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Oxygen supply and exchange > anticoagulation therapeutics > Flashcards

anticoagulation therapeutics Flashcards

1
Q

major steps in haemostasis

A

vascular spasm
formation of platelet plug - platelet adhesion to damaged collagen
conversion to a clot by reinforcement with fibrin
tissue repair

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2
Q

ADP
serotonin
TxA2

A

sticky platelets
vasoconstrictor
vasoC and activates

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3
Q

why doesn’t the platelet plug spread along the vessel

A

prostacyclin - from intact endothelium inhibits platelet adhesion and aggregation

NO - from intact endothelium inhibits platelet adhesion

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4
Q

liver role in clotting

A

bile salts in bile cause gi tract to absorb vitK

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5
Q

fibrinolytic

A

fibrinolytic drug, also called thrombolytic drug, any agent that is capable of stimulating the dissolution of a blood clot (thrombus). Fibrinolytic drugs work by activating the so-called fibrinolytic pathway.

clot busters

Eminase (anistreplase)
Retavase (reteplase)
Streptase (streptokinase, kabikinase)
t-PA (class of drugs that includes Activase)

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6
Q

Background. Heavy menstrual bleeding (HMB) is an important physical and social problem for women. Oral treatment for HMB includes antifibrinolytic drugs which are designed to reduce bleeding how

A

which are designed to reduce bleeding by inhibiting clot‐dissolving enzymes in the endometrium.

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7
Q

what is an anticoagulant

A

Drug that interrupts the process involved in the formation of blood clots

called blood thinner

anticoagulants are different to antiplatelet medicines, such as aspirin and clopidogrel.
because They act on components of the clotting cascade!

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8
Q

how do antiplatlets work

A

reduce the ability of the platelets to stick together and reduces the risk of clots forming

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9
Q

4 ways we can quantify clotting capability

A

measure platlets
calculate INR ( standardised)
measure prothrombin time
measure ATPR

Platelet count = maximal strength of clot and time to stop bleeding reflected by this

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10
Q

prothrombin time

A

time to initiate coagulation (evaluates intrinsic pathway)

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11
Q

ATPR

A

measures effectiveness of reinforcing the clot (evaluates contact pathway)

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12
Q

what is the INR

what should your value be if taking a blood thinner

A

INR = Ratio of patient’s Prothrombin time to the normal population

between 2-3

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13
Q

prothrombin is made where

A

liver

precusor for thrombin

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14
Q

do warfarin and heparin need measuring with blood tests

A

yes

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15
Q

4 types of DOACs

A

rivaroxaban (Xarelto)
dabigatran (Pradaxa)
apixaban (Eliquis)
edoxaban (Lixiana)

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16
Q

which anticoagulant is a pentasaccharide

how does heparin work - what factors and what does it activate

A

heparin - encourages body natural clot lysis to break down clots that have formed acting of 10a and 2a preventing fibrin clot formation by activating antithrombin h=which is the bodys natural anticlht protein

heparin essentially brings antithrombin and factor 10 close together to speed up the reaction

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17
Q

difference between unfractioned and LMWH

A

LMWH enoxaparin binds less avidly to plasma proteins and therefore has increased bioavailability and duration of action - lower risk of osteoporosis and lower risk of HIT

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18
Q

when is unfractioned heparin preferred

A

in patients with renal impairment

LMWH stable in all types of general and orthopaedic surgery

19
Q

what is fondarparinux more similar to

A

LMWH

20
Q

what factors does heparin act on

A

factor 10a and 2a( thrombin)

21
Q

what factor converts prothrombin to thrombin

A

fact 10a

22
Q

what is the bodies natural anticoagulant

does heparin speed up or slow this process

what is the special role of unfracitonated heparin

A

antithrombin - bind to factor 10a and inhibits it.
heparin speeds up this process

unfractioned binds to antithrombin causing antithrombin to bind to both 10a and 2a means it can stop clotting in 2 places - forms a ternary complex
the other forms cannot to this

23
Q

unfractionated

IV infusion
Effective immediately
Short half life
Most likely to cause HIT
APTR monitored
A

LMWH/fondaparinux

SC injection
Effective after 1 hour
Longer half life – renally excreted
HIT even rarer with LMWH
Doesn’t require monitoring
24
Q

you can use heparin

DVT
PE
Acute MI
VTE prophylaxis
During Haemodialysis 
During open heart surgery
(Safe to use in pregnancy)

what are contraindications and complication s

A 
Haemorrhagic disorders
Thrombocytopaenia
Severe HTN
Surgery / lumbar puncture
Trauma
Spinal or epidural anaethesia (for treatment dose)
Acute bacterial endocarditis
Heparin-induced thrombocytopenia (HIT)
-> autoimmune attack on platelets
 resulting in degradation 
~ reversed on discontinuation. 
Counter-intuitively causes increased thrombotic events

Hypersensitivity reactions
Hyperkalaemia

25
Q

how does warfarin work

A

acts on vit k and block 1972 and protein C and S

vitamin K is only active in it’s reduced form. Vitamin K reductase reduces Vitamin K which activates gamma-glutamyl carboxylase. Gamma glutamyl carboxylase then converts glutamic acid to Gamma-carboxy-glutamic acid which produces factor 2,7,9, 10 protein C+S.
warfarin binds to vit k reducatase enzyme in order to inactivate it

26
Q

what enzyme does warfarin bind to

why do we give heparin at first too

A

vit k reducatase enzyme inactivating it

This means there is a decreased production in the reduced form (active form) of vitamin K. This leads to the deactivation of gamma glutamyl carboxylase which impairs the conversion of glutamic acid to gamma carboxy-glutamic acid and this suppresses the clotting factors 2, 7, 9, 10, and protein C + S.
Interestingly, 2,7,9,10 are clotting factors, but protein C + S are actually anticoagulant!! So this means initially warfarin can actually be pro-thrombotic because C+S are blocked. This is why when starting warfarin we often cover with heparin for a few days.

27
Q

drugs that potentiate warfarin effects

A

metronidazole and co-trimazole- inhibit hepatic drug metabolism

aspirin - inhibit platelet function

cephalosporins - inhibit reduction of vit k

broad spectrum antibtiocis - dreads avaivbilty of vitamin k - gut bacteria contain it k

28
Q

what drugs inhibit the effect of warfarin

A

rifampicin and carbamazepine - induce hepatic P450 enzymes

cholestyramine reduce warfarin absorption in the gut

29
Q

when should we use warfarin

A

DVT
PE
AF in those at risk of embolisation
Mechanical prosthetic heart valves

Pregnancy/48hrs post partum
Haemorrhagic/recent ischaemic stroke
Severe renal/hepatic disease
Peptic ulcer/GI bleed
Severe Hypertension
Recent surgery

Initially prothrombotic
Bleeding → increased risk due to interactions
Teratogenic- disordered bone development
Skin necrosis

30
Q

target inr during anticoagulant therapy

when can it be allowed to be more

A
  1. 5 ( 2.0-3.0 )
  2. 5-3.5 - mechanical mitral heart valve
  3. 0.4.0 - anti phospholipid syndrome, recrurent DVT Nad or PE , first generation heart valves
31
Q

81 year old male comes to you because he’s been experiencing palpitations.

You feel his pulse and he has an irregularly irregular heart rate

You explain that this can increase his risk of strokes so he will need something to ‘thin his blood’. What will you use?

won’t take warfarin either what do you give

A

DOAC

32
Q

what do DOACs do

A

inhibit factor 10a - apixaban , rivaroxaban , edozaban - this is the propagation phase

in the fibrin formation phase dabigatran can inhibit factor 2a ( thrombin)

33
Q

which DOac is the most bioavialbke

A

riavaroxaban

34
Q

when should a DOAC be used

A

Same as warfarin
(but cannot use a DOAC if mechanical heart valve - warfarin only!!)

contraindications

Acute bleeding Coagulopathies
Severe renal insufficiency
Preg/breastfeeding
 Severe hypertension
Endocarditis

complciatons

Dapbigatran-
 GI disturbance, diarrhoea, 
 GI bleed risk
Rivaroxaban- constipation, headaches
Apixaban- lower risk of GI bleeds than others
35
Q

which doac is most preferred and why

A

Apixaban = lowest bleeding profile so now preferred amongst physicians. dabigatran worse than warfarin! Originally didnt have reversal agents (unlike warfarin so often pts preferred warfarin) but now there are things for some of them, def for edoxaban.

36
Q

what is a fibrinolytic drug

A

fibrinolytic drug, also called thrombolytic drug, any agent that is capable of stimulating the dissolution of a blood clot (thrombus)

37
Q

most common fibrinolytic drug

A

altepase - recombinant tPA

38
Q

how is d-dimer formed and what conditions can it detect

A

D-dimers are unique FSPs that are formed when cross-linked fibrin is lysed by plasmin

DVT
PE
Venous sinus thrombosis
Aortic dissection
Disseminated intravascular coagulation
39
Q

antifibrinolytics example what does it do

A

tranezamic acid

Anti-fibrino-lytics means something that STOPS the breakdown of a clot. So the opposite of everything else we’ve been learning about. In this case, it STOPS plasminogen from converting to plasmin in order to STOP fibrinolysis (clot splitting).

40
Q

what is dalteparin

A
  • heparin –> anticoagulant
41
Q

if your on an heparin infusion what range of ATPR should you have

A

1.5

42
Q

low platelet called

A

thorombocytopenia

43
Q

complication of taking heparin when platelets get low

A

HIT

Oxygen supply and exchange (24 decks)

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