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RUSVM Physiology I 2016 > Blood > Flashcards

Blood Flashcards

1
Q

What are the characteristics of blood?

A

Viscosity- thicker and flows slower
Temperature- higher than tissues, redistributes
Alkaline - pH 7.35-7.45 (arterial more alkaline due to less CO2)

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2
Q

Functions of blood

A

Clotting
Immune response
Transport -nutrient, gasses, wastes, hormones, heat
Regulation - water, electrolytes, temp and acidity

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3
Q

How does blood maintain a relatively stable pH?

A

Buffering
Carbonic anhydrase coverts CO2 to H2CO3
CO2 + H2O <==> H2CO3 <==> H+ and HCO3-
Hemoglobin binds H+

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4
Q

How do plasma proteins maintain water balance?

A

Starlings forces.
Colloid osmotic pressure promotes reabsorption of fluid from tissues.
Prevent excessive loss of plasma proteins

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5
Q

What are the classes of plasma proteins?

A

Albumins
Globulins
Fibrinogen

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6
Q

Function of albumins

A

Major contributor to ontonic pressure of plasma

Important in transport of fatty acid

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7
Q

What are the types of Globulins and what is their main function?

A

Transport globulins- binding hormones or small molecules for transport in the body

Immunoglobulins- antibodies in immune response

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8
Q

What is the function of fibrinogens?

A

Blood clotting

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9
Q

Where are albumins and fibrinogens produced?

A

Liver

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10
Q

Where are immmunoglobulins produced?

A

Lymphocytes

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11
Q

What are the primary differences between blood plasma and interstitial fluid?

A

Concentration of dissolved proteins

Levels of respiratory gases

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12
Q

What is the process of producing formed elements of the blood called?

A

Haemopoiesis or hematopoiesis

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13
Q

Where does hematopoiesis take place?

A

Bone marrow

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14
Q

All formed elements in blood are derived from what type of cell?

A

pluripotent hematopoietic stem cell

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15
Q

The pluripotent hematopoietic stem cell can differentiate into which two types of cells?

A

Lymphoid stem cell

Colony forming unit

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16
Q

A colony forming unit can form what types of cells?

A

Erythrocytes
Leukocytes
Megakaryocytes (platelets)

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17
Q

How are erythrocytes formed?

A

CFU-S differentiates into CFU-E, produces hemoglobin.Under the influences of erythropoietin CFU-E develops into a recticulocyte (no nucleus). Recticulocytes leave the bone marrow. Recticulocyte loses ER, mitochondria, and ribosomes to become a mature RBC.

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18
Q

CFU-GM forms what types of cells?

A

Granulocytes and Monocytes

= basophils, eosinophils, neutrophils, monocytes.

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19
Q

CFU-M forms what types of cells?

A

Megakaryocytes which form platelets (influenced by thrombopoietin)

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20
Q

Lymphocyte stem cells form what?

A

T lymphocytes and B lymphocytes

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21
Q

What are the characteristics of RBC?

A

Flat
Biconcave
Disc-shaped

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22
Q

The characteristics of the RBC allows for what functions?

A

High surface area for diffusion of O2
Narrow shape for diffusion of O2 between exterior and interior of cell (Ficks Law)
Bending of cell to travel through capillary

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23
Q

Ficks Law

A

Diffusion rate is proportional to the partial pressure of O2, proportional to SA of diffusion, and inversely proportional to thickness of the membrane (distance travelled)

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24
Q

Describe the process of erythrocytes degradation

A

RBC have no nucleus and cannot replace enzymes. Membrane proteins are degraded over time and the integrity of the plasma membrane decreases. RBC travel through narrow vessels of spleen and membrane ruptures. Macrophages phagocytose RBC and hemoglobin is recycled

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25
Q

What is anemia?

A

Reduction below normal isn’t he O2 carrying capacity of blood and is characterized by a low number of RBC

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26
Q

What is a hematocrit?

A

Ratio of RBC volume to total volume of blood

Aka Packed cell volume

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27
Q

What are the 3 causes of anemia?

A

Decreased rate of erythropoiesis
Excessive loss of erythrocytes
Deficiency in hemoglobin concentration of RBC

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28
Q

Anemia due to a deficiency of a factor required for erythropoiesis

A

Nutritional anemia

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29
Q

What nutritional factors may be lacking in nutritional anemia?

A

Iron- not enough for Hb synthesis

Folic Acid- critical for stem cell division and maturation of RBC

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30
Q

What type of anemia results from an inability to absorb vitamin B12?

A

Pernicious anemia
B12 required for development of RBC
Intrinsic factor lacking preventing sufficient absorption from GI tract

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31
Q

What is aplastic anemia?

A

Failure of bone marrow to produce adequate amounts of RBC
Toxic chemicals
Radiation exposure
Bone marrow cancer

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32
Q

Renal anemia is caused by what?

A

Erythropoietin(stimulant for RBC production) is not released from the kidney

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33
Q

A substantial blood loss causes what kind of anemia?

A

Hemorrhagic anemia

34
Q

An immunohemolytic disease would cause what type of anemia?

A

Haemolytic anemia

- autoimmune disease

35
Q

Anemia resulting from low RBC would have what effect on the circulatory system?

A

Decrease in blood viscosity -> decreased total peripheral resistance -> increased flow -> increased venous return and preload
Cardiac hypertrophy
Heart failure
Law of LaPlace

36
Q

What is Polycythemia

A

Excess amount of circulating RBC

37
Q

In polycythemia, what happens to hematocrit?

A

Increase in RBC

70% hematocrit (same total volume, higher percentage being RBC)

38
Q

What two conditions can cause and elevated hematocrit?

A

Polycythemia

Dehydration

39
Q

Elevated hematocrit in dehydration is due to what?

A

Decreased plasma volume
Amount of RBC remains the same
Increased blood viscosity

40
Q

Primary polycythremia

A

Tumor-like condition where bone marrow is producing excessive RBC

41
Q

Secondary polycythremia

A

Physiological response

Erythropoietin released by kidney in response to low O2 in tissues. (Often seen in at high altitudes)

42
Q

What effect can polycythremia have on the CVS?

A

Increase RBC -> increase viscosity -> increased total peripheral resistance -> increase afterload -> more work for heart ->
Cardiac hypertrophy
Heart failure
Law of LaPlace

43
Q

Hemoglobin structure

A

4 nonprotien haem groups

Porphyrin ring

44
Q

How are platelets produced

A

In bone marrow. CFU-M forms megakaryocytes. Shedding of cytoplasm making platelets. The remaining nucleus of megakaryocyte is engulfed my macrophage.

45
Q

What is platelet production called?

A

Thrombopoiesis

46
Q

What is thrombopoietin and what does it do?

A

Peptide hormone that accelerates platelet production and stimulates megakaryocytes production.

47
Q

What is the function of platelets?

A

Transport chemicals- clotting factors
Form platelet plug
Contraction- actin and myosin filaments to reduce clot size

48
Q

What are the three responses to tissue injury that maintain hemostasis

A

Vascular spasm
Platelet plug formation
Clotting/coagulation

49
Q

What happens in vascular spasm?

A

Cutting/damage to vascular wall triggers contraction of smooth muscle
Slows blood flow and minimizes blood loss

50
Q

What changes can be seen in the endothelium during vascular spasm

A

Contract and exposure of underlying basement membrane
Release of chemical factors
Contraction of blood vessels

Become sticky- opposing endothelial walls stick together

51
Q

What is the process of platelet plug formation

A

Damaged endothelial wall with exposed collagen of basement membrane
Platelets bind to collagen and vonWillenbrand factor
Platelets change shape and extend projections
Synthesize clotting factors

52
Q

What molecules do platelets produce?

A 
ADP
Thromboxane A2
Serotonin 
Ca2+
Platelet derived growth factor
53
Q

What role does ADP play in the platelet plug?

A

Stimulus for platelet aggregation and change in shape
Released by damaged endothelium and activated platelets
Projections and sticky platelets

54
Q

What role does thromboxane play in the platelet plug?

A

Stimulates ADP release, platelet aggregation, and contraction of smooth muscle

55
Q

What role does serotonin play in the platelet plug

A

Assist thromboxane in vasoconstriction

56
Q

What role does Ca2+ play in platelet plug?

A

Aggregation and clotting

57
Q

What role does platelet derived growth factor play in the platelet plug?

A

Promote vessel repair- stimulate division of endothelial, smooth muscle, and fibroblast cells

58
Q

How is platelet plug formation regulated

A

Positive feedback - ADP, thromboxane and Ca2+ feedback to stimulate each other

Prostacyclin limits platelet growth

59
Q

What enzyme converts fibrinogen to fibrin?

A

Thrombin

60
Q

What is the purpose of fibrin?

A

Forms a network covering injured tissue. Seal of damaged blood vessel

61
Q

Where are most procoagulants produced?

A

Liver

62
Q

What are procoagulants?

A

Precursors to an enzyme that are converted to active forms by a clotting factor

63
Q

What is the functions of anticoagulants?

A

Prevent clotting

64
Q

What do coagulants do?

A

Convert inactive molecules in clotting to active forms

65
Q

Why is vitamin K important to clotting process?

A

Vitamin K must be present in liver to synthesize 4 clotting factors (prothrombin, proconvertin, christmas factor, stuart-proper factor)

66
Q

At what steps of fibrinogen to fibrin formation is Ca2+ involved?

A

Prothrombin is converted to thrombin by prothrombinase and Ca2+.
Thrombin converts fibrinogen to fibrin
Fibrin converted to fibrin fibers by thrombin and Ca2+

67
Q

What initiates the intrinsic pathway of clotting?

A

Exposure of blood to collagen fibers

68
Q

What initiates extrinsic clotting pathway?

A

Trauma to vessel wall causing release of tissue factor (thromboplastin)

69
Q

Exposure of blood to collagen causes activation and release of what? (Intrinsic clotting pathway)

A

Activation of factor XII and release of platelet phospholipids

70
Q

How is coagulation regulated

A

Positive feedback- formation of thrombin from factors VIII and V, thrombin activates factors and production of thrombin

Negative feedback- thrombin produces protein C which prevents its formation by deactivating factors

71
Q

What is the purpose of clot retraction?

A

Pull edges of damaged tissue together

Reduces size of damaged area making it easier for fibroblasts and smooth muscle to complete repairs

72
Q

The process of clot removal is called…

A

Fibrinolysis

73
Q

What converts fibrin into soluble fibrin fragments?

A

Plasmin

74
Q

What turns plasminogen into plasmin?

A

Plasminogen activator

75
Q

What activates plasminogen activator?

A

Thrombin inhibits plasminogen activator inhibitors (i-PA). Active PA can convert plasminogen to plasmin

76
Q

What factors prevent clotting from occurring all the time?

A

Smoothness of vessel wall
Substance on inside of wall
Thrombomodulin

77
Q

What is the purpose of thrombomodulin?

A

Sequesters thrombin and activates protein C (prevent thrombin formation)

78
Q

Name anticoagulants

A

Prostacyclin
Tissue plasminogen activator
Anti-thrombin III
Heparin

79
Q

How does prostacyclin inhibit clotting?

A

Released by healthy endothelial cells

Opposes ADP platelet stimulation -> no platelet aggregation

80
Q

What is the action of anti-thrombin III?

A

Inhibits production of several procoagulants, including thrombin

81
Q

How does Heparin inhibit clot formation?

A

Released by basophils, mast cells, and endothelial cells.

Increased activation of anti-thrombin III (anticoagulant )

82
Q

How does Warfarin decrease clotting?

A

Block the use of vitamin K in the liver

Decreased synthesis of clotting factors

RUSVM Physiology I 2016 (2 decks)

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