inside them?

answer

granules holding many of the molecules needed for blood clotting, ADP, PDGF, (platelet derived growth factor), mitochondria, glycogen for energy which they burn in glycolysis, and many surface receptors

question

what are some things that will cause a signal to happen in a platelet? can these signals be amplified?

answer

ADP, serotonin, shear forces, thrombin, epinephrine, plasmin, PAF, Tx A2. these signals can be amplified.

question

what are two receptors on platelets

that allow them to adhere to the subendothelium and aggregate together, and how do they work?

answer

GpIIb-IIIa binds to fibrinogen which forms a bridge between platelets expressing GpIIb-IIIa, this creates aggregation. GpIb/IX/V binds to von Willebrand factors which bind to collagen on the subendothelium, allowing adhesion of the platelets expressing GpIb to the subendothelium. GpIIb-IIIa can also bind to von Willebrand factors.

question

how do GpIIb-IIIa and GpIb/IX/V bind to fibrinogen and vWF, (von willebrand factor)?

answer

GpIIb-IIIa and GpIb/IX/V bind to RGD, (arginine, glycine, aspartate), that is found on both fibrinogen and vWF

question

what is another function of vWF in coagulation?

answer

vWF also carries factor VIII in circulation, (one of the co-factors in the blood clotting cascade)

question

why would a deficiency in vWF cause more problems than a deficiency in GpIb/IX/V?

answer

with a deficiency in GpIb/IX/V, adhesion wouldn't work but clotting could still work, but with a deficiency in vWF, Factor VIII would not be present since vFW carries it, and therefore blood clotting could not occur

question

where do vWFs come from?

answer

weibel-palade bodies in platelet cells and endothelial cells or synthesized by the liver

question

can vWF bind 2 platelets together?

answer

yes

question

how is arachidonic acid released inside platelet or endothelial cells?

answer

on the cell membrane, phospholipids w/arachidonic acid in position 2 are cleaved by PLA2, (phospholipase A2),

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what do leukotrienes do?

answer

vasoconstrition, dialtion, vascular permeability

question

what enzymes synthesize arachidonic acid into prostaglandins or leukotrienes inside platelet or endothelial cells?

answer

arachidonic acid is made into prostaglandins via cyclooxygenase or into leukotrienes via lipoxygenases

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what happens to arachidonic acid once cleaved in the prostaglandin pathway of both platelet and endothelial cells?

answer

phospholipase A2 cuts arachidonic acid from the #2 postion, (of 3 on the FA), which then folds up and PGH synthase,(includes cyclooxygenase as the 1st component), carries out the next rxn, creating PGH2 - common intermediate in both platelet or endothelial cells

question

where does arachidonic acid come from?

answer

linoleic acid, omega 6 FA, (essential b/c human body can't make double bonds that far out). aside: if people ate more omega 3, there might be another molecule in the #2 position, which may help people with RA or other inflammatory diseases

question

what happens to PGH2 in platelet cells?

answer

an enzyme makes PGH2 into thromboxine A2, a prostaglandin that is a very powerful vasoconstrictor

question

what happens to PGH2 in endothelial cells?

answer

PGH2 is made by another enzyme which makes prostacyclin, (PGI2), a prostaglandin which is a very good vasodialator

question

what is the general hemostatic pattern with platelets and endothelial cells?

answer

platelets do something first and endothelial cells come back and do something later

question

what does aspirin, (salicylic acid), do in terms of the prostaglandin pathway? what do ibuprofen and other NSAIDs do?

answer

ASA blocks cyclooxygenase permanently via methylation, ibuprofen and other NSAIDs only do this reversibly.

question

what is COX-1 and where is it found? COX-2? are they produced constitutively? what do drugs intended to cause less stomach irritation target?

answer

COX is cyclooxygenase. COX-1 is found often in the stomach and is constitutive. COX-2 is inflammation-induced. drugs intended to cause less stomach irritation target COX-2.

question

what is the danger in taking too much ASA?

answer

COX permanently blocked in platelets cannot be replaced because platelets do not have nuclei, (however endothelial cells do have nuclei and are thus capable of creating more COX)

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how do platelets control vascular diameter?

answer

platlets can release serotonin and thromboxane A2 which vasoconstrict

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how do endothelial cells control vascular diameter?

answer

endothelial cells release endothelins which vasoconstricts, and nitric oxide and prostacyclin, (PGI2), which vasodialate

question

what happens to the phospholipids on the inside of the cell plasma membrane once arachidonic acid is cleaved from the #2 position? what charge do they now have?

answer

flipases move the newly negatively charged phospholipids to the extracellular surface, creating a negative charge important for the blood clotting process

question

what are characteristics of the blood coagulation cascade?

answer

an ordered series of rxns, specificity of enzymes, amplification of effects, 2 independent but converging pathways

question

how is thrombin, (IIa) formed?

answer

prothrombin, (II), is held to the outer surface of the cell membrane by Ca++ and the enzyme Xa cuts it in 2 places, via cofactor V, releasing thrombin, (IIa)

question

what is factor V activated by? where does it bind? what inactivates it?

answer

factor V is activated by thrombin, (so is factor XIII), to Va. it binds to the receptors on the platelet surface. activated protein C,

(APC), inactivates factor V to Vi, (factor XIII is inactivated similarly).

question

how do Ca++ ions bind factors to the cell surface?

answer

b/c flipase flipped the negatively charged phospholipids out onto the surface, Ca++ can bind to them. various factors have negative carboxyl groups that can then bind to Ca++, attaching them to the cell surface

question

how are factors II,VII,IX,X,C, and S prepared to attach to cell Ca++ ions on the cell surface? where does this happen?

answer

factors II,VII,IX,X,C, and S have glutamate residues with one carboxyl group, and then vit K adds another, giving them the right amount of negativity to bind to Ca++. this happens in the liver.

question

how does coumarin or wafarin keep factors II,VII,IX,X,C, and S from binding to the cell surface?

answer

vitamin K is oxidized during activation of factors, and must be reduced before the next rxn. coumarin derivatives, (warfarin/dicoumarol), block the reductases and thus inhibit the recycling of vit K.

question

what do the negatively charged phospholipids exposed to the external side of activated platelets help to do?

answer

concentrate reactants, achieve 2 dimensional diffusion, and orient the reactants for enzymatic reaction

question

how does a soft fibrin clot form?

answer

the center of fibrinogen has little little alpha and beta fibrinopeptides that are cut off by thrombin, leaving a very sticky middle portion that lines up with other

fibrin molecules to create non-covalent bonds. the clot becomes hard when the bonds become covalent via factor XIII. side note: fibrinopeptides are important to inflammation.

question

how is the soft fibrin clot, (non-covalent), made into a hard fibrin clot, (covalent)?

answer

a lysine from one fibrin is bound to the glutamine of another covalently via a peptide bond created by transglutaminase, (factor XIIIa, a ligase)

question

what activates factor XIIIa?

answer

thrombin

question

what is the relationship between factor XIIa and kallikrein? what is the cofactor for this rxn?

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factor XII is highly sensitive to activation and it changes prekallikrein to kallikrein. kallikrein then changes more factor XII to factor XIIa. the cofactor for this rxn is high molecular weight kininogen, (HMWK), which kallikrein takes a little peptide from to form bradykinin, (another inflammatory molecule)

question

what cells are at the core of anti-coagulation?

answer

endothelial cells

question

how is thrombin inactivated?

answer

endothelial cells make thrombomodulin, which thrombin binds to, this leads to activation of protein C, (APC), and APC inactivates factor Va->Vi as well as factor VIIIa->VIIIi

question

what happens with factor

V Leiden?

answer

there is a mutation in factor V where protein C, (APC), cannot inactivate factor V, and there is more clotting

question

how is a clot proteolyzed?

answer

plasminogen is activated by plasminogen activator, (PA), to plasmin. plasmin is a protease which cuts the clot into small pieces.

question

what is the regulation of plasmin enacted by?

answer

PAI blocks plasminogen activator, (PA), and alpha2-AP blocks plasmin itself

question

what are plasmin activators? where are they made? are there plasmin activators

that can be given to patients?

answer

TPA, (tissue plasminogen activator), made in vascular endothelial cells. there is also SEU, (single chain eurokinase). streptokinase can be injected and works as a plasmin activator.

question

where do inhibitors of protease enzymes come from? what are the two basic kinds?

answer

clotting enzymes and others are produced in the liver and circulate in the blood. the inhibitors usually either inactivate or trap blood clotting factors. inactivation is usually enacted in the "suicide substrate" method, where the complex of inhibitor+clotting factor is cleared from circulation

question

what does alpha2-macroglobulin do?

answer

a large molecule acts as a trap for clotting factors. it is shaped like a mouth with residues that attract clotting factors, that alpha2-macroglobulin folds over, trapping them. the clotting

factors are still active, just no longer free, and the complex is cleared from circulation.

question

what are serpines?

answer

suicide inhibitors of serine proteases, that enzymes bind to, but the bond is irreversible and the complex is cleared from circulation

question

what are some examples of serpines?

answer

alpha1-protease inhibitor, (alpha1P1), antithrombinIII, (ATIII), plasminogen activator inhibitor, (PAI-1, PAI-2), alpha1-antiplasmin, (alpha1AP), and C1-Inh

question

what is alpha1-protease inhibitor do, what is it related to?

answer

alpha-1PI inhibits many clotting factors, it was formerly

called alpha1-antitrypsin. it is a serpin.

question

what does antithrombin III do?

answer

inhibits mostly factor X and thrombin. it is a serpin. it can also inhibit IX, XI, and XII

question

what does C1-Inhibitor do?

answer

C1-Inh inhibits most everything along the intrinsic pathway

question

what do the protease inhibitors have in common?

answer

they are all serine inhibitors, b/c protease has a serine in it

question

what is the tissue factor pathway inhibitor? what is it made by?

answer

TF is the co-factor for the extrinsic pathway, (factor VII->VIIa and VIIa activates factor X). endothelial cells produce TF, thus inhibiting factors VIIa and Xa

question

what does heparin do, where does it come from? what are the different types?

answer

heparin can be made in endothelial cells or it can be administered to pts. it binds to antithrombinIII, (ATIII), to enhance its inhibitory activity, (by conformational changes in ATIII and actually pulling in thrombin or factor Xa). there is high and low molecular weight, (HMW+LMW). HMW also activates PAI but LMW is used clinically

question

what are 2 tests for primary hemostasis?

answer

platelet count, to determine # of thrombocytes, (looking for thrombocytopenia). bleeding time is tested blotting every 15 sec until bleeding stops, this can help assess clotting factors and platelet count.

question

what is the PTT?

answer

partial thromboplastin, (phosphoplipid), time -> tests the intrinsic and common pathways. it is done by putting the pt's plasma, a phospholipid, kaolin, and Ca++ into a test tube. 2 electrodes move towards each other until a bloot clot forms, and then the machine stops. this tests for heparin or severe deficiencies of the common or instrinsic pathway. it is relatively slow, as it goes from factor XII to XI, X, prothrombin, fibrin, (25-27 sec avg).

question

how does the PTT measure effects of heparin?

answer

heparin enhances antithrombin III, which primarily inhibits

factor Xa and thrombin, (factor IIa), in the common pathway. it also inhibits factors IXa, XIa, and XIIa of the intrinsic pathway. thus if heparin is present, it should take longer for the clot to form

question

what is the PT test? how is it done and what does it measure?

answer

prothrombin time. in a test tube the pt's plasma, phospholipid, tissue factor, (cofactor for extrinsic pathway), and Ca++ are mixed. this tests the pt's common and extrinsic pathways and is used to test the effect of coumadin and the presence of deficiences. this test takes a shorter time, (VII->VIIa, X->Xa, II->IIa ~15 secs)

question

what is the INR?

answer

international normalized ration, which is used to standardize PT from various labs. it is calculated by dividing the pts PT/PT notmal mean. a ratio of 1 = normal, around 10-12 sec, a ratio of 2 means

the pt is 2x normal, (20-24 sec). 3x-4x is probably too much coumadin.

question

what does coumadin do?

answer

blocks action of vitamin K in the liver, post-translational additon of a gamma carboxyl group on factors II, (thrombin), VII, IX, X, and proteins S and C, (S is C's cofactor). this takes time as the liver is making new blood clotting factors

question

what test would you use for a pt with a factor VIII deficiency?

answer

PTT

question

what test would you use for a pt with a PF4, (platelet factor 4), deficiency?

answer

neither

question

what test would you use for a pt with a factor VII deficiency?

answer

question

what test would you use for a pt with a factor XII deficiency?

answer

question

what test would you use for a pt on heparin?

answer

PTT

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question

what test would you use for a pt on coumadin?

answer

coagulation Essay Example

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