CVS 2 and Blood Flashcards

Question

Venulues?

Answer 1

- capacitance vessels (store charge) - 20-200 microns - constrict in response to: 1. sympathetic stimulation 2. adrenaline 3. muscle and abdominal pumps

Answer 2

Occur by: diffusion - most important (98% of all exhange) - depends on 1. capillary permeability to substance (P) 2. capillary surface area (S) 3. concentration gradient (C outside - C inside) which is Fick's Law Rate of diffusion J = -PS(Co-Ci) filtration - movement of water between plasma and interstitial fluid - determined by rate and direction of H2O passage through pores - Starling forces transcytosis - least important

Answer 3

high - lipid-soluble - fatty molecules - steroid hormones moderate - small, charged particles (water, ions) poor - larged charged particles

Answer 4

Outward forces driving filtration: 1. hydrostatic pressure of blood in capillary (Pc) KEY FACTOR 2. interstitial fluid colloid osmotic pressure (πif) - substance which excerts highest osmotic pressure is protein (suspended in colloid) Inward forces: - hydrostatic pressure of interstitial fluid (Pif) - plasma colloid osmotic pressure (πp) Net filtration pressure (NFP) = [(Pc + πif) – (Pif + πp)] Starling equation Volume flux across capillary wall (Jv) = k[(Pc + πif) - (Pif + πp)] k (in Starling equation) is filtration co-efficient; reflects differing permeability of capillaries to water (no., size of pores) As sum of forces [(Pc + πif) – (Pif + πp)] is (NFP), therefore Jv = k x NFP Hydrostatic pressure of blood in capillary changes depending on where we are on the capillary bed!! Ideal capillary: - some only filter - some only absorb do EXAMPLES!!

Answer 5

- in caveolae and vesicles - the transport of large, lipid-insoluble molecules - venous end, muscle > lung > brain - caveola → vesicle → release - post-capillary venules - cavern/tunnel LOOK AT DIAGRAM!!

Answer 6

Lymphatic vessels: Capillaries - closed-end, highly permeable - large gaps between endothelial cells - only way protein can leave Vessels - similar to veins; thin layer of smooth muscle in wall - separated into segments (lymphangion) by valves Nodes (lymph nodes) - concentration of lymphocytes (white blood cells) and other immune system cells - phagocytic cells (macrophages) ‘clean’ lymph before it is returned to blood

Answer 7

1. motor cortex ("gotta run") 2. hypothalamus 3. cardovascular control centre 4a. sympathetic stimulation - increased rate - increased force - increased CO 4b. diversion of increased CO to muscle 4c. immediate vasodilation in muscle

Answer 8

1. metabolic dilation - increased flow - capillary recruitment - releases K+, adeonsine, CO2, lactate --> decreases pH Also: 2. local histamine release - vasodilation - increased capillary permeability - increased lymph flow 3. adrenaline release - increased cardiac outputt - dilation of coronary, muscle vessels - stretch receptors in muscle - reflex activation of CV centre 4. muscle pump - maintains venous return 5. temp increase - dilation of skin vessels - sympathetic stimulation of sweat glands

Answer 9

transport of: - nutrients - metabolites - excretory products - gases - hormones (e.g. adrenaline) - cells of a non-respiratory function (e.g. white blood) also: - transmission of force - coagulation - maintenance of cell homeostasis

Answer 10

- 8% of body weight - 3 types of specialised cell compartments 1. red cells (erythrocytes) 2. white cells (leukocytes) 3. platelets - all suspended in plasma (3L) What is in plasma? - 90% water - electrolytes - plasma proteins (7g%) - nutrients (waste products, hormones, gases) Albumins (4.5g%) - binds substances for transport through plasma - osmotic pressure for plasma - helps maintain plasma volume Globulins (2.5g%) - binding/transporting certain substances - contribute to blood clotting Fibrinogens (0.3g%) - blood clotting

Answer 11

Adults have ~7,000 white blood cells per microlitre of blood (7000/mm^3) Can be polymorphonuclear leukocytes/granulocytes: - have multilobed nuclei - formed in bone marrow - released into circulation when required - protects body against invading organisms These include: 1. Neutrophils (not stained) - can clearly see multilobed nuclei - 50-80% - phagocytic cells - engulf/digest microorganisms, abnormal cells, etc. - chemotaxic (migrates to chemicals produced by inflamed tissue) Neutrophilia - 5x increase in number of neutrophils - substances produced by inflamed tissue enters blood stream, transported to bone marrow and stores neutrophils to circularing blood 2. Basophils - blue dye - dense granules, nucleus is difficult to see - <4% -non-phagocytic - release toxic molecules that damage invaders - release histamine, heparin, etc into blood which contribute to allergic reactions 3. Eosinophils - red dye - granules in cytoplasm (pink) - 1-4% - phagocytic - attach to parasites and release toxic substances from granules - defence is weak and may be harmful OR/ Can be agranulocytes: - single, large non-segmented nucleus (few granules) Include: 1. Monocytes - generally larger cells - kidney-shaped nucleus - 2-8% - spend 10-20 hours in blood transit to target tissue - in tissue, they become macrophages - very phagocytic - can be fixed or wandering - first line of defence - dead neutrophils, dead macrophages, etc. = pus 2. Lymphocytes - round nucleus (occupies most of cell) - 20-40% - derived from lymphoid stem cells in bone marrow - function in immune system - live for 100-300 days In immune system - B lymphocytes produce antibodies which target antigens - each antigen stimulates B lymphocytes to secrete antibodies, which target it for later destruction - T lymphocytes don't prodyce antibodies, directly destroy cells (cell-mediated immune response) - null cells are large granuluar lymphocytes, function in nonspecific defence similar to T

Answer 12

Glandular fever Infection with Epstein-Barr virus - infectious mononucleuosis Leukopenia/agranulocytosis - bone marrow stops producing WBC - allow invasion by resident bacteria Leukaemia - greatly increased numbers of abnormal white cells - most WBC are myeloblasts or immature leukocytes - some nucleated red blood cells also present

Answer 13

All takes 5-7 days 1. Proerythroblasts 2. Basophilic erythroblast 3. Polychromatic erythroblast 4. Reticulocyte 5. Mature red blood cell - down the line, they become smaller - becomes pinker with increasing amounts of haemoglobin - nuclear chromatin becomes progressively more condensed - nucleus is extruded, producing a reticulocyte (RNA, capable of synthesising haemoglobin)

Answer 14

Control of erythropoiesis - state of tissue oxygenation is basic regulator of red cell production - any condition that causes quantity of O2 transported to tissues will increase production of RBC - major factor is not concentration of RBC but functional ability to transport oxygen Factors that decrease oxygenation 1. haemorrhage 2. destruction of bone marrow 3. high altitudes 4. disease of circulation (e.g. cardiac failure) 5. pulmonary disease Erythropoietin (EPO) - stimulates erythropoiesis - 90% found in liver - stimulates production of proerythroblasts from myeloid committed stem cells in bone marrow - causes cells to pass more rapidly through different erthyroblast stages so production of new cells is sped up - production of cells continues as long as person remains hypoxic or until enough red blood cells are produced - testosterone increases basal rate of ethropoiesis by raising level of EPO secretion

Answer 15

Vitamins B12 (cobalamin) & folic acid - essential for DNA production in red cells Folic acid - found in leafy plants, yeast & liver - easily destroyed by cooking B12 ‐ water soluble, only in animal products - only absorbed from intestine bound to intrinsic factor ‐ a glycoprotein released by cells in stomach - stored in liver - released to bone marrow & other tissues - minimum amount of B12 required each day – 1‐3g - normal store about 1000x this amount Iron (liver & bone marrow) - 4-5g - 65% haemoglobin - 4% myoglobin - 15-30% stored in liver - 10% absorbed into blood - Fe2+ ions absorbed easier than Fe3+ ions, aided by vit C - free iron bind with apotransferrin to form transferrin Can destroy erthrocytes - after 120 days, destroyed in spleen; phagocytosed by macrophages - haemoglobin is catabolised

Answer 16

- deficiency of haemoglobin 1. nutritional anemia - iron deficiency (microcytic), B12/folic acid deficiency (megaloblastic) 2. pernicious anemia - lack of intrinsic factor -> B12 deficiency (megaloblastic anemia) 3. haemorrhagic anemia - blood loss 4. aplastic anaemia - bone marrow failure (e.g. radiation) 5. haemolytic anaemia - fragile RBC (e.g. spherocytosis, sickle cell, thalassemia)

Answer 17

Antigens: A or B, A = Type A B = Type B A and B = Type AB (universal recipient, no antibodies) Neither = Type O (universal donor, anti-A and anti-B antibodies) Antibodies in plasma Anti-B = A Anti A = B Neither = AB Both = O Antibodies - develop after birth from food and bacteria exposure Incompatibility - recipient antibodies attack donor antigens - causes agglutination, transfusion reaction

Answer 18

- Either Rh + (81% of Australias) - or Rh - (no Rh antigen) Antibodies: Rh– individuals develop anti-Rh antibodies after exposure (e.g., transfusion, pregnancy) Erythroblastosis Fetalis (Hemolytic Disease of Newborn): - Rh– mother, Rh+ baby → mother’s antibodies attack baby’s RBCs. - affects later pregnancies (3% second baby, 10% third). Symptoms: - anemia - jaundice - brain damage (bilirubin) Prevention: - inject Rh antibodies into mother post-delivery to destroy fetal RBCs before immune response

Answer 19

Haemostasis - to stop bleeding, body's clotting mechanism - veins contain blood at lower pressure so venous bleeding is less rapid/more easily controlled Steps: 1. Vascular spasm - vessel wall contraction from pain, smooth muscle spasm or chemical factors from traumatised tissue - platelets release thromboxane A2 and serotonin 2. Formation of platelet plug - platelets adhere to exposed collagen, swell and release ADP, serotonin and thromboxane A2 - ADP makes platelets sticky -> aggregation -> plug - prostacyclin (from endothelium) limits plug to injury site - small hole - plug can stop blood loss - large hole - blood clot + plug is required 3. Formation of blood clot through coagulation - blood into solid gel/clot/thrombus - consists of fibrin - clotting occurs around platelet plug, solidifying blood remaining in wound channel 4. Clot retraction - platelets contract (actin/myosin), pull vessel edges together, exude serum 5. Replacement of clot with fibrous tissue or dissolution - replaced by fibrous tissue (fibroblasts, 1–2 weeks) or dissolved (plasminogen → plasmin via tissue plasminogen activator, digests fibrin)

Answer 20

1. Prothrombin activation formation Intrinsic pathway: - Factor XII activated by collagen → cascade (XII (Hageman)→ XI → IX → X) → prothrombin activator (1–6 min) Extrinsic pathway: - Tissue factor (from damaged tissue) → Factor III & IV → extrinsic thromboplastin activates factor X → prothrombin activator (15 sec) 2. Formation of thrombin - Prothrombin → thrombin (via prothrombin activator) 3. Formation of fibrin - Fibrinogen → fibrin (via thrombin); fibrin mesh traps cells, forms clot - creates meshwork of fibrin fibres, which creates a clot that adheres to damaged vessels

Answer 21

- formed in bone marrow (megakaryocytes) - 200,000-500,000 per cubic milimetre - no nucleus, contain granules (ADP, serotonin, thromboxane A2) - adhere to damaged vessels to form a plug

Answer 22

Vitamin K deficency - needed for clotting factors - caused by liver disease, bile blockage - causes bleeding disorders Haemophilia - genetic (X-linked recessive) - Type A (80%): lack factor VIII - Type B: lack factor IX Symptoms: - uncontrolled bleeding - bruising - joint/muscle hemorrhage Treatment: - replace missing factors VIII or IX Thrombocytopenia - low platelets (<50,000/microlitres) Symptoms: - bleeding from small vessels, petechiae Causes: - cancer - infections, autoimmunity (idiopathic thrombocytopenic purpura) Treatment: - platelet transfusion for severe cases

Answer 23

Thrombus - abnormal clot in vessel Embolus - free-dloating clot (e.g. stroke, pulmonary embolism) Causes: - immobility - genetics - smoking - high cholesterol - obesity - diabetes - stress - atherosclerosis - slow blood flow Treatment - anticoagulants to restore flow - remove thrombus/embolus

Answer 24

Aspirin - inhibits thromboxane A2 - which reduces platelet aggregation (300mg/day) Warfarin - inhibits vitamin K activation - lowers clotting factors (e.g. prothrombin) - decreases coagulant activity of blood to 20% of normal within 24 hrs Intravenous heparin (IV) - produced by basophils & mast cells - activates antithrombin III - inactivates thrombin, factor X - increases clotting time 5x - destroyed by heparinase Thrombolytic therapy - t-PA/streptokinase --> activates plasminogen --> plasmin --> dissolve clots

Answer 25

Silicone - prevents platelet factor/factor XII activation Heparin - used outside body - calcium binders (e.g. oxalate, citrate) - binds Ca2+ to prevent coagulation