Platelets, Blood Coagulation And Blood Grouping.AshutoshYadav223
This powerpoint presentation includes information regarding Platelets and its function , Blood coagulation and haemostasis, and blood grouping system.
This presentation is created by a medical student.
Coagulation of blood right from haematopoiesis, platelets, endothelial injuries, development of clotting factors, coagulation cascade, applied aspect of coagulation related disorders and much more.
Haemostasis + Steps of blood clotting (coagulation)Mohammed Alawad
(slide 9. includes an amazing GIF that shows the process)
__ Get in presentation format: https://drive.google.com/file/d/1XVfSmRoB40angMGIw7DJC-FUxp6MUPw7/view?usp=sharing
A very simple presentation on Haemostasis and its mechanism + Steps of blood clotting
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
Platelets, Blood Coagulation And Blood Grouping.AshutoshYadav223
This powerpoint presentation includes information regarding Platelets and its function , Blood coagulation and haemostasis, and blood grouping system.
This presentation is created by a medical student.
Coagulation of blood right from haematopoiesis, platelets, endothelial injuries, development of clotting factors, coagulation cascade, applied aspect of coagulation related disorders and much more.
Haemostasis + Steps of blood clotting (coagulation)Mohammed Alawad
(slide 9. includes an amazing GIF that shows the process)
__ Get in presentation format: https://drive.google.com/file/d/1XVfSmRoB40angMGIw7DJC-FUxp6MUPw7/view?usp=sharing
A very simple presentation on Haemostasis and its mechanism + Steps of blood clotting
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
Hemostasis and coagulation of blood by Pandian M, Tutor, Dept of Physiology, ...Pandian M
DEFINITION Hemostasis
STAGES OF HEMOSTASIS
VASOCONSTRICTION
PLATELET PLUG FORMATION
COAGULATION OF BLOOD DEFINITION
FACTORS INVOLVED IN BLOOD CLOTTING
SEQUENCE OF CLOTTING MECHANISM
BLOOD CLOT
ANTICLOTTING MECHANISM IN THE BODY
ANTICOAGULANTS
PHYSICAL METHODS TO PREVENT BLOOD CLOTTING
PROCOAGULANTS
TESTS FOR BLOOD CLOTTING
APPLIED PHYSIOLOGY
Hemostasis is the mechanism that leads to cessation of bleeding from a blood vessel. It is a process that involves multiple interlinked steps. This cascade culminates into the formation of a “plug” that closes up the damaged site of the blood vessel controlling the bleeding.
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.
Similar to Anticoagulation theory 2_students_ (20)
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
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
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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.
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!
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
2. Coagulation Basics
• Ability of the body to control flow of blood
following vascular injury is needed for survival
• Hemostasis: process of blood clotting and
then the subsequent dissolution of the clot
following repair of injured tissue
4. Hemostasis
• Maintains circulating blood in fluid state
• Disrupts blood flow due to vessel injury to
minimize anoxia and cellular death
• Facilitates maintenance of vascular integrity
following injury
6. Hemostasis
• Complex interaction of cellular components
and plasma proteins that once activated,
result in clot formation to plug the vessel
injury
• Has components necessary for limiting
excessive formation of clots and those
necessary for dissolving the clots over time
7. Hemostasis
• Balance between procoagulants and down
regulators
• Perturbation of this balance results in either
bleeding or pathologic clot formation
– You either don’t clot when you need to or clot
when you don’t need to
12. Primary Hemostasis
• Process of forming a platelet plug at the sit of
vessel injury
• Consists of vasoconstriction and platelet
adhesion
13. Vasoconstriction (Vascular phase)
• “Tightening” of blood vessels to divert blood
flow around the damaged vessel
• Enhances contact activation of platelets and
coagulation factors
14. Platelet Adhesion (Platelet phase)
• Platelets become activated and aggregate at
the site of injury, forming a temporary, loose,
platelet plug
15. Secondary Hemostasis
• To stabilize the initially loose platelet plug, a
sequence of enzymatic reactions is initiated
which culminates in fibrin strands forming at
the platelet plug
• Fibrin mesh (clot) is formed and entraps the
plug
16. Coagulation phase
• Fibrin-forming system
• Coagulation factors interact with each other
to form a fibrin clot
• Reinforces the platelet plug
17. Coagulation Factors
• Proteins normally present in the blood
• Most are produced by the liver
• Normally “turned off” (inactive)
• Designated by roman numerals
• Common names are significant of patients’
last names who were deficient with the factor
• “a” signals the factor in its “active” form
18. Coagulation Cascade
• Sequence of biochemical reactions that form
an insoluble gel (clot)
• Converts fibrinogen to fibrin
• Domino or waterfall effect
• Each factor is converted into its active form by
the preceding factor
19. ENDOTHELIALDAMAGE
Endothelium secretes VWF which makes platelets stick to the injured
vessel and cause platelet aggregation
Endothelium secretes Tissue Factors that
activate the Extrinsic system
EXTRINSIC SYSTEMINTRINSIC SYSTEM
Factor VII
XII CONTACT HMK
XIIa
KAL
XI XIa
IX IXa
ENDOTHELIUM
Ca++
Plasminogen
Plasmin
Stable Fibrin Clot Fibrin Degradation
Products
Fibrin
XIIIa
Thrombin
+ PF3 Factor VIIa
X Xa
V + Ca++ + PF3
Prothrombin
Fibrinogen
Factor XIIIActivated Protein C
Protein C
Protein S
Ca++
Tissue Factor
VIII
VIII
Antithrombin III
20. Extrinsic Pathway
• Activated when endothelial cells are injured and tissue
factor is released
• Activated Factor VII and tissue factor bind to form a
complex
– This complex, plus calcium, activates Factor X
Tissue Factor
VII VIIa
Ca+
X Xa
(Protrombin) II IIa (Thrombin)
Fibrinogen Fibrin
PF3 Ca++
21. Intrinsic Pathway
• Requires clotting factors
VIII-XII
• Initiation occurs when
factor XII is exposed to a
negatively charged
surface
– Termed the contact
phase
• Exposure of collagen to a
vessel surface is the
primary stimulus for the
contact phase
Prekalikrein Kalikrein
XII XIIa
XI XIa
IX IXa
X Xa
PF3 Ca++
22. Common Pathway
• Activated by either extrinsic or intrinsic pathway
• When Factor Xa binds to the platelet surface, a complex
is formed composed of platelet phospholipid, calcium
and Factor Va
– Complex converts prothrombin to thrombin which in turn
converts fibrinogen to fibrin
X Xa
(Prothrombin) Thrombin
Fibrinogen Fibrin
PF3
Ca++
23. Clot Generation
• Endothelial damage vWF platelets stick
to endothelium (adhesion) exposure of
collagen fibrils stimulates platelets to stick
together (aggregation)
• Activation of coagulation
– Tissue factor on the surface of monocytes and
endothelium activate various factors that lead to
the formation of thrombin
24. Clot Generation
• Thrombin changes properties of fibrinogen
polymerization fibrin meshwork clot
• Fibrinolysis: dissolution of the fibrin clot
– Initiation of clot lysis begins concurrently with the
activation of the clotting cascade
• Endothelium plasminogen plasmin
degrades fibrin FDP
25. Fibrinolysis
• Body’s way of keeping coagulation from becoming
excessive and occluding the blood vessels
• Function of plasmin that circulates as the inactive
proenzyme plasminogen
Fibrinogen
Soluble
Fibrin
Insoluble (stable)
Fibrin Clot
FDPs Plasminogen
Plasmin
Tissue
Plasminogen
Activator
D
26. Regulation
• Balance between coagulation and fibrinolytic
processes must be maintained
– Otherwise, excess clotting or fibrinolysis will occur
• Body has inhibitors to regulate the system
Antithrombin
Protein C
Protein S
Plasmin Inhibitor
STOP
27. ENDOTHELIALDAMAGE
Endothelium secretes VWF which makes platelets stick to the injured
vessel and cause platelet aggregation
Endothelium secretes Tissue Factors that
activate the Extrinsic system
EXTRINSIC SYSTEMINTRINSIC SYSTEM
Factor VII
XII CONTACT HMK
XIIa
KAL
XI XIa
IX IXa
ENDOTHELIUM
Ca++
Plasminogen
Plasmin
Stable Fibrin Clot Fibrin Degradation
Products
Fibrin
XIIIa
Thrombin
+ PF3 Factor VIIa
X Xa
V + Ca++ + PF3
Prothrombin
Fibrinogen
Factor XIIIActivated Protein C
Protein C
Protein S
Ca++
Tissue Factor
VIII
VIII
Antithrombin III
28. Venous Thrombotic Event (VTE)
• Thrombophilia
– Hypercoagulable state due to inherited
(hereditary/genetic) defects or acquired defects in
one or several factors of the coagulation cascade
• Thrombophilia causes DVT (deep vein
thrombosis) or PE (pulmonary embolism)
29. Thrombotic Alert #1
• How many patients in the US are diagnosed
with deep vein thrombosis each year?
More than 500,000
30. Thrombotic Alert #2
• How many pulmonary embolisms are
diagnosed each year in the US?
More than 630,000
31. Thrombotic Alert #3
• How many deaths are attributed to PE each
year?
Approximately 200,000 deaths
34. Hereditary/Genetic Irreversible
Factor I (Fibrinogen)
• Afibrinogenemia
– Total absence of measurable fibrinogen
– Rare congenital disorder
• Hypofibrinogenemia
– Below normal levels of fibrinogen
– Treated by cryoprecipitate or FFP
• Dysfibrinogenemia
– Altered structure of the fibrinogen molecule
– Usually asymptomatic but has been associated
with both bleeding and thrombotic events
35. Factor V (Proaccelerin)
Gene Defect
• Cofactor in coagulation cascade
• Deficiency causes bleeding but…
– Factor V mutation (Factor V Leiden) causes
thrombotic events due to impaired degradation of
Factor V resulting in continued thrombin
generation
• Most common cause of thrombophilia
36. Defects in Prothrombin Gene
• Second most common cause of thrombophilia
• Prothrombin does not break down
– Keeps on activating thrombin to convert
fibrinogen into a fibrin clot
37. Defects of Methyl Tetrahydrofolate
Reductase (MTHFR) Enzyme
• MTHFR breaks down homocysteine
• Deficiency of MTHFR increases homocysteine,
leading to thrombosis
• Acquired homocysteinemia is due to
deficiency of folate, vitamins B6 and B12
39. Factor VIII (Antihemophilic Factor)
• Composed of a coagulant portion and vWF
(vonWillebrand Factor)
• Acute phase reactant
– Increase in inflammation, stress, pregnancy and
infection which can lead to clot formation
• Defect or absence of coagulant portion causes
classic Hemophilia A
• Deficiency in vWF portion causes
vonWillebrand’s Disease