indelible, noxious, glib temerity

warfarin band naems

jantovan, coumadin

clopidogrel band names

plavix

Dipyridamole + aspirin

aggrenox

Dabigatran band name

pradaxa

cilostazol band name

Pletal

Dipyridamole

Persantine

Apixaban band name

eliquis

rivaroxaban band name

xarelto

edoxaban band name

savaysa

Bivalirudin band name

angiomax

Abxicimab band name

reopro

heparin brand name

heparin

Enoxaparin band name

lovenox

Prasugrel

efficient

Alteplase band name

Activase

Tenecteplace band name

TNKase

Reteplase band name

Retavase

what are the three big steps in clotting cascade

1. injury, platelet plug forms around exposed collagen of blood vessel

2. coag cascade - all the coag factors create thrombin, fibrin to form mesh over platelet plug

3. clot stabilize by factor 8— connects fibrin

what drug is low MW heparin

ennoxaparin (lovenox)

• doesn’t have to just be IV

what is fibrin

a protein mesh from fibrinogen that holds clot together

• “fabric”

• “stronger” clot

what is thrombus

the whole clot, with platelets, fibrin, RBCs, WBCs

what is fibrinolysis

breaking down a blood clot

what is an embolous

blood clot taht is in circulation/clogged smaller vessels

• just where it is NOT supposed to be

what is thrombin

the ENZYME that converts fibrinogen into fibrin '

activates clotting factors

what is Venous Thromboembolism (VTE)

general term for clots in veins

• includes DVT and PE

• means clot (thrombo) and traveling clot (embolism)

what is deep vein thrombosis (dvt)

clot in a deep vein, legs

• presents as leg swelling, pain , warmth, redness

what is PE pulmonary embolism

clot travels to lungs

• presents as short breath, chest pain, tachy, low oxygen

• usually from breakage of DVT clot into lung circulation

pulmonary embolism more s/s?

symtpoms!

• Cough

  ▪ Chest pain/tightness

  ▪ Shortness of breath

  ▪ Palpitation

  ▪ Hemoptysis- (coughing up blood)

  ▪ Dizziness/lightheadedness

signs

• Tachypnea

  ▪ Tachycardia

  ▪ Diaphoresis (increased sweating)

  ▪ Distended neck veins

  ▪ Cyanosis (blue discoloration of hands)

  ▪ Hypotension

  ▪ Decreased oxygen saturation

DVT s/s!

symptoms

• Unilateral pain and swelling

  ▪ Warmth

  ▪ Erythema

signs

• Dilated superficial veins

  ▪ Homans sign (pain in the back of knee

  when flexing the foot of the affected

  leg

antiplatelet agents (list brand/gen)

Aspirin- salicylates

➢ Clopidogrel, prasugrel , ticlodipine, ticagrelor , cangrelor – ADP inhibitors (thienopyridine)

➢ Abiciximab, epitifibatide, tirofiban – Antagonist of GPIIb/IIIa receptors

➢ Dipyridamole – Phosphodiesterase inhibitors

➢ Epoprostenol- synthetic PGI2

➢ Vorapaxar - Protease Activated Receptor 1 (PAR1)

Anticoagulants list brand/gen

Unfractionated heparin (UFH)

❖ LMWH : enoxaparin, delteparin, tinzaparin

❖ Synthetic factor Xa inhibitor: fondaparinux

❖ Direct Xa inhibitor: rivaroxaban, apixaban, edoxaban

❖ Direct thrombin inhibitors (DTIs): argatroban, lepirudin, desirudin, bivalirudin, dabigatran

❖ Warfarin

list Thrombolytic agents

1st generation: Streptokinase, urokinase

✓ 2nd generation: Alteplase (tPA), reteplace, tenecteplace

WHAT two things to platelets stick to after injury

collagen— uses GP Ia

von Willebrand factor (vWF) via GP Ib

what binds collagen and platelets

GP 1a

what binds von Willy with platelets right after injury

GP 1b

what do activated platelets release once bound to collagen or von Willy

• Thromboxane A2 (TXA2)

• ADP

• Serotonin (5-HT)

• Platelet factor 4

used to activate/recruit even more platelets!

what factor is mostly IV

factor 2!

what two factors join platelets together

fibrinogen and von Willy

how many plaetlets does bennett want us to know

150,000 to 400,000

what is the MAIN chemical for platelet aggregation at end of cascade

GP IIb/IIIa

what does thomboxane A2 cause

vasoconstriction, promote PLT aggregationw

what do prostacyclins do

promote vasodilation, inhibit plaetlet aggreagation

what is the common precursor for prostacylins AND thrombozane A2

prostaglandins

• prostaglandins also cause PGD,PGE, PGF

what is box warning for cox 1 inhibitors

GI bleeding

what is box warning for COX2 inhibitors

CV events, MI risk

what is only COX-2 only inhibitor out there rn

celebrex (celecoxib)

what is common precursor for leukotrienes, prostacyclins, thromboxanes

arachidonic acid!!

what do leukotrienes cause

vasoconstriction, bronchospasm, increased permability

what factors oppose platelet aggreagation

prostaglandins

increased cAMP

what promotes platelet aggregation

decreased PGI (prostglandins), decreased cAMP

increased ADP, serotoinin, Ca+, thrombin, epinephrine

increased PGH2 that can become TXA2 (even though this is also the precursor to PGH 2)

what does aspirin stop to decrease clots

COX-1 to stop thromboxane formation— less plt recruitment/activation

which drugs stop plt recruitment/activation by decreasing ADP? what does ADP do to recruit more platelets

ticlopidine

clopidogrel

prasugrel

cangrelor

tricagrelor

• all of these block p2Y12 receptors that ADP hits to activate platelets

turns on GP IIb/IIIa receptors to recruit more platelets and hit p2Y12 receptors (the activation factor)

what enzyme breaks ATP into cAMP

adenylyl cyclase

what enzyme breaks cAMP into AMP? why is this bad/needs to be inhibited

phosphodiesterases

• means that less cAMP to inhibit aggregation

what effect does more Ca have platelets? how does this work

Ca increases platelet activation and aggregation

• Ca releease changes Plt shape and activates GP IIb/IIIa receptors that allows for cross linking

which substances more adhesion? which more activation/aggregation?

adhesion: serotonin, thromboxanes, ADP

act/agg: GP Ilb/IIIa

aspirin MOA, how does this effect clot formation?

inhibit cyclo-oxygenase (Cox) and PGH2 synthesis

• decrease TXA2 in favor of PGI2

what is another name for thrombin

factor 2!!

aspirin indications

thromboprophylaxis (80 mg); acute MI; mini strokes; atrial

fibrillation (if oral anticoagulant is contraindicated)

aspirin ADRs

bleeding, GI and duodenal ulcer, hypersensitivity rxn, tinnitus

ddi aspirin

anticoagulant, antiplatelet, alcohol ( cause GI ulceration), decrease effect of BB, furosemide, thiazide

preg category for aspirin in trimester 1/2? third trimester?

• c

  • d for last tri

what blood level of aspirin represents overdose? how does this present?

serum salicylate > 200 mcg/mL (salicylism: tinnitus, NV, agitation

hyperventilation, metabolic acidosis, CNS depression)

what is term for aspirin overdose

salicylism

what is salicylim (aspirin overdose) treated with

sodium bicarbonate, saline, charcoal

what are the Thienopyridines (one example) and thier MOA?

• ADP inhibitor— blocks those P2Y12 receptors

• clopidogrel is the one to watch here

what kind of drug is epoprostenol (flolan)

prostacyclin analog (PGI2)

• which is antiplatelet— like prostacyclin, binds to vascular smooth muscle cells and platelets to activate adenylate cyclase, increasing cAMP that stops platelet aggregation

  • recall cAMP stopped PLT agg by upreg GP 2b/3a expression

ok so pgh2 is the common PROSTAGLADIN precursor for many things. what is the new clarity point on the substance cause is ANTI CLOTTING (what kind of prostagladin is anti clotting)

PGI1— prostacyclin

what is the main indication of Epoprostenol

HTN, not so much for anti-PLT acitivty

• activation of cAMP causes massive vasodilation

what is the bennett indication for epoprostenol (flolan)

dialysis patient who can’t take heparin, severe pulmonary HTN and circulatory shock

• not bc its a good antiplt

• its infused INTO dialysis and can work in the blood without having to be activated by going into the patients body/ quick acting

  • used for quick clotting in active bleed patient

what is half life for epoprotsenol and why important

6 minutes- rapidly hydrolyzed.

what are the four laboratory tests

1. prothrombin time

2. international normalized ratio

3. activated partial thromboplastin time

4. thrombin time

prothrombin time what measures

time to fibrin clot after adding tissue factor

prothrombin time what used for

• monitors warfarin

  • monitors extrinsic and common pathways

INR what measures

compares patients prothrombin to normal prothrombin

INR what is rnomal

1

what is normal prothrombin time

11-15 seconds

what IS thromboplastin (used to initiate clotting in clotting factor tests)

tissue factor or factor 3 and phospholipids that accelerates thrombin made from prothrombin

what does activated partial thromboplastin time measure

time to clot after adding prothrombin with calcium and phospholipids

what pathways does act part thromboplastin time act on, and waht is main drug

instrinsic+common

measures warfarinw

avg time for act part thromboplastin time

25-35 seconds

thrombin time what is it

time required to convert fibrogen to fibrin (equates to time required for clot formation after thrombin is added to plasma)

what is avg thrombin time

7-12 seconds

what is thrombin time used to measure

used to monitor therapy that is generally anticoag, such as antifibrinolytic

what is half life of warfarin

36-42 hours

what is warfarin onset of action

3-5 days

• full effect in 8-15 days bc some clotting factors have longer t-halves than others

what is typical BW for anticoags

Pts receiving epidural,

spinal anesthesia, or

undergoing spinal

puncture are at risk of

hematomas and

paralysis.

which antiplatelet is specifically mentioned as a prodrug

clopidogrel

clopidogrel ADRs

bleeding, thrombocytopenic pupura, rash, d, n, hemtaological toxicities

clopidogrel DDI

omperazole

nsaids

warfarin

what does clopidogrel do with omeprazole and why

inhibit CYP2c19

higher rate of CV events

what does clopidogrel do with nsaids

increases risk of GI bleeding

what does clopidogrel do with warfarin

both are cyp2c19 substrates. increases risk of bleeding

BW for clopidogrel

poor metabolizers (PM— its an allele) of CYP2C19 exhibit higher

cardiovascular problems than normal CYP2C19 metabolizer.

what need to associate with clopidogrel

thienopyridine

p2y12

adp inhibitor

which two we want to increase for less clot

cAMP, PGI2 (prostacyclin)

what do we want to decrease to decrease clotting

ADP

PDE

TXA2

Ca, IP3

what class is ticlodipine/what drug is similar to

clopidogrel— antiplatelet

how to give clopidogrel to poor metabolism

decrease dose or split and give BID

adrs of ticlodipine (other p2y12 inhibitor)

bleeding, thrombocytopenic purpura, rash, diarrhea, nausea, leukopenia