G oo d M

orning..

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Story of Band-Aid invention

• By Earle Dickson in 1920.

• He worked for a company that manufactured gauze and

adhesive tape called Johnson & Johnson.

•Earle Dickson was Married to Josephine Dickson

•We will never know the reason, but it is a fact that

Josephine Dickson was accident prone.

•During the first week that she was married to Earle

Dickson, she cut her self twice with the kitchen knife.

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After that, it just went from bad to worse. It seemed that
Josephine was always cutting herself.

The dressing made by him would come off easily while she was
working

One day her husband had an idea. He sat down with some tape
and gauze and a pair of scissors. Then he cut the tape into strips.
In the middle of each strip he stuck a little square of gauze.

From then on, whenever Josephine had an accident, ready-made

bandages were on hand for her to use quickly and without a lot
of fuss.

At Johnson & Johnson, they heard about these new bandages

that could be put on in thirty seconds.
Soon the company was making them to sell on a small scale.

Four years later, in 1924, the company installed machines for

mass producing the new product, and the trade name BAND-
AID was adopted
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Hemostasis & Blood
Coagulation

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 Contents
o Introduction
o Definition- Hemostasis
- Coagulation
o Basic units of Hemostasis and Coagulation

o Hemostasis- Primary Hemostasis

- Secondary Hemostasis
o Coagulation Cascade.
o Factors controlling coagulation
o Fibrinolytic pathway.
o Applied aspects
o Investigations
o Refferences
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 Introduction
• Coagulation is a complex process by which blood
forms clots. It is an important part of hemostasis

• Human body has amazing protective mechanisms

to combat all sorts of injuries to body.

• Bleeding has to be stopped as early as possible to

prevent further complication

• Whenever vessel is severed, hemostasis is

achieved by
- Vascular spasm
- Formation of Platelet plug
- Formation of Blood clot
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- Growth of fibrous tissue intoPage
the clot.
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 Definitions
• Hemostasis : Defined as prevention of blood loss
By Willium F Ganong

o Blood coagulation  the sequential process by which

the multiple coagulation factors of blood interact in the
coagulation cascade, resulting in formation of an
insoluble fibrin clot.
Medical Dictionary

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 Hemostasis
• Primary hemostasis: Vasoconstriction and platelet
plug together produce the immedieate stopping of
hemorrhage ( within say few seconds to few
minutes ). This phase is called Primary
hemostasis.

• Secondary hemostasis. Formation of fibrin clot

over platelet plug is designated as secondary
hemostasis.

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Serial events after blood loss
• Constriction of small arterioles. Achieved by two
mechanisms
i) Neural- by action of sympathetic vasoconstrictor
nerves.
ii) Locally released chemicals – serotonin and
endothelin.

• Adhesion: Platelets adhere to damaged vessel wall

and are activated. Ultimately platelet plug is formed.
This plug seals the vessel.

• These two events taken togather constitute Primary

hemostasis
.
• Time between onset of bleeding and primary
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hemostasis is called bleeding time. Page 9
• Finrin clot develops over platelet plug by a
mechanism called Coagulation.

• This fibrin clot bolsters the platelet plug. This

event is called as secondary hemostasis and it
stabilizes the platelet plug.

• Fibrinolytic mechanism : After few days clot is

lysed and recanalization of the vessel again
occurs.

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 Injury to blood vessel and damage to endothelium

Exposure of Collagen
Von Willebrand F

Adhesion of Platelets to collagen

Activation of Platelets

Secretion of Serotonin Secretion of ADP & Formation of

Thromboxane A2 Prothrombin activator

Aggregatoin of
Platelets
Blood Clotting

Vasoconstriction Formation of
Platelet plug

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 Basic units of Hemostasis and
Coagulation
• Blood : The fluid that circulates in the heart,
arteries, capillaries, and veins of a vertebrate animal
carrying nourishment and oxygen to and bringing
away waste products from all parts of the body

• Vascular wall :

• Platelets : a minute colorless anucleate disklike

body of mammalian blood that is derived from
fragments of megakaryocyte cytoplasm, that is
released from the bone marrow into the blood, and
that assists in blood clotting by adhering to other
platelets and to damaged epithelium—called also
blood platelet, thrombocyte
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 Vessel wall or Endothelium
• The endothelium is the thin layer of cells that lines
the interior surface of blood vessels,[1] forming an
interface between circulating blood in the lumen and
the rest of the vessel wall.
• These cells are called endothelial cells. Endothelial
cells line the entire circulatory system, from the
heart to the smallest capillary.

• The endothelium normally provides a non-

thrombogenic surface because it contains heparan
sulfate which acts as a cofactor for activating
antithrombin III, a protease that cleaves several
factors in the coagulation cascade.

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 Platelets
• Non- nucleated
• During hemostasis inactive platelets become active.
• Normal count : 1.5 to 4 lacs per Micro liter.
• Less than 40,000 is called critical count.
• Pools : Red bone merrow, blood and spleen
• Morphology :
-Diameter- 2-4 Microns
- When inactive- Disc shaped
-When active- Become spherical.

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 Membrone

Outer Inner Lipoprotein

glycocalyx layer.

Lipid molecules which are

Glycoproteins. Receptors of
phospholipids-Precursors of
membrane are glycoprotiens
TxA2,

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• Cytosol – Granules
- Tubules
- Contractile elements
- Mitochondria Fibronectin,
- Golgi apparatus ADP,V,ATP,
Factor VII, 5
HT,
PF4, PDGF,
histamine
• Granules- Alfa granulae- and Ca.

Dense granules-

• So platelets also called as “Tiny pharmaceutical

bags”

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• Tubules- Open and Dense
Open- communicate with ECF
Dense- donot communicate with exterior.

Contractile clements_ Actin and Myosin- action of

these help in producing pseudopods.

Platelets donot have DNA or RNA.

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 Functions of Platelets

• Adheison: Platelets have receptors for collagen.

So bind to subendothelial collagen at the site of
injury. This is reinforced by Von Willebrand
factor

• Aggregatoin: Following adhesion platelet get

activatec and secrete ADP and Thromboxane
A2 which attract other platelet to form a lump of
platelets.

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 Development of Platelet
• In RBM from pluripotent stem cells

Committed stem cell

CFU

Promegakaryoblast

Megakaryoblast

Megakaryocyte

Platelets.
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 Coagulation factors :
I. Fibrinogen
II. Prothrombin
III. Tissue Thromboplastin
IV. Ca
V. Proaccelerin or Labile factor
VI. Not Present
VII. Proconvertin or Stable factor
VIII. Antihemophelic factor
IX. Christmas facotr or Plasma thromboplastin
component or AHF B
X. Staurt facotor
XI. Plasma thromboplastin anticedent
XII. Hageman factor or glass factor
Freestabilizing
XIII. Fibrin Powerpoint Templates
factor or Laki Larland factor.
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 Coagulation cascade
• Coagulation of blood is secondary hemostasis.
Occurs little after platelet plug formation.

• There are procoagulant substances in blood which

are proenzymes in nature. Once process of clotting
starts these proenzymes become activated one after
another in a sequential manner. Final end product is
fibrin. Fibrins are thread like structures .

• Large number of fibrin threads crisscross with each

other and blood cells are entangled in the fibrin
network. Fibrin thread containing blood cells is
known as clot.

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• Ultimately fibrin must be formed. This is formed
from precursor fibrinogen. Thrombin acts on
fibrinogen to form fibrin. Thrombin is present as
prothrombin which is activated to thrombin by
factor Xa.

• Xa is produced by one of the two major pathways.

– Intrensic or Extrensic pathway.

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• Triggering mechanism for Intrensic pathway-
injury to vessels leading to contact of factor XII
with the subendothelial tissue of the blood vessel.

• Triggering mehcanism for extrensic pathway –

release of tissue thromboplastin from the injured
vascular and other cells.

• Fibrin formed is stabilized by XIIIa.

• Clot formed is soft and friable. After clot

retraction
Freeyellowish
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This fluid is serum.
 Intrinsic Pathway Extrinsic Pathway
XII contact with subendothelium Release of Tissue thrombopolastin

XII XIIa
VII VIIa
XI XIa
VIIIa,PL,Ca

Common Pathway
IX IXa
X Xa
Xa, PL, Va, Ca

Prothrombin Thrombin

Fibrinogen Fibrin
XIIIa

Stable Fibrin
 Inhibitors of Coagulation
• Clot formed remains confined to the site of injury.
How???
i) Naturally occurring anticoagulants- Antithrombin
- Heparin
- Protein C
- Protein S
ii) TFPI : Tissue factor pathway inhibiors.
iii) Thrombomodulin:
iv) Fibrinolytic mechanism.

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 Fibrinolytic Pathway

Present in liver and

Plasminogen circulating blood

Plasminogin is adsorbed on the clot

Local endothelial cells produce plasminogen

activator.

Plasminogen Plasmin

Breaksdowns the fibrin threads

( tPA: tissue Engulfed

plasminogen by the RES
activator
and Urokinase)
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 Role of Vit K, Liver, vWF,

• Vit K:
- Essential for activation of factors II, VII, IX, X

- Sourses: - Vegetables ( Cabbage)

- Intestinal flora

- Deficiency is seen in- Comatose patient

- New borns
- Obstructive juandice

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 Role of Liver
• Synthesizes factors II,VII,IX,X, I, V, XI

• Also synthesize : antithrombin III, heparin,

protein C & protein S.

• So in real life liver failure may be associated

with excessive bleedign as well as intravascular
coagulation

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 Role of vWF
• It is synthesized by Megakaryocyte and vascular
endothelium

Functions-

-Acts a bridge
betweenplatelet and
- Acts as a carrier
denuded
for factor VIII
subendothelium.

-between platelet and

platelet.

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Applied aspects

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 Investigations
• Bleeding time: - Ivy method- 7-11mins
- Duke’s method-1-4 mins

• Clotting time- Wright cappillary tube method- 1-7

mins
- Lee and white method-5-10 mins

• Prothrombin time ( PT)

Normal value- 10-20 seconds ( Quick method)
Defect in extrinsic and common pathway.
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• Activated partial thromboplastin time ( APTT)
Normal value- 40 sec
Defect in intrinsic and common pathway.

• Platelet count : 150,000 to 400,000cells/cu mm

• Clot retraction time : 30-60 mins

• Cappillary fragility test : more than 10 petechiae/

inch

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 Conclusion
• Hemostasis & coagulation are the body’s best
mechanisms to prevent blood loss from the body.
• Many bleeding and clotting disorders manifest
mainly in oral cavity.
• Thorough medical history and investigations help in
identifying those persons at risk of increased
bleeding after surgery.
• Those people at risk must be identified prior to
minor or major surgery to prevent further
complication
• Thorough understanding of hemostatic and
coagulation will help in us to determine the
appropriate test and treatment.
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 Refferences
• Arthur C Guyton. Text book of medical physiology.
8th ed

• Chaudhuri. Text book of Concise medical

physiology. 4th ed

• Willium F Ganong. Review of Medical physiology.

12th ed

• K. Sembulingam. Essentials of medical physiology

• www.wikipedia .com

• Google immages

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