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a. Pharm Exam 1(w-13) > blood thinners > Flashcards

blood thinners Flashcards

0
Q

heparins:

  1. what is heparin & where does it occur naturally?
  2. what are the 2 types of heparins?
  3. where do commercially prepared heparins come from?
A
  1. heprain is a slufated mucopolysaccharide stored in the granules of mast cells
  2. commercially prepared heparin comes from bovine lung or porcine intestinal mucosa
  3. heparin can be:
    - –a.can be unfractionized (standard heparin) or
    - –b. low molecular weight (lovenox etc.)
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1
Q

heparins:

  1. how do heparins work and what factors do they inactivate?
  2. how does unfractionated heparin work?
A

it acts as a co-factor with antightombin (AT) to inactivate factors II, IX, X, XI & XII (2, 9,10,11,12)
to inactivate thrombin (factor II), heparin must bind simultaneously to thrombin and antithrombin; since unfractionated heparin has a longer chain, it can simultaneously inactivate factors II and X in a 1:1 ratio.

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2
Q

heparins:

how long of a polysaccharide chain is standard (unfractionated heparin)?

A

> 18 monosaccharide units

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3
Q

heparins:

which factor do LMWHs work on better?

A

factor Xa more than factor II(thrombin) because the chain is too short to bridge antithrombin to thrombin

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4
Q

heparins:

how is LMWH made

A

by depolymerization of unfractioned porcine heparin

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5
Q

heparins:

why can’t you monitor LMWHs with a PTT?

A
  • UF heparin works on factor IIa whichaffects factor II (thrombin)
  • LMW heparin works on factor Xa, which a PTT does not monitor
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6
Q

heparins:

does protamine work on UFH and LMWH?

A

it works completely on UFH and partially on LMWF

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7
Q 
heparins:
how are heparin doses determined:
1. theraputic doses:
2. prophylactic doses:
3. which one depends on renal function for adjustment?
A
  1. based on body weight
  2. prophylactic doses are fixed (ex. 5,000 u q 12 hrs)
  3. LMWH doses are based on renal fxn
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8
Q

heparins:

if the PTT doesnt work on the LMWH, then why not use an Anti Xa?

A

it is inconclusive and expensive

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9
Q

heparins:
when to stop blood thinners prior to surgery:
1. UFH:
2. LMWH:

A
  1. unfractionated heparin: 2 hours

2. low molecular weight heparin: 12 hours

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10
Q 
heparins:
adverse effects of UFH and LMWH:
1. hemotological:
2. other:
3. why the increase in liver enzymes?
A
  1. hematological:
    - - bleeding,
    - - HIT
  2. osteoporosis, hyperkalemia, increased AST & ALT
  3. broken down in liver
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11
Q

heparins:
what are advantages and disadvantages of LMWH?
1. advantages:
2. disadvantages:

A
  1. advantages:
    - high bioavailability via SQ route
    - lower incidence of HIT; no need to monitor PTT
    - ideal during pregnancy (not teratogenic)
  2. disadvantages:
    - require dose adjustemt if renal issues,
    - cannot be on patients with HIT,
    - longer half life may prolong risk of bleeding,
    - not fully reversed with protamine,
    - more expensive
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12
Q

protamine:
1. where does it come from?
2. MOA:
3. clinical use
4. side effects:

A
  1. salmon sperm
  2. protamine is a polycationic molecule that binds to the negatively charged polyanionic heparin forming a stable 1:1 protamine: heparin complex
  3. full reversal of UFH or partial reversal of LMWH
  4. bradycardia, hypotension, anaphylactoid reaction, circulatory collapse, capillary leak, noncardiogenic pulmonary edema, flushing, nausea, vomiting, dyspepsia
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13
Q

protamine cont.

what causes the anaphalyctoid side effects ?

A
  1. prior exposure d/t NPH insulin (NPH=neutral protamine hagedorn)
  2. fish allergies
  3. vasectomized men (1/3 of them) have anti protamine IgG
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14
Q

protamine dose:

  1. how much protamine works on how much heparin?
    - - how much protamine works on how much LMWH (lovenox)?
  2. how fast should protamine go in? what are side effects of too much protamine?
A
  1. 1 mg protamine for every 100 units of heparin remaining in the patient (1 mg protamine only antagonizes 1 mg LMWH)
  2. infusion rate=5 mg/ min max (avoid excess protamine d/t weak anticoagulant effect and platelet inhibition)
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15
Q

pharmacokinetics of protamine:

  1. onset:
  2. duration:
  3. elimination:
  4. t1/2:
  5. what can sometimes happen? what is the treatment?
A
  1. O: 5 minutes
  2. D: 2 hours
  3. Elim: reticuloendothelial system
  4. t 1/2: 20 minutes
  5. heparin rebound may occur and cause need for protamine gtt
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16
Q

direct thrombin inhibitors (DTI)

  1. action; what is the difference between DTIs and LMWHs/UFHs?
  2. examples:
  3. how long before surgery should DTIs be discontinued?
A
  1. directly inhibits thrombin as opposed to LMWH ane UFH work indirectly
  2. examples: lepirudin, argatroban
  3. (pradaxa) 1-2 days before surgery inf creat clearance is > or equal to 50 ml/min; 3-5 days if CrCl is less than 50 ml/min
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17
Q

elimination of direct thrombin inhibitors (DTIs):

  1. argatroban:
  2. lepirudin, dabigatran, desirudin, bivalirudin:
A
  1. hepatic

2. renal

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18
Q

DTIs: Pradaxa:

  1. what if patient needs major surgery or spinal; is 3-5 days long enough?
  2. is there an antidote
  3. dialysis patients: how much is left after?
A
  1. consider longer holds (?? 1 week even) is complete hemostasis is needed.
  2. there is no antidote, FFP, PCC or recombinant factor VIIa has not been proven to reverse DTIs
  3. dialysis removes 60% in 2-3 hours
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19
Q

DTIs:

  1. how is bleeding risk from dabigatran (pradaxa) assessed?
  2. why is the test not done usually?
  3. what test can be done?
A
  1. ECT (ecarin clotting time).
  2. test is expensive and not available at all hospitals
  3. PTT or TT (thrombin time) can be used for their negative predictive value (i.e. if they are at baseline, the patient can go to surgre).
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20
Q

DTIs:

  1. which ones are IV?
  2. Which are PO?
  3. which are SQ?
A
  1. IV:
    a. Argatroban–halflife: 39-51 hrs.–elimination: hepatic–monitoring: PTT/ACT–effect on INR: moderate to significant
    b. Lepirudin–halflife: 1.3 hours–elimination: renal–monitoring: PTT–effect on INR: none to slight
    c. Bivalirudin–halflife: 30 min–elimination: enzymatic and renal–monitoring: PTT/ACT–effect on INR: slight to moderate
  2. PO:
    - Dabigatran (pradaxa)–halflife: 13-17 hours–elimination: renal–monitoring: NONE–effect on INR: slight to none
  3. SQ:
    - Desirudin–halflife: 2-3 hours–elimination: renal–monitoring: PTT–effect on INR: slight to moderate
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21
Q

Fraction Xa inhibitors:

2 types of action (and brand names);

A

indirect acting (Fondaparinux) and direct acting (Rivaroxaban, Apixaban)

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22
Q

Indirect Factor Xa Inhibitors:
Fondaparinux (Arixtra)
1. pharmacology:
2. it has the same end result as heparins, but how is it different (as far as what it doesnt inhibit)?

A
  1. synthetic pentasaccharide linds to antithrombin (AT) causing binding and inhibition to Xa
    - —inhibition of factor Xa disrupts coagulation cascade which inhibits thrombin formation and thrombus formation
  2. compared to heparins, ther is no direct action on thrombin (factor IIa) or platelet factor 4 (therefore less chance of HIT).
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23
Q 
pharmacokinetics of Fondaparinux:
-absorption:
-distribution:
-metabolism:
-excretion:
t 1/2 time:
A
  • absorption: sub q=100%
  • distribution: 94% bound to antithrombin
  • metabolism: minimal
  • excretion: renal (77% excreted unchanged)
  • –contraindicated in crcl is <30 ml/min
  • t 1/2 time=17-21 hours (does not significantly bind to plasma proteins).
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24
Q

Indirect factor Xa inhibitors: Arixtra-

  1. advantages:
  2. clinical uses:
A
  1. good alternative to UHF or LMWH;
    - -safer profile on platelets
    - -given sq daily
    - -possibly more effective than lovenox in preventing dvt post orthopedic procedures
  2. clinical uses: tx of or prevention of dvt
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25
Q

DIRECT factor Xa Inhibitors: Rivaroxam (Xarelto)–

  1. route:
  2. action:
A

Xarelto:

  1. action: oral direct Xa inhibitor
  2. Inhibits the active site of FXa directly without need for antithrombin as a cofactor by inhibiting bound and free factor Xa
  3. FDA approved for :
    - prophylaxis of DVT post hip or knee
    - reduction of CVI and thromboembolis in nonvalvular a-fib
    - treatment of DVT
    - treatment of PE
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26
Q

Direct factor Xa inhibitors: Xarelto-

-pharmacokinetics:

A
  • pharmacokinetics:
  • given orally, bioavailability=80%
  • food does not affect bioavailability
  • protein binding=92-95%
  • cMAX=2 to4 hours
  • metabolized by CYP3A4
  • substrate for transporter P-glycoprotein
  • dual elimination (renal 1/3 and hepatic 2/3)
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27
Q

Xarelto: (Rivaroxaban)

  1. adverse effects:
  2. use around spinal or epidural
  3. use around surgery
A

Xarelto: (Rivaroxaban)

  1. adverse effects: bleeding, mild increase in liver enzymes (ALT), nausea, fever, vomiting
  2. use around spinal or epidural:
    - -do not remove epidural cath for 18 hours post last administration
    - -hold next dose for 6 hours post removal
    - -if traumatic puncture; delay next dose for 24 hours
    - -less risk of spinal hematoma than with NSAIDS or platelet inhibitors
  3. use around surgery:
    - -stop 24 hours prior to surgery
    - -restart when adequate homeostasis re-established
    - -start 6-10 hrs post orthopedic procedure when adequate homeostasis re-established
28
Q

Direct factor Xa inhibitors: Xarelto therapy:

  1. route/ frequency:
  2. food & drug interactions:
  3. onset
  4. theraputic window:
  5. efficacy similar to …
  6. more effective than…
  7. bleeding rates in comparison to other agents?
  8. antidote?
A
  1. orally q day
  2. less interactions than coumadin
  3. rapid onset
  4. wide theraputic window
  5. efficacy similar to coumadin with afib
  6. more effective than lovenox in post hip/knee arthroplasty
  7. comparable bleeding rates
  8. no antidote (or specific reversal agent)
29
Q

Direct factor Xa inhibitor: Apixaban (Eliquis)

  1. pharmacology:
  2. pharmacokinetics:
    - -bioavailability:
    - -onset:
    - -t1/2:
    - -elimination:
    - -metabolism:
    - -FDA approved for:
A
  1. pharmacology: selective direct inhibitor of free and clot associated factor Xa
  2. pharmacokinetics:
    - -bioavailability: 66%
    - -onset: 1-3 hours
    - -t1/2: 13 hours
    - -elimination: renal (27%); fecal & biliary (73%)
    - -metabolism: cyp3A4
    - -FDA approved: for recudtion of CVI and thrombus in patients with nonvalvular afib
30
Q

apixapan (Eliquis) use around surgery:

  1. when to discontinue before elective surgery or procedure with HIGH RISK of bleeding:
  2. when to discontinue before elective surgery or procedure with LOW RISK of bleeding:
  3. guidelines for use around spinal/epidural:
A
  1. 48 hours
  2. 24 hours
  3. no guidelines for use around spinal/epidural
31
Q

Direct factor Xa inhibitors: apixaban (eliquis)

  1. route, frequency:
  2. drug/ food interactions
  3. onset:
  4. theraputic window:
  5. efficacy with a-fib:
  6. efficacy with post knee or hip arthroplasty
  7. efficacy as a blood thinner:
A
  1. orally, bid
  2. less drug or food interactions than coumadin
  3. rapid onset
  4. wider theraputic window
  5. superior to coumadin in a-fib
  6. just as effective as lovenox with post knee or hip arthroplasty
  7. comparable bleeding to current agents
  8. no specific reversal
32
Q

vitamin K antagonist: coumadin-

  1. mechanism of action:
  2. what factors are hindered?
  3. what natural anticoagluants are also hindered by warfarin?
A
  1. warfarin bind to vitamin K epoxide reductase (VKOR) and interferes with hepatic regeneration of natural vitamin K1 (quinone) from its inactive. this causes hepatic production of partially carboxylated or decarboxylated proteins with reduced procoagulant properties
  2. factors II, VII, IX, X are all inhibited (2,7,9,10)
  3. protein C and protein S (which are also vitamin k dependent)
33
Q

how long does it take for coumadin to deplete enough functional factors (II & X) that the patient is anticoagulated?

A

5 days

34
Q

vit K antagonists: coumadin:

  1. what is coumadin isomer mix?
  2. which isomer is more potent R or S?
  3. absorption rate?
  4. protein binding?
  5. metabolism:
  6. theraputic response:
A
  1. racemic (equal parts R & S warafin isomers)
  2. S isomer is more potent
  3. full absorption in 90 min
  4. protein binding 97-99% (mostly to albumin)
  5. hepatic metabolism
  6. response varies of genetics, illnes, drug interactions,diet and clotting factors
35
Q

vit K antagonist (warfarin)

adverse effects:(3)

A
  1. bleeding
  2. skin necrosis (rare)
    - -thrombosis of venules and capillaries within sq fat
    - -??associated with protein c defeciency
    - -more common in middle aged, obese females
  3. purple toe syndrome (rare)
    - -warfarin may induce formation of cholesterol micro-emboli with subsequent occlusion and infarct of dremal arterioles with concomitant cyanosis
36
Q

vit k antags (coumadin)

  1. monitoring:
  2. dietary considerations
A
  1. International normalized ratio (INR); usually kept between 2 & 3
  2. avoid foods that may antagonize effects:
    - —soy and fiber bind coumadin in the gut and prevent absorption (dont eat these within 4 hours of coumadin)
37
Q

vit k antags: coumadin
pre-procedural bridging of coumadin:
1. when to stop coumadin?
2. what is started and when?
3. when is last dose of replacement before surgery?
4. when are coumadin and replacement restarted post op?

A

1-stop coumadin 5 days prior
2-start LMWH 3 days prior
3-give last LMWH 24 hours prior
4-start coumadin and LMWH no earlier than 8 hours post procedure

38
Q

vit K antag: coumadin-

who will get bridge therapy (7 different scenarios)

A
  1. mechanical mitral valve
  2. caged ball or tilting disc aortic valve prosthesis
  3. stroke or TIA in past 3 months
  4. afib with CHADS2 score of 5-6
  5. rheumatic heart valve disease
  6. DVT in past 3 mos
  7. hx of severe thrombphilia
39
Q 
vit K antag: coumadin-
reversal:
1. what is used for immediate reversal?
2. what about vitamin k; how long does it take to take effect:
--IVPB:
--PO:
--SQ:
A
  1. immediate reversal use PCC (prothrombin complex concentrate) or FFP
  2. vitamin K onset:
    - -IVPB=8 hours
    - -PO=24 hours
    - - SQ= up to 72 (delayed and poor absorption)
40
Q

Fibrinolytics:

  1. action:
  2. uses
  3. name the 3 commonly used thrombolytics:
A
  1. axn: act as plasminogen activators and catalyze plasminogen to plasmin conversion which in turn cleaves fibrin
  2. uses: to lyse already formed clots
  3. Alteplase (activase); Reteplase (retavase); Tenecteplase (TNKase)
41
Q

fibrinolytics:
1. clinical indications:
2. contraindications:

A
  1. indications:
    - -STEMI
    - -CVI (alteplase only)
    - -PE (alteplase only)
    - -acute arterial occlusions (low dose)
    - -catheter clearance (low dose)
  2. contraindications:
    - -intracranial disease
    - -uncontrolled HTN
    - -major surgery or trauma
42
Q

antiplatelet therapy:

5 types:

A
  1. cyclooxygenase inhibitors (ASA and NSAIDs)
  2. antiplatelet P2Y12 inhibitors (Plavix, Ticlid, Effient, Brilinta)
  3. GP IIb-IIIa inhibitors (Integrilin, Reapro)
  4. Cliostazol (Pletal) [reversible phosphodiesterase (PDE) inhibitor]
  5. Dipyridamole (Persantine, Aggrenox) also a [reversible phosphodiesterase (PDE) inhibitor]
43
Q

antiplatelet: ASA
1. what is COX used for?
2. what does asa do to COX?
3. which cox does low dose ASA work most on? why is that good?

A
  1. platelets use arachadonic acid to form thromboxane A2 which induces platelet formation and causes vasoconstriction; this is the opposite action of PGI2 (prostacyclin)which inhibits platelet aggregation and causes vasodilation.
  2. ASA blocks platelet cyclooxygenase keeping it from forming thromboxane A2 from arachadonic acid which reduces platelet aggregation
  3. low dose ASA inhibits more platelet cox 1 than vessel wall endothelial cox2 (cox 2 is where prostacyclin is made from).
    - - this is good because prostacycline helps ASA do its job (it is also an anti platelet aggregate)
44
Q 
action of ASA: (4 things)
1-
2-
3-
4-
A
  1. anti inflammatory- blocks cox activity
  2. analgesic-inhibits pain at subcortical level
  3. antipyretic
  4. antiplatelet irreversibly blocks platelet aggregation by destroying COX enzymes. since platelets have no nucleus to make new COX enxymes it lasts the duration of the platelet (7 days).
45
Q

asa dosing:

–is low dose equal to high dose

A

low dose is equal to high dose but initially the patient with coronary stents will want to be on 325 mg for several months then reduce to 160 or 81 mg

46
Q

asa side effects:

A
  1. most common: gastropathy (intolerence, bleeding, ulcerations)
  2. least common: hepatotoxicity, sensitivity (i.e bronchospasm or asa sensitive asthma); renal toxicity (hypertension, edema); tinnitus (with high dose); reyes syndrome (in young persons)
47
Q 
antiplatelet meds:
when to stop the drug prior to surgery:
1. ibuprofin, orudis, indicin, voltaren:
2. naproxen, dolobid, clinoril
3. mobic, relafen (nambumetone)
4. pletal (cliostazol)
5. dipyridamole (persantine)
6. persantine + asa (aggrenox)
A 
antiplatelet meds:
when to stop the drug prior to surgery:
1. ibuprofin, orudis, indicin, voltaren: 1 day
2. naproxen, dolobid, clinoril: 2-3 days
3. mobic, relafen (nambumetone): 10 days
4. pletal (cliostazol): 2-3 days
5. dipyridamole (persantine): 2-3 days
6. persantine + asa (aggrenox): 7 days
48
Q

antiplatelet P2Y12 inhibitors:

  1. 2 categories
  2. name brands and category
A
  1. thieno-pyridines (3) and cyclopentyl-triazolo-pyrimidines (1)
  2. Ticlid (ticlopidine); Plavix (clopidogrel); Effient (prasugrel) are thieno pyridines
    - –Brilinta (ticagrelor) is the only cyclopentyl-triazolo-pyrimidine
49
Q

antiplatelet p2y12

  1. action:
  2. clinical use:
  3. which one is rarely used (anymore)?
A
  1. thienopyridines (plavis etc.) irreversibly block ADP reveptor (P2Y12) on the platelets inhibiting aggrigation by activating the glycoprotein IIb-IIIa pathway.
  2. used on patients with acute coronary syndromes. Off label use includes: CVi, PAD and coronary stent placement
  3. ticlodipine is rarely used anymore d/t risk of neutropenia and its delayed onset.
50
Q

antiplatelet p2y12

  1. which ones are prodrugs?
  2. when are the drugs stopped before surgery?
A
  1. clopidogrel (plavix) and prasugrel (effient)

2. 5 days prior

51
Q

antiplatelet p2y12
side effects
1. theinoyridines:
2. cycloental-triazolo-theinopyrimidines:

A
  1. GI symptoms (nausea, diarrhea), bleeding, TTP

2. brilinta can cause DIB and increased serum uric acid and creatnine

52
Q

antiplatelet P2Y12

some persons will not respond to plavix, why?

A

2-3% of blacks and whites as well as 10-15% of asians have a polymorphic cyp2c19 which cannot metabolize plavix into a prodrug

53
Q

Platelet GP IIb-IIIa receptor antagonist:

  1. name the agents:
  2. what is the action
  3. clinical use:
A
  1. (abciximab) reapro; (eptifibatide) integrillin; (tirofiban) aggrastat
  2. blocks IIb/IIIa receptor on platelet surface preventing fibrinogen from binding to activated platelets
  3. used in cath lab
54
Q

GPIIb/IIIa antagonists
action:
1. which ones are reversible antagonism:
2. which one lasts the longest (12-24 hours)
3. which ones are not broken down by plasma proteases?

A
  1. integrilin and aggrastat
  2. reapro
  3. integrilin (renal); aggrastat (renal and billiary)
55
Q

what is the structure of:

  1. abciximab (reapro)
  2. integrillin (eptifibatide)
  3. aggrastat (tirofiban)
A

what is the structure of:

  1. abciximab (reapro)-an antibody
  2. integrillin (eptifibatide)-a synthetic non-peptide
  3. aggrastat (tirofiban)- a synthetic peptide
56
Q

-

A
  • bleeding (1-4%)

- thrombocytopenia (3-5%) (occurs more with reapro than with integrilin or aggrastat).

57
Q

herbal products with MAJOR antithrombotic properties:

A

Garlic,Ginger,Ginkoba, Danshen, Dong Quai, Evening Primrose, Feverfew, Policosanol, Wintergreen

58
Q

neuraxial anesthesia and thromboprophylaxis:

1. Nsaids:

A

neuraxial anesthesia and thromboprophylaxis:

1. Nsaids: no contraindication

59
Q

-2. antiplatelets:

A
  1. antiplatelets: stop ticlid 14 days prior; plavix 7days prior; ticagrelor 5 days prior; reapro, integrilin (etc) 8-48 hrs prior
60
Q
  1. SQ heparin
A

-3. SQ heparin: delay next dose, caution if >10,000 u/day

61
Q
  1. IV heparin:
A

-4. IV heparin: can start 1 hour post neuraxial; remove 2-4 hours post last dose or drip stopped

62
Q
  1. LMWH:
A

-5. LMWH: can remove catheter 2 hours prior to first dose; wait 24 hours after last dose for neuraxial

63
Q
  1. coumadin:
A

-6. coumadin: when INR <1.5

64
Q
  1. fondaparineux (arixtra):
A

-7. fondaparineux (arixtra): needle 36 hrs post last dose

65
Q
  1. DTIs (argatroban, lepirudin, pradaxa):
A

-8. DTIs (argatroban, lepirudin, pradaxa): avoid d/t insufficient data

66
Q
  1. thrombolytics (alteplase etc)
A

-9. thrombolytics (alteplase etc): ABSOLUTE contraindication

67
Q
  1. herbals:
A

-10. herbals: no evidence of mandatory, but be aware of interaction risk

a. Pharm Exam 1(w-13) (2 decks)

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