Hemostasis is the process of preventing blood loss from broken blood vessels. It is achieved through three main mechanisms: vascular constriction, platelet plug formation, and blood coagulation. Vascular constriction occurs when smooth muscle contracts after vessel wall trauma. Platelets aggregate at the injury site to form a plug and provide clotting factors. Blood coagulation activates clotting factors through the extrinsic and intrinsic pathways, ultimately converting prothrombin to thrombin which converts fibrinogen to fibrin forming a clot. Clots are dissolved by plasmin which degrades fibrin, and several factors prevent excessive clotting.
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.
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 presentation deals with the basics of hemorrhage i.e. classification, etiology. It also covers the mechanism of hemostasis and the various methods to achieve hemostasis.
Hope you like it! Suggestions and feedback will always be well appreciated. :)
Blood platelets (or thrombocytes) are very small, 2-4 μm in diameter, non-nucleated, membrane-bound cells derived from the cytoplasm of megakaryocytes in the red bone marrow.
Each megakaryocyte can produce 2,000–5,000 platelets
Even though platelets like RBCs have no nucleus, their cytoplasm is packed with granules containing a variety of substances that promote blood clotting.
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.
Platelets
Disc-shape cell fragment with no nucleus
Platelets are the cell fragments pinched off from megakaryocytes in red bone marrow
Platelets are important in preventing blood loss
Platelet plugs
Promoting formation and contraction of clots
Platelets--Life History
Platelets form in bone marrow by following steps:
myeloid stem cells eventually become megakaryocytes whose cell fragments form platelets.
Short life span (5 to 9 days in bloodstream)
They are formed in bone marrow.
They remain few days in circulating blood.
Aged ones are removed by fixed macrophages in liver and spleen.
Normal count: 2-4 lacs per mm3 of blood.
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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!
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
2. • Hemostasis
• means prevention of blood loss from a broken blood vessel
• achieved by several mechanisms:
• vascular constriction
• platelet plug formation
• blood coagulation
3. Vascular Constriction
• trauma to vessel wall causes the smooth muscle to
contract
• contraction results from
• local myogenic spasm
• factors from the traumatized tissues & platelets
• nervous reflexes
4. Platelets (thrombocytes)
• smallest (1-4 µm in diameter) formed elements of blood
• anuclear fragments of megakaryocytes
• a single megakaryocytes typically produces about 1000
platelets
• develop in response to hormone thrombopoietin
• they are removed from circulation by the tissue macrophages
• 150,000-300,000/µl
• half life 5 to 12 days
6. Functions of platelets
1. serotonin released by platelets contributes to the
vasoconstriction
2. platelets aggregate to plug the vascular injury
3. platelets provide the clotting factors
4. contractile protein of the platelets bring about clot
retraction
5. platelets have a growth factor which stimulates mitosis
in the vascular wall
7.
8. Blood Coagulation
• coagulation of blood occurs due to activation of clotting
factors
• occurs in three major stages:
• Formation of prothrombin activator
• Extrinsic pathway
• Intrinsic pathway
• Conversion of prothrombin to thrombin
• Conversion of fibrinogen to fibrin
9.
10.
11. Dissolution of clots
• clot is composed of a meshwork of fibrin fibers running in
all directions & entrapping blood cells, platelets, & plasma
• a large amount of plasminogen is also trapped in the clot
• tissue plasminogen activator (t-PA) converts plasminogen
to plasmin
• plasmin digests fibrin fibers & some other protein
coagulants such as Factors I, II, V, VIII, & XII
12. Prevention of blood clotting
endothelial surface factors
a. smoothness of endothelial cell surface, which prevents
contact activation of the intrinsic clotting system
b. a layer of glycocalyx on the endothelium which repels
clotting factors & platelets
c. thrombomodulin binds thrombin
• thrombomodulin- thrombin complex also activates protein C
that inactivates Factors V & VIII
13. Fibrin
85 to 90% of the thrombin becomes adsorbed to the fibrin fibers
↓
prevent the spread of thrombin
↓
prevents the excessive spread of clot
Antithrombin III
thrombin that does not adsorb to the fibrin fibers soon combines
with antithrombin III
14. Bleeding disorders
• liver diseases can depress the clotting system
• vitamin K deficiency can lead to serious bleeding tendencies
Hemophilia
• abnormality or deficiency of Factor VIII & IX
• abnormality is located on the sex chromosome X
almost never will a woman have hemophilia because at least one
of her 2 X chromosomes will have appropriate gene
Purpura
• a group of disease that occurs due to thrombocytopenia
15. Blood coagulation tests
• Bleeding Time
• time from the onset of bleeding till the stoppage of bleeding (1-5
min)
• Clotting Time
• time from the onset of bleeding till the clot formation (2-8 min)
• Prothrombin Time
• time required for coagulation to take place (12-16 s)
16. Anticoagulants
• anticoagulants act by binding calcium ions- in vitro
(sodium citrate, potassium oxalate & EDTA)
• Heparin is another popular anticoagulant- in vivo & in
vitro
• Vitamin K antogonists such as Dicumarol & Warfarin are
suitable as anticoagulants-in vivo
17. References
• Review of Medical Physiology, 22/E Ganong
• Textbook of Medical Physiology, 14/E Guyton & Hall
• Understanding Medical Physiology, 4/E Bijlani &
Manjunatha
