Hemostasis occurs in three stages: vasoconstriction, platelet plug formation, and coagulation. During vasoconstriction, blood vessels constrict to decrease blood loss. Platelets then adhere to collagen at the injury site and form a temporary platelet plug. Finally, fibrin threads form and attach to the platelet plug, blocking blood loss completely. Coagulation disorders like hemophilia can result from deficiencies in specific clotting factors and cause prolonged bleeding.
Hemostasis and coagulation of blood For M.Sc & Basic Medical Students by Pand...Pandian M
Blood coagulation
Mechanism of coagulation
STAGES OF HEMOSTASIS
Coagulation of blood
Factors involved in blood clotting
Enzyme cascade theory
Mechanisms for formation of prothrombin activator
Fibrinolysis
Anticlotting mechanism in the body
Applied physiology
the objectives from this ppt :-
1.Define haemostasis.
2.Describe the main mechanisms that prevent blood loss after an injury.
3.Describe role of platelets in haemostasis.
4.Outline the mechanism of platelet plug formation.
5.Describe the mechanisms of blood coagulation.
Hemostasis and coagulation of blood For M.Sc & Basic Medical Students by Pand...Pandian M
Blood coagulation
Mechanism of coagulation
STAGES OF HEMOSTASIS
Coagulation of blood
Factors involved in blood clotting
Enzyme cascade theory
Mechanisms for formation of prothrombin activator
Fibrinolysis
Anticlotting mechanism in the body
Applied physiology
the objectives from this ppt :-
1.Define haemostasis.
2.Describe the main mechanisms that prevent blood loss after an injury.
3.Describe role of platelets in haemostasis.
4.Outline the mechanism of platelet plug formation.
5.Describe the mechanisms of blood coagulation.
Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Phys...Physiology Dept
Definition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation
White blood cells & Immunity (The Guyton and Hall Physiology)Maryam Fida
Leukocytes or WBCs are the mobile units of the body’s immune defense system.
Immunity is the body’s ability to resist or eliminate potentially harmful foreign materials or abnormal cells.
WBC count: 5000 to 11000/ul of blood
GRANULOCYTES
Polymorphonuclear neutrophils 60-70%
Polymorphonuclear eosinophils 2-3%
Polymorphonuclear basophils 0.4%
NON-GRANULOCYTES
Monocytes 5.3%
Lymphocytes 30%
Granulocytes and monocytes are formed and stored only in bone marrow
Lymphocytes and plasma cells are formed and stored mainly in various lymphoid tissue such as lymph node, spleen, thymus and tonsils as well as in bone marrow.
GRANULOCYTES
4 to 8 hours in blood and 4 to 5 days in tissues
MONOCYTES
Monocytes also have a short transit time:
10 to 20 hours in blood and In tissue they swell to much larger size to become tissue macrophages.
LYMPHOCYTES
weeks to months
neutrophil
. 60-70% of leukocytes
nucleus: 2-5 lobes
Counting the number of lobes and grouping them is called Arneth count.
Shift to left means (increase no of young and predominant WBCs) e.g During acute infection.
Shift to right means, old cells are predominant. e.g During recovery phase
NEUTROPENIA
Decrease in neutrophils count
Typhoid
AIDS and viral hepatitis
Kalazar fever
Bone marrow depression by drugs and radiations
NEUTROPHILIA
Increase in neutrophils count
Appendicitis , Tonsillitis, Pneumonia
Burns, Hemorrhage, MI, Pain
Hypoxia, Pregnancy
BASOPHIL
Their cytoplasmic granules take up basic dyes and appear deep blue
MAST CELLS are derived from basophils under the influence of interleukins 3 and 4
Under many allergic conditions basophils and mast cells bursts and releases
Histamine
Bradykinin
Serotonin
Slow reacting substance of anaphylaxis
Heparin
Lysosomal enzymes
It is the capacity of the human body to resist and destroy the invading organisms or toxins.
Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Phys...Physiology Dept
Definition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation
White blood cells & Immunity (The Guyton and Hall Physiology)Maryam Fida
Leukocytes or WBCs are the mobile units of the body’s immune defense system.
Immunity is the body’s ability to resist or eliminate potentially harmful foreign materials or abnormal cells.
WBC count: 5000 to 11000/ul of blood
GRANULOCYTES
Polymorphonuclear neutrophils 60-70%
Polymorphonuclear eosinophils 2-3%
Polymorphonuclear basophils 0.4%
NON-GRANULOCYTES
Monocytes 5.3%
Lymphocytes 30%
Granulocytes and monocytes are formed and stored only in bone marrow
Lymphocytes and plasma cells are formed and stored mainly in various lymphoid tissue such as lymph node, spleen, thymus and tonsils as well as in bone marrow.
GRANULOCYTES
4 to 8 hours in blood and 4 to 5 days in tissues
MONOCYTES
Monocytes also have a short transit time:
10 to 20 hours in blood and In tissue they swell to much larger size to become tissue macrophages.
LYMPHOCYTES
weeks to months
neutrophil
. 60-70% of leukocytes
nucleus: 2-5 lobes
Counting the number of lobes and grouping them is called Arneth count.
Shift to left means (increase no of young and predominant WBCs) e.g During acute infection.
Shift to right means, old cells are predominant. e.g During recovery phase
NEUTROPENIA
Decrease in neutrophils count
Typhoid
AIDS and viral hepatitis
Kalazar fever
Bone marrow depression by drugs and radiations
NEUTROPHILIA
Increase in neutrophils count
Appendicitis , Tonsillitis, Pneumonia
Burns, Hemorrhage, MI, Pain
Hypoxia, Pregnancy
BASOPHIL
Their cytoplasmic granules take up basic dyes and appear deep blue
MAST CELLS are derived from basophils under the influence of interleukins 3 and 4
Under many allergic conditions basophils and mast cells bursts and releases
Histamine
Bradykinin
Serotonin
Slow reacting substance of anaphylaxis
Heparin
Lysosomal enzymes
It is the capacity of the human body to resist and destroy the invading organisms or toxins.
This is the power point that explains about the blood and blood cells. Power point describes about the mechanism of coagulation and defense cells of our circulatory system.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. Hemostasis
Hemostasis is defined as arrest or stoppage of bleeding.
Stages of hemostasis:
When a blood vessel is injured, the injury initiates a series of reactions, resulting in
hemostasis. It occurs in three stages
1. Vasoconstriction
2. Platelet plug formation
3. Coagulation of blood.
„VASOCONSTRICTION
• Immediately after injury, the blood vessel constricts and decreases the loss of
blood from damaged portion.
• Usually, arterioles and small arteries constrict. Vasoconstriction is purely a local
phenomenon. When the blood vessels are cut, the endothelium is damaged and
the collagen is exposed. Platelets adhere to this collagen and get activated.
• The activated platelets secret serotonin and other vasoconstrictor substances
which cause constriction of the blood vessels.
• Adherence platelets to the collagen is accelerated by von Willebrand factor. This
factor acts as a bridge between a specific glycoprotein present on the surface of
platelet and collagen fibrils.
3. „
PLATELET PLUG FORMATION
• Platelets get adhered to the collagen of ruptured blood vessel and secrete adenosine
diphosphate (ADP) and thromboxane A2.
• These two substances attract more and more platelets and activate them. All these
platelets aggregate together and form a loose temporary platelet plug or temporary
hemostatic plug, which closes the ruptured vessel and prevents further blood loss.
• Platelet aggregation is accelerated by platelet activating factor (PAF).
„COAGULATION OF BLOOD
• During this process, the fibrinogen is converted into fibrin. Fibrin threads get
attached to the loose platelet plug, which blocks the ruptured part of blood vessels
and prevents further blood loss completely.
4.
5.
6. Coagulation of Blood
Coagulation or clotting is defined as The process in which blood loses its
fluidity and becomes a jelly-like mass few minutes after it is shed out or
collected in a container.
Clotting Factors
Coagulation occurs through a series of reactions due to the activation of a
group of substances. The substances necessary for clotting are called Clotting
factors.
7. Thirteen clotting factors are identified:
Factor I Fibrinogen
Factor II Prothrombin
Factor III Thromboplastin (Tissue factor)
Factor IV Calcium
Factor V Labile factor (Proaccelerin or accelerator globulin)
Factor VI Presence has not been proved
Factor VII Stable factor
Factor VIII Antihemophilic factor (Antihemophilic globulin)
Factor IX Christmas factor
Factor X Stuart-Prower factor
Factor XI Plasma thromboplastin antecedent
Factor XII Hageman factor (Contact factor)
Factor XIII Fibrin-stabilizing factor (Fibrinase).
8. Stages of Blood Clotting
1.Formation of Prothrombin Activator
2. Conversion of Prothrombin into Thrombin
3. Conversion of Fibrinogen into Fibrin
Stage 1: Formation of Prothrombin Activator:
• Formation of prothrombin activator occurs through 2 pathways:
i.Intrinsic pathway – initiated by platelets within the blood
ii.Extrinsic pathway – initiated by tissue thromboplastin formed from injured tissues
Stage 2: Conversion of Prothrombin into Thrombin:
• Blood clotting is all about thrombin formation. Once thrombin is formed, it definitely leads to
clot formation.
• Prothrombin activator that is formed converts prothrombin into thrombin in the presence of
calcium(factor IV).
• Once formed, thrombin initiates the formation of more thrombin molecules. Factor V in turn
accelerates formation of both extrinsic and intrinsic prothrombin activator, which converts
prothrombin into thrombin. This effect of thrombin is called positive feedback effect.
Stage 3: Conversion of Fibrinogen into Fibrin :
• Thrombin converts inactive fibrinogen into activated fibrinogen which is called fibrin
monomer. Fibrin monomer polymerizes with other monomer molecules and form loosely
arranged strands of fibrin.
• Later these loose strands are modified into dense and tight fibrin threads by fibrin- stabilizing
factor (factor XIII) in the presence of calcium ions. All the tight fibrin threads are aggregated
to form a meshwork of stable clot.
9.
10. Intrinsic Pathway for the Formation of Prothrombin Activator
In this pathway, the formation of prothrombin activator is initiated by platelets, which
are within the blood itself
Sequence of Events in Intrinsic pathway
i. During the injury, the blood vessel is ruptured. Endothelium is damaged and collagen
beneath the endothelium is exposed.
ii. When factor XII (Hageman factor) comes in contact with collagen, it is converted into
activated factor XII in the presence of kallikrein and high molecular weight (HMW)
kinogen.
iii. The activated factor XII converts factor XI into activated factor XI in the presence of
HMW kinogen.
iv. The activated factor XI activates factor IX in the presence of factor IV (calcium).
v. Activated factor IX activates factor X in the presence of factor VIII and calcium.
vi. When platelet comes in contact with collagen of damaged blood vessel, it gets
activated and releases phospholipids.
vii. Now the activated factor X reacts with platelet phospholipid and factor V to form
prothrombin activator. This needs the presence of calcium ions.
viii. Factor V is also activated by positive feedback effect of thrombin.
11. Extrinsic Pathway for the Formation of Prothrombin Activator
In this pathway, the formation of prothrombin activator is initiated by the tissue
thromboplastin, which is formed from the injured tissues.
Sequence of Events in Extrinsic Pathway
i. Tissues that are damaged during injury release tissue thromboplastin (factor III).
Thromboplastin contains proteins, phospholipid and glycoprotein,which act as proteolytic
enzymes.
ii. Glycoprotein and phospholipid components of thromboplastin convert factor X into
activated factor X, in the presence of factor VII.
iii. Activated factor X reacts with factor V and phospholipid component of tissue
thromboplastin to form prothrombin activator. This reaction requires the presence of
calcium ions.
12. Blood Clot
• Blood clot is defined as the mass of coagulated blood which contains RBCs, WBCs
and platelets entrapped in fibrin meshwork.
• RBCs and WBCs are not responsible for clotting. However, when clot is formed these
cells are trapped in it along with platelets.
Clot Retraction
• After the formation, blood clot starts contracting and 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
https://youtu.be/4DrJjvpaeLs
13. Fibrinolysis
Lysis of blood clot inside the blood vessel is called fibrinolysis. It helps to remove the
clot from lumen of the blood vessel. This process requires a substance called plasmin or
fibrinolysin.
Formation of Plasmin
• Plasmin is formed from inactivated glycoprotein called plasminogen. Plasminogen is
synthesized in liver and it is incorporated with other proteins in the blood clot.
• Plasminogen is converted into plasmin by tissue plasminogen activator (t-PA),
lysosomal enzymes and thrombin.
• The t-PA and lysosomal enzymes are released from damaged tissues and damaged
endothelium.
• Thrombin is derived from blood. The t-PA is always inhibited by a substance called t-
PA inhibitor. It is also inhibited by factors V and VIII.
• Besides t-PA, there is another plasminogen activator called urokinase plasminogen
activator (u-PA). It is derived from blood.
14. Sequence of Events Involved in the
Activation of Plasminogen
1. During intravascular clotting, the endothelium
of the blood vessel secretes a thrombin-binding
protein, the thrombomodulin. It is secreted by the
endothelium of all the blood vessels, except the
minute vessels of brain.
2. Thrombomodulin combines with thrombin and
forms a thrombomodulin-thrombin complex
3. Thrombomodulin-thrombin complex activates
protein C
4. Activated protein C inactivates factor V and VIII
in the presence of a cofactor called protein S
5. Protein C also inactivates the t-PA inhibitor
6. Now, the t-PA becomes active
7. Activated t-PA and lysosomal enzymes activate
plasminogen to form plasmin. Plasminogen is also
activated by thrombin and u-PA
15.
16. „ANTICLOTTING MECHANISM IN THE BODY
Under physiological conditions, intravascular clotting does not occur. It is because of the
presence of some physicochemical factors in the body.
1. Physical Factors
i. Continuous circulation of blood.
ii. Smooth endothelial lining of the blood vessels.
2. Chemical Factors – Natural Anticoagulants
i. Presence of natural anticoagulant called heparin that is produced by the liver
ii. Production of thrombomodulin by endothelium of the blood vessels (except in brain
capillaries).
• Thrombomodulin is a thrombin-binding protein. It binds with thrombin and forms a
thrombomodulin-thrombin complex. This complex activates protein C. Activated protein C
along with its cofactor protein S inactivates Factor V and Factor VIII. Inactivation of these
two clotting factors prevents clot formation
iii. All the clotting factors are in inactive state.
17.
18.
19.
20.
21.
22.
23. Uses
EDTA is used as an anticoagulant both in vivo and in vitro. It is:
i. Commonly administered intravenously, in cases of lead
poisoning.
ii. Used as an anticoagulant in the laboratory (in vitro).
• 0.5 to 2.0 mg of EDTA per mL of blood is sufficient to preserve
the blood for at least 6 hours. On refrigeration, it can preserve
the blood up to 24 hours.
24.
25. Mechanism of action
• Oxalates combines with calcium and forms insoluble
calcium oxalate. Thus oxalates removes calcium from
blood and lack of calcium prevents coagulation.
• Earlier sodium and potassium oxalates were used.
• Nowadays, mixture of ammonium oxalate and
potassium oxalate in the ratio of 3 : 2 is used.
• Each salt is an anticoagulant by itself. But potassium
oxalate alone causes shrinkage of RBCs. Ammonium
oxalate alone causes swelling of RBCs. But together,
these substances do not alter the cellular activity.
26. i. It is used to store blood in the blood bank as:
a. Acid citrate dextrose (ACD): 1 part of ACD with 4 parts of
blood.
b. Citrate phosphate dextrose (CPD): 1 part of CPD with 4
parts of blood.
ii. Citrate is also used in laboratory in the form of formol-
citrate solution (Dacie’s solution) of RBC and platelet count.
27.
28.
29. 1. Hemophilia
• Hemophilia is a group of sex-linked inherited blood disorders, characterized by
prolonged clotting time. However, the bleeding time is normal. Usually, it affects
the males, with the females being the carriers.
• Because of prolonged clotting time, even a mild trauma causes excess bleeding
which can lead to death.
• Damage of skin while falling or extraction of a tooth may cause excess bleeding
for few weeks.
• Easy bruising and hemorrhage in muscles and joints are also common in this
disease.
Causes of hemophilia
• Hemophilia occurs due to lack of formation of prothrombin activator. That is why
the coagulation time is prolonged.
• The formation of prothrombin activator is affected due to the deficiency of factor
VIII, IX or XI.
Clotting time is the time
interval from oozing of
blood after a cut or injury till
the formation of clot.
30. Types of hemophilia
• Depending upon the deficiency of the factor involved ,hemophilia is classified into
three types:
i. Hemophilia A or classic hemophilia: Due to the deficiency of factor VIII. 85% of
people with hemophilia are affected by hemophilia A.
ii. Hemophilia B or christmas disease: Due to the deficiency of factor IX.15% of
people with hemophilia are affected by hemophilia B.
iii. Hemophilia C or factor XI deficiency: Due to the deficiency of factor XI. It is a
very rare bleeding disorder.
Symptoms of hemophilia
i. Spontaneous bleeding.
ii. Prolonged bleeding due to cuts, tooth extraction
and surgery.
iii. Hemorrhage in gastrointestinal and urinary tracts.
iv. Bleeding in joints followed by swelling and pain
v. Appearance of blood in urine.
Treatment for hemophilia
Effective therapy for classical hemophilia involves
replacement of missing clotting factor.
31. 2. Purpura
• Purpura is a disorder characterized by prolonged bleeding time. However, the clotting time
is normal. Characteristic feature of this disease is spontaneous bleeding under the skin
from ruptured capillaries.
• It causes small tiny hemorrhagic spots in many areas of the body. The hemorrhagic spots
under the skin are called purpuric spots (purple colored patch like appearance). That iswhy
this disease is called purpura.
• Blood also sometimes collects in large areas beneath the skin which are called ecchymoses.
Types and causes of purpura
Purpura is classified into three types depending upon the causes:
i. Thrombocytopenic purpura
Thrombocytopenic purpura is due to the deficiency of platelets
(thrombocytopenia). In bone marrow disease,platelet production
is affected leading to the deficiency of platelets.
ii. Idiopathic thrombocytopenic purpura
Purpura due to some unknown cause is called idiopathic thrombocytopenic purpura. It is
believed that platelet count decreases due to the development of antibodies against platelets,
which occurs after blood transfusion.
iii. Thrombasthenic purpura
Thrombasthenic purpura is due to structural or functional abnormality of platelets. However,
the platelet count is normal. It is characterized by normal clotting time, normal or prolonged
bleeding time but defective clot retraction.
(BT) is the time interval
from oozing of
blood after a cut or
injury till arrest of
bleeding.
32. 3. von Willebrand Disease
• von Willebrand disease is a bleeding disorder, characterized by excess bleeding
even with a mild injury.
• It is due to deficiency of von Willebrand factor, which isa protein secreted by
endothelium of damaged blood vessels and platelets. This protein is responsible
for adherence of platelets to endothelium of blood vessels during hemostasis
after an injury. It is also responsible for the survival and maintenance of factor VIII
in plasma.
• Deficiency of von Willebrand factor suppresses platelet adhesion. It also causes
deficiency of factor VIII. This results in excess bleeding, which resembles the
bleeding that occurs during platelet dysfunction or hemophilia.
„ THROMBOSIS
Thrombosis or intravascular blood clotting refers to coagulation of blood inside the
blood vessels. Normally, blood does not clot in the blood vessel because of some
Factors. But some abnormal conditions cause thrombosis.
Causes of Thrombosis
1. Injury to blood vessels
During infection or mechanical obstruction, the endothelial lining of the blood
vessel is damaged and it initiates thrombosis.
2. Roughened endothelial lining
In infection, damage or arteriosclerosis, the endothelium becomes rough and this
initiates clotting.
33. 3. Sluggishness of blood flow
Decreased rate of blood flow causes aggregation of platelets and formation of thrombus. Slowness
of blood flow occurs in reduced cardiac action, hypotension, low metabolic rate, prolonged
confinement to bed and immobility of limbs.
4. Agglutination of RBCs
Agglutination of the RBCs leads to thrombosis. Agglutination of RBCs occurs by the foreign antigens
or toxic substances.
5. Toxic thrombosis
Thrombosis is common due to the action of chemical poisons like arsenic compounds, mercury,
poisonous mushrooms and snake venom.
6. Congenital absence of protein C
Protein C is a circulating anticoagulant, which inactivates factors V and VIII. Thrombosis occurs in the
absence of this protein. Congenital absence of protein C causes thrombosis and death in infancy.
Complications of Thrombosis
1. Thrombus
During thrombosis, lumen of blood vessels is occluded. The solid mass of platelets, red cells and/or
clot, which obstructs the blood vessel, is called thrombus. The thrombus formed due to
agglutination of RBC is called agglutinative thrombus.
2. Embolism and embolus
Embolism is the process in which the thrombus or a part of it is detached and carried in bloodstream
and occludes the small blood vessels, resulting in arrests of blood flow to any organ or region of the
body. Embolus is the thrombus or part of it, which arrests the blood flow. The obstruction of blood
flow by embolism is common in lungs (pulmonary embolism), brain (cerebral embolism)
or heart (coronary embolism)
34. 3. Ischemia
Insufficient blood supply to an organ or area of the body by the obstruction of blood vessels
is called ischemia.Ischemia results in tissue damage because of hypoxia (lack of oxygen).
Ischemia also causes discomfort, pain and tissue death. Death of body tissue is called
necrosis.
4. Necrosis and infarction
Necrosis is a general term that refers to tissue death caused by loss of blood supply, injury,
infection, inflammation, physical agents or chemical substances.
Infarction means the tissue death due to loss of blood supply. Loss of blood supply is usually
caused by occlusion of an artery by thrombus or embolus and sometimes by atherosclerosis .
Area of tissue that undergoes infarction is called infarct. Infarction commonly occurs in heart,
brain, lungs, kidneys and spleen.
ATHEROSCLEROSIS:
A build up of cholesterol plaque in the walls of
arteries, causing obstruction of blood flow. Plaques
may rupture, causing acute occlusion of the artery
by clot.