Blood, Hemostasis, and Lymphatics Flashcards
1
Q
What are characteristics of an erthyrocyte?
A
- biconcave disc; greatest SA to volume ratio of a simple shape (nucleus is ejected during development which leaves this shape)
- strong, flexible membrane
- no nucleus (no DNA)
- lack mitochondria; generate ATP anaerobically (constantly regenerating these because they can’t repair themselves)
- hemoglobin
2
Q
What is hemoglobin? Where is it most highly saturated? What conditions increase the release of oxygen?
A
- polypeptide chains; two beta and two alpha chains for a total of 4 chains
- each chain connects to iron-containing heme group
- iron combines reversibly with oxygen; means that it can offload oxygen once it is attached to it
- 97% saturation at the lungs of hemoglobin, 75% at tissue
- in times of higher oxygen demands, more oxygen can be released (eg. when body temp goes up, increase in CO2, decrease in pH)
- increase in CO2 and decrease in pH happens in metabolically active tissue which allows for the offloading of oxygen
- tissue oxygen buffer system helps to maintain the partial pressure of oxygen in the tissues
3
Q
Where is oxygen saturation the greatest in the circulation?
A
- greatest in systemic arteries
- decreases with deoxygenated blood in systemic veins
- curve can be shifted under various conditions; red line indicates easier oxygen offloading
4
Q
Describe the process of erythropoiesis
A
- starts as pluripotent stem cell
- differentiates into myeloid stem cell then further differentiates into a proerythroblast
- nucleus is ejected and becomes a reticulocyte
- reticulocytes enter the bloodstream from red bone marrow through sinusoid capillaries
- takes 1-2 days for erythrocyte to mature
5
Q
Describe the life cycle of an erthyrocyte. What causes anemia?
A
- production occurs in bone marrow (axial skeleton, ribs, pelvis, in infant it will also occur in long bones)
- last 120 days before they are damaged or ruptured
- liver and spleen play a role in phagocytosis and recycling some of the products from the degradation (particularly iron)
- anemia may result if destruction>production
-liver damage may lead to jaundice
6
Q
What stimulates red blood cell production? How can kidney damage affect this?
A
- hypoxia- body is looking for ways to meet oxygen demand by body tissues
- hypoxia can result because of lack of RBCs (blood donation)
- kidney releases erythropoietin to stimulate bone marrow to produce more RBCs
- this increases oxygen carrying capacity of system
- with kidney damage, might not be able to release enough erythropoietin and meet the oxygen demands so in this case injections of erythropoietin may be given
- decreased perfusion to the kidney; kidney senses lower oxygen levels because kidney perfusion itself is reduced so as a result it will release erythropoietin
7
Q
How does the ABO blood typing system work?
A
- red blood cells have antigens on them
- antigen: any substance that causes an antibody response to be generated
- antibodies are floating in plasma
- ABO system looks at which antigens are present on the red blood cells
8
Q
What antigens/antibodies are contained in Type A blood?
A
- RBC has A antigen
- anti-B antibody in plasma
- in the plasma we don’t have an antibody that reacts against antigen on the RBC because this would be incompatible
9
Q
What antigens/antibodies are contained in Type B blood?
A
- B antigen
- anti-A antibody
10
Q
What antigens/antibodies are contained in Type AB blood?
A
- A and B antigens
- neither antibody
11
Q
What antigens/antibodies are contained in Type O blood?
A
- neither A nor B antigen
- both anti-A and anti-B antibody
12
Q
How can blood typing be conducted to determine blood type?
A
- take a blood sample and mix with different antisera which contain the antibody
- if you treat a type A blood sample with anti-A serum, you get agglutination reaction where RBCs clump together and on reaction with the anti-B serum
13
Q
What is cross matching?
A
-take a donor’s red blood cells and mix them with a patient’s serum to see if there is a reaction
14
Q
What is screening?
A
- recipient’s serum is tested against a panel of red blood cells
- based on which blood cells it reacts with you can determine the type
15
Q
What is hemolytic disease of newborn?
A
- if an individual is pregnant and is Rh-, and fetus is Rh+ at birth there is a possibility of a leak between fetal and maternal circulation so Rh+ RBCs will enter into Rh- individual
- as a result, this individual will start to develop antibodies against these Rh+ RBCs
- for Rh- individual it is not a problem because they don’t have Rh+ RBCs
- it becomes a problem at a subsequent pregnancy if the next fetus is Rh+, the antibodies in Rh- individual could pass to the second fetus and attack RBCs of the newborn
- can administer RhoGAM to bind up the antibodies in the Rh- prior to subsequent pregnancies
16
Q
What are compatible blood donors for each blood type?
A
24
Q
What occurs during platelet plug formation?
A
- platelet adhesion to collagen fibres and damaged endothelium
- activation: liberated ADP, serotonin, and thromboxane A2
- ADP makes platelets stick together and also acts as a vasoconstrictor along with thromboxane A2
- platelet aggregation
26
Q
Describe the positive feedback of blood clotting
A
- Broken blood vessel with exposed binding sites for platelets (stimulus)
2a. Platelets bind to the blood vessel (detectors)
2b. Binding of platelets to blood vessel leads to activation of the platelets (control centre) - Platelets release substances which attract more platelets (effectors)
- Platelets attract further platelets- effectors now provide the stimulus
- Platelets plug up the whole and growth of clot is limited by anticlotting chemicals like prostacyclin and prostaglandin I2 and the absence of binding sites
27
Q
Describe the pathways that start clot formation.
A
Extrinsic (outside of blood vessel):
- rapid
- tissue trauma which releases tissue factor (thromboplastin)
- in the presence of calcium it becomes activated 10
- in the presence of factor 5 and calcium, activation of prothrombinase
Intrinsic (inside the blood vessel eg. damage to endothelium):
- longer
- release of activated 12 and activated platelets
- in the presence of calcium and platelet phospholipids, activated 12 is converted to activated 10
- in the presence of platelet phospholipids and factor 5 (in presence of calcium), results in activation of prothrombinase
28
Q
Describe the common pathway
A
- prothrombinase in the presence of calcium converts prothrombin to thrombin
- thrombin is key to formation of insoluble fibrin
- thrombin with calcium acts on fibrinogen (soluble) to make loose fibrin threads (insoluble)
- factor 13 will be activated, activated 13 will help make loose fibrin threads into strengthened fibrin threads
36
Q
How does lymphatic system drain interstitial fluid?
A
- lymphatic capillary is in interstitial space
- lymphatic capillary is thin walled, has many valves
- single layer of endothelium
- anchroing filaments
- excess buildup of fluid will pull on the anchoring filaments which will start to open the spaces between the endothelial cells which allows fluid to move into lymphatic capillaries
- lymphatic capillaries have some smooth muscle to help it move through
39
Q
What is the main lymph drainage route?
A
- drainage into cisterna chyli then left thoracic duct
- enters back into cardiovascular system at the junction between the internal jugular vein and the subclavian vein
- right lymphatic duct comes from upper body and enters cardiovascular system at junction between right internal jugular vein and right subclavian vein
