Blood Flashcards
2 main components of blood
Plasma (55%)
Formed Elements (45%)
6 components of plasma
proteins
amino acids
wastes
nutrients
gases
electrolytes
Formed Elements
Includes erythrocytes (red blood cells), leukocytes (white blood cells) and platelets.
Function of Erythrocytes (Red Blood Cells)
- Deliver Oxygen to Cells
- Remove Carbon Dioxide from Cells
Function of Leukocytes (White Blood Cells)
- Defends the body from diseases (foreign pathogens, toxins, bacteria).
- Divided into granulocytes and agranulocytes.
Granulocytes
- Cytoplasm CONTAINS very fine granules .
- Consist of neutrophils, basophils and eosinophils.
Agranulocytes
- Cytoplasm DOES not contain granules .
- Consist of lymphocytes and monocytes.
Neutrophils
Recognise, engulf snd destroy pathogens via phagocytosis
Release preformed granules ( hydrolytic enzymes, antimicrobial
proteins).
Eosinophils
- target extracellular pathogens that are too large to be engulfed by phagocytosis eg. parasites
- Facilitate allergic Reactions
Basophils
Contains granules of histamine which are released to initiate an allergic response
Lymphocytes
Specialised WBC that defends against specific pathogens
7 Function of Platelets
- Secrete vasoconstrictors that constrict blood vessels when damaged
- Form temporary platelet plugs to stop bleeding
- Includes clotting factors to promote blood clotting
- Dissolve blood clots when no longer needed
- Digest and destroy bacteria
- Secrete chemicals that attract neutrophils and monocytes to sites of inflammation
- Secrete growth factors to maintain the lining of blood vessels
What happens if there are too few red blood cells
- Reduced oxygen carrying capacity
- Increased risk of hypoxia (oxygen deprivation)
What happens if there are too many red blood cells
- Increases blood viscosity
- Increases resistance to flow through blood vessels
- Increases risk of blood clotting
Steps for Feedback Loop of RBC
- Stimulus: Decrease O2 carrying ability.. Due to ..
- Decreased RBC Count
- Decreased amount of haemoglobin
- Decreased availability of O2 - Receptors: Receptors in the Kidney respond to low oxygen levels.
- Kidney’s increase EPO secretion into the bloodstream.
- EPO circles in higher numbers. - Control Center: Stimulates proerythroblasts activating bone marrow to produce reticulocytes (immature RBC).
- Effectors: Reticulocytes enter circulating blood resulting in a larger number of red blood cells in circulation.
- Response: Increased oxygen delivery to tissues
- Return to homeostatic levels.
3 Steps in Haemostasis
- Vascular Spasm
- Platelet Plug Formation
- Coagulation
Vascular Spasm
- Blood vessels respond to injury by contracting (vasoconstriction)
- Acts to decrease blood flow to the area of injury (restricts blood loss) enabling for other steps of
haemostasis to occur
Platelet Plug Formation
- Occur via a positive feedback cycle.
- Platelets come into contact with exposed collagen.
- Platelets adhere to exposed collagen. Platelets develop
pseudopods - Cytokines are released (Thromboxane, ADP, 5HT)
- Cytokines activates and attract more platelets to the site
of injury - More platelets aggregate into the region resulting in
formation of plug - Act through positive feedback loop to activate more
platelets
Coagulation
Phase 1:
- Both pathways are triggered by tissue damaging events and vitamin K is necessary for normal clotting factor production
- Both pathways lead to production of factor X
- Intrinsic (slower) = activated by injury that occurs within the blood vesse. This begins the activation of factor XII (12)
- Extrinsic (Faster) = Activated by exposed blood to tissue (RELEASES, factor 7). Production of factor X that similarly produces prothrombin activator
Phase 2: Common Pathway to Thrombin
- The production of factor X and Prothrombinactivator cleaves Prothrombin to Thrombin. 3.
Phase 3: Common Pathway to Fibrin Mesh
- Thrombin catalyses the transformation of Fibrinogen to Fibrin.
- Fibrin molecules band together to form long hair-like insoluble strands
- Glue platelets together to form a structural web
- In presence of calcium, factor XIII (crosslinking enzyme), tightly binds fibrin to stabilise the fibrin
mesh.
Fibrinolysis
- Process that removes unneeded clots when healing has occurred
- Crucial process as clots continually form and need to be degraded to prevent clogging of blood vessels
Antithrombotic Drugs
- reduce the formation of blood clots
- For Example: Warfarin, and Aspirin
Warfarin Action
Warfarin blocks Vitamin K epoxide reductase, and prevents the activation of the vitamin K related factors such as prothrombin which is involved in clotting cascade.
Aspirin Action
- Aspirin blocks cyclooxygenase enzymes, preventing the release of thromboxane.
- Decreases the amount of platelet activation and aggregation.
Monocytes
Monocytes in blood differentiate into macrophages
HAEMOSTASIS
A mechanism that leads to the cessation of bleeding from a blood vessel.
Fast, localised and controlled.
STEPS OF HAEMOSTASIS:
(1) INJURY TO THE BLOOD VESSEL
- causes disruption to the endothelium, exposing the connective tissue under the endothelium.
- Causes collagen fibres to be exposed to blood and platelets.
(2) PLATELET PLUG FORMATION
- Platelets resultantly become activated (because of exposure to collagen fibres).
- Platelets RELEASE ADP, which activates other platelets.
- Causes platelets to swell and stick together to form a plug – positive feedback cycle.
- Reduces the blood loss at the site of injury.
(3) COAGULATION (process of a liquid changing to a solid/semi-solidstate.)
- Fibrin forms a mesh that traps RBC and platelets, allowing the formation of a clot.
- Activation of Fibrogen to fibrin. Fibrin covalently linked mesh that
contracts and retards RBC movement.
- COAGULATION CASCADE – release of clotting factors. Blood goes from liquid to a gel.
