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hemostasis drugs Flashcards

1
Q

what is hemostasis

A

process that halts bleeding after injury to a blood vessel
- formation of platelet plug
- production of fibrin
(clotting cascade with many plasma proteins)

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2
Q

hemostasis modifier agents

A
  1. anticoagulants
    - inhibit the action of clotting factors
    - prevent clot formation
  2. antiplatelet drugs
    - inhibit platelet aggregation
    - prevent platelet plugs
  3. thrombolytic drugs
    - break down existing clots
  4. hemostatic agents
    - promote blood coagulation
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3
Q

coagulation pathway simplified

A
  • ends with fibrin (p.p. chain activated)
  • amplification down the chain
  • thrombin changes fibrinogen into fibrin
  • factor 10 activates thrombin
  • intrinsic and extrinsic pathway (converge at common point)
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4
Q

anticoagulants “blood thinners”

A

used prophylactically to prevent:
- clot formation (thrombus)
- embolus

does not break existing clot just stops one from getting bigger

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5
Q

anticoagulants indications

A

prevent clot formation:
- MI (block in cardiac artery)
- unstable angina (clot/block)
- a fib (SVD which increases risk of clot bc slower moving blood)
- DVT
- indwelling devices (mechanical heart valves)
- pulmonary embolism

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6
Q

types of anticoagulants

A
  • heparin
  • low molecular weight heparins (LMWH)
  • warfarin (PO)
  • direct acting oral anticoagulants (DOAC - factor X and thrombin)
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7
Q

anticoagulants contraindications

A
  • known drug allergy
  • acute bleeding process
  • thrombocytopenia (decreased platelets in circulation)
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8
Q

anticoagulants adverse effects

A

bleeding risk:
- gum bleed
- nosebleeds
- unusual bleeding
- anemia/low Hct
- tarry stools (GI bleeding, ulcers)

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9
Q

heparin

A

indirectly inhibits activity of multiple proteins on cascade
- thrombin
- factor Xa
- other factors in intrinsic pathway

from natural pathway

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10
Q

why is heparin dosage unpredictable

A

all molecules are a different lengths and size
- want to inhibit coagulations to the right degree

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11
Q

how is heparin dosage monitored

A

monitored by activated partial thromboplastin times (aPTT)
- measures the intrinsic pathway
- aPTTs need to be 1.5-2.5 x greater than control (40sec)
- blood test to measure how long it takes for coagulation

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12
Q

heparin characteristics

A
  • given parenteral (SC or IV)
  • effective within minutes
  • short half life (1-2 minutes)
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13
Q

heparin adverse effects

A

heparin induced thrombocytopenia (HIT)
- binds to platelets and brings antibodies around it which may activate and bring platelets together
- leading to lower amount of circulating platelets

hypersensitivity reactions
- fever, chills, urticaria

anticoagulant effects reversed by protamine sulfate (antidote)

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14
Q

LMWHs

A

low molecular weight heparins
- enoxaparin
- tinzaparin
- dalteparin

predictable anticoagulant response
- do not require frequent lab monitoring (given at home, SC every 12 hrs)

less thrombocytopenia then heparin (protamine sulphate antidote)

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15
Q

which plasma protein does lmwh inhibit

A

factor X

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16
Q

other anticoagulants

A

danaparoid
- alternative to heparin
- SC or IV

fondaparinux
- synthetic
- SC or IV

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17
Q

client implications: heparin

A
  • double check dose with another nurse
  • give SC in areas with more fat (abdomen)
  • rotate injection site
  • protamine sulphate antidote
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18
Q

client implications: LMWH

A
  • SC in abdomen
  • rotate sites below umbilicus
  • protamine sulphate antidote
19
Q

oral anticoagulants: warfarin

A
  • vitamin K antagonist
  • vit K makes clotting factors ready for action: VII, IX, X, pro-thrombin (liver)
  • warfarin doesn’t effect proteins already in plasma just the cells being made in the liver
  • effects depends on clotting factors turnover (protein degradation)
  • max effect may take 3-5 days (starts within 24 hours)
  • patients may be started on 5 days LMWH + warfarin (then LMWH withdrawn)
20
Q

warfarin continued

A
  • orally only
  • dosage variable between individuals
  • monitored by clotting lab test
    - prothrombin time (PT - coagulation time)
    - INR (international normalization reference ratio - desired goal to be in range)
  • PT/INR (measure activity of extrinsic pathway)
21
Q

PT/INR values

A

PT therapeutic level is 1.3-1.5 times the control level

target INR range 2-3x control (2.5-3.5 if mechanical heart valves)

22
Q

what does excessive dietary vitamin k do to warfarin effectiveness

A

warfarin less effective bc more vitamin k to help clotting factors

23
Q

what happens to warfarin effectiveness when too little vitamin k

A

dosage becomes too high (INR levels too high)

24
Q

what happens if there is warfarin excess

A

give an antidote (vitamin k)
- IV slow infusion: 4-8 hour effect
- PO: within 24 h

25
Q

warfarin contraindications

A

pregnancy
- risk of fetal bleeding, teratogenicity, spontaneous abortion
- can cross BBB

26
Q

client education anticoagulants

A
  • maintain intake of vitamin k constant (tomatoes, dark leafy green vegetables)
  • wear medical alert bracelt
  • consult physician before taking other drugs or OTC products (many drug-drug interactions bc its metabolized by CYP enzymes)
27
Q

client education: warfarin

A
  • may be started while client still on heparins (until PT/INR indicate adequate coagulation)
  • full therapeutic effect takes several days
  • monitor PT/INR regularly
28
Q

Direct-Acting Oral Anticoagulants (DOACs) advantages

A
  • rapid onset and offset
  • fixed doses
  • no blood test
  • few drug-drug interactions
  • no dietary concerns
  • lower risk of bleeds
29
Q

DOACs: direct thrombin inhibitor

A

Dabigatran
- po administration (with LMWH for DVT)
- GI disturbance (N&V, pain, bloating)

30
Q

DOACs: direct factor Xa inhibitors

A

rivaroxaban
- apixaban
- betrixaban
- edoxaban

PO administration

31
Q

anticoagulant adverse effectse

A

increased bleeding (mild to life threatening)

32
Q

all anticoagulants: client education

A
  • importance of regular lab testing where necessary)
  • signs of abnormal bleeding (gums, nosebleeds, bruising, heavier menstrual bleeding, in vomit/stools/urine/sputum, abdominal pain)
33
Q

antiplatelet agents

A

taken prophylactically
- stop agents that activate platelets (ADP, TXA2)
- prevent platelet action

34
Q

acetylsalicylic acid (antiplatelet)

A

inhibit COX pathway (for thromboxane A2)
- irreversible inhibition of COX in platelets

risk for stomach problems and ulcers
used for heart attack, MI, stroke, cardiac arteries blocked

pentoxifylline

35
Q

clopidogrel (prasugrel, ticlopidine)

A
  • irreversible ADP receptor blocker (antagonist)
  • effect lasts lifetime of platelet
36
Q

ticagrelor

A

reversible ADP receptor blocker (antagonist)

37
Q

antiplatelet drugs indications

A

antithrombotic effects
- reduce MI risk
- reduce stroke risk

38
Q

aspirin + clopidogrel combination

A

produces additive antiplatelet activity
- increased bleeding potential

39
Q

thrombolytic agents

A

drugs that break down preformed clots
- recombinant tissue plasminogen activator (tPA)
- activate plasminogen to become plasmin which eats away existing clots

40
Q

thrombolytic agents examples

A
  • alteplase
  • tenecteplase
  • reteplase
41
Q

thrombolytic agents: mechanism of action

A

activate fibrinolytic system to break down clot in blood vessel (plasminogen –> plasmin)

re-establish blood flow to
- heart muscle (MI)
- brain (stroke)

42
Q

thrombolytic agents: indications

A
  • acute MI
  • arterial thrombolysis
  • DVT
  • occlusions of shunts or catheters
  • pulmonary embolus
43
Q

thrombolytic agents contraindications

A
  • allergy
  • concurrent use of other anticoagulation
44
Q

thrombolytic agents adverse effects

A

bleeding
- internal
- intracranial
- superficial
other effects: N&V, hypotension, anaphylactoid reactions, dysrhythmias

pharm (28 decks)

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