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NUR 326 > module 5 > Flashcards

module 5 Flashcards

1
Q

what is thrombogenesis

A

the formation of blood clots, a normal body defense mechanism to prevent blood loss. it is life saving in the case of hemorrhage and life threatening in the case of thrombus obstruction

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2
Q

What us the sequence that has to occur for blood clotting?

A

When there is a blood vessel injury, the blood is exposed to sub endothelial cells. That triggers XIIs activation to XIIa, this active version XIIa activates facotr XI to its active form factor XIa. Which along with ca+ Activates factor IX to its active form IXa. Factor 9 activates factor 10 which converts prothrombin to thrombin which converts fibrinogen to fibrin

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3
Q

arterial thrombosis

A

occurs when platelets initiate the process followed by fibrin formation which causes RBCs to be trapped in the fibrin and obstruct blood flow. this is usually associated with atherosclerotic plaques, hypertension, and turbulent blood flow.

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4
Q

venous thrombosis

A

when platelet aggregation combines with fibrin and attaches tot he RBC. venous thrombosis is usually associated with venous stasis. when blood flows slowly, thrombin and other procoagulant substances become concentrated and initiate the clotting process.

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5
Q

which is more likely to travel and why? a venous or arterial thrombosis

A

a venous thrombosis because there is no atherosclerosis on the walls of the venous vessels making the clots less cohesive.

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6
Q

where do arterial blood clots likely manifest?

A

cerebral arteries: stroke
pulmonary arteries: pulmonary embolism
cardiac system: MI

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7
Q

what can venous blood clots lead to

A

DVT. these are often times (50%) asymptomatic

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8
Q

what do anticoagulants do

A

prevent formation of new clots and prevent extension of existing ones. DO NOT DISSOLVE
-allow the blood to thin so it is easier for the blood to get by the clot

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9
Q

antiplatelets

A

prevent platelet aggregation and are mainly used to prevent arterial thrombosis

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10
Q

thrombolytic drugs

A

attack and dissolve blood clots already formed

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11
Q

what are anticoags used for

A

prevention of both venous and arterial thrombosis

venous: DVT and PE
arterial: MI, CVA, those with artificial heart valves

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12
Q

heparin

A

natural anticoagulant produced by mast cells
if used before thrombus formation
-combines with a natural anti coag in the blood called antithrombin and inhibits factors 9, 10, 11, and 12 which stops prothrombin to covert to thrombin thus preventing the formation of a clot
if used after clot production
1. inhibits additional coagulation by inactivating thrombin which stops fibrinogen to convert to fibrin. it inhibits factor five and 8 and platelet aggregation to stop the clot from increasing in size

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13
Q

the therapeutic effect of heparin

A

prolongs clotting time. so if you have a pt with a stroke must find out if it is a hemorrhaging or ischemic stroke which can be done with a CT scan. ask the pt what peds they’re on and when the symptoms started

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14
Q

heparin contraindications

A

active bleeding
history of HIT: heparin-induced thrombocytopenia. the normal platelet levels are 150-300
adverse effect: cause bleeding

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15
Q

antidot for heparin

A

protamine sulfate

proat-amine sulfate

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16
Q

watch out for these herbs when taking heparin

A

chamomile, garlic, ginger, ginkgo, ginseng, and high dose vitaE

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17
Q

how ware heparin doses determined

A

an activated partial thromboplastin time or an aPTT is drawn. the normal values of aPTT that indicate normal coagulation are 25-35 seconds, but with those on heparin, we are looking for therapeutic values which are higher. therapeutic values are 45-70 seconds

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18
Q

what is the difference between heparin and LMWH?

A

LMWH like Lovenox inactivate factor Xa like heparin but are less able to inhibit thrombin.

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19
Q

indications for LMWH

A

DVT, PE, prevent complications of MI, ischemic complications of unstable angina.
-no need to monitor PTT but monitor platelet counts

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20
Q

contraindications of LMWH

A

hemorrhagic stroke, ulcers, blood abnormalities, low platelet count, those having surgery on eyes, brain or spine

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21
Q

enoxaparin

A

lovenox: LMWH
route: subq
it is often used after patients come off heparin and are going to be discharged home but want to sustain anticoag effects.

22
Q

patient teaching heparin

A

monitor for indication of bleeding such as bruised gums. abdomen pain, coffee-ground emesis, and tarry stools
-avoid NSAIDs, aspirin, or meds with salicylates

23
Q

patient teaching fo enoxaparin

A

provide instruction for self administration
do not expel air bubble: it is there to make sure the full dose is given
also teaching given to those with heparin

24
Q

Direct thrombin inhibitors

A

dabigatran (Pradaxa) a type of anticoag

action: inhibit thrombin which inhibits thrombus formation, prevents stroke, and prevents embolism with patient with A-Fib,
- if the patient is going in for an angioplasty it is given with ASA

25
Q

when would a direct thrombin inhibitor be used

A

if a patient cannot take heparin.

for this drug, therapeutic drug monitoring is not necessary but platelet count is. there is a risk with pregnancy

26
Q

adverse effects of dabigatran

A

bleeding, dyspepsia, abdominal pain, gastritis, and anemia

27
Q

what type of anticoagulant is warfarin

A

a vitamin k antagonist

it is the most commonly used oral anticoagulant and is the prototype vitamin k antagonist

28
Q

action of warfarin

A

coumadin
acts in the liver to prevent the synthesis of vitamin k-depending factors such as 2, 7, 9, and 10.
check LFTs because it works in the liver

29
Q

route and dose for coumadin

A

it is oral and its dosage is adjusted according to the INR. it must be given at the same time every day

30
Q

what is the normal INR

A

1.3-2 this number repots prothrombin time

a therapeutic PT value is approximately 1.5 times the normal persons or 18 seconds longer.

31
Q

antidote for warfarin

A

vitamin K

32
Q

drugs that decrease the effects of warfarin

A

chlordiazepoxide, haloperidol, IV lipid emulsions, spironolactone

33
Q

drugs that increase the effects of coumadin

A
34
Q

drugs that increase the effects of coumadin

A

acetaminophen (high dose), allopurinol. amiodarone, aspirin, antibiotics like cephalosporins

35
Q

herbs that increase effects of warfarin

A

chamomile, garlic, ginkgo, green tea, and turmeric

36
Q

herbs that decrease the effects of warfarin

A

foods with vitamin k such as broccoli, bruss, cabbage, cauliflower, kale, lettuce, mustard

37
Q

nursing implications for warfarin

A

monitor INR: if they’re on long term coumadin, ask if they are able to get their lab draws every week
the teaching of signs of bleeding like those for heparin, no alcohol, OTC meds, or herbals, no aspirin or NSAIDs

38
Q

direct factor Xa inhibitors

A

a category of anticoagulant
inhibit platelet activation and the formation of firing by inhibiting factor Xa.
include rivaroxaban (xarelto), apixaban (eliquis)

39
Q

uses for direct factor 10 inhibitors

A

treatment and secondary prevention of venous thromboembolism and in stroke prevention in patients with nonvalvular a fib, treatment of PE, pos op after hip or knee surgery

40
Q

adverse effects of rivaroxaban and apixaban

A

bleeding
contraindication: allergy
monitoring INR isnt necessary

41
Q

what increases the effects of xaralto

A

aspirin, vitamin E

42
Q

what increases the effects of Xarelto

A

estrogen, prgestins, CYP3A4

43
Q

herbs that increase effects of ribaroxaban

A

alfalfa, biberry, grapefruit juice

44
Q

what are antiplatelet drugs used for?

A

prophylactic use in ARTERIES for prevention of platelet aggregation leading to MI, stroke, or repeat MI or STROKE
-long term low dose aspirin therapy is an example. must be stopped 7 days before surgery due to prolonged antiplatelet activity

45
Q

what is the most widely used drug for the prevention of MI, stroke, and people with prosthetic valves>

A

ASA. if the patient suspect’s MI, chew an aspirin
antiplatelet with an adverse effect of tinnitus
-caffeine may increase absorption, corticosteroids will increase its excretion and decrease effects, ASA can reduce the effects of beta-blockers acting against hypertension

46
Q

clopidogrel

A

Plavix: prototype
indefinitely blocks the ADP receptors on platlets
contraindicated for bleeding especially in the brain and stomach

47
Q

drugs that increase the effects of clopidogrel

A

aspirin, NSAIDS, platlet inhibitors, thrombolytics, atorvastatin, rifamipn

48
Q

drugs that decrease the effects of clopidogrel

A

amidoarone, antibiotidcs, omeprazole, SSRIs

49
Q

abciximab

A

reo pro
antiplatelet that prevents binding of fibrinogen on active platlets
contraindicated with bleeding

50
Q

prasugrel and ticagrelor

A

prasugrel Efficient: improved cardiac outcome for acute coronary syndromes
ticagrelor: Brilliant: ADP receptor antagonist
uses: reduce Cardiovascular death, MI, and stroke in thosewith history of them. decrease stent thrombosis as well
BLACK BOX: fatal hemorrhage bot are more potent than clopidogrel

51
Q

thrombolytics

A 
alteplase tPA or Activase: prototype and given to patients in the ER with ischemic stroke
purpose: to dissolve thrombi that have already formed
uses: 
Acute severe thromboembolic disease
After acute MI
Stroke (must be used in 3-4.5 hours)
 Pulmonary embolus
 DVT
Noncoronary artery occlusion

NUR 326 (7 decks)

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