Blood

Question 1

What is hemoglobin?

Answer 1

A molecule consisting of 2 alpha and 2 beta polypeptide chains

4 Heme groups which contain an Iron ion that binds O2

Question 2

How is the majority of the oxygen transported in the blood?

Answer 2

98.4% of O2 is transported bound to Hemoglobin

Question 3

What does oxygenated blood look like?

Answer 3

Bright red

Question 4

What does deoxygenated blood look like?

Answer 4

Dark red

Question 5

What does Hemoglobin also bind to?

Answer 5

Carbon dioxide

Hydrogen ions

Carbon monoxide

Question 6

Where are erythrocytes produced?

Answer 6

In the bone marrow

Derived from hemopoietic stem cells

Question 7

What stimulates the production of erythrocytes?

Answer 7

Erythropoietin secreted from the kidneys under conditions of hypoxia (low oxygen level in the blood flowing through the kidneys)

Question 8

Simple description of erythrocyte differentiation

Answer 8

1. Erythropoietin triggers hematopoietic stem cells to differentiate into erythrocytes
2. Cells begin to produce hemoglobin gradually becoming redder
3. Developing erythrocytes lose nuclei and organelles

Question 9

What three vitamins/ compounds are needed for erythrocyte production?

Answer 9

Iron

Folic acid

Vitamin B12

Question 10

What is folic acid AND Vitamin B12 needed for in erythrocyte production?

Answer 10

Necessary for DNA replication and thus cell proliferation

Question 11

What organ filters old erythrocytes?

Answer 11

SPLEEN

Spleen macrophages filter blood by phagocytosis of old, fragile RBCs

Hemoglobin is catabolized by removing heme from iron creating bilirubin

Question 12

What organ destroys old erythrocytes?

Answer 12

LIVER

Metabolizes by-products from brreakdown of erythrocytes

Question 13

Describe Hemoglobin catabolism

Answer 13

1. Heme is removed from the globin part (protein)
2. Globin (alpha and beta polypeptides) broken down into amino acids and recycled
3. Iron is removed from the hemoglobin leaving heme which is now called biliverdin
4. Biliverdin is broken down into bilirubin is released into the bloodstream bound to albumin
5. Travels to the liver for further metabolism into bile

Question 14

How is iron recycled?

Answer 14

Heme molecules are toxic to the body and must be broken down

Heme oxygenase breaks heme into biliverdin and Fe2+

Fe2+ leaves the macrophage and is converted to Fe3+

Fe3+ binds to transferrin and is transported into through the blood as T-iron

Transferrin goes from the GI tract to the bone marrow or from the liver to the bone marrow

Question 15

Name three places where ferritin is stored

Answer 15

Liver (Ferritin iron (F-iron))

Spleen

Small intestine

Question 16

Where is bilirubin converted to bile?

Answer 16

Liver

Question 17

How is some bile secreted?

Answer 17

In the form of feces and in the urine

Question 18

What are the two types of stem cells produced from hemopoietic stem cells?

Answer 18

Myeloid stem cells

Lymphoid stem cells

Question 19

What leukocytes develop from myeloid stem cells?

Answer 19

Neutrophil

Basophil

Eosinophil

Macrophage/ Monocyte

Platelets/Megakaryocytes

Erythrocytes

Question 20

What leukocytes develop from Lymphoid stem cells?

Answer 20

Lymphocytes

B cells/ plasma cells

Cytotoxic T cells

Natural killer cells

Helper T cells

Question 21

What are the clinical causes of dietary anemia?

Answer 21

Low iron

Low Vitamin B12 (pernicious anemia

Question 22

What is the cause of hemolytic anemia?

Answer 22

Hemolytic =destruction of RBCs

Malaria

Sickle cell anemia

Question 23

What is the cause of aplastic anemia?

Answer 23

Aplastic= bone marrow does not produce new cells, body susceptible to infection and bleeding

Bone marrow defect

Question 24

What is the cause of renal anemia?

Answer 24

Kidney disease

Kidneys produce erythropoietin to trigger RBC production

Diseased kidneys = little to no erythropoietin

Question 25

What is the cause of hemorrhagic anemia?

Answer 25

YOU ARE BLEEDING MY GUY

Question 26

How do we prevent the blood from clotting?

Answer 26

Healthy endothelial cells produce Nitric oxide and Prostacyclin (PGI2) which inactivate platelets This prevents the spread of a platelet plug (platelet aggregation)

Question 27

List the 5 steps in hemostasis

Answer 27

Vascular spasm Platelet plug formation Coagulation Clot retraction and repair Fibrinolysis

Question 28

`Vascular spasm

Answer 28

Damage to the endothelium can lead to blood loss To prevent blood loss the vessel contracts to minimize blood loss by decreasing the diameter of the vessel (**⇑⇑⇑⇑ Resistance & ⇓⇓⇓⇓ Flow**) Sympathetic innervation and Intrinsic vascular response

Question 29

What is the intrinsic vascular response in vascular spasm?

Answer 29

Intrinsic vascular response: Endothelial cells will release endothelin which binds to receptors on the smooth muscle below and cause it to contract

Question 30

Platelet plug formation

Answer 30

Blood vessel damage Exposure of subendothelium Von Willebrand factor secreted by endothelial cells bind to collagen fibers Injured endothelial cells cannot secrete nitric oxide and prostacyclin so platelets become activated and clotting factors are activated Platelets bind to Von Willebrand factor Platelets secrete ADP, Thromboxane A2, Seratonin

Question 31

What is the function of ADP and Thromboxane A2 in Platelet plug formation

Answer 31

ADP and Thromboxane A 2 increase the stickiness of the platelets in circulation and activate them drawing them to the site of injury. Causes = Platelet aggregation Use a Positive feedback loop

Question 32

What specific protein causes the platelets to stick together?

Answer 32

Fibrinogen

Question 33

Describe the Coagulation cascade | (Intrinsic)

Answer 33

1. **Factor 12** comes in contact with the platelets or collagen and becomes **factor 12a** 2. **Factor 12a** activates **factor 11 → Factor 11 a** 3. **Factor 11 a** activates **factor 9 → factor 9a** 4. **Factor 9 a** and **factor 8** will come together with platelet factor 3 and Ca2+ forming a complex that converts **factor 10 to 10 a** 5. **Factor 10 a** will react with **factor 5,** platelet factor 3, and Ca 2+ to activate **Prothrombin activator** 6. **Prothrombin activator** will convert **Factor 2 (prothrombin) into factor 2a (thrombin)** 7. **Thrombin** will cause soluble **fibrinogen to polymerize** into fibrin (insoluble) causing blood to become jelly-like to slow blood flow 8. Factor 13 (**fibrin stabilizing factor**) will **cross-link** the fibrin to form a **fibrin mesh** to hold down the platelet plug to prevent it from dislodging and traveling (embolism)

Question 34

How do the intrinsic and extrinsic coagulation pathways differ?

Answer 34

**Intrinsic pathway is activated through exposed endothelial collagen** **Extrinsic pathway is activated through tissue factor (Factor 3) released into the blood by endothelial cells after external damage**.

Question 35

Extrinsic coagulation cascade

Answer 35

Tissue damage causes the release of tissue factor (Factor 3) Factor 3 will interact with factor 7 which will stimulate the activation of factor9 Factor 7 converges on the common pathway where facto 10 is activated Factor 10a binds to factor 5, platelet factor 3 and Ca2+ to activate the prothrombin activator

Question 36

What is the common factor between the intrinsic and extrinsic pathways?

Answer 36

Conversion of Factor 10 into 10a

Question 37

Write of the coagulation cascade shortcut

Answer 37

Question 38

Clot retraction and repair

Answer 38

Platelets contain actin and myosin that allows them to contract and pull the edges of the endothelial cells closer together Platelets will secrete platelet-derived growth factors to help renew damaged smooth muscle Platelets secret vascular endothelial growth factor replenishes the endothelial lining

Question 39

Fibrinolysis

Answer 39

Tissue plasminogen activator (tPA) on endothelial cells which converts/ cleaves plasminogen into plasmin Plasmin begins to digest/ cut up the fibrin mesh and busts up the clot to prevent the blood vessel from becoming occluded

Question 40

What 3 factors limit the formation of clots to prevent occlusions of blood vessels?

Answer 40

Anticoagulants Tissue Factor pathway inhibitor (Extrinsic pathway inhibitor) Thrombomodulin

Question 41

How do anticoagulants limit clot formation in low doses?

Answer 41

Anticoagulants are chemicals that inhibit blood clotting or coagulation. Low doses of aspirin acts by inhibiting the formation of Thromboxane A 2 (produced by activated plateletes to increase aggregation) thereby decreasing platelet aggregation and platelet plug formation

Question 42

How do anticoagulants limit clot formation in high doses?

Answer 42

Aspirin decreases the formation of prostacyclin (inactivates platelets) which increases the likelihood of clot formation

Question 43

How do tissue factor pathway inhibitor limit clot formation?

Answer 43

Secreted during the initial phase of clotting by healthy endothelial cells Inhibits the extrinsic pathway so that not so much factor 10 is activated and ultimately fibrin mesh formed Clot size does not occlude the blood vessel

Question 44

How do Thrombomodulin limit clot formation?

Answer 44

Thrombomodulin binds to thrombin forming the thrombomodulin-thrombin complex Thrombin cannot convert fibrinogen into fibrin Complex activates protein C (anticoagulant) that inhibits both intrinsic and extrinsic pathways

Question 45

Explain hemophila and clot formation disorders

Answer 45

Genetic disorder caused by a deficiency of gene for specific coagulation factor Most commonly Factor 8 or 9 is deficient

Question 46

Explain how von Willebrand's disease affects clotting

Answer 46

Genetic bleeding disorder where there is a deficiency in vWf making it hard to form a platelet plug due to reduced levels vWf is also a plasma carrier for factor 8 so its absence makes factor 8 more unstable and quick to break down Low factor 8 levels

Question 47

How does Vitamin K affect clotting?

Answer 47

Clotting factors are made in the liver and vitamin K is needed for the synthesis of many of the proteins necessary in blood clotting