Blood and Inflammation Flashcards
Erythropoietin
Protein drives RBC differentiation
Erythropoietin released from kidneys in response to hypoxia (e.g. oxygen deficiency secondary to haemorrhage, loss of RBCs, insufficient haemoglobin, reduced oxygen, increased demands)
Erythropoietin → stimulates rapid maturation of committed RBCs, increased circulating reticulocyte count within 2 days (testosterone enhances production -> higher RBC count in males
ERYTHROPOIESIS
(RBC differentiation)
Requires Vitamins B12 & B9
Iron deficient Anaemia;
Most common causes
- Parasites
- Dietary deficiency
- Blood loss
- Malabsorption
- Pregnancy
Signs and symptoms:
- Fatigue
- Pale appearance
- Shortness of breath
- Irritable
- Light headed
- Glossitis/red beefy tongue
- Recurrent mouth ulcers
- Candida infections -> Angular cheilosis
- Poor wound healing
- Burning mouth symptoms
WBCs
= leukocytes, leave blood stream via diapedesis
[Never Let Monkeys Eat Bananas] - (greatest proportion to least)
Haemostasis
= Prevention of blood loss; whenever a vessel is severed or ruptured, haemostasis achieved by several different mechanisms:
- Vessel Injury
- Vascular Spasm
- Platelet plug formation
Platelets adhere to damaged endothelium (platelet plug) and degranulate. Plug activation is regulated by Von Willebrand Factor (found in plasma). Platelets adhere to the collagen fibers in the wound, becoming spiky and sticky. They release chemicals (ADP, serotonin) causing more platelets to stick to the plug and cause further vasoconstriction creating a feedback loop. Clotting factors become activated and begin deposition of fibrin, creating a meshwork. - Coagulation
Coagulation reinforces the clot, which is formed by the transformation of soluble fibrinogen → insoluble fibrin. RBCs and platelets stay trapped in the mesh.
Thrombus
clot that develops and persists in an unbroken blood vessel
- May block circulation, leading to tissue death
Embolus
- Pulmonary emboli impair body’s ability to obtain oxygen
- Cerebral emboli can cause strokes or transient ischaemic attacks (TIA – temporary disruption in blood supply to part of the brain)
- Cardiac emboli can cause MI (myocardial infarction)
Thromboembolism
Deep vein thrombosis
Immobility → high risk .’. put on prophylaxis (measure taken to maintain health and prevent disease/the spread of)
- Aspirin: Antiprostaglandin, inhibits thromboxane A2
- Heparin: Anticoagulant, used clinically for pre and postoperative cardiac care
- Warfarin: used for those prone to atrial fibrillation
- New agents becoming available e.g. Rivaroxaban (Factor Xa inhibitor)
Thrombocytopenia
= too few platelets
- Causes spontaneous bleeding
- Due to suppression or destruction of bone marrow (e.g. malignancy, radiation)
- Platelet count
Impaired liver function
– liver produces vitamin K which produces essential clotting factors
- Impairs ability to produce procoagulants e.g. Vitamin K (necessary for Prothrombin, factor 7, 9, 10)
- Causes are vitamin K deficiency, Hepatitis, cirrhosis, injury
Von Willebrand Disease
- Most common hereditary coagulation disease
- Type 1 (autosomal dominant), Type 2 (autosomal dominant), Type 3 (autosomal recessive), Platelet type (autosomal dominant)
- Deficiency of VWF found in plasma and subendothelial connective tissue; von Willebrand factor mediates the binding of glycoprotein Ib (GPIb) to collagen. This binding helps mediate the activation of platelets and formation of primary hemostasis.
Haemophilias
(group of hereditary genetic bleeding disorders that impair the body’s ability to control blood clotting)
- Symptoms: Prolonged bleeding, especially in joint cavities
- Treated with plasma transfusions and injection of missing factors
- 2 most common deficiencies are factor VIII (A = 1/5000 males) and IX (B 1/30,000 males)
- Both X-linked recessive with occasional spontaneous mutations – affects more males than females
Blood Groups
Based on presence of 2 major antigens in RBC membranes; A and B.
Rhesus Factor
Rh+ 85% dominant in population
Rh- 15% recessive
Describes presence of Rhesus antigen D
Haemolytic disease of newborn – Rh+ foetus, Rh- mother, can lead to anti-rhesus antibodies from mother attacking the foetal blood cells causing haemolytic anaemia .’. RhoGAM test at 28 weeks
Plasma
Components: 90% Water 8% solutes: PROTEINS: Albumin (60%), Alpha/Beta/Gamma globulins, Fibrinogens GAS ELECTROLYTES =Transport Medium ORGANIC NUTRIENTS: Carbohydrates, amino acids, lipids, vitamins HORMONES METABOLIC WASTE: CO2, Urea etc.
