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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
what is the molecular weight of low molecular weight heprins
2000 to 6000 daltons
26
waht si the advantage of using low molecular weight heprin
no monitoring and less side effects - less likely to cause thrombocytopenia the uses are the same as UF heprin
27
what is an example of a low molecualr weight heprin
enoxaparin this is more Xa selective thatn inbiiting thormbin
28
what is the action of warfarin
acts to prevent the formation of active clottings factors 7 9 10 and 2 (protrombin) inhibits the syntheiss of vitamin k dependent clotting facotors
29
formation of the clotting factors is dependent on what
dependent on the presense of vitamin k
30
what is the mechanism of action of warfain
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
31
what is the therapeutic use of warfain
dvt prophhylaxis and treatment embolism prophylaxis and treatment atrial fibrilation - prophylaxis of systemic embolism
32
why is afib concering for thromboembolism
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
33
what are side effects of warfarin
bleeding contraindicated in pregnancy
34
what is the antidote for warfarin
vitamin k1
35
can warfarin be used in pregnancy
causes fetal malformation striculy contraindicated category x
36
what are considerations for warfarin use
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
37
why must warfarin be overlapped with heprin
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
38
what are food and drug interactions with warfarin taht increaes the activity of warfarin and why
most nsaids cimetidne (macrolides and azoles) these drugs inhibit cytochrome p450 enzumes thus preventing warfarin metabolism this increaseing the activity of warfarin
39
what are food and drug interactins with warfarin that decrease the activity of warfarin and why
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
40
what is the action of dabigatran
direct thrombin inhibitor
41
what is the action of rivaroxaban
factor xa inhibitor
42
what are dabigatran and rivaroxaban uses
commonily used in prolypaxis treatment of a fib now replacing warfarin in treatment of DVT and pulmonary embolism long term therapy
43
dpes pt time need to be monitored with rivaroxaban dabigatran
prothrombin time does not need to be obtained
44
what are considerations with dabigatran and rivaroxaban
bleeding major concern do not require pt monitoring faster onset of action than warfarin limited drug to drug interaction compared iwth warfarin
45
what is the mechanism of action of aspirin and clopidogrel
inhibits platelet aggregation or prevents platelet activation
46
platelets have thormboxane a2 receptors on their surface and adp receptors what happens when thromboxin A two binds
binding of the thromboxin AII to the thromboxane receptor or adp to its receptor initiates platelet activation that leads to aggregation
47
the flbrinogen recetpor on platelets is called waht and what does it do
glycoprotein 2b3a receptor which recognizes fibrinogen on tohe platelets
48
stimulation by thromboxin a2 or adp causes waht
a cross linking of the platelets resulting in platelet aggregation
49
what does aspirin do
inhibits the cyclooxygenase 1 (cox1) enzyme and inhibits the formation of thrombozin A2 this inhibition if irreversable
50
what does clopidogrel do
inhibits the binding of adp to adp receptor and inhibits platelet aggregation
51
what are therapeudic uses fo aspirina nd clopidogrel
acture coronoary syndrome such as mi or unstable angina adjunct to percutaneous coronary intervention prophylaxis of transient ischemic attacks
52
why are aspirin and clopidogrel mandatory after mi
if it requires percutaenous cornonary intervention such as angioplasty or stenting goal to prevent new clot formation in colonary arteries
53
what are the side effects/considerations of aspirin and clopidogrel
gi in aspirin clopodogrel is a produg which requires the activatio of cyp450 enzymes - requires hepatic metabolism blood disorders (thrombotic thrombocytopenia, purpura, agranulocytosis
54
hemostasis is controleld by what
coagulation cascase and platlet aggredation
55
coagulation cascade results in the formation of what
fibrin clot
56
fibrin clot can be inhibtiied by what
anticoagulatns such as warfarin/heprin/noas such as riveroxiban and dabigatron
57
effect of antiogoaulation is monitored in vitro and manifests as
pt time in warfarin
58
platelet aggregatioon results in the formation of
platelet plug
59
platelet plug can be inhibtied by
antithormbotics like cox inhibitors and adp r antagonists
60
the effect of antithombotics manifests as
increased bleedig time
61
what is the antidote of warfarin
viatmin k1
62
what ios the antidote of heprin
protamine so4
63
when blood levels of lipids are elevated what can this lead to
lead to development of coronary artery disease
64
what is the biochemistry of lipoprotein
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
what are apolipoproteins
are a key part of the lipoprotein they rovide structure activate enzymes and serve as ligands ofr receptors
66
waht is the ligand for the LDL recepotr
apob100
67
what is the rate limiting step in cholesterol synthesis
hdm coa reductase enzyme is the rate limiting step in cholesterol synthesis
68
hdm coa reductase results in waht
leads to teh production of VLDL that are secreted by the hepatocytes into the blood stream
69
what is the composition of VLDL
triglyceride rich about 80% cholesterol
70
one VLDL is in the blood what happens q
they are acted upon by lipoprotein lipase these lipases revmoe the rriglycerisdes rseulting the for thefmatio fo free fatty acids
71
what do free fatty acids do
along with glucose are used as an energy source for the body
72
what is the structure of LDL
cholesterol rich protein triclyceride poor carry 60-70% of palsma cholesterol arise from metabolism of vldl remant
73
how is cholesterol delivered throughout the body
LDL binds to the LDL receptor and becomes internalized
74
what is cholesterol used by cells for
used by cells for making biological membranes, in steroid formation , in myelin formation and for bile salts
75
ldl can be deposited in teh intimal space of arteries such as
coronary arteries
76
LDL is removed by what
removed by ldl receptors in teh liver or peripheral tissues or deposeited into intimal space of coronary, carotid or peripharla arteries
77
HDl is involed in what
reverse cholesterol transport which takes excess cholestroll and returns it to the hapatocytes this is how we remove choleserol from the body
78
HDL possesses waht kind of effects
posesses anti aterogentic effects
79
when there is an incraese in LDL cholesterol then waht
there is a greater risk for cad
80
when we decrease LDL then what
we decrease the risk fo coronary artery diease
81
when LDL is deposited in the intimal space, what happens
ldl becomes oxidized leading to the formation fo atherscleroti cplaque this initiates an inflammatory cascade
82
what are risk factors for dyslipidemia
hypertension, smoking, diabetes, stress and genetic factors
83
what is the goal of therapy for dyslipidemia
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
what are examples of drugs for dyslipidemia
statins niacin fibrates bile acid sequestrants cholesterol absorption inhibitors
85
what are examples of statins
atorvastatin (lipitor) and pravastatin (pravachol)w
86
what is the pharmacology of statins
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
overall waht do stains do
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
what are side effects of statins
liver toxicity initially rhabdomyolysis msucle pain and weakness insulin resistance - incrase a1c contra indiceted in pregnacy
89
what are statins contraindicated in oregnacy
inhibit cholesterol synthesis which is required for fetal developent
90
what is the pharacolgy of niacin
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
what are the two forms of niacin
crystalline niacin systained release niacin
92
wahta are side ffects of crystalized niacin
flusing and itching this is prostaglandin mediated so treat with aspirin
93
what are side effects of niacin in sustained release form
hepatotoxicity so have to monitor liver function annually
94
why is niacin contraindicated in pregnancy
teratogeinc effects
95
what arre examples of the fibrates
clofibrate and gemfibrozil
96
what is the pharmacolgoy of fibrates
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
what are ppars
nuclear receptors that stimulate the transcription of specific genes following ligand binding
98
what are the side effects of fibrates
rhabdomyalysis especially when given with statins
99
what is an example of bile acid sequesterants
cholestyramine
100
what is the pharmacology of bile acid sequestrants
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
what are the side effects of bile acid sequesterants
potential increase of hmg coa reductase expression and stimualte cholestol synthesis so combine with statin therapy constipation and bloating
102
what is an example of cholesterol absorption inhibitor
ezetimibe (zetia)
103
what is the pharmacology of cholesterol absorption inhibitors ezetimibe
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
why would you combine ezetimbine witih statin
further decrease ldl levels both decrease in cholesterol absoption stain prevents compensatory increase in cholesterol in liver from hmg coa reductase upregualtion
105
side effect of zetia
side effect from combo w statin
106

Pharmacology (6 decks)

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