Lecture 9 - Blood Flashcards
1
Q
What is the movement of O2 in the body?
A
from blood to tissues
2
Q
What is the CO2 movement in the body?
A
from tissues to the blood
3
Q
What is the blood made of?
A
-formed elements (45% mostly RBC)
-plasma (55%)
4
Q
What are the formed elements in blood?
A
-erythrocytes (RBCs)
-leukocytes (WBCs)
-platelets
5
Q
What does hematocrit mean?
A
the # RBCs in the total volume of blood
6
Q
What should the blood pH be?
A
7.35-7.45
7
Q
What is the temperature of the blood?
A
38º C, warmer than the body temp
8
Q
Average blood volume
-male
-female
A
-5-6L
-4-5L
9
Q
What is the general pathway for O2 distribution by the blood?
A
from lungs to heart to target
10
Q
How do nutrients get distributed by the blood?
A
the digestive tract to target
11
Q
How does metabolic waste get distributed by the blood?
A
lungs and kidneys to the esophagus to uruter
12
Q
How do hormones get distributed by the blood?
A
from endocrine glands to target
13
Q
What does blood regulate?
A
-body temp
-pH in tissues (bicarbonate ions)
-fluid volume (osmotic pressure)
14
Q
What and how does the blood protect the body?
A
-blood loss = proteins + platelets clot to stop bleeding
-infection = antibodies, proteins, and leukocytes stop the spread of viruses
15
Q
What are the main plasma proteins?
A
-albumin
-alpha globulins
-beta globulins
-y globulins
16
Q
What are plasma waste products?
A
-lactic acid
-urea
-creatine
17
Q
What are the plasma’s organic nutrients?
A
-glucose
-carbohydrates
-amino acids
18
Q
What are the electrolytes found in the plasma? (5)
A
-Na+
-K+
-Ca2+
-Cl-
-H3CO2
19
Q
State the 2 respiratory gases found in the plasma
A
-O2 & CO2
20
Q
What is special about the structure of an erythrocyte?
A
has no nucleus
21
Q
How do erythrocytes transport gas?
A
O2 binds to iron on the heme on the polypeptide of the hemoglobin
-always at full capacity
22
Q
What is the erythrocyte plasma membrane made of?
A
spectrin
23
Q
What makes an erythrocyte so flexible?
A
-spectrin, actin and myosin
24
Q
How do RBCs not consume the O2 it carries?
A
The ATP of the RBC is made anaerobically
25
Why are hemoglobins not free in circulation?
many negative consequences
-increase osmotic pressure
-lose Hb to tissues
-increase blood viscosity
-damage kidneys
26
What is the structure of hemoglobin (Hb)?
1 Hb
= 2 alpha polypeptide + 2 beta polypeptide chains
= 4 heme groups
= 4 iron
= 4 O2
27
How does the affinity O2 affinity increase/decrease?
once one O2 bind/unbind, the affinity increase/decreases to bind/unbind the rest
28
What are oxyhemoglobin and deoxyhemoglobin?
-with O2 from lungs
-no O2 from tissues
29
What is carbaminohemoglobin?
a compound of Hb and CO2 where the CO2 binds to the peptide backbone
30
What does CO2 get converted to?
HCO3 in erythrocytes by carbonic anhydrase
31
What is the word for blood cell formation?
hematopoiesis
32
Where does hematopoiesis occur in the body?
-red bone marrow
=axial skeleton + girdles (hips)
=humerus + femur (largest bones)
33
How much hematopoiesis in mL is made a day?
30mL/day
34
What is erythropoiesis?
production of RBCs
35
What are the steps of erythropoiesis?
1. hemocytoblasts (formed elements)
2. proerythroblasts
3. early erythroblasts (ribosome synthesis)
4. late erythroblasts (Hb accumulation)
5. normoblasts
6. reticulocytes (ejection of the nucleus)
7. erythrocytes
36
How long is the process of erythropoiesis?
15 days
37
What is it called when there are too few RBCs?
-tissue hypoxia
=run out of O2 in the tissues
38
What happens when there are too many RBCs?
-increase in blood viscosity
=make blood flow hard, too thick
39
How is erythropoiesis controlled and maintained?
-hormonally controlled (erythropoietin)
-relies on iron, amino acids, vitamin B
40
Where is erythropoietin made?
kidneys
41
Why would erythropoietin be released?
-hypoxia (O2 levels low, demand more O2)
42
What would an increased amount of erythropoietin do?
-increase RBCs in circulating blood
-increase O2 carrying ability
-increase reticulocyte count = rate RBC synthesis
43
What is the homeostatic response to low O2 levels in blood?
1. kidney release EPO
2. stimulate red bone marrow
3. enhanced erythropoiesis = increase RBC count
4. increase O2 carrying
5. increase until normal
44
Why do dialysis patients become anemic?
no EPO is produced so there is no RBC production
45
What does erythropoiesis require to function?
-proteins, lipids, carbohydrates
-iron, vitamin B12, folic acid
46
Where does the body store iron?
-hemoglobin (65%)
-liver
-spleen
-bone marrow
47
Where is the intracellular iron?
-ferritin
-hemosiderin
48
Where is circulatory iron?
loosely bound to transferrin or eaten by haptoglobin
49
What is the lifespan of an erythrocyte?
100-120 days
50
Why do RBCs become rigid and fragile?
degeneration of backbone with no regeneration
51
Where do dying RBCs go?
trapped in spleen and eaten by macrophages
52
What happens to the heme of the hemoglobin when RBC is eaten?
1. degraded to bilirubin
2. liver bilirubin into intestine bile
3. intestine bile metabolizes into urobilinogen
4. urobilinogen to stercobilin feces leaves the body
53
What happens to the globin of hemoglobin when RBC is eaten?
-metabolized into amino acids and released into circulation
54
What happens to the iron from hemoglobin when RBC is eaten?
-salvaged for reuse, attach to ferritin and hemosiderin
55
What happens to the hemoglobin released into the blood?
captured and phagocytized by haptoglobin
56
What is anemia?
-erythrocyte disorder
-low O2 carrying ability
57
What are the signs/ symptoms of anemia?
-fatigue, paleness, shortness of breath, chills
58
What are the types of anemia where there is insufficient RBCs + explanation?
1. hemorrhagic (acute/chronic blood loss)
2. hemolytic (prematurely ruptured RBC)
3. aplastic (destruct/inhibit red bone marrow)
59
What are the types of anemia where there is decreased hemoglobin content + explanation?
4. iron-deficiency (loss iron, no intake, no absorption)
5. pernicious (no B12, no intrinsic factor)
60
What are the types of anemia where there is abnormal hemoglobin + explanation?
6. thalassemias (faulty globin of Hb)
7. sickle-cell (defective gene)
61
What is polycythemia?
-excess RBC = increased blood viscosity
62
What are the 3 main polycythemia conditions + definitions?
1. polycythemia vera = naturally make too much
2. secondary polycythemia = smoker/burn victim
3. blood doping/EPO abuse = drugs/ enhancers
63
What are leukocytes?
-white blood cells
-a complete cell that is <1% blood volume
-responds to bacterial or viral invasion
64
What are platelets?
-megakoryocytes
-clotting factors and enzymes
65
What regulates platelets?
thrombopoietin
66
What inactivates platelets?
nitric oxide (NO) and prostacyclin
67
What is the genesis of platelets?
-hemocytoblast
-megakaryoblast
-promegakaryocyte
-megakaryocyte
-platelet
68
How is blood homeostasis maintained?
1. vascular spasms
-smooth muscle contract
-vasoconstriction
2. platelet plug
-collagen exposed
-platelet adhere
3. coagulation
-fibrin mesh
69
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
70
What are the steps to platelet plug formation?
1. damage to blood vessel
2. release von Willebrand factor (VWF) = adhere to collagen
3. release thromboxane A2
4. stick to exposed collagen
5. release serotonin and ADP = attract more platelets
71
What kind of homeostatic process is the platelet plug formation?
positive feedback chain
72
What is the process of homeostatic coagulation?
1. intrinsic/extrinsic pathway
2. prothrombin activator (PA)
3. prothrombin to thrombin
4. thrombin catalyzes fibrinogen to fibrin mesh
73
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
74
What is unique about the extrinsic pathway of coagulation?
-requires tissue factor
-for larger events and vessel damage
-less steps = much faster
75
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)
76
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
]
77
How does clot retraction work?
-pull together and stabilize the clot by squeezing serum out
78
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)
79
How does clot removal work?
-digestion = plasmin (plasminogen) which is activated by tissue plasminogen activator (tPA) and released by endothelial cells
80
What causes the inhibition of clotting factors? (2 things)
-fibrin + thrombin = anticoagulant
-antithrombin III = thrombin inactivator
81
What causes an increase in antithrombin III activity?
-heparin
82
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
83
What is the name of a type of thrombus?
embolus
-free floating thrombus in the blood
-can block and get stuck in smaller vessels
84
How do you prevent undesirable clots? (3 drugs)
-aspirin (inhibit thromboxane A2)
-heparin (inhibit thrombin)
-warfarin (inhibit vitamin K)
85
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
86
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
87
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
88
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.
89
When are blood transfusions used?
-blood loss is substantial (15-30% weakness + 30% shock)
90
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
91
What blood groups are used for legalities?
M, N, Duffy, Kell, Lewis
92
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
93
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
94
How many Rh agglutinogens (antigens) are there?
50 different
95
What are the 3 most common Rh blood groups?
C, D, E
96
How do you know there is an Rh agglutinogen present on the RBC?
Rh+
97
How are anti-Rh antibodies formed?
-not spontaneous
-Rh- individual receives Rh+ blood
98
What causes a transfusion reaction in Rh blood groups?
a 2nd exposure to Rh+ blood
99
What is the hemolytic disease of the newborn?
=erythroblastosis fetalis
-Rh- mom
-> 1st child (Rh+) = okay
-> 2nd child (Rh+) = antibodies attack
100
What is the treatment for hemolytic disease of the newborn?
=RhoGAM drug (passively immunize Rh- mom)
-pre-birth transfusions
-after-birth exchange transfusions
101
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
