Lecture 18: Bkood Flashcards
1) Plasma
What does it contain?
What is the function of plasma proteins?
Water Nutrients Wastes Dissolved gases Salts Plasma proteins
Functions of plasma proteins: -Transport eg hormone-binding proteins) -buffers pH -immunity -blood coagulation (fibrinogen ➡fibrin) -produce osmotic pressure (especially albumin) Eg slide 7
List the major components of blood
Erythrocytes (red blood cells)
Platelets (cell fragments ➡clotting)
Leukocytes (white bc)
Plasma (fluid)
Plasma vs Serum
Serum = fluid from clotted blood
- plasma minus blood cells, platelets, plasma clotting proteins
- clear, thin, sticky
- they can be stored for research (contains antibodies)
Production of blood cells and platelets
Look at slide 9 and learn it
Erythrocytes (red blood cells)
What is their function
What is their anatomy?
Function:
- major function is to transport O2 to tissues and CO2 away from tissues
- constitutes more than 90% of all blood cells
- lasts 120 days in circulation
Anatomy:
- no nucleus
- no cell division so can’t replicate them selves
- no DNA or RNA so no protein to repair tissue damage
- no organelles
- including mitochondria so no aerobic metabolism
- sacs of haemoglobin
- pigmented protein
Erythrocyte function: O2 and CO2 transport
Has transport reactions are reversible ➡ uptake and unloading of gasses in tissues and lungs
Oxygen reversibility binds to heme groups of hemoglobin
Hb + O2 ➡⬅ Hb.O2
Carbon dioxide and water reversibly converted to carbonic acid by carbonic anhydrase (CA) enzyme
CO2 + H20 ⬅CA➡ H2CO3 ⬅➡ H+ + HCO3-
Carbon dioxide can also bind with haemoglobin (completes O2)
Both gases also dissolve in plasma, small proportion but important for tissue exchange
Hemoglobin
Hb is a protein made up of one globin groups (4 polypeptide chains) and 4 heme groups
-each polypeptide chain has one heme group, which contains one iron ion (Fe2+ that can bind one O2 molecule)
-colour depends on O2 saturation (pink when saturated, dark bluish-red without oxygen)
Hb concentration quite constant, erythrocyte number mainly determines gas carriage)
Erythrocyte production
Mature RBC cannot replicate or repair themselves
Need constant replacement
How?
Kidney (reduced O2 transport leads to increased secretion of erythropoietin (EPO) ➡ EPO ➡ bone marrow (increased erythrocyte production ➡ blood (increased number of circulating erythrocytes. Increased O2 transport
Erythrocyte production is determined by tissue oxygen, not erythrocyte number
Nutrition and erythrocyte production. What should you be consuming to allow for normal erythrocyte production?
Iron:
- component of hemoglobin
- efficiently recycled, released from heme during destruction of ageing erythrocytes
- transported in the blood by transferrin complex (iron + protein)
- stored in liver, spleen, bone marrow
- used in bone marrow to make new hemoglobin
- dietary intake required to match iron loss through urine, sweat, intestinal and skin cells
Folic acid
Vitamin B12
Both necessary for DNA replication therefore cell replication
Filtering and destruction of erythrocytes
What 2 structures are involved and what do they do?
Spleen
- filters old erythrocytes
- broken into components by macrophages (iron, bilirubin, amino acids)
Kidneys: -excrete 5% of bile in urine Liver -metabolises bilirubin ➡ bile GI tract -excretes 95% of bile in faeces
Jaundice = unusually high level of plasma bilirubin
-causes include excessive erythrocyte destruction, failing/ immature liver, blocked bile duct between liver and intestine
The hematocrit
What effects it?
What are the outcomes if it is high or low?
Hematocrit= % packed erythrocytes by volume
It is an indicator of the oxygen carrying capacity of the blood
Normal range = 37-52
Influenced by sex, age, physical activity, nutrition, lactation, altitude, emotional state
Sympathetic activity mobilises erythrocytes from spleen ➡ increased haematocrit
Increased hematocrit ➡ increased blood viscosity ➡ increased resistance to blood flow (makes heart work harder)
Anemia
What is it?
How does it come about?
Anemia= decreased in oxygen carrying capacity of the blood
Anemia usually caused by insufficient erythrocytes or insufficient iron
Erythrocyte ➡ hemoglobin molecule ➡ heme ➡ iron atom ➡ oxygen molecule
Explain the erythrocyte deficiency kind of anemia
Insufficient production of erythrocytes
- deficiency of vitamin B12/folic acid ➡ inadequate DNA synthesis and stem cell division (pernicious anemia)
- reduced erythropoietin in kidney disease ➡ reduced production of RBCs (renal anemia)
- bone marrow defect eg after chemotherapy, radiation (aplastic anemic)
Excessive loss or destruction of erythrocytes (production can’t keep up)
- bleeding
- increased RBC destruction (haemolytic anemia)
- antigen-antibody binding
- fragile erythrocytes ➡ increased destruction in capillaries
- malaria
- sickle cell anemia
Explain the iron-deficiency anemias
Insufficient iron intake
-dietary insufficiency (dietary anemia)
-reduced GI absorption
Excessive iron loss (reduction in iron recycling)
-increased loss due to bleeding, GI ulcers, GI tumours, heavy menstruation
Anemia and cardiac output
Some anemias are associated with reduced numbers if erythrocytes
Up to a point, decreased oxygen transport is compensated by increased blood flow.
Check out slide 20
Leukocytes (white blood cells)
Types?
Function
Anatomy
Five types: lymphocyte, monocyte, basophil, eosinophil, neutrophil
Overall function is body defence:
-defend against pathogens
-identify and destroy cancer cells
-phagocytosis of debris from dead or injured cells
Transported in blood but perform most functions in tissues
All have nucleus, organelles but no pigment
Present in blood (small numbers), bone marrow and tissues
-infection ➡ increased production of Leukocytes and massive release if Leukocytes from marrow into blood
Memorise the shit out of slide 22
Important
Platelets
- Smallest cell-like structures in blood, do not move out of the blood
- no hemoglobin (no pigment), no nucleus (no mitosis), some organelles, actin and myosin (contraction)
- main function is hemostasis
- produced in bone marrow, break off from cytoplasm of megakaryocytes
- stored in spleen, sympathetic activation ➡ contraction of spleen capsule ➡ mobilisation
- destroyed macrophages after approx 10 days
Blood cell summary
Learn slide 24
Do it
Hemostasis
What is it
It is cessation of bleeding after injury to a blood vessel
Inadequate hemostasis ➡ hemorrhage after minor injury
Excessive hemostasis ➡ excessive formation of blood clots
Hemostasis involves 3 main steps:
Vascular spasm
Platelet plug formation
Clot formation
Hemostasis
A) vascular spasm
Vascular spasm= contraction of an injured blood vessel
-function is to reduce blood loss until plug/clot is formed
-contraction of vascular smooth muscle ➡ increased resistance ➡ decreased blood loss
Extensive injury ➡ maximal vascular spasm
Contraction is cause by:
- sympathetic activation
- intrinsic vascular response (damage tissue releases vasoactive substance)
- response of smooth muscle cells to mechanical impact
Hemostasis
B) platelet plug formation
After tissue damage, platelet plug forms around damaged site to prevent blood loss
Refer to slide 27 for a more detailed explanation
Real platelets:
Hemostasis
C) blood clott formation
Blood is converted into a solid gel called a blood clott
(Clotting = coagulation, clot = thrombus
Refer to slide 29 (must)
Fibrinogen, thrombin and factor XIIIa present in plasma in inactive form (coagulation factors) ➡ require activation (by coagulation cascade) prior to clot formation.
Describe the coagulation cascade- intrinsic and extrinsic coagulation pathways
Intrinsic pathway
- mediated entirely by factors within the blood
- clotting occurs when blood contacts non-endothelial tissue (collagen, glass, plastic)
Extrinsic pathway:
- requires factor III from damaged tissue.
- proceeds rapidlym triggers the intrinsic pathway
- important for clotting outside vessels
Final common pathway:
Both activate factor X ➡ thrombin activation ➡ fibrin stabilisation (clot)
Factors limiting blood clot formation
Thrombomodulin
- forms complex with thrombin
- prevents thrombin from converting fibrinogen ➡ fibrin
- instead, complex activates anticoagulants that inhibit intrinsic and extrinsic pathways
Tissue factor pathway inhibitor:
-inhibits the extrinsic coagulation pathway
Anticoagulants:
-endothelial surface and plasma proteins
Healthy endothelial cells actively prevent both platelet plug formation and blood clot formation.
Dissolving a clot
Requires another cascade initiated by exposure of collagen
Stuff to look at on slide 32
Fibrinogen makes clot fibrous, plasminogen reverts clot back to plasma.
What are some alteration to hemostasis? Eg hemophilia?
Hemophilia:
- reduce clotting
- usually lack of factor VIII
Von willebrands disease:
- reduced platelet plug formation
- low level of vWf
- secondary effect on factor VIII, reduced clotting
Aspirin:
- low doses inhibit thromboxane A2 formation➡ reduced plug formation
- high doses inhibit prostacyclin ➡ increased plug formation (and clotting risk)
