SOK Blood Physiology Hemostasis & Platelet Function (1-2020)

Dr Khaled Abdelfattah A. Abulfadle

Assistant Professor of Physiology
Zagazig College of Medicine, Egypt
khafadle@[Link]
Hemostasis [Link]
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Platelet Function SOK Physiology Group on
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Introductory Case:
A 42-year-old patient is scheduled for surgery that will likely require a
transfusion. Because the patient has a rare blood type, an autologous
blood transfusion is planned. Prior to surgery, 1500 ml of blood is
collected. The collection tubes contain calcium citrate to prevent
coagulation.

Learning Objectives
At the end of this chapter, you should be able to:
1. Define plasma, serum, hemostasis, homeostasis and thrombosis.
2. Outline steps of hemostasis.
3. Discuss functional structure of the platelet.
4. Describe role of platelets in hemostasis.
5. Enumerate clotting factors.
6. Discuss intrinsic and extrinsic pathways of blood clotting.
7. Describe the interrelation between the types of hemostatic
mechanisms.
8. Enumerate factors normally prevent intravascular clotting
(thrombosis).
9. Outline causes of thrombosis.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Important Definitions: (See Table-1)

Plasma It is the liquid portion of the blood. It can clot on standing (Why?).
Serum It is the liquid left over after blood has clotted. It cannot clot on standing (Why?).
Hemostasis It is the physiologic (normal) protective process by means of which blood loss is
limited following minor vascular injury i.e. it is the stoppage of bleeding in case of a
small vascular injury.
Homeostasis It is the process by which the internal environment of the body is kept constant e.g.
calcium homeostasis means factors that maintain blood calcium level constant (9-11
mg/dl).
Thrombosis It is a pathologic process in which blood clots inside blood vessels.
Table-1: Important definitions.

Hemostasis (Hemo= Blood, Stasis= Stop): (See Table-2 and Figures 1-2)

Definition It is a physiological process by means of which bleeding from a small vascular injury
is stopped.
Mechanism of 1. Role of extravascular factors:
hemostasis a. Physical effects: of skin and elastic tissue in closing the injured blood vessel.
b. Biochemical effects: of released substances from tissue (e.g. tissue thromboplastin,
clotting factor III) in activation of clotting.
2. Role of injured vessel wall:
Effect: local vasoconstriction (VC) i.e. local vascular spasm.
Mechanism of local VC:
a. Chemical theory: released vasoconstrictor substances (as serotonin and
ADP) from injured tissue and activated platelets.
b. Nervous theory: pain from injury causes sympathetic stimulation.
c. Myogenic theory: smooth muscle of injured vessel responds by contraction
(inherited myogenic property).
Importance of local VC:
a. It decreases amount of blood loss from injured area.
b. It helps contact activation of platelets (plug formation) and clotting factors
(clot formation).
c. It helps healing of injured vessel (via approximation of injured ends).
3. Role of platelets (platelet function): See later.
4. Role of clotting factors (blood coagulation): See later.
5. Healing of vessel wall: helped by approximation of injured ends and released
growth factors e.g. platelet derived growth factor (PDGF) released from platelets. (See
later)
6. Role of fibrinolytic system (fibrinolysis, clot dissolution): See later.
Factors affecting They include:
hemostasis 1. Tissues surrounding injured vessel.
2. Injured vessel.
3. Platelets.
4. Clotting factors.

Figure-1: Factors affecting

hemostasis

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)

Figure-2: Mechanism of hemostasis.

Table-2: Hemostasis.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Platelets (Thrombocytes): (See Table-3 and Figures 3-7)

Definition They are small, membrane-bounded, anucleated cytoplasmic fragments derived from
megakaryocytes.
Normal platelet 150,000 - 400,000/mm3 (average 300,000/ml).
count
Normal life span 5–10 days (short life span). Why?
Formation of Site of platelet formation: in the bone marrow.
platelets Origin of platelets: megakaryocytes (giant cells in the bone marrow).
Mechanism of formation of platelets: pinching off bits of cytoplasm of
megakaryocytes and extruding them into the circulation.

Figure-3: Formation of platelets.

Regulation of platelet formation:

1. Colony-stimulating factors (CSFs): control the production of megakaryocytes.
2. Thrombopoietin:
Nature: it is a circulating protein factor.
Origin: liver and kidneys.
Functions:
a. It facilitates megakaryocyte maturation.
b. Platelets have thrombopoietin receptors on their surfaces.
Distribution of the formed platelets:
60 % - 75 %: are in the circulating blood.
The remaining 25% - 40 %: are mostly in the spleen. Thus, splenectomy (removal
of the spleen) increases platelet count i.e. thrombocytosis.
Platelet structure 1. It has a ring of microtubules around their periphery and an extensively invaginated
(contents) membrane with a canalicular system in contact with the extracellular fluid (ECF).
2. Its membrane contains receptors for:
a. Thrombopoietin.
b. Collagen.
c. Von Willebrand factor (VWF).
d. Adenosine diphosphate (ADP).
e. Fibrinogen.
3. Its cytoplasm contains:
a. Actin, myosin, glycogen and lysosomes.
[Link]:
1) Dense () granules:
They are smaller, denser and less numerous granules than the specific
granules.
They contain non-protein substances (serotonin, histamine, calcium, ADP and
ATP) secreted in response to platelet activation.
Function: these substances facilitate platelet adhesion and vasoconstriction
in the area of the injured vessel.

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SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
2) Specific granules (α-granules):
They are the largest and the most numerous granules in the platelets.
They contain proteins other than the hydrolases in lysosomes i.e.
a. Clotting factors: fibrinogen (I), V, VIII, Von Willebrand factor (VWF),
heparin antagonist (platelet factor 4 i.e. PF4) and XIII.
b. Plasminogen and plasminogen activator inhibitor.
c. Platelet activating factor (PAF).
d. Platelet-derived growth factor (PDGF):
Origin: it is produced by platelets, macrophages and endothelial cells.
Function:
1. It stimulates wound healing.
2. It is a potent mitogen for vascular smooth muscle.
3) -granules: they are similar to lysosomes found in other cells and contain several
hydrolytic enzymes.
4) -granules: function in clot resorption during the later stages of vessel repair.

(a)

(b)

Figure-4: Structure (contents) of platelets.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Platelet factors:
1. Platelet activating factor (PAF).
2. Platelet derived growth factor (PDGF).
3. Platelet factor 3 (PF3, platelet membrane phospholipid).
4. Platelet factor 4 (PF4, heparin antagonist).
Von Willebrand factor (VWF):
1. Increases platelet adherence by forming a bridge between platelet surface receptors
and collagen in the subendothelial matrix.
2. Regulates circulating levels of factor VIII.

Figure-5: Role of VWF in platelet adhesion.

Functions of Platelets share in all steps of hemostasis i.e.
platelets (Role of 1. They help initiating local vascular spasm.
platelets in 2. They form a platelet plug (see below) to stop bleeding from small damaged vessels.
hemostasis) 3. They help initiating the clotting process.
4. They release Ca2+, thrombasthenin and ADP causing clot retraction.
5. They release platelet derived growth factor (PDGF) which stimulates growth of
the vascular endothelial cells, smooth muscles and fibroblasts which help the
repair of the damaged vessels.
6. They help limiting clot formation (share in fibrinolytic system).
Formation of Aim: formation of a mechanical plug to close the minute vascular injury.
platelet plug Steps of formation of platelet plug:
1) Platelet adhesion:
Following blood vessel injury, platelets adhere to the exposed subendothelial
collagen and myofibrils.
It depends on:
a. Surface membrane glycoporteins (platelet receptors for collagen and VWF).
b. Von-Willebrand factor (See before).
2) Platelet activation: adhered platelets become activated i.e. become swollen,
more sticky, and irregular with numerous processes which facilitate the
interaction (aggregation) between adjacent platelets.

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SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
3) Platelet release reaction:
Platelets enzymes form thromboxane A2 which is released in the blood.
Thromboxane A2 decreases platelet cAMP which causes contraction of the
contractile proteins of platelets resulting in release of the contents of platelets
such as ADP, serotonin, VWF, fibrinogen and platelet factors.
4) Platelet aggregation:
Released ADP and thromboxane A2 cause more activation of platelets and make
them adhere to each other i.e. aggregation leading to further release and more
aggregation and so on (a positive feedback mechanism).
The result is the formation of platelet plug which closes the injured area.
5) Platelet plug: at first, the plug is loose then, becomes firm and tight by
contraction of platelets contractile proteins and by fibrin threads (after their
formation) which attached to the injured vessel wall forming a tight plug.

Figure-6: Platelet plug formation.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Control of platelet plug formation:
The normal endothelial cells around the injury, release prostacyclin (PGI2) which
causes limitation of the plug to the site of injury by antagonizing thromboxane A2
actions i.e. PGI2 causes:
a. Inhibition of platelet aggregation.
b. Vasodilatation.
Importance of the platelet plug:
1. It stops blood loss from small vessels.
2. It closes the minute ruptures of very small vessels, which occur hundreds of times
daily.
3. The chemicals released from the plug help other mechanisms of hemostasis as
following:
a. Serotonin and thromboxane A2 cause local vascular spasm.
b. After platelet aggregation, the membrane phospholipid (platelet factor 3),
factor V, and fibrinogen are exposed and initiate intrinsic clotting.
c. Factor XIII helps in stabilization of the blood clot.
d. Platelet factor 4 (heparin antagonist) neutralizes heparin and prevents its
inhibitory effect on blood clot.
e. PDGF helps healing of injured vessel wall.
f. Plasminogen helps resorption of the clot (fibrinolysis).
Steps of hemostasis may be divided into:
1. Primary hemostasis:
a. Local vascular spasm.
b. Platelets plug formation.
2. Secondary hemostasis:
a. Activation of clotting cascade.
b. Stabilization of fibrin.
3. Tertiary hemostasis: dissolution of fibrin clot (fibrinolysis)
Variations in 1. Purpura:
platelet count a. Thrombocytopenic purpura: is
characterized by easy bruisability and
multiple subcutaneous hemorrhages
secondary to decrease platelet count.
b. Thrombasthenic purpura: it occurs
when the platelet count is normal or
even increased, but platelets are of
abnormal function.
2. Thrombocytosis: increased platelet count Figure-7: Purpura.
which predisposes to thrombotic events.
Table-3: Platelets.

Blood Coagulation (Blood Clotting): (See Tables 4 & 4a and Figures 8-13)

Definitions Blood clot: is a network of insoluble fibrin entangling blood cells.

Blood clotting: is the formation of a blood clot.
Clotting factors Definition: factors that share in the clot formation.
Sites of synthesis:
1. Liver.
2. Megakaryocytes.
3. Macrophages.
4. Endothelial cells.
Types (classification) of clotting factors:
1. Fibrinogen group (I, V, VIII and XIII):
Formed in liver and megakaryocytes.

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SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Thrombin reacts with them.
Utilized during coagulation, so they are absent in the remaining serum.
V and VIII lose their activity in the stored cold blood (restored on blood
warming).
2. Prothrombin group (II, VII, IX and X):
Formed in liver and needs vitamin K (vitamin K dependent group).
Not utilized during coagulation (except II).
Stable and preserved in the stored blood.
3. Contact group (XI and XII):
XI needs vitamin K to be used by liver.
Stable and preserved in stored blood.
HMWK and prekallikerin are also
contact factors.
4. Factor IV (calcium): Figure-8: Clotting factors classification.
9-11 mg/100 ml plasma (50% ionized).
It is required for conversion of prothrombin to thrombin
Its removal by citrate or oxalate or absorption by EDTA will prevent clotting.
5. Factor III (thromboplastin):
a. Tissue factor: released from tissue damage (the brain and lung are rich in this
factor) to trigger the extrinsic clotting system.
b. Platelet factor: released from platelet as phospholipids (platelet factor 3) to
trigger the intrinsic clotting system.
Protein C and protein S are natural anticoagulants that are vitamin K related.

Figure-9: Clotting factors.

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SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Steps of blood [1] Formation of prothrombin activator (Xa, PF3, IV and Va):
clotting A-Extrinsic pathway (cascade, chain): (it starts by a tissue factor from outside
the blood)
Duration: it takes few seconds (short duration).
Mechanism:
1. Injury of the blood vessels and surrounding tissue causes release of tissue
thromboplastin (lipoprotein mixture) which activates factor VII which
stimulates factor X in the presence of Ca++ (factor IV).
2. Activated factor X with factor Va and tissue phospholipids (PF3) and
calcium (IV) form enzyme complex called prothrombin activators.
Factors affecting the extrinsic pathway:
1. Degree of tissue injury.
2. Quantities of factors VII, V and X.

B-Intrinsic pathway (cascade) of blood clotting: (it starts by contact activation of

both contact factors and platelets inside the blood)
Duration: it takes 2-10 minutes (longer duration than extrinsic mechanism).
Mechanism:
Stimulus: contact of the blood with;
1. Subendothelial collagen in injured blood vessel.
2. A wettable surface as test tube.
Effect:
1. Contact activation of:
a. Factor XII to active XII (XIIa), helped by kallikrein.
b. Platelets to release platelets phospholipids (PF3).
2. Factor XIIa activates factor XI to active XI (XIa), in presence of high
molecular weight kininogen (HMWK).
3. Then, factor XIa activates factor IX to active IX (IXa).
4. Factors IXa, VIIIa and PF3 (platelet phospholipids), in presence of calcium
ions (factor IV), activate factor X to active factor X (Xa).
5. Activated factor X (Xa) with factor Va, platelet phospholipids and calcium,
form an enzyme complex called prothrombin activator.
[2] Conversion of prothrombin to thrombin:
Mechanism: by the prothrombin activator (Xa, PF3, IV and Va), the prothrombin
(II) is changed into thrombin (IIa).
Actions (functions) of thrombin (IIa):
1. It increases platelet adhesion and aggregation.
2. It activates some of the clotting factors (V, VII and VIII) which are required
for its formation.
3. It acts on prothrombin itself producing more thrombin (positive feedback
effect)
4. It increases conversion of fibrinogen to fibrin threads (acts as a proteolytic
enzyme).
5. It activates factor XIII, thus helps in stabilization of the clot.

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SOK Blood Physiology Hemostasis & Platelet Function (1-2020)

Figure-10: Thrombin functions.

[3] Conversion of fibrinogen to fibrin:

Thrombin splits small negatively charged peptide fragments from the
fibrinogen molecules.
This results in:
1. Removal of the repulsive forces from the fibrinogen molecules.
2. Polymerization of the remainder of the splitted fibrinogen molecules to form
fibrin polymers (threads).

Figure-11: Clotting cascades

(pathways).

[4] Clot formation:

Fibrin threads adhere to the injured blood vessel wall forming loose net like
meshwork that traps the blood cells forming red soft blood clot.
Stabilization of the blood clot by the activated factor XIII (fibrin stabilizing
factor, XIIIa) which is activated by thrombin (IIa).
Mechanism: factor XIIIa strengthens (stabilizes) the fibrin clot by forming
strong bonds between fibrin polymers.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)

Figure-12: Clot formation.

[5] Clot retraction:
Definition: the fibrin clot contains large number of platelets which are attached to
both fibrin threads and subendothelial collagen, and contract by their contractile
proteins (actin, myosin and thrombasthenin).
Control of clot retraction: it is stimulated by thrombin (IIa) and calcium ions
(IV) released from the platelets.
Importance of clot retraction:
1. It causes the fibrin meshwork to shrink and to become stronger.
2. It makes the clot denser and stronger.
3. It pulls the edges of the wound together facilitating the repair (healing) of the
injury.
4. It squeezes a clear yellowish serum from the clot.
Clot dissolution Definition: it is the system by means of
(fibrinolysis, which the temporary fibrin clot is
fibrinolytic systematically and gradually dissolved as
system) the vessel heals.
Mechanism: the clot is slowly dissolved
by the fibrin splitting enzyme called
plasmin.
Steps:
1. Plasminogen is the inactive precursor
that is activated by factor XII
(Hageman factor).
2. Plasmin gets trapped in clot and
slowly dissolves it by breaking down
the fibrin meshwork.
Importance of fibrinolytic system:
a. It restores normal blood flow.
b. It localizes clot formation. Figure-13: Fibrinolytic system.
c. It prevents the intravascular thrombosis.
Role of calcium in hemostasis: calcium ions (clotting factor IV) are required for each step in
the clotting process except for the first two reactions of the intrinsic pathway. Therefore,
adequate levels of calcium ions (9-11 mg/dl) are necessary for normal clotting. In reality,
plasma calcium levels never fall low enough (below 4 mg/dl) to impair the clotting processes
since death would have resulted from other causes (most notably tetany of the respiratory
muscles) long before. However, it is possible to prevent the coagulation of blood removed
from the body and stored in vitro by reducing the calcium ion concentration of the plasma.
This can be achieved by the addition of substances such as EDTA (chelation of calcium) or
citrate (deionization of calcium).
Table-4: Blood coagulation.

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Factors Normally Prevent Intravascular Clotting: (Factors that keep blood in a fluid form in the cardiovascular system
i.e. Factors that prevent thrombosis i.e. Natural anticoagulant mechanisms) (See Table-5 and Figure-14)

Types of natural I-Vascular factors normally prevent intravascular clotting i.e. Role of smoothness of
anticoagulant endothelium in prevention of thrombosis:
mechanisms 1. It prevents contact activation of factor XII.
2. The protein that covers the endothelium has negative charges which repel
negative charged platelets and clotting factors.
3. Thrombomodulin (protein) which covers endothelium binds with thrombin
preventing its action and this complex activates protein-C that acts as an
anticoagulant.
4. Release of prostacyclin i.e. PGI2 (major inhibitor of platelets aggregation) from
the healthy endothelium.

Figure-14: Role of smoothness of endothelium in prevention of thrombosis.

II-Intravascular factors normally prevent intravascular clotting i.e. Role of the blood
itself in prevention of thrombosis:
1. Effect of normal blood flow:
It removes activated clotting factors by the circulating blood into the liver,
spleen and the bone marrow to be inactivated.
2. Anti-thrombin action of fibrin and anti-thrombin III:
a. Fibrin: adsorbs about 90% of thrombin formed during blood clotting
(preventing its spread into the blood causing more coagulation).
b. Anti-thrombin III: combines with the remaining 10% of formed thrombin (and
factor Xa) inhibiting them.
3. Protein C and protein S (natural anticoagulants formed in the liver in
presence of vitamin K):
a. Protein C:
It is activated by thrombin.
It inhibits the clotting factors V and VIII.
It stimulates fibrinolysis.
b. Protein S: potentiates the effect of protein C.
4. Heparin:
Nature: it is a negatively charged mucopolysaccharide.
Origin: it is secreted by mast cells and basophil cells (in minute amounts).
Site of action: in vivo and in vitro.
Actions of heparin:
a. It inhibits platelet aggregation.
b. It combines with anti-thrombin III helping in inhibition of thrombin.
c. It inhibits factors IXa, Xa and XIa.
d. It stimulates fibrinolysis.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
e. It stimulates (activates) lipase enzyme to hydrolyze lipids and prevent its
deposition in blood vessels. So, it prevents development of atherosclerosis
(lipemia clearing effect).
5. Plasmin (fibrinolysin): causes breakdown of fibrin, fibrinogen (I), prothrombin
(II), V, VIII and XII.
6. Alpha2-macroglobulin: binds to and inhibits coagulation factors.
7. Alpha1-antitrypsin: inactivates factor XIa and thrombin.
Importance of 1. In normal state: they prevent blood clotting.
natural 2. In cases of injury:
anticoagulant a. They limit the process of blood coagulation to the site of injury.
mechanisms b. They help recanalization of thrombosed blood vessels.
Hematoma:
Definition: it is an accumulation of blood within soft tissues.
Causes:
1. Traumatic damage to vessels (common).
2. Follows spontaneous rupture following disease (occasionally).
Thrombosis:
Definition: it is the formation of a solid tissue mass of blood within the circulatory
system.
Pathophysiology: there are three ways in which a thrombosis can occur (Virchow's
triad):
1. Abnormalities of the vessel wall e.g. atheroma, direct injury or inflammation.
2. Abnormalities of blood flow e.g. stagnation (in veins) or turbulence (in arteries).
3. Abnormalities of blood components e.g. smokers (the clotting factors more readily
bind to the endothelial lining) or post-partum (newly synthesized cofactors are in
varying concentrations).
Disseminated intravascular coagulation:
Definition: it is a serious complication of septicemia, extensive tissue injury, and other
diseases in which fibrin is deposited in the vascular system and many small- and
medium-sized vessels are thrombosed.
Pathophysiology: the increased consumption of platelets and coagulation factors
causes bleeding to occur at the same time. The cause of the condition appears to be
increased generation of thrombin due to increased tissue factor activity without
adequate tissue factor inhibitory pathway activity.
Table-5: Factors that normally prevent intravascular clotting.

Case Discussion:
Case Presentation: necessary for normal clotting. In reality, plasma
A 42-year-old patient is scheduled for surgery that calcium levels never fall low enough (below 4 mg/dl)
will likely require a transfusion. Because the patient to impair the clotting processes since death would
has a rare blood type, an autologous blood have resulted from other causes (most notably tetany
transfusion is planned. Prior to surgery, 1500 mL of of the respiratory muscles) long before. However, it
blood is collected. The collection tubes contain is possible to prevent the coagulation of blood
calcium citrate to prevent coagulation. removed from the body and stored in vitro by
Case Discussion: reducing the calcium ion concentration of the plasma.
Calcium ions (clotting factor IV) are required for This can be achieved by the addition of substances
each step in the clotting process except for the first such as EDTA (chelation of calcium) or citrate
two reactions of the intrinsic pathway. Therefore, (deionization of calcium).
adequate levels of calcium ions (9-11 mg/dl) are
Summary:
Hemostasis is the physiologic protective process blood clots inside blood vessels.
by means of which blood loss is limited Platelets are small, membrane-bounded,
following minor vascular injury. anucleated cytoplasmic fragments derived from
Thrombosis is a pathologic process in which megakaryocytes.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
Dense granules in the platelet contain non-protein muscles and fibroblasts which help the repair of
substances (serotonin, histamine, calcium, ADP the damaged vessels.
and ATP) which are secreted in response to Calcium ions (clotting factor IV) are required for
platelet activation. each step in the clotting process except for the
Platelet derived growth factor (PDGF) stimulates first two reactions of the intrinsic pathway.
growth of the vascular endothelial cells, smooth Hematoma is an accumulation of blood within
soft tissues.
Examples of Self-Assessment Questions:
SEQs: C. 20 mg/dl.
1-Define: plasma, serum, homeostasis, hemostasis D. 4 mg/dl.
and thrombosis. E. 15 mg/dl.
2-Outline mechanism of hemostasis. 16-Which one of the following is the normal
3-Discuss platelet contents and functions. thrombocytic count?
4-Discuss role of platelets in hemostasis. A. 3000 /mm3.
5-Describe the extrinsic cascade of blood clotting. B. 30000 /mm3.
6-Discuss the intrinsic pathway of blood clotting. C. 300000 /mm3.
7-Outline fibrinolytic system. D. 3000000 /mm3.
8-Mention role of calcium in hemostasis. E. 30000000 /mm3.
9-Discuss factors normally prevent intravascular 17-Which one of the following is the site of
clotting. synthesis of thrombopoietin?
10-Mention pathophysiology of thrombosis. A. Spleen.
B. Placenta.
MCQs: C. Stomach.
11-Which of the following initiates the D. Liver.
coagulation cascade in vivo? E. Pancreas.
A. Factor XII. 18-Which one of the following is present in
B. Thrombin. specific granules of platelets?
C. Tissue factor. A. Serotonin.
D. Factor X. B. Fibrinogen.
E. Prekallikerin. C. Calcium.
12-What does von Willebrand factor do? D. ADP.
A. Binds platelets to each other. E. ATP.
B. Binds platelets to the subendothelial collagen. 19-Thrombocytopenic purpura occurs due to:
C. Binds platelets to the phospholipid surface. A. Increase in RBCs count.
D. Carries factor VII. B. Decrease in RBCs count.
E. Cleaves factor V. C. Increase in platelet count.
13-Which one of the following anti-clotting D. Decrease in platelet count.
substances acts on factors V and VIII? E. Increase in WBCs count.
A. Anti-thrombin III. 20-Which one of the following clotting factors
B. Protein C. blood is normally devoid of it?
C. Anti-heparin. A. II.
D. Plasmin. B. III.
E. t-PA. C. IV.
14-Which of the following is a cofactor? D. V.
A. XII. E. XIII.
B. X. 21-Which one of the following clotting factors is
C. VIII. the fibrin stabilizing factor?
D. VII. A. II.
E. II. B. III.
15-Which of the following is the normal level of C. IV.
blood calcium? D. V.
A. 10 mg/dl. E. XIII.
B. 6 mg/dl.

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 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
22-Which one of the following clotting factors 30-Hageman factor is a synonym for which
represents calcium ions? clotting factor?
A. II. A. XII
B. III. B. X
C. IV. C. VII
D. V. D. V
E. XIII. 31-The contact group of clotting factors include:
23-Which one of the following clotting factors is a A. II
member of prothrombin group of blood B. IV
clotting factors? C. XI
A. VII. D. XIII
B. III. 32-The fibrinogen group of clotting factors
C. IV. include:
D. V. A. II
E. XIII. B. VII
24-Hemophilia A occurs secondary to deficiency C. IX
of which one of the following clotting factors? D. XIII
A. VII. 33-Which one of the following factors prevents
B. VIII. blood clotting?
C. IV. A. Thromboplastin
D. V. B. Thrombomodulin
E. XII. C. Thrombasthenin
25-Which of the following is a character of D. Thrombopoietin
heparin? 34-Which one of the following clotting factors is
A. It stimulates platelet aggregation. vitamin K independent?
B. It has in-vivo and in-vitro actions. A. II
C. It is secreted by neutrophil cells. B. IV
D. It is a positively charged mucopolysaccharide. C. VII
E. It inhibits lipase enzyme.
D. IX
26-Tissue plasmin activator is essential for:
35-The activity of which clotting factor is lost in
A. wound healing.
stored cold blood and restored by blood
B. allergy response.
warming?
C. immunity.
A. II
D. dissolving blood clot.
B. IV
27-Which of the following will not coagulate when
C. VIII
placed separately on four slides?
D. IX
A. Blood serum
36-Which of the following is a part of primary
B. Blood plasma
hemostasis?
C. Blood from pulmonary vein
A. Local vascular spasm
D. Blood from lymphatic tissue
B. Activation of clotting cascade
28-Heparin antagonist is a synonym for:
C. Stabilization of fibrin
A. Platelet activating factor
B. Platelet derived growth factor D. Fibrinolysis
C. Platelet factor 3 MEQs:
D. Platelet factor 4 37-A 42-year-old patient is scheduled for surgery
29-Which one of the following increases platelet that will likely require a transfusion. Because
count? the patient has a rare blood type, an autologous
A. Storage of blood in blood bank blood transfusion is planned. Prior to surgery,
B. Splenectomy 1500 mL of blood is collected. The collection
C. Exposure to viral infection tubes contain calcium citrate to prevent
D. Appendicectomy coagulation.
a. How citrate prevents coagulation?
b. Mention role of calcium in hemostasis.

Dr Khaled A Abulfadle [Link] 16

 SOK Blood Physiology Hemostasis & Platelet Function (1-2020)
References: Human Physiology, Integrated approach, by Dee
Dr Khaled Abulfadle Physiology Site, Unglaub Silverthorn, 7th edition, 2016.
Link: [Link] Insights in Physiology, by Sudha Vinayak
Dr Khaled A Abulfadle YouTube Channel, Khanorkar, 1st edition, 2012.
[Link] Medical physiology, A systems approach, by
1FtBROicx4gkDDA Hershel Raff, 2011.
SOK Physiology Group on Facebook: Oxford handbook of medical sciences, Second
[Link] edition, 2011.
475141/ Physiology by Linda S Costanzo, 7th edition,
SOK Physiology Group on Telegram: 2019.
[Link] Principles of anatomy and physiology, by
Berne & Levy Physiology, 7th edition, 2018. Tortora, 14th edition, 2014.
Case files Physiology, Lange series, 2nd edition, Vander’s Human Physiology: The Mechanisms of
2009. Body Function, 15th edition, 2019.
Color atlas of Physiology, 7th edition, 2015.
Essentials of Medical Physiology by K MCQs Answer Key
Sembulingam, 6th edition, 2012. 11-C. 12-B. 13-B. 14-C. 15-A. 16-C.
17-D. 18-B. 19-D. 20-B. 21-E. 22-C.
First aid for the USMLE step 1, 2019.
23-A. 24-B. 25-B. 26-D. 27-A. 28-D.
Ganong's Review of Medical Physiology, 26th 29-B. 30-A. 31-C. 32-D. 33-B. 34-B.
Edition, 2019. 35-C. 36-A.
Guyton & Hall Textbook of Medical Physiology
13th edition, 2016.
Human Physiology, by Stuart Ira Fox, 14th edition,
2016.

Dr Khaled A Abulfadle [Link] 17