Lecture 9 - Blood Flashcards
What is the movement of O2 in the body?
from blood to tissues
What is the CO2 movement in the body?
from tissues to the blood
What is the blood made of?
-formed elements (45% mostly RBC)
-plasma (55%)
What are the formed elements in blood?
-erythrocytes (RBCs)
-leukocytes (WBCs)
-platelets
What does hematocrit mean?
the # RBCs in the total volume of blood
What should the blood pH be?
7.35-7.45
What is the temperature of the blood?
38º C, warmer than the body temp
Average blood volume
-male
-female
-5-6L
-4-5L
What is the general pathway for O2 distribution by the blood?
from lungs to heart to target
How do nutrients get distributed by the blood?
the digestive tract to target
How does metabolic waste get distributed by the blood?
lungs and kidneys to the esophagus to uruter
How do hormones get distributed by the blood?
from endocrine glands to target
What does blood regulate?
-body temp
-pH in tissues (bicarbonate ions)
-fluid volume (osmotic pressure)
What and how does the blood protect the body?
-blood loss = proteins + platelets clot to stop bleeding
-infection = antibodies, proteins, and leukocytes stop the spread of viruses
What are the main plasma proteins?
-albumin
-alpha globulins
-beta globulins
-y globulins
What are plasma waste products?
-lactic acid
-urea
-creatine
What are the plasma’s organic nutrients?
-glucose
-carbohydrates
-amino acids
What are the electrolytes found in the plasma? (5)
-Na+
-K+
-Ca2+
-Cl-
-H3CO2
State the 2 respiratory gases found in the plasma
-O2 & CO2
What is special about the structure of an erythrocyte?
has no nucleus
How do erythrocytes transport gas?
O2 binds to iron on the heme on the polypeptide of the hemoglobin
-always at full capacity
What is the erythrocyte plasma membrane made of?
spectrin
What makes an erythrocyte so flexible?
-spectrin, actin and myosin
How do RBCs not consume the O2 it carries?
The ATP of the RBC is made anaerobically
Why are hemoglobins not free in circulation?
many negative consequences
-increase osmotic pressure
-lose Hb to tissues
-increase blood viscosity
-damage kidneys
What is the structure of hemoglobin (Hb)?
1 Hb
= 2 alpha polypeptide + 2 beta polypeptide chains
= 4 heme groups
= 4 iron
= 4 O2
How does the affinity O2 affinity increase/decrease?
once one O2 bind/unbind, the affinity increase/decreases to bind/unbind the rest
What are oxyhemoglobin and deoxyhemoglobin?
-with O2 from lungs
-no O2 from tissues
What is carbaminohemoglobin?
a compound of Hb and CO2 where the CO2 binds to the peptide backbone
What does CO2 get converted to?
HCO3 in erythrocytes by carbonic anhydrase
What is the word for blood cell formation?
hematopoiesis
Where does hematopoiesis occur in the body?
-red bone marrow
=axial skeleton + girdles (hips)
=humerus + femur (largest bones)
How much hematopoiesis in mL is made a day?
30mL/day
What is erythropoiesis?
production of RBCs
What are the steps of erythropoiesis?
- hemocytoblasts (formed elements)
- proerythroblasts
- early erythroblasts (ribosome synthesis)
- late erythroblasts (Hb accumulation)
- normoblasts
- reticulocytes (ejection of the nucleus)
- erythrocytes
How long is the process of erythropoiesis?
15 days
What is it called when there are too few RBCs?
-tissue hypoxia
=run out of O2 in the tissues
What happens when there are too many RBCs?
-increase in blood viscosity
=make blood flow hard, too thick
How is erythropoiesis controlled and maintained?
-hormonally controlled (erythropoietin)
-relies on iron, amino acids, vitamin B
Where is erythropoietin made?
kidneys
Why would erythropoietin be released?
-hypoxia (O2 levels low, demand more O2)
What would an increased amount of erythropoietin do?
-increase RBCs in circulating blood
-increase O2 carrying ability
-increase reticulocyte count = rate RBC synthesis
What is the homeostatic response to low O2 levels in blood?
- kidney release EPO
- stimulate red bone marrow
- enhanced erythropoiesis = increase RBC count
- increase O2 carrying
- increase until normal
Why do dialysis patients become anemic?
no EPO is produced so there is no RBC production
What does erythropoiesis require to function?
-proteins, lipids, carbohydrates
-iron, vitamin B12, folic acid
Where does the body store iron?
-hemoglobin (65%)
-liver
-spleen
-bone marrow
Where is the intracellular iron?
-ferritin
-hemosiderin
Where is circulatory iron?
loosely bound to transferrin or eaten by haptoglobin
What is the lifespan of an erythrocyte?
100-120 days
Why do RBCs become rigid and fragile?
degeneration of backbone with no regeneration
Where do dying RBCs go?
trapped in spleen and eaten by macrophages
What happens to the heme of the hemoglobin when RBC is eaten?
- degraded to bilirubin
- liver bilirubin into intestine bile
- intestine bile metabolizes into urobilinogen
- urobilinogen to stercobilin feces leaves the body
What happens to the globin of hemoglobin when RBC is eaten?
-metabolized into amino acids and released into circulation
What happens to the iron from hemoglobin when RBC is eaten?
-salvaged for reuse, attach to ferritin and hemosiderin
What happens to the hemoglobin released into the blood?
captured and phagocytized by haptoglobin
What is anemia?
-erythrocyte disorder
-low O2 carrying ability
What are the signs/ symptoms of anemia?
-fatigue, paleness, shortness of breath, chills
What are the types of anemia where there is insufficient RBCs + explanation?
- hemorrhagic (acute/chronic blood loss)
- hemolytic (prematurely ruptured RBC)
- aplastic (destruct/inhibit red bone marrow)
What are the types of anemia where there is decreased hemoglobin content + explanation?
- iron-deficiency (loss iron, no intake, no absorption)
- pernicious (no B12, no intrinsic factor)
What are the types of anemia where there is abnormal hemoglobin + explanation?
- thalassemias (faulty globin of Hb)
- sickle-cell (defective gene)
What is polycythemia?
-excess RBC = increased blood viscosity
What are the 3 main polycythemia conditions + definitions?
- polycythemia vera = naturally make too much
- secondary polycythemia = smoker/burn victim
- blood doping/EPO abuse = drugs/ enhancers
What are leukocytes?
-white blood cells
-a complete cell that is <1% blood volume
-responds to bacterial or viral invasion
What are platelets?
-megakoryocytes
-clotting factors and enzymes
What regulates platelets?
thrombopoietin
What inactivates platelets?
nitric oxide (NO) and prostacyclin
What is the genesis of platelets?
-hemocytoblast
-megakaryoblast
-promegakaryocyte
-megakaryocyte
-platelet
How is blood homeostasis maintained?
- vascular spasms
-smooth muscle contract
-vasoconstriction - platelet plug
-collagen exposed
-platelet adhere - coagulation
-fibrin mesh
How is the platelet plug only formed where it is needed?
-Nitric oxide (NO) and prostacyclin (PGIs) stop spreading
-swift removal by normal blood flow
-inhibition of activated clotting factors
What are the steps to platelet plug formation?
- damage to blood vessel
- release von Willebrand factor (VWF) = adhere to collagen
- release thromboxane A2
- stick to exposed collagen
- release serotonin and ADP = attract more platelets
What kind of homeostatic process is the platelet plug formation?
positive feedback chain
What is the process of homeostatic coagulation?
- intrinsic/extrinsic pathway
- prothrombin activator (PA)
- prothrombin to thrombin
- thrombin catalyzes fibrinogen to fibrin mesh
What is special about the intrinsic pathway of coagulation?
-occurs in the blood itself
-occurs without the addition of anything
-small events
-multiple steps = slower
What is unique about the extrinsic pathway of coagulation?
-requires tissue factor
-for larger events and vessel damage
-less steps = much faster
Draw out the diagram of phase 1 of coagulation
-intrinsic
-extrinsic
-(X -> Xa)
-Ca2+, (V -> Va), PF3 (platelet factor 3) addition to Xa = prothrombin activator (PA)
Draw out phase 2 and phase 3 of coagulation
phase 2 [
-Prothrombin + PA = thrombin
]
phase 3 [
-Fibrinogen + thrombin = fibrin
-(XIII -> XIIIa)+ Ca2+ + thrombin + fibrin = cross-linked mesh
]
How does clot retraction work?
-pull together and stabilize the clot by squeezing serum out
What are the 3 clot repair options and how?
=promote healing vessel wall (platelet-derived growth factor)
=CT patch-up (fibroblasts)
=restore endothelial lining (vascular endothelial growth factor)
How does clot removal work?
-digestion = plasmin (plasminogen) which is activated by tissue plasminogen activator (tPA) and released by endothelial cells
What causes the inhibition of clotting factors? (2 things)
-fibrin + thrombin = anticoagulant
-antithrombin III = thrombin inactivator
What causes an increase in antithrombin III activity?
-heparin
What is the name of a common thromboembolic condition and its definition?
thrombus
-clot develops and persists in unbroken bv
-causes a block in circulation
What is the name of a type of thrombus?
embolus
-free floating thrombus in the blood
-can block and get stuck in smaller vessels
How do you prevent undesirable clots? (3 drugs)
-aspirin (inhibit thromboxane A2)
-heparin (inhibit thrombin)
-warfarin (inhibit vitamin K)
What is the bleeding disorder where there are insufficient platelets?
-definition
-cause
-symptoms
-treatment
=thrombocytopenia
-not enough platelets in circulation
-destruction/ suppression of bone marrow
-bruising
-whole blood transfusion
What is the bleeding disorder where there is an inability to synthesize procoagulants?
-definition
-cause
-symptoms
=liver disease
-inability to make procoagulants
-liver disease, no procoagulants synthesize, no absorb fat
-vitamin k deficiency, hepatitis and cirrhosis
What is a bleeding disorder where there is a lack of clotting factors?
-how is it passed down
-treatments
=hemophilias
A - no factor VIII (most common/ severe)
B - no factor IX (more severe)
C - no factor XI (mild type)
- A and B are X-linked, C is autosomal recessive
- blood transfusions, injection of missing factors
Why is hemophilia C a more mild form of the disease in comparison to Hemophilia A/B?
Hemophilia C lacks factor XI which is where the extrinsic pathway can help the intrinsic pathway.
Hemophilia A and B lack factors VIII and IX which cannot be helped and therefore cause a larger problem.
When are blood transfusions used?
-blood loss is substantial (15-30% weakness + 30% shock)
How do the human blood groups differ?
-by the presence or absence of glycoprotein antigens on the surface of the RBC membranes
-unique to the person
-foreign if transfused
-30 varieties
What blood groups are used for legalities?
M, N, Duffy, Kell, Lewis
For ABO blood groups where are the following located?
-antigens
-agglutinins (antibodies)
-antigens A/B located on the surface of RBC
-anti- A/B located in the plasma
Draw out the ABO blood group table
-blood group (4)
-RBC antigens (agglutinogens)
-illustration
-plasma antibodies (agglutinins)
-blood that can be recieved
look at notes
How many Rh agglutinogens (antigens) are there?
50 different
What are the 3 most common Rh blood groups?
C, D, E
How do you know there is an Rh agglutinogen present on the RBC?
Rh+
How are anti-Rh antibodies formed?
-not spontaneous
-Rh- individual receives Rh+ blood
What causes a transfusion reaction in Rh blood groups?
a 2nd exposure to Rh+ blood
What is the hemolytic disease of the newborn?
=erythroblastosis fetalis
-Rh- mom
-> 1st child (Rh+) = okay
-> 2nd child (Rh+) = antibodies attack
What is the treatment for hemolytic disease of the newborn?
=RhoGAM drug (passively immunize Rh- mom)
-pre-birth transfusions
-after-birth exchange transfusions
What happens when mismatched blood is infused?
=transfusion reactions
-donor cells attached by host agglutinins
-diminished O2 carrying
-clot = no flow
-free Hg in bloodstream = kidney
