Ch 16 Blood part 2 Flashcards
3 stages of hemostasis
- Vasoconstriction
- Formation of platelet plug
- Coagulation
Hemostasis Stage 1
Vasoconstriction:smooth muscle contraction
- triggered by paracrine release from endothelium
- reduce outward flow of blood
- lasts 30 mins
Hemostasis Stage 2
Formation of platelet plug
- platelets exposed to collagen develop spikes
- platelets stick together at site of damage
What prevents activation of platelets
Blood vessel endothelial cells
- physical barrier to collagen and basement membrane molecules
- Endothelial cell surface (-) and platelets (-)
- Secrete prostacyclin and nitric oxide (inhibit platelet activation)
- Express CD39
CD39
Enzyme that converts ADP (activator of platelets) to AMP by removing a phosphate
-Inhibits platelet activation
Prep of basement membrane (blood vessel endothelial cells)
-Part of Stage 2
Secretion of Von Willebrand’s factor
-Binds to collagen and to platelets to form a very strong layer to resist force of flowing blood
Platelet Release Action
-Part of Stage 2
Activation leads to Degranulation of vesicles containing ADP, serotonin(vasoconstrictor), thromboxane A (activates platelets and vasocontrictor)
- Platelets become stick and signal other platelets to do the same
- Creates layers of platelets in the plug
What initiates coagulation?
-Part of Stage 2
Platelets bind to fibrinogen and fibrinin
Hemostasis Stage 3
Coagulation: conversion of blood from liquid to gel
- Cascade that results in activation of fibrin
- Platelets contract to pull sides of vessel together
- Clots are dissolved by plasmin
Fibrin
Polymerized into meshwork to traps other cells at the site
- activated during coagulation
- Clot stabilized by crosslinking proteins via factor 13
- Clot retraction
Thrombus
blood clot
Clot retraction
Contraction of entire mass, bringing edges together
Healing process of blood clots
XII activates Kallikrein (plasminogin activator)
Converts plasminogin into active plasmin
Plasmin digests fibrin into small chains
Dissolution of the clot
Anticoagulants
Thrombin bound to fibrin no longer activates fibrinogen Heparin Chelators Citric Acid EDTA
Heparin
A glycosaminoglycan prevents clotting by activation antithrombin III (inactivator of thrombin)
- Can be released by mast cells
- Clinical use as anticoagulant
Chelators
Molecules that bind to metal ions (Ca, Mg) and prevent their binding elsewhere
-Citric acid
Coumarin
Pharmacologic anticoagulant
- Precursor for many anticoagulants like Warfarin
- Found in leeches
Warfarin (Coumadin)
Cause vit K deficiency
- Prevents formation of gamma carboxyglutamate-high Ca binding form of glutamate
- Must be administered and monitored over several days and then regularly afterward
- Rat poison
Hemophilia
Lack of clotting factor -VIII=type A -IX=type B -Prolonged Bleeding from injury and spontaneous internal bleeding Treatment: injections of clotting factor
Septicemia
Infection of the blood “blood poisoning”
Usually stem from prior injury or infection
Symptoms: fever, chills, elevated heart beat, shallow breathing, flushed skin
Treatment: IV antibiotics
Anemia
Reduced O2 carrying capacity of the blood
- Iron deficiency
- Hemorrhagic, Pernicious, Hemolytic
Pernicious Anemia
Reduced vit B12
Hemolytic Anemia
Early destruction of RBCs (malaria, sickle cell)
Blood Doping
Erythropoietin injections to increase O2 carrying capacity
-Used by athletes
Risks: heart must pump harder, increase risk of clots, stroke, heart attack, high bp