coagulants in detail with all drugs, mechanism of action, advantages, adverse effect, contraindication with example and pictures.
in simplified manner , easy to understand
2. Haemostasis & blood coagulation involve
complex interactions between the injured
vessel wall, platelets & coagulation factors
For blood to clot, a cascading series of
proteolytic reactions is started by.
1. Contact activation of Hageman factor:
intrinsic system.
Slow and takes several minutes to activate
factor X.
3. 2. Tissue thromboplastin-
extrinsic system.
Needs a tissue factor.
Activates factor x in seconds.
Clotting factors are present in the plasma in the
inactive form.
↓partial proteolysis.
Active protease ----→ activates next factor.
Antithrombin, protein C, protein S, antithromboplastin
and the fibrinolysin system ---- oppose coagulation
& lyse formed clot
4.
5.
6. These are agents which promote coagulation
and are indicated in the haemorrhagic
states.
Fresh whole blood/plasma provide all the
factors needed for coagulation.
8. 1. Vitamin K:
K1 [ from plants]-phytonadione.
K2 [ from bacteria]-Menaquinones
K3 [ synthetic] Fat soluble- Menadione,
-Acetomenaphthone
Water soluble- Menadione
sod.bisulfite
- Menadione
sod.diphosphate
9. Fat soluble, required for the synthesis of
clotting factors.
Daily requirements: it is uncertain, variable
amount becomes available from colonic
bacteria. 50-100μg/day
Dietary sources: green leafy vegetables.
Liver, cheese etc.
10. Action: acts as a cofactor at a late stage in
liver during synthesis of coagulation proteins-
II, VII, IX & X.
11. Fat soluble forms
are absorbed from
intestine via lymph
and require bile
salts for
absorption.
Stored mainly in
liver.
Metabolites are
excreted in bile or
urine.
12. liver disease,
obstructive jaundice
malabsorption,
long term antimicrobial therapy
13. I. Dietary deficiency >5-10mg/day
oral/parenteral vit K
II. Prolonged antimicrobial therapy
III. Obstructive jaundice/malabsorption
syndromes >vit K 10mg/day i.m./orally
IV. Liver disease(cirrhosis, viral hepatitis)
V. Newborns>vit K 1mg i.m.
VI. Overdose of oral anticoagulants:K1.dose
depends on the severity of bleeding &
hypoprothrombinaemia
VII. Prolonged high dose salicylate therapy.
15. Fibrinogen- control bleeding in
haemophilia, Antihaemophilic globulin
(AHG) deficiency & acute fibrinogenemic
states
16. concentrated human AHG prepared from
pooled human plasma.
Used to control bleeding in haemophiliacs
ADVERSE EFFECTS: fever with chills,
headache and skin rashes.
17. Ethamsylate:
It decreases capillary bleeding when
platelets are adequate; probably exerts
antihyaluronidase action & improves
capillary wall stability, but does not stabilize
fibrin.
It is used in capillary bleeding in
menorrhagia, after abortion, PPH, epistaxis,
haematuria, malena,after tooth extraction.
SE:nausea,rash,headache,fall in BP
18. Desmopressin:
Releases factor VIII & von Willebrand’s
factor from vascular endothelium.
Used to control bleeding in haemophilia and
von willebrands’s disease
21. These are substances used to stop bleeding
from a local & approachable site. Effective
on oozing surfaces.
E.g. bleeding following tooth extraction,
abrasion, epistaxis, etc.
22. 1. Thrombin- obtained from bovine
plasma. It is applied as dry powder
on the bleeding surface. Used in
haemophilia, neurosurgery, skin
grafting.
23. 2. Fibrin-obtained from human plasma and is
dried; it is used as sheets or foam for
covering or packing bleeding surfaces. It is
left in situ.
24. 3. Gelatin foam- spongy gelatin.
- Moistened with saline or thrombin solution
& used for packing wounds.
- Absorbed in 1-2 months. It is left inside.
25. 4. Russels viper venom- applied locally. Acts as
thromboplastin. Used to stop external
bleeding in haemophiliacs
5. Vasoconstrictors .-0.1% solution adrenaline
To stop epistaxis.
6. Astringent- tannic acid or metallic salts.
Bleeding gums,bleeding piles.