Haemostasis involves three main processes: vasoconstriction, temporary haemostatic plug formation by platelets, and definitive plug formation through blood coagulation. Platelet adhesion and aggregation leads to a temporary plug, while coagulation involves clotting factors that ultimately convert fibrinogen to fibrin for a solid clot. Several factors regulate haemostasis, including the endothelium, circulating anticoagulants, liver synthesis of clotting factors, and vitamin K which enables procoagulant synthesis. Disruptions can lead to bleeding disorders or thrombosis.
Here's important & condensed ppt slides about hemostasis and its orchestrated steps and cogulation cascade, roles of endothelium,platelets and Coagulation protiens....!
Here's important & condensed ppt slides about hemostasis and its orchestrated steps and cogulation cascade, roles of endothelium,platelets and Coagulation protiens....!
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 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
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 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 normal physiological mechanism by which blood in fluid state in vascular system normally and prevention of bleeding by Hemostasis by complex interactions of blood vessels wall, plasma proteins and platelets.
US E-cigarette Summit: Taming the nicotine industrial complexClive Bates
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TEST BANK For Williams' Essentials of Nutrition and Diet Therapy, 13th Editio...kevinkariuki227
TEST BANK For Williams' Essentials of Nutrition and Diet Therapy, 13th Edition Schlenker & Gilbert, Verified Chapters 1 - 25, Complete Newest Version.pdf
TEST BANK For Williams' Essentials of Nutrition and Diet Therapy, 13th Edition Schlenker & Gilbert, Verified Chapters 1 - 25, 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
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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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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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.
3. HAEMOSTASIS
Definition – spontaneous arrest or stoppage of bleeding
from injured blood vessel by physiological process.
3 processes
Vasoconstriction
Formation of temporary haemostatic plug formation
Formation of Definitive haemostatic plug formation
Saturday, May 14, 2016
4. VASOCONSTRICTION
Immediate –
Direct effect of injury
Proportionate to the
degree of trauma.
Later by humoral
Release of 5- HT by
bound platelets to the
collagen
Saturday, May 14, 2016
5. FORMATION OF TEMPORARY
HAEMOSTATIC PLUG FORMATION
Platelet adhesion
Platelet activation
Platelet aggregation
Formation of
temporary
haemostatic plug
Inhibition of further
plug formation.
Saturday, May 14, 2016
6. PLATELET ADHESION
After injury platelets
contacts with collagen &
damaged endothelium
Swell, becomes irregular &
protrudes Pseudopodia.
Contractile proteins contracts
& releases granules.
Platelets becomes sticky &
adhere to collagen.
Saturday, May 14, 2016
8. PLATELET AGGREGATION
Activated sticky
platelets stick to each
other & forms
Aggregation
It is also increases by
Platelet Activating
Factor (PAF) released
by neutrophils,
Monocyte & platelets
cell membrane lipids.
Saturday, May 14, 2016
10. INHIBITION OF FURTHER
PLUG FORMATION.
Prostacycline from
membrane
phospholipids
Inhibit Thromboxane
formation
Saturday, May 14, 2016
11. FORMATION OF DEFINITIVE
HAEMOSTATIC PLUG FORMATION
Temporary plug
converted to definitive
plug by Process of
blood coagulation.
Results in formation of
tight unyielding seal
Saturday, May 14, 2016
12. COAGULATION OF BLOOD
Through out life blood – in
fluid state but when
removed or shed or
collected in container
become jelly like – clot
Fluidity – necessary for
circulation.
Coagulation – protect
from excessive bleeding.
Saturday, May 14, 2016
13. COAGULATION OF BLOOD
Clotting factors
Mechanism of coagulation
Role of calcium in blood coagulation.
Role of vitamin –k, liver and vascular wall in
haemostasis and coagulation.
Blood clot retraction
Blood in fluid state
Thrombosis
Saturday, May 14, 2016
14. CLOTTING FACTORS
I – FIBRINOGEN
Soluble
Mol wt – 3,40,000
Dalton
6 polypeptide chain
Conc. – 0.3 gm/100 ml
It is converted into
fibrin in the presence of
enzyme thrombin
Saturday, May 14, 2016
15. CLOTTING FACTORS
II- PROTHROMBIN
Inactive precursor of
thrombin.
Mol wt 69000 dalton.
Synthesized in liver in
the presence of vitamin
K.
Conc. is 40 mg / 100
ml.
Saturday, May 14, 2016
16. CLOTTING FACTORS
III – THROMBOPLASTIN
Also called tissue factor or tissue thromboplastin
Released in extrinsic pathway.
Saturday, May 14, 2016
17. CLOTTING FACTORS
IV – CALCIUM
Essential in all stages of coagulation.
Saturday, May 14, 2016
18. CLOTTING FACTORS
V – LABILE FACTOR / PROACCLERIN
Required for formation of protrombin activator
Consumed during clotting so absent in serum.
Saturday, May 14, 2016
19. CLOTTING FACTORS
VII – STABLE FACTOR / PROCONVERTIN
For activation of factor X in extrinsic pathway.
Saturday, May 14, 2016
20. CLOTTING FACTORS
VIII – ANTI-HAEMOPHYLLIC FACTOR A / ANTI-
HAEMOPHLIC GLOBULIN.
Protein of b globulin type, synthesized in liver.
Activation of factor x
Deficiency causes classical Haemophilia.
Inherited disease in which CT prolonged.
Saturday, May 14, 2016
21. CLOTTING FACTORS
IX – ANTI-HAEMOPHILIC FACTOR B/ PLASMA
THROMBOPLASTIC COMPONENT
First discovered in patient named Christmas.
Saturday, May 14, 2016
22. CLOTTING FACTORS
X –STUART-PROWER FACTOR
Along with active factor V, Ca and phopholipid forms a
complex – Prothrombin activator.
Formed in both extrinsic & intrinsic pathway.
Saturday, May 14, 2016
23. CLOTTING FACTORS
XI – PLASMA THROMBOPLASTIN
ANTICEDENT / ANTI-HAEMOPHILIC FACTOR C
Its deficiency causes hemorrhagic state.
Saturday, May 14, 2016
24. CLOTTING FACTORS
XII – HAGEMAN FACTOR/ GLASS FACTOR /
CONTACT FACTOR
Activated when comes in contact with electronegative
surface or glass or rough surface.
Its activation initiate intrinsic pathway.
Saturday, May 14, 2016
25. CLOTTING FACTORS
XIII – FIBRIN STABILIZING FACTOR /
FIBRINASE / LAKI LORAND FACTOR
Required for activation of fibrin polymer along with Ca.
Saturday, May 14, 2016
29. DIFFERENCE .
INTRINSIC
PATHWAY.
Begins in blood itself.
Much slower take 2-6
min.
Initiated by activation
of factor XII.
EXTRINSIC
PATHWAY.
Begins with trauma to
the vascular wall or
tissue outside the
vessel wall.
Explosive in nature
takes 15 sec.
Initiated by activation
of factor III.
Saturday, May 14, 2016
30. CONVERSION OF
PROTHROMBIN TO THROMBIN
Prothrombin –
Inactive precursor of
thrombin.
Mol wt 69000 dalton.
Synthesized in liver in
the presence of
vitamin K.
Conc. is 40 mg / 100
ml.
Saturday, May 14, 2016
31. THROMBIN.
Saturday, May 14, 2016
Proteolytic enzyme.
Amount of thrombin
produced during
clotting of 1 ml of
blood is sufficient to
coagulate 3 liters of
blood.
32. I – FIBRINOGEN
Soluble
Mol wt – 3,40,000 Dalton
6 polypeptide chain
Conc. – 0.3 gm/100 ml
It is converted into fibrin in the presence of enzyme
thrombin
Saturday, May 14, 2016
33. FIBRINOGEN TO FIBRIN.
Proteolysis
Polymerization .
Stabilization of fibrin polymers.
Saturday, May 14, 2016
34. BLOOD CLOT RETRACTION.
Clot is meshwork of fibrin
with entrapped blood cells ,
platelets & plasma.
Contractile proteins – Actin,
myosin & thrombosthenin.
Compress fibrin meshwork
squeeze out serum.
Clot reduced to 40% of
original volume.
Saturday, May 14, 2016
35. ROLE OF CALCIUM.
Except for first 2 steps Ca required for all steps.
Ca removal causes Anticoagulation.
e.g. use of oxalates & citrates.
Saturday, May 14, 2016
36. ROLE OF VITAMIN K.
Chemical structure.
Naphthoquinone derivatives.
Fat soluble , insoluble in water.
Sources.
Food , bacterial flora.
Role of vitamin K
Synthesis of coagulants like Prothrombin.
Factor VII , IX & X & circulatory anticoagulant
protein.
Saturday, May 14, 2016
37. ROLE OF VITAMIN K.
Deficiency causes serious hemorrhages.
Its due to
Obstructive jaundice
Newborn babies.
Chronic diarrhoea.
Side effects of antibiotics.
Saturday, May 14, 2016
38. ROLE OF LIVER.
Synthesis of procoagulants – site of synthesis of
factor V,VII,IX,X, Prothrombin & fibrinogen
Removal of activated procoagulants.
Synthesis of anticoagulants like – heparin, anti
thrombin III & protein C
Saturday, May 14, 2016
40. ROLE OF BLOOD VESSELS.
Coagulant role
Von Willebrand factor
(VWF)
Tissue factor.
Plasminogen activator.
Sub endothelial tissue –
collagen fibres
Causes platelet
aggregation
Intrinsic pathway
activation.
Saturday, May 14, 2016
41. BLOOD IN FLUID STATE
Velocity of circulation.
Surface effect of
endothelium.
Glycocalyx
Circulatory
anticoagulants.
Fibrinolytic mechanism.
Removal of activated
clotting factors.
Saturday, May 14, 2016
42. VELOCITY OF CIRCULATION.
Blood is in constant motion due to pumping by
heart & at constant velocity
Decrease in velocity
Intravascular clotting
Saturday, May 14, 2016
45. FIBRINOLYTIC MECHANISM.
Protein C
Inactivates inhibitor of
TPA
Increases Plasmin
formation
Acts as Fibrinolytic
Saturday, May 14, 2016
46. REMOVAL OF ACTIVATED
CLOTTING FACTORS.
Liver plays an important role
Removes activated clotting factors
Prevents Intravascular Clotting
Saturday, May 14, 2016
47. THROMBOSIS
Def.– Intravascular
clotting of blood & clot
so formed is thrombus
Thrombus – Def –
Solid mass formed in
the living heart or
blood vessel from the
constituents of blood.
Saturday, May 14, 2016
48. THROMBOSIS
Virchow’s triad which
predisposes to
thrombus formation.
Predisposing factors
Endothelial injury
Alteration of blood flow
Hypercoagulability of
blood
Saturday, May 14, 2016
49. ENDOTHELIAL INJURY
It occurs in
Ulcerated plaques in
advanced
atherosclerosis,
Haemodynamic stress in
HT
Arterial diseases
DM
Hypercholesterolemia
Saturday, May 14, 2016
50. ALTERATION OF BLOOD FLOW
Turbulence / stasis blood
flow
Platelet contact with
endothelium
Initiate thrombosis
(especially venous
thrombosis in leg veins
after major operations)
Saturday, May 14, 2016
51. HYPERCOAGULABILITY OF
BLOOD
Increase Platelet count
& adhesiveness.
Increase Coagulation
factors as fibrinogen,
prothrombin
factors,Via,VIIa,Xa
Decrease coagulation
inhibitors – Antithrombin
III & fibrinogen
degradation product.
Saturday, May 14, 2016
52. THROMBOGENESIS
Adherence of platelets
Activation of coagulation system
Entanglement of RBC with WBC – so clot mass is
mainly formed by entangled RBC & WBC.
Saturday, May 14, 2016
53. THROMBI
Red - mainly venous
Soft, red & Gelatinous
White – mainly arterial
Pale & firm
Mixed or laminated –
consists of alternate
white & red Layers –
Lines Of Zahn.
Saturday, May 14, 2016
54. EFFECTS OF THROMBI
Ischemia and Infarction
Clot in Intact vessel decrease blood supply (Ischemia)
Cell death (Infarction)
Thromboembolism
Dislodged clot in distant vessel & block circulation
Pulmonary & Cerebral Embolism
Saturday, May 14, 2016
55. PREVENTION OF THROMBI
Drugs – decrease platelet adhesion; Aspirin,
Dextran
Anticoagulants – Heparin, Dicoumarol
Intermittent compression or electrical
stimulation of calf muscle
Saturday, May 14, 2016