Heamology Flashcards
Hat is blood
Blood is a type of connective tissue
Red blood cells (erythrocytes)
White blood cells (leukocytes)
Platelets – cell fragments
Plasma – fluid part of blood
How much adult has blood in avarice
4 to 6 liter
The amount of blood depend on what
Size of person
Amount of adipose
Concentration of ion
Females tend to have less than males
The composition of blood; Hematocrit
The percentage of red blood cells Normal is about 45%
• White cells and platelets = 1%
• Plasma = 54%
Erythrocytes
Transport oxygen
Small bi concave shape
No nucleus
Life span 120 days
Hemoglobin is a pigment in ABCs
Erythropoietin (epo) regulates production of ABCs
Type of hemoglobin
Oxyhemoglobin carries oxygen; bright red
Deoxyhemoglobin does not carry oxygen; darker red
Carries carbon dioxide, so also called carboxyhemoglobin
Anemia – low RBC count
White blood cells (WBC)
leucocytes
Granulocytes
Neutrophils (50-70%) – destroy bacteria, viruses, and toxins in the
bloodstream (phagocytes)
• Eosinophils (1-4%) – get rid of parasitic infections such as worm infections
• Basophils (1%) – control inflammation and allergic reactions
Agranulocytes
Monocytes (2-8%) – destroy bacteria, viruses, and toxins in blood
• After leaving blood and entering tissues, differentiate into macrophages
• Lymphocytes (20-40%) – provide immunity for the body (cell killing, production
of antibodies etc)
WBC count normally —-to——cells / ml3 of blood Leukocytosis
5000 to 10000
Leukocytosis
Elevated WBC count, usually due to infection
Leukopenia
Low WBC count, usually due to some viral infections and other conditions
Platelets
Fragments of cells found in the bloodstream (no nuclei); also called thrombocytes
• Important in the clotting process of blood
• Have receptors for binding collagen, adenosine di-phosphate (ADP) and other factors in blood vessel wall which trigger clotting/clumping
• Normal count - 130,000 to 360,000 platelets per cubic millimeter of blood
Plasma
Liquid portion of blood composed mostly of water, with; protein (albumin globulin
Fibrinogen)
Nutrients
Gases electrolytes waste product ‘]
Globulins
Transportandimmunedefense-,andglobulins
• and globulins; transport proteins and enzymes including hormones, transferrin, complement
proteins, prothrombin, plasminogen
• globulins include the immunoglobulins (antibodies e.g., IgG, IgA, IgE, IgM)
Nutrients in plasma are composed of what
• Aminoacids
• Glucose
• Nucleotides
• Lipidsfromthedigestivetract
Fibrinogen
neededforbloodclotting
Gases in plasma are composed ofclat
oxygen,carbondioxide,andnitrogen
Haematopoiesis
• Generation of blood cells from a
common stem cell / progenitor
Bone marrow of adults (liver and spleen in foetus)
• Regulated by various hormones and cytokines
• Erythropoietin
• Granulocyte-macrophage
colony stimulating factor (GM- CSF)
Haemostasis
– the physiological control of bleeding (versus thrombosis, which is a result pathological clots or thrombi)
What clot do
An injured blood vessel must induce the formation of a blood clot to prevent blood loss and to allow healing
also remain localized to prevent widespread clotting within intact vessels
The formation of a localized clot at the site of vessel injury is accomplished by several, temporally overlapping what stages
Primary haemostasis – platelet plug formation Secondary haemostasis – clotting cascade
Why Localized vasoconstriction occurs
response to injury to limit blood loss
What neurogenic do
control sympathetic innervation
secretion of endothelium-derived
vasoconstrictors such as endothelin
What happens following vasoconstriction
primary haemostasis occurs
Results of Primary haemostasis
formation of a primary haemostatic plug composed of aggregated platelets
What is Platelets
are activated and adhere to the exposed sub- endothelial matrix
• Platelet activation involves both a change in shape of the platelet and the release of secretory granule contents from the platelet
The secreted granule substances recruit other platelets, causing more platelets to adhere to the sub- endothelial matrix and to aggregate with one another at the site of vascular injury
Platelet adhesion is mediated initially by two molecular interactions;
von Willebrand factor (vWF), a large multimeric protein secreted by both activated platelets and the injured endothelium and binds both to surface receptors on platelets (glycoprotein lb [GPIb]) and to the exposed collagen
• Platelet glycoprotein VI (GPVI) interacts directly with collagen in the exposed vessel wall
What required • Both the GPIb:vWF:collagen interaction and the GPVI:collagen interaction
for initiation of primary haemostasis
During platelet aggregation, fibrinogen cross-links platelets to one another by binding to GPIIb–IIIa receptors on platelet membranes
Activated platelets
undergo shape change and granule release, recruiting and activating more platelets
How Platelet recruitment and aggregation is mediated
by the release of soluble platelet factors, including adenosine diphosphate (ADP) and thromboxane A2 (TxA2)
• ADP helps platelets to become “sticky” and adhere to one another
• TxA2 is also a potent vasoconstrictor
How Tissue factor, helps
expressed on activated endothelium, is a critical initiating component in the coagulation cascade (secondary haemostasis)
At this stage there is a soft plug formed of aggregated platelets, which is subsequently / simultaneously reinforced by fibrin deposition and crosslinking (clotting cascade)
What happens during secondary heamostasis
also known as the coagulation cascade, tissue factor complexes with coagulation factor VII to initiate the coagulation cascade
The coagulation cascade is a sequence of what
enzymatic events;
• most plasma coagulation factors circulate as inactive proenzymes, (synthesized by the liver), which are proteolytically cleaved, and activated, by activated factors that
precede them in the cascade
• The result of this cascade is the activation of thrombin
What thrombin serve
two pivotal functions in haemostasis:
• It converts soluble fibrinogen to an insoluble fibrin polymer that
forms the matrix of the clot
• It induces more platelet recruitment and activation
• Fibrin clot formation (secondary haemostasis)
overlaps temporally with platelet plug formation (primary haemostasis) - each process reinforces the other
Haemostasis is highly regulated and restricted to the site of vascular injury; the size of the primary and secondary haemostatic plugs is restricted, so the vascular lumen remains patent
• After vascular injury, the endothelium surrounding the injured area participates in five separate mechanisms that limit the initiation and propagation of the haemostatic process to the vicinity of the injury. These mechanisms involve;
• Prostacyclin (PGI2) (and nitric oxide) which block platelet aggregation and adhesion
• Heparin and antithrombin III combine as potent inhibitors of thrombin
• Proteins C and S block activation of factors V and VIII in clotting cascade
• Tissue factor pathway inhibitor (TFPI) – blocks/limits action of tissue factor
• Tissue-type plasminogen activator (t-PA) – converts plasminogen to plasmin which breaks down fibrin (fibrinolysis); several inhibitors to control plasmin
An introduction to haematology - part two
Thrombosis
• Thrombosis is the pathologic extension of haemostasis; the fundamental process is similar but without the tight control
• In thrombosis, coagulation reactions are inappropriately regulated so that a clot uncontrollably enlarges and occludes the lumen of a blood vessel
• The pathologic clot is now termed a thrombus; may produce pain, swelling in periphery; chest pain/heart attack
• Three major factors predispose to thrombus formation; endothelial injury, abnormal blood flow, and hypercoagulability.
• These three factors influence one another and are collectively known as Virchow’s triad
What is Thrombosis
is the pathologic extension of haemostasis; the fundamental process is similar but without the tight control
In thrombosis, coagulation reactions are inappropriately regulated so that a clot uncontrollably enlarges and occludes the lumen of a blood vessel
The pathologic clot is now termed a thrombus what is produce
may produce pain, swelling in periphery; chest pain/heart attack
What is Three major factors predispose to thrombus formation;
endothelial injury, abnormal blood flow, and hypercoagulability.
These three factors influence one another and are collectively known as
Virchow’s triad
Endothelial injury is the dominant influence on what
thrombus formation in the heart and the arterial circulation (associated with atherosclerosis)
How can Endothelial injury impact
Can affect the veins – low flow, close to the valves e.g., deep vein thrombosis (DVT)
I possible causes of endothelial injury
Changes in shear stress associated with hypertension or
turbulent flow
• hyperlipidaemia
• elevated blood glucose in diabetes mellitus
• traumatic vascular injury, including atherosclerotic plaque
rupture and some infections
Hypercoagulability is generally less common, but can be an important factor in some patients; abnormally heightened coagulation response to vascular injury, resulting from either primary (genetic) disorders or secondary (acquired) disorders
How drug can help formation of thrombus
prevent and/or reverse thrombus formation fall into three classes: antiplatelet agents, anticoagulants, and thrombolytic agen
