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Components of blood and blood clotting mechanism
1.
2.
3. COMPONENTS OF BLOOD AND
BLOOD CLOTTING MECHANISM
BY DR.PRITAM CHATTERJEE
1ST YEAR MDS
DEPARTMENT OF PUBLIC HEALTH DENTISTRY
NAVODAYA DENTAL COLLEGE HOSPITAL RAICHUR
4. CONTENTS
• INTRODUCTION
• PROPERTIES OF BLOOD
• COMPOSITION OF BLOOD
• FUNCTION OF BLOOD
• CONSTITUENTS OF PLASMA
• PLASMA PROTEINS
• RED BLOOD CELLS
• WHITE BLOOD CELLS
• PLATELETS
• HEMOSTASIS
• BLOOD COAGULATION
• BLOOD CLOT
• TESTS FOR BLOOD CLOTTING
• ANTICOAGULANT DRUGS
• MANAGEMENT OF PATIENTS ON ANTICOAGULANT THERAPY
• CONCLUSION
• REFERENCE
5. INTRODUCTION
Blood is a connective tissue in fluid form. It is considered
as the ‘fluid of life’ because it carries oxygen from lungs
to all parts of the body and carbon dioxide from all parts
of the body to the lungs. It is known as ‘fluid of growth’
because it carries nutritive substances from the digestive
system and hormones from endocrine gland to all the
tissues. The blood is also called the ‘fluid of health’
because it protects the body against the diseases and
gets rid of the waste products and unwanted substances
by transporting them to the excretory organs
6. PROPERTIES OF BLOOD
1. Color: Blood is red in color. Arterial blood is scarlet
red because it contains more oxygen and venous
blood is purple red because of more carbon
dioxide.
2. Volume: Average volume of blood in a normal adult
is 5 L. In a newborn baby, the volume is 450 ml.
In females, is about 4.5 L.
It is about 8% of the body weight in a normal
young healthy adult.
7. PROPERTIES OF BLOOD
Reaction and pH: Blood is slightly alkaline and its
pH in normal conditions is 7.4.
Specific gravity:
Specific gravity of total blood : 1.052 to 1.061
Specific gravity blood cells : 1.092 to 1.101
Specific gravity of plasma : 1.022 to 1.026
Viscosity:
Blood is five times more viscous than
water.
8. COMPOSITION OF BLOOD
Blood contains both extracellular fluid (the fluid in plasma)
and intracellular fluid (the fluid in the red blood cells)
The most important difference between these two
compartments is the higher concentration of protein in
the plasma
Donnan effect, the concentration of
positively charged ions (cations) is slightly
greater (≈2 percent) in the plasma than in the
interstitial fluid.
9.
10.
11. FUNCTIONS OF BLOOD
1. NUTRITIVE FUNCTION
2. RESPIRATORY FUNCTION
3. EXCRETORY FUNCTION
4. TRANSPORT OF HORMONES AND ENZYMES
5. REGULATION OF WATER BALANCE
6. REGULATION OF ACID-BASE BALANCE
7. REGULATION OF BODY TEMPERATURE
8. STORAGE FUNCTION
9. DEFENSIVE FUNCTION
12. Plasma is a straw-colored clear liquid
part of blood
SERUM=PLASMA-FIBRINOGEN.
Substance Normal value
Glucose 100 to 120 mg/dL
Creatinine 0.5 to 1.5 mg/dL
Cholesterol Up to 200 mg/dL
Plasma proteins 6.4 to 8.3 g/dL
Bilirubin 0.5 to 1.5 mg/dL
Iron 50 to 150 µg/dL
Copper 100 to 200 mg/dL
Calcium 9 to 11 mg/dL
4.5 to 5.5 mEq/L
Sodium 135 to 145 mEq/L
Potassium 3.5 to 5.0 mEq/L
Magnesium 1.5 to 2.0 mEq/L
Chloride 100 to 110 mEq/
Bicarbonate 22 to 26 mEq/L
14. „MOLECULAR WEIGHT
Albumin : 69,000
Globulin : 1,56,000
Fibrinogen : 4,00,000
. Osmotic pressure / colloidal osmotic/ oncotic pressure.
25 mm Hg.
Albumin plays a major role in exerting oncotic pressure.
„SPECIFIC GRAVITY
Specific gravity of the plasma proteins is 1.026.
„BUFFER ACTION
Acceptance of hydrogen ions is called buffer action. The
plasma proteins have 1/6 of total buffering action of the
blood.
15. „ORIGIN OF PLASMA PROTEINS
„IN EMBRYO
Synthesized by the mesenchyme cells.
The albumin is synthesized first
„IN ADULTS
synthesized mainly from reticuloendothelial cells of liver.
also from spleen
bone marrow,
disintegrating blood cells
general tissue cells.
Gamma globulin is synthesized from B lymphocytes.
16.
17. CLINICAL SIGNIFICANCE OF PLASMA PROTEINS
PROTEINS INCREASE DECREASE
Total proteins
Hyperproteinemia:
1. Dehydration
2. Hemolysis
3. Acute infections
4. Respiratory distress
syndrome
5. Excess of glucocorticoids
6. Leukemia
7. Rheumatoid arthritis
8. Alcoholism
Hypoproteinemia:
1. Diarrhea
2. Hemorrhage
3. Burns
4. Pregnancy
5. Malnutrition
6. Prolonged starvation
7. Cirrhosis of liver
8. Chronic infections like
chronic hepatitis or
chronic nephritis
Albumin 1. Dehydration
2. Excess of glucocorticoids
3. Congestive cardiac failure
1. Malnutrition
2. Cirrhosis of liver
3. Burns
4. Hypothyroidism
5. Nephrosis
6. Excessive intake of water
18. CLINICAL SIGNIFICANCE OF PLASMA PROTEINS
PROTEINS INCREASES DECREASES
Globulin 1. Cirrhosis of liver
2. Chronic infections
3. Nephrosis
4. Rheumatoid arthritis
1. Emphysema
2. Acute hemolytic anemia
3. Glomerulonephritis
4. Hypogammaglobulinemia
Fibrinogen 1. Acute infections
2. Rheumatoid arthritis
3. Glomerulonephritis
4. Myocardial infarction
5. Stroke
6. Trauma
1. Liver dysfunction
2. Use of anabolic steroids
3. Use of phenobarbital
A/G ratio 1. Hypothyroidism
2. Excess of glucocorticoids
3. Hypogammaglobulinemia
4. Intake of high carbohydrate
or protein diet
1. Liver dysfunction
2. Nephrosis
23. Surface area : 120 sq µ
Volume : 85 to 90 cu µ
Organells absent: DNA
Mitochondria
Golgi apparatus
Cytoskeleton:
actin-=======ankyrin =====spectrin.
Absence of spectrin results in
hereditary spherocytosis.
41. PLATELETS/THROMBOCYTES
.„NORMAL COUNT
Normal platelet count is 2,50,000/cu mm of blood.
„PHYSIOLOGICAL VARIATIONS
1. infants -1,50,000 to 2,00,000/cu mm) and reaches normal level at 3rd
month after birth.
2. Sex: There is no difference in the platelet count
between males and females. In females, it is reduced
during menstruation.
3. High altitude: Platelet count increases.
4. After meals: After taking food, the platelet count
increases.
42. PLATELETS/THROMBOCYTES
CELLULAR MORPHOLOGY
Diameter : 2.5 µ (2 to 4 µ)
Volume : 7.5 cu µ (7 to 8 cu µ).
CELL MEMBRANE
Glycoproteins
Phospholipids
MICROTUBULES
CYTOPLASM
Proteins
Enzymes
Hormonal Substances
Platelet Granules
Alpha granules
Dense granules.
63. i. Thrombin converts inactive fibrinogen into
activated fibrinogen due to loss of 2 pairs of
polypeptides from each fibrinogen molecule.
The
activated fibrinogen is called fibrin monomer.
ii. Fibrin monomer polymerizes with other
monomer
molecules and form loosely arranged strands
of
fibrin.
iii. Later these loose strands are modified
into dense
and tight fibrin threads by fibrin-stabilizing
factor
(factor XIII) in the presence of calcium ions
64. Blood clot is defined as the mass of coagulated blood
which contains RBCs, WBCs and platelets entrapped in
fibrin meshwork
65. After the formation, the blood clot starts contracting. And
after about 30 to 45 minutes, the straw-colored serum
oozes out of the clot. The process involving the contraction
of blood clot and oozing of serum is called clot retraction.
Contractile proteins, namely actin, myosin and
thrombosthenin in the cytoplasm of platelets are
responsible for clot retraction.
66.
67.
68.
69.
70.
71. {modified Ivy’s method} {Lee & White method}
N = 1-6 mts N = 6-10 mts in glass
• platelet plug N = 20-60 mts in siliconized tubes
Prolonged in:
Thrombocytopenia Measures intrinsic &
Thrombasthenia common pathway
Von-Willebrand’s disease
72. calcium
• oxalated blood from patient clot
tissue thromboplastin
. N = 12 secs
• measures extrinsic & common pathway
1. Oral anticoagulant drugs
2. Liver disease, obstructive jaundice
3. Vit K deficiency
4. Deficiency of factor VII , X, V, II
SPECIFIC FOR FACTOR VII
[ With X & V APTT is also prolonged]
74. •PLASMA + THROMBIN CLOT
•Assesses fibrinogen
• Normal duration of thrombin time is 12 to 20 seconds.
•Prolonged in :
Hypofibrinogenemia
Dysfibrinogenaemia
75.
76. • This is an inhibitor of thrombin, its action being potentiated by
heparin.
• Congenital antithrombin III deficiency is inherited as an autosomal
dominant.
• Heterozygotes may suffer from recurrent DVT, pulmonary embolism,
and mesenteric thrombosis.
• Homozygotes present in childhood with severe arterial and venous
thrombosis.
77. NATURAL ANTICOAGULANTS
• Protein C and protein S
• These are synthesised in the liver and are dependant on vitamin K.
• Protein C degrades factors Va and VIIIa and promotes fibrinolysis by
inactivating plasminogen-activator inhibitor I.
• Protein S is a cofactor for protein C and enhances its activity.
• Hereditary protein C defciency may occur, patients being more
susceptible to DVT, PE, superficial thrombophlebitis, and cerebral
venous thrombosis
79. ANTICOAGULANT DRUGS
Warfarin is a coumarin derivative which is administered orally.
• It is a vitamin K antagonist and in effect induces a state analogous
to vitamin K deficiency.
• It interferes with the activity of factors II, VII, IX and X. It delays
thrombin generation, thus preventing the formation of thrombi.
• Warfarin is usually administered for 3–6 months following DVT or
PE
• Lifelong warfarin is required for recurrent venous thromboembolic
disease,some prosthetic heart valves, congenital deficiency of
antithrombin III, deficiency of protein C or protein S,
80. ANTICOAGULANT DRUGS
„EDTA
Ethylenediaminetetraacetic acid (EDTA) is a strong
anticoagulant. It is available in two forms:
i. Disodium salt (Na2
EDTA).
ii. Tripotassium salt (K3
EDTA).
„OXALATE COMPOUNDS
„CITRATES
Sodium, ammonium and potassium citrates are used as
anticoagulants.
81. MANAGEMENT OF PATIENTS ON
ANTICOAGULANT THERAPY IN DENTAL
PRACTICE
DRUG BLEEDING ELECTIVE EMERGENCY
RISK SURGERY SURGERY
1 .HEPARIN Low / Moderate Discontinue high dose Same as elective
Give low dose heparin
High risK Discontinue 6 – 12 hrs Discontinue
2. L M W H -- Discontinue 12 – 24 hrs before surgery especially in high risk
82. MANAGEMENT OF PATIENTS ON
ANTICOAGULANT THERAPY
DRUG BLEEDING ELECTIVE EMERGENCY
RISK SURGERY SURGERY
3. Warfarin LOW Adjust dose to I N R < 2.5 Discontinue warfarin
MODERATE ADJUST DOSE TO INR < 2.5. Discontinue warfarin
HIGH Discontinue & allow P T to Discontinue warfarin
normalize. Substitute with heparin .
83. MANAGEMENT OF PATIENTS ON
ANTICOAGULANT THERAPY
Aspirin:
•Discontinue 1 week before surgery.
•Platelet transfusion
•DDAVP In emergency surgery
Fibrinolytics:
• Wait for half life
6 min for TPA
23 min for Streptokinase
16 min for Urokinase
84. CONCLUSION
The more exotic these approaches become, the more one is compelled
to emphasize that gentle handling, precise dissection and accurately
applied haemostasis constitute much the art of surgery.
Injecting, burning, stuffing, and scorching wounds is not likely to lead
to a higher plateau of accomplishment.
John A Collins , M.D
85. REFERENCE
*GANONGS REVIEW OF MEDICAL PHYSIOLOGY 23RD EDITION
*GUYTAN AND HALL BOOK ON MEDICAL PHYSIOLOGY
*ESSENTIALS OF MEDICAL PHYSIOLOGY BY DR SEMBULINGAM
*HEMATOLOGY IN NUTSHELL
*JOURNAL OF HEMATOLOGY 2019
*JOURNAL OF HEMATOLOGY AIIMS 2017
*GENERAL PHARMACHOLOGY BY KD TRIPATHI
*JOURNAL OF IAMB FOR MANAGEMENT OF PATIENTS ON
ANTICOAGULANT THERAPY