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General Physiology > Blood > Flashcards

Blood Flashcards

1
Q

What is hemoglobin?

A

A molecule consisting of 2 alpha and 2 beta polypeptide chains

4 Heme groups which contain an Iron ion that binds O2

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2
Q

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

A

98.4% of O2 is transported bound to Hemoglobin

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3
Q

What does oxygenated blood look like?

A

Bright red

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4
Q

What does deoxygenated blood look like?

A

Dark red

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5
Q

What does Hemoglobin also bind to?

A

Carbon dioxide

Hydrogen ions

Carbon monoxide

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6
Q

Where are erythrocytes produced?

A

In the bone marrow

Derived from hemopoietic stem cells

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7
Q

What stimulates the production of erythrocytes?

A

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

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8
Q

Simple description of erythrocyte differentiation

A
  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
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9
Q

What three vitamins/ compounds are needed for erythrocyte production?

A

Iron

Folic acid

Vitamin B12

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10
Q

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

A

Necessary for DNA replication and thus cell proliferation

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11
Q

What organ filters old erythrocytes?

A

SPLEEN

Spleen macrophages filter blood by phagocytosis of old, fragile RBCs

Hemoglobin is catabolized by removing heme from iron creating bilirubin

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12
Q

What organ destroys old erythrocytes?

A

LIVER

Metabolizes by-products from brreakdown of erythrocytes

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13
Q

Describe Hemoglobin catabolism

A
  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
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14
Q

How is iron recycled?

A

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

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15
Q

Name three places where ferritin is stored

A

Liver (Ferritin iron (F-iron))

Spleen

Small intestine

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16
Q

Where is bilirubin converted to bile?

A

Liver

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17
Q

How is some bile secreted?

A

In the form of feces and in the urine

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18
Q

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

A

Myeloid stem cells

Lymphoid stem cells

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19
Q

What leukocytes develop from myeloid stem cells?

A

Neutrophil

Basophil

Eosinophil

Macrophage/ Monocyte

Platelets/Megakaryocytes

Erythrocytes

20
Q

What leukocytes develop from Lymphoid stem cells?

A

Lymphocytes

B cells/ plasma cells

Cytotoxic T cells

Natural killer cells

Helper T cells

21
Q

What are the clinical causes of dietary anemia?

A

Low iron

Low Vitamin B12 (pernicious anemia

22
Q

What is the cause of hemolytic anemia?

A

Hemolytic =destruction of RBCs

Malaria

Sickle cell anemia

23
Q

What is the cause of aplastic anemia?

A

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

Bone marrow defect

24
Q

What is the cause of renal anemia?

A

Kidney disease

Kidneys produce erythropoietin to trigger RBC production

Diseased kidneys = little to no erythropoietin

25
Q

What is the cause of hemorrhagic anemia?

A

YOU ARE BLEEDING MY GUY

26
Q

How do we prevent the blood from clotting?

A

Healthy endothelial cells produce Nitric oxide and Prostacyclin (PGI2) which inactivate platelets

This prevents the spread of a platelet plug (platelet aggregation)

27
Q

List the 5 steps in hemostasis

A

Vascular spasm

Platelet plug formation

Coagulation

Clot retraction and repair

Fibrinolysis

28
Q

`Vascular spasm

A

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

29
Q

What is the intrinsic vascular response in vascular spasm?

A

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

30
Q

Platelet plug formation

A

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

31
Q

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

A

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

32
Q

What specific protein causes the platelets to stick together?

A

Fibrinogen

33
Q

Describe the Coagulation cascade

(Intrinsic)

A
  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)
34
Q

How do the intrinsic and extrinsic coagulation pathways differ?

A

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.

35
Q

Extrinsic coagulation cascade

A

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

36
Q

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

A

Conversion of Factor 10 into 10a

37
Q

Write of the coagulation cascade shortcut

A
38
Q

Clot retraction and repair

A

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

39
Q

Fibrinolysis

A

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

40
Q

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

A

Anticoagulants

Tissue Factor pathway inhibitor (Extrinsic pathway inhibitor)

Thrombomodulin

41
Q

How do anticoagulants limit clot formation in low doses?

A

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

42
Q

How do anticoagulants limit clot formation in high doses?

A

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

43
Q

How do tissue factor pathway inhibitor limit clot formation?

A

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

44
Q

How do Thrombomodulin limit clot formation?

A

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

45
Q

Explain hemophila and clot formation disorders

A

Genetic disorder caused by a deficiency of gene for specific coagulation factor

Most commonly Factor 8 or 9 is deficient

46
Q

Explain how von Willebrand’s disease affects clotting

A

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

47
Q

How does Vitamin K affect clotting?

A

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

General Physiology (7 decks)

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