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Pharmacology > Mod 4 Anticoagulation > Flashcards

Mod 4 Anticoagulation Flashcards

1
Q

hemostasis involves pathways what what

A

bring about a cessation of bleeding

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2
Q

in clot formation there are intrinsic and extreins pathways that converge where and do what

A

these pathways converge on the step where prothrombin factor II is converted to thrombin factor IIa by factor Xa
thrombin then acts on fibrinogen to produce fibring
this is monomeric fibring that then becomes cross linked to form the clot

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3
Q

red clots result when

A

result when red blood cells become trapped in the fibrin mesh
these usually occur on the venous side of the circulation and can result in thromboembolism

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4
Q

drugs taht act on red clot part of the pathway care called what

A

anticoagulants

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5
Q

what does warfarin do

A

inhibits the syntheiss of prothrombin by inhibting the formation of active vitamin K

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6
Q

what does unfractionated hpring do

A

inhibtis btoh the activation of prothrombin by factor Xa and the activity of thrombin

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7
Q

low molecular weight fractionated heprins are more selective in inhibting what

A

factor Xa

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8
Q

what is an example of selective Xa inhibtior

A

xarelto (rivaroxoban) and thomin inhibitors sich as dabatran (pradaxa)

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9
Q

drugs that prevent platelet aggregation do what

A

prolong the bleeding time

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10
Q

without platelet aggregation what happens

A

no plug is formed and the bleeing time is prolonged

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11
Q

platelets for what kind of clot

A

white clot that is typically found on the arterial side and can lead to embolism

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12
Q

drugs taht inhibit platlet aggregation include

A

aspirin and clopidogrel

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13
Q

what does aspirin do

A

inhibtis cycooygenase enzyme thus inhibiting the production fo thromboxi AII

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14
Q

what does clopidogrel do

A

inhibits the binding of ADP to its receptor site on platelets thus inhibiting platelet activation

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15
Q

unfractionated heprin is a mixture of what

A

acid mucoolysaccharide

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16
Q

since unfractionated heprin is unfractuonated what can the molecular weight be

A

can range anywhere from 2000-30000 daltons

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17
Q

what is the mechanism of action of heprin

A

antithrombin III (naturally occuring protein found in blood) binds to rhombin producing an inactive complex and this process normally occurs slowly
when heprin binds to antithrombin, it causes a 1000 fold incraese in teh rate of the reaction
once the heprin antithrombin thrombin complex is fomred, heprin can dissocated and bind to other antithrombin proteins causing more complexes to be formed

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18
Q

what is one advantage of heprin to warfarin

A

it acts immediately
heprin is normally given intravenously
sometimes given subcutaneously
never given IM becuase of the risk of hematoma formation

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19
Q

what is the pharmacology of unfractionated heprin

A

ufh inhibits factors IIa (thrombin) and Xa

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20
Q

what are the therapeutic uses of heprin

A

dvt prophalaxis and treatmetn
embolism prophylax and treatment pulmonary
percutantoes coronary intervetntion, blod transfusions, dialysis

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21
Q

what are the side effects of heprin

A

bleeding - avoid bleeding diathesis/uncontrolled bleeding
thrombocytopenia

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22
Q

what is the antidote for heprin

A

protamie sulfate

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23
Q

how does protamine sulfate work

A

excessive bleeding with unfractionated heprin can be treated with protamine sulfate that binfs to heprin and prvents heprin from binding to antithombin

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24
Q

what is thrombocytopenia

A

most serious side effect of unfractionated heprin
results from a drop in platelets
if this occurs then heprin treatment must immediately be stopped

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25
Q

what is the molecular weight of low molecular weight heprins

A

2000 to 6000 daltons

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26
Q

waht si the advantage of using low molecular weight heprin

A

no monitoring and less side effects - less likely to cause thrombocytopenia
the uses are the same as UF heprin

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27
Q

what is an example of a low molecualr weight heprin

A

enoxaparin
this is more Xa selective thatn inbiiting thormbin

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28
Q

what is the action of warfarin

A

acts to prevent the formation of active clottings factors 7 9 10 and 2 (protrombin)
inhibits the syntheiss of vitamin k dependent clotting facotors

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29
Q

formation of the clotting factors is dependent on what

A

dependent on the presense of vitamin k

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30
Q

what is the mechanism of action of warfain

A

vitamin k epoxide reductase is an enyme that converts oxidized inactive vitamin K to reduced active vitamin K
vitamin k serves as a cofactor in the synthesis of the clotting factors such as prothrombin

inhibit virtamin k epoxide reductase
as a result there is no vitamin k available to use for the synthesis of clotting factors

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31
Q

what is the therapeutic use of warfain

A

dvt prophhylaxis and treatment
embolism prophylaxis and treatment
atrial fibrilation - prophylaxis of systemic embolism

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32
Q

why is afib concering for thromboembolism

A

results in the pooling of blood in the atria and can result in the developemnt of thromboembolism
this can cause embolism of cerebral vesles and stroke
warfarin prior to and following afib treatment

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33
Q

what are side effects of warfarin

A

bleeding
contraindicated in pregnancy

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34
Q

what is the antidote for warfarin

A

vitamin k1

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35
Q

can warfarin be used in pregnancy

A

causes fetal malformation
striculy contraindicated
category x

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36
Q

what are considerations for warfarin use

A

oral bioavailabilty - can be oral and good for outpt use
dalyaed onset of action so must overlap with heprin
must monitor prothrombin time (pt)
warfain undergores microsomal metabolism (cyp 2c9)
cyp 2c9 inhibitors will prolong the warfarin pt time

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37
Q

why must warfarin be overlapped with heprin

A

clotting cascade proteins have long half life of 4-6 hours for factor 7 up to 60 ohurs for protrhombin
so even if you inhibit the synthesis of new clotting factors with warfain, you still have clotting facotrs that are already present in the blood
as a result onet of warfarin actin can be delayed for days for even weeks
improtant when starting warfarin to overlap therapy with heparin

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38
Q

what are food and drug interactions with warfarin taht increaes the activity of warfarin and why

A

most nsaids
cimetidne (macrolides and azoles)
these drugs inhibit cytochrome p450 enzumes thus preventing warfarin metabolism this increaseing the activity of warfarin

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39
Q

what are food and drug interactins with warfarin that decrease the activity of warfarin and why

A

phenobarbital
bile acid resins
vitamin k foods
induce cyp405 enzymes increasing warfarin metabolism reducing warfarin activity
need to incrase dose of warfarin if take cyp450 inducler

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40
Q

what is the action of dabigatran

A

direct thrombin inhibitor

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41
Q

what is the action of rivaroxaban

A

factor xa inhibitor

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42
Q

what are dabigatran and rivaroxaban uses

A

commonily used in prolypaxis treatment of a fib
now replacing warfarin in treatment of DVT and pulmonary embolism long term therapy

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43
Q

dpes pt time need to be monitored with rivaroxaban dabigatran

A

prothrombin time does not need to be obtained

44
Q

what are considerations with dabigatran and rivaroxaban

A

bleeding major concern
do not require pt monitoring
faster onset of action than warfarin
limited drug to drug interaction compared iwth warfarin

45
Q

what is the mechanism of action of aspirin and clopidogrel

A

inhibits platelet aggregation or prevents platelet activation

46
Q

platelets have thormboxane a2 receptors on their surface and adp receptors what happens when thromboxin A two binds

A

binding of the thromboxin AII to the thromboxane receptor or adp to its receptor initiates platelet activation that leads to aggregation

47
Q

the flbrinogen recetpor on platelets is called waht and what does it do

A

glycoprotein 2b3a receptor which recognizes fibrinogen on tohe platelets

48
Q

stimulation by thromboxin a2 or adp causes waht

A

a cross linking of the platelets resulting in platelet aggregation

49
Q

what does aspirin do

A

inhibits the cyclooxygenase 1 (cox1) enzyme and inhibits the formation of thrombozin A2
this inhibition if irreversable

50
Q

what does clopidogrel do

A

inhibits the binding of adp to adp receptor and inhibits platelet aggregation

51
Q

what are therapeudic uses fo aspirina nd clopidogrel

A

acture coronoary syndrome such as mi or unstable angina
adjunct to percutaneous coronary intervention
prophylaxis of transient ischemic attacks

52
Q

why are aspirin and clopidogrel mandatory after mi

A

if it requires percutaenous cornonary intervention such as angioplasty or stenting
goal to prevent new clot formation in colonary arteries

53
Q

what are the side effects/considerations of aspirin and clopidogrel

A

gi in aspirin
clopodogrel is a produg which requires the activatio of cyp450 enzymes - requires hepatic metabolism
blood disorders (thrombotic thrombocytopenia, purpura, agranulocytosis

54
Q

hemostasis is controleld by what

A

coagulation cascase and platlet aggredation

55
Q

coagulation cascade results in the formation of what

A

fibrin clot

56
Q

fibrin clot can be inhibtiied by what

A

anticoagulatns such as warfarin/heprin/noas such as riveroxiban and dabigatron

57
Q

effect of antiogoaulation is monitored in vitro and manifests as

A

pt time in warfarin

58
Q

platelet aggregatioon results in the formation of

A

platelet plug

59
Q

platelet plug can be inhibtied by

A

antithormbotics like cox inhibitors and adp r antagonists

60
Q

the effect of antithombotics manifests as

A

increased bleedig time

61
Q

what is the antidote of warfarin

A

viatmin k1

62
Q

what ios the antidote of heprin

A

protamine so4

63
Q

when blood levels of lipids are elevated what can this lead to

A

lead to development of coronary artery disease

64
Q

what is the biochemistry of lipoprotein

A

lipoproteins have an inner hydrophobic core with cholesterol esterase and triglycerides
there are different ratios of cholesterols and triglycerides in lipoprotiens
there is also an outer hydrophillic coat with phospholipiids unsterifed cholesterole (free) and apolipoproteins

65
Q

what are apolipoproteins

A

are a key part of the lipoprotein
they rovide structure activate enzymes and serve as ligands ofr receptors

66
Q

waht is the ligand for the LDL recepotr

A

apob100

67
Q

what is the rate limiting step in cholesterol synthesis

A

hdm coa reductase enzyme is the rate limiting step in cholesterol synthesis

68
Q

hdm coa reductase results in waht

A

leads to teh production of VLDL that are secreted by the hepatocytes into the blood stream

69
Q

what is the composition of VLDL

A

triglyceride rich
about 80% cholesterol

70
Q

one VLDL is in the blood what happens q

A

they are acted upon by lipoprotein lipase
these lipases revmoe the rriglycerisdes rseulting the for thefmatio fo free fatty acids

71
Q

what do free fatty acids do

A

along with glucose are used as an energy source for the body

72
Q

what is the structure of LDL

A

cholesterol rich protein
triclyceride poor
carry 60-70% of palsma cholesterol
arise from metabolism of vldl remant

73
Q

how is cholesterol delivered throughout the body

A

LDL binds to the LDL receptor and becomes internalized

74
Q

what is cholesterol used by cells for

A

used by cells for making biological membranes, in steroid formation , in myelin formation and for bile salts

75
Q

ldl can be deposited in teh intimal space of arteries such as

A

coronary arteries

76
Q

LDL is removed by what

A

removed by ldl receptors in teh liver or peripheral tissues or deposeited into intimal space of coronary, carotid or peripharla arteries

77
Q

HDl is involed in what

A

reverse cholesterol transport which takes excess cholestroll and returns it to the hapatocytes
this is how we remove choleserol from the body

78
Q

HDL possesses waht kind of effects

A

posesses anti aterogentic effects

79
Q

when there is an incraese in LDL cholesterol then waht

A

there is a greater risk for cad

80
Q

when we decrease LDL then what

A

we decrease the risk fo coronary artery diease

81
Q

when LDL is deposited in the intimal space, what happens

A

ldl becomes oxidized leading to the formation fo atherscleroti cplaque
this initiates an inflammatory cascade

82
Q

what are risk factors for dyslipidemia

A

hypertension, smoking, diabetes, stress and genetic factors

83
Q

what is the goal of therapy for dyslipidemia

A

goal for therapy are to improve lipiprotein profules and reduce palque formation and stabilize existing plaques
like to reduce 20% of ldl during treatment

84
Q

what are examples of drugs for dyslipidemia

A

statins
niacin
fibrates
bile acid sequestrants
cholesterol absorption inhibitors

85
Q

what are examples of statins

A

atorvastatin (lipitor) and pravastatin (pravachol)w

86
Q

what is the pharmacology of statins

A

stains inhibit hmg coa reductase thus inhibtiiign the early rate limiting step in cholesterol biosynthesis
decrease in hepatic vldl and plasma ldl and will cause an increase in teh expression of ldl receptors
with an incraese in ldl receptors there is more ldl taken up into hepatocytes and less blood cholesterol

87
Q

overall waht do stains do

A

inhibt hmg coa resuctase
reduce choleserol synthesis
decrease plasma ldl levels (20-25%)
increaed expression fo ldl receptors
small change in hdl and triglyceride?

88
Q

what are side effects of statins

A

liver toxicity initially
rhabdomyolysis msucle pain and weakness
insulin resistance - incrase a1c
contra indiceted in pregnacy

89
Q

what are statins contraindicated in oregnacy

A

inhibit cholesterol synthesis which is required for fetal developent

90
Q

what is the pharacolgy of niacin

A

vit b3
decreaes vldl secretion from hepatocytes this reduced blood ldl
reduced triglycerides 35-40%
reduced plasma ldl levels (20-30%0
increases plasma hdl levels (30-40%)

91
Q

what are the two forms of niacin

A

crystalline niacin
systained release niacin

92
Q

wahta are side ffects of crystalized niacin

A

flusing and itching
this is prostaglandin mediated so treat with aspirin

93
Q

what are side effects of niacin in sustained release form

A

hepatotoxicity so have to monitor liver function annually

94
Q

why is niacin contraindicated in pregnancy

A

teratogeinc effects

95
Q

what arre examples of the fibrates

A

clofibrate and gemfibrozil

96
Q

what is the pharmacolgoy of fibrates

A

these drugs bind to peroxosome proliferator activated receptors (PPAR)
this causes increased expression of ldl receptors
leads to modest decrase in ldl and decrease in triglycerides

97
Q

what are ppars

A

nuclear receptors that stimulate the transcription of specific genes following ligand binding

98
Q

what are the side effects of fibrates

A

rhabdomyalysis especially when given with statins

99
Q

what is an example of bile acid sequesterants

A

cholestyramine

100
Q

what is the pharmacology of bile acid sequestrants

A

bile acid sequensterants become retained in the lumen of the gut
in the gut they bind to bile acids and prevent to absorptin
this stimulates the coversoin of cholesterol to bile acids in the liver and thus a decrease in cholesetrol synthesis
this leads to compensatory increase in ldl receptor expression
decrase in plasma ldl levels
since bile acid sequenterants decrese choleserol levels there can be a conpensatory increase in hmg coa reductase
this is situation where statin that inhbits hmg coa reductase might be coadminsitered

101
Q

what are the side effects of bile acid sequesterants

A

potential increase of hmg coa reductase expression and stimualte cholestol synthesis so combine with statin therapy
constipation and bloating

102
Q

what is an example of cholesterol absorption inhibitor

A

ezetimibe (zetia)

103
Q

what is the pharmacology of cholesterol absorption inhibitors ezetimibe

A

resuced cholesrol absorpiton (inhibit intestinal absorpiton of choelsterol)
reduces ldl levls plasma and leads to a compensatory increase in hepatic LDL receptor expression do increased liver ldl
little to no effect on triglycerides and hdl

104
Q

why would you combine ezetimbine witih statin

A

further decrease ldl levels
both decrease in cholesterol absoption
stain prevents compensatory increase in cholesterol in liver from hmg coa reductase upregualtion

105
Q

side effect of zetia

A

side effect from combo w statin

106
Q
A

Pharmacology (6 decks)

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