B&l: Test 2: Taube : Final Review

Front 1

if you have arthritis, why do you take a COX 2 inhibitor..what is one risk?

Back 1

inhibit COX 2 because it is associated with inflammation, and COX 1 will not be affected and thus you won't have GI bleed

With time COX2 inhibitors alone can lead to risk for MI

Front 2

If you are on a Cox 2 inhibitor and taking an ASA for prevention of MI...what is this the equivalent of?

Back 2

taking Ibuprofen.. because the ASA gives you the GI effects that you were trying to avoid with Ibuprofen, but you have to take the ASA to prevent MI with a COX2!

Front 3

Patients who do not receive ____ within 48 h of onset of an acute MI are 27% more likely to die in the hospital than those who do.

Back 3

aspirin

Front 4

biggest side effect of asprin?

Back 4

GI irritation and bleeding

inhibits COX1 that inhibits the synthesis of prostaglandins that promote secretion of bicarb and mucous

Front 5

Clopidogrel is what kind of agent?

Back 5

ADP Receptor Antagonists

stops platelet aggregation

Front 6

Prasugrel is what kind of agent?

Back 6

ADP Receptor Antagonists

stops platelet aggregation

Front 7

Abciximab is what kind of agent?

Back 7

GP IIb/IIIa Receptor Antagonists

stops platelet aggregation

Front 8

Clopidogrel vs Abciximab

How it is given

Back 8

Clopidogrel: Oral

Abciximab: IV

Both stop platelet agg

Front 9

Which agents may be used for the secondary prevention of an acute MI?

Abciximab
Aspirin
Clopidogrel
Dalteparin

Back 9

Aspirin
Clopidogrel

Front 10

Which of the following agents may be used to prevent thrombosis during PCI (percutaneous intervention)?

Abciximab
Aspirin
Clopidogrel
Dalteparin
Warfarin

Back 10

Abciximab
Aspirin
Clopidogrel
Dalteparin

NOT WARFARIN because it takes a while to work

this is a person getting an angioplasty done

getting rid of the endothelial layer, really need a lot of anti-platelet action

Front 11

Streptokinase is what kind of agent?

Back 11

Thrombolytics

turn plasminogen into plasmin

Front 12

what kind of drugs are

Alteplase (Activase)
Reteplase (Retavase)
Tenecteplase (TNKase)

Back 12

recombinant t-PA

tissue type plasminogen activator

Front 13

clinical uses for Thrombolytics

Back 13

STEMI
Deep vein thrombosis
Pulmonary embolism
Stroke (ischemic)

Front 14

why do you NOT use thrombolytics for unstable angina or NSTEMI

Back 14

risk of bleeding is too high

Front 15

Adverse effects of streptokinase? 3

Back 15

bleeding
Allergic-anaphylactic reaction
Hypotension

Front 16

A 62 year old male. Swelling of leg. He has tenderness in popliteal fossa, calf and ankle swollen. No injury, chest pain or SOB. He started medical therapy, was sent home, and was told that a nurse would come to his house for the next few days to check his INR. Six days later he most likely developed which of the following side-effects...

Hypotension
Bleeding
GI Ulcer
HIT type 2
Osteoporosis
Purple Toes

Back 16

he likely has a DVT

so he is either taking LMW heparin or fondoparanox (spelling)

Hypotension-streptokinase- X
Purple Toes-Warfarin-X (occurs several weeks later)
Osteoporosis-Long Term Heparin-X
GI Ulcer- Aspirin- X
HIT type 2- Unfractionated Heparin-X

BLEEDING- Correct

Front 17

What type of drug is Dabigatran? administered how?

Back 17

ORAL thrombin inhibitor

alternative to warfarin

Front 18

will you use lepirudin for the chronic treatment of atrial fib?

Back 18

NO

it is IV

remember this is a Recombinant derivative of hirudin (leech)

Front 19

When would you use a direct thrombin inhibitor?

Back 19

HIT

Front 20

MOA of Warfarin? (general)

Back 20

Vitamin K antagonist

thus it blocks 1972, and protein C and S

(10, 9, 7, 2)

Front 21

How does warfarin act as a Vitamin K antag?

Back 21

Vitamin K epoxide must be reduced so that you have the form of Vitamin K that can act as a co-factor for clotting factors

warfarin blocks this reduction

Front 22

how is warfarin administered?

Back 22

ORAL mainly (can be IV)

Front 23

Why does it take so long to get a peak anticoagulant effect of warfarin?

Back 23

Long half life of pre-existing clotting factors because it doesn't do anything to the clotting factors that are already made and released from the liver

have to wait for those to go away before you have an effect from the warfarin

Front 24

how do you monitor Warfarin?

Back 24

PT Time

but have to used standardized PT time which is the INR

Front 25

What are some examples of when warfarin can be used? 5

Back 25

A fib

DVT

Prosthetic heart valves

People at risk following surgery, trauma or cancer

STEMI (post MI)

Front 26

A patient is scheduled for an angioplasty. What anticoagulant may be administered just prior to the procedure? 3

also, why is aspirin not correct here?

Back 26

Bivalirudin

Unfractionated heparin

Enoxaparin (LMWH)

Asprin is NOT CORRECT- it is not an anticoagulant, it is antiplatelet (even though it would be used in an angioplasty)

91

Front 27

side effects of warfarin (2)

Back 27

Bleeding
Skin necrosis--from widespread thrombosis
---Occurs early in therapy (within the first 10 days)
Possibly due to reduced activity of Protein C

Front 28

Purple toe syndrome is a result of using what drug?

Back 28

Warfarin

due to Release of cholesterol microemboli from atheromatous plaques

Usually occurs within 3-10 weeks

Front 29

when is warfarin most teratogenic?

Back 29

1st trimester

Front 30

why is warfarin contraindicated in pts with hepatic disease and chronic alcoholism?

Back 30

affects the liver (clotting factors are there)

Front 31

if a person Develops HIT, can you use warfarin alone as alternate therapy?

Back 31

NO!

When used alone, it can cause venous limb gangrene or multicentric skin necrosis
The rapid loss of the endogenous anticoagulant, protein C, can cause a hypercoagulated state

Front 32

67 year old lady with HTN, CKD, chest pain, SOB. Has UTI, put on Unfractionated heparin for suspicion of PE...also had exacerbation of HF. Got on Ceftriaxone. On hospital day 7, platelet count drops, aPTT prior was 28s is now 57s what drug change would you most likely make? stop the heparin and add....

Enoxiparin
Leparudin
Aspirin
Warfarin
Protamine sulfate

Back 32

Enoxiparin (LMWH)
Leparudin (direct thrombin inhibitor)
Aspirin (anticoag)
Warfarin
Protamine sulfate (antidote for too much heparin)

she most likely developed HIT

so stop the Unfractionated heparin and start a direct thrombin inhibitor (so Leparudin)

Front 33

what 2 things cause activation of platelets?

Back 33

ADP

and Thromboxane (TxA2)

Front 34

what type of agent is aspirin?

Back 34

Irreversibly inhibits cyclooxygenase
Greater inhibition of COX-1 than COX-2

Blocks the production of TxA2
Platelets

Front 35

does aspirin work more on TxA2 or PGI2?

Back 35

TxA2-->Cyclooxygenase is inhibited for the life of the platelet

wheras in endothelial cell-->Cyclooxygenase is inhibited for 6-8 hours

Front 36

Why is cyclooxygenase inhibited for only a short time in endothelial cells and forever in the platelet?

Back 36

endothelial cells have a nucleus, which is critical for producing new proteins, thus they are able to produce more COX, and platelets cant do this

Front 37

what does ibuprofen do when used with aspirin? why?

Back 37

ibuprofen negates the beneficial affects of aspirin

they fight for the spot on Cox 1, and in the evening when they have both been used up Cox 1 is open and hasnt had the irreversible effects of aspirin

so you have to separate the dose

Front 38

COX 2 inhibitors can have what effect on the heart?

Back 38

causes more MIs and strokes; not cardioprotective

get rid of prostacyclin you have unopposed stuff from the thromboxane

Front 39

3 uses for Aspirin?

Back 39

STEMI, NSTEMI or Unstable angina
--Primary and secondary prevention
--Acute treatment

Percutaneous coronary intervention (PCI)
--Acute
--Chronic treatment afterwards

Embolic stroke
--Prevention
--Acute treatment