DRUGS AFFECTING

BLOOD
I. Haematinics

I. Coagulants

II. Anticoagulants

III.Fibrinolytics (Thrombolytics)

IV.Antifibrinolytics

V. Antiplatelet drugs (Antithrombotics)

 Hemostasis is the spontaneous arrest of bleeding
from the damage blood vessels.

 Process is a complex takes place in b/w injured

vessel & clotting factors.

 Clotting factors are proteins synthesized by liver.

 Coagulants / hemostatics. -
 The drugs which promote coagulation- used to control &
treat haemorrhagic states.
 Used locally/systemically.
 Local hemostatics- styptics.
 Physical methods like pressure, tourniquet or ice can control
bleeding.
Styptics- used in bleeding sites.
 Adrenaline- 1:10,000 soln, placed in tooth sockets, nasal
packs. Vasoconstrictor. C.I in CVD pt’s.
 Thrombin dusting powder- skin grafting.
- obtained from cattle / human plasma
 Fibrin- human plasma, used in covering/packing bleeding
surfaces.

 Gelatin- with thrombin to control bleeding wounds.

 Thromboplastin powder- used in surgery.

 Astringents like FeCl3, tannic acid are used in bleeding

gums / sites.
Coagulants used systemically-
 Vit K- fat soluble, essential for synthesis of clotting factors.

 Vit.K1- present in food from plant source.

 Vit.K2 (menadione) - produced by in GUT by bacteria

 Vit.K3- synthetic compound used therapeutically.

 Vit K is essential for the biosynthesis of clotting factors-

Prothrombin & factors II, VII, IX & X by the liver.
 Heparin-

M.A.O- activates antithrombin III which binds to C.F ( Xa, IIa, IXa, XIa,
XIIa, XIIIa ) & inactivates them by forming stable complexes.
Actions- powerful anticoagulant - acts instantaneously both in
vivo & vitro.
PK-
 Not effective orally, Given IV/SC.
 IM- causes hematomas.
 I.V inj- Quick onset of action, peak in 5-10min & C.T
returns to normal by 2-4hr’s.
 Rx is monitored by aPTT or CT.
 A/V- Bleeding, Hypersensitivity, Thrombocytopenia, Alopecia,
Osteoporosis.

 Heparin over dosage-Continues bleeding.

 Mild cases - stop heparin adm, short acting.
 Sever cases – Protamine sulphate, obtained from fish sperm, given
I.V- 1mg neutralizes 100 U of heparin.
 Its self acts as a weak anticoagulant, So avoid overdose. Protamine is
a strong basic ptn’ which binds & neutralises strong acids by forming
stable complexes, which doesn't have anticoagulant activity. Whole
blood transfusion is required.
Oral Anticoagulants-
 Warfarin– is most commonly used.
 Anti coagulant action is by interfering with synthesis of
Vit K dependent clotting factors in liver.
 Acts only in vivo.
 Over dosage- haemorrhage is main hazard.

 Bleeding in the intestines/brain.

 Episodes of epistaxis & bleeding gums.

 Teratogenic effects & skin necrosis.

Treatment depends on severity-
 Stop anticoagulant therapy.

 Fresh blood transfusion

 Antidote- Vit.K1.

 It helps in activation of clotting factors.

 IV adm- response develops after several hours.

 In emergency- fresh whole blood encounters the effects of

anticoagulant.
Uses of anticoagulants-
 They prevents extension of thrombus but can’t destroy the
clot which is already formed.
 Heparin is a short & fast acting- for starting Rx .
 Warfarin is a long & slow acting- for maintenance Rx &
oral use
1. Venous thrombosis & pulmonary embolism.
2. Post operative, post stroke & bed ridden pt’s.
3. Rheumatic valvular diseases.
4. Unstable angina- reduces the risk of MI.
5. Vascular surgery, artificial valves & haemodialysis
CI to Anticoagulant therapy-
 Bleeding disorders including thrombocytopenia.

 Severe hypertension.

 Malignancies

 Bacterial endocarditis.

 Liver & kidney diseases.

 Heparin Warfarin
Naturally occurring, animal source- Ox Synthetic.
lung & pig intestine.
Active in Vivo & in Vitro In Vivo
Adm parentally I.V/S/C Adm Orally
Acts by + antithrombin III & inactivates Acts by inhibiting Vit-K dependent
X a, II a, IX a, XI a, XII a, XIII a clotting factors II, VII, IX & X

Has rapid onset action, short duration Has slow onset & long acting

Monitored by aPTT Monitored by INR

Over dosage- Protamine Over dosage by Vit.K

X Placental barrier, safe during Crosses barrier, teratogenic.
pregnancy
Used mainly to initiate therapy Used maintenance therapy
Expensive Not expensive
Thrombolytics / Fibrinolytics -

Uses-
1. Acute MI- IV adm reduces the mortality rate.
2. Deep vein thrombosis & pulmonary embolism.
Antifibrinolytics -
 Inhibits plasminogen activation & prevents fibrinolysis.
Epsilon-amino carpic acid (EACA) & Tranexamic acid.

 To controls bleeding due to overdose of fibrinolytics

 To reduce the bleeding after prostrate surgery.

 After tooth extraction in haemophiliacs.

 After tonsillectomy & menorrhagia.

Antiplatelet drugs/ antithrombotics -

 Platelets forms –initial plug at the site of vascular injury &

also involved in atherosclerosis.

 By X platelet function, thrombosis & atherosclerotic

vascular disease can be prevented.

 E.g., aspirin, dipyrimidamole, sulphinpyrazone, ticlopidine.

Uses-
1. Acute MI-aspirin + Thrombolytics.
 Aspirin long term use reduces reinfraction in MI.
2. Angina pectoris/ unstable angina
3.In prosthetic heart valves, valvular heart diseases & coronary
by pass implants.

4. Cerebral thrombosis- in Pt’s with TIA- aspirin reduces the

incidence of stroke & decreases mortality.
Hypolipidemis -
 Hyper lipoproteinemias - Cholesterol / T.G’s
carrying lipoproteins in the plasma is elevated above
normal.

 Increased lipoproteins- fastens the atherosclerosis &

risk of MI.

 RX Hyper lipoproteinemias – B. wt reduction + low

cholesterol diet + Hypolipidemis .
Hypolipidemics –
1. HMG CoA reductase inhibitors- Lovastatin,
Simvastatin, Pravastatin.

2. Fibric acid- Gemfibrozil, Clofibrate, fenofibrate.

3. Bile acid binding agents- Cholestyramine,

Colestipol.

4. Antioxidant- Probucol.

5. Miscellaneous- Nicotinic acid, Neomycin.

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