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Anatomy and Physiology > Red Blood Cells > Flashcards

Red Blood Cells Flashcards

1
Q

What can regulate temperature, ICF water concentration, electrolyte concentration, and acid base balance?

A

Blood

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2
Q

What substance makes up the vast majority of plasma?

A

Water

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3
Q

Where are albumin and fibrinogen produced?

A

The liver

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4
Q

Where are blood cells produced in the fetus?

A

Bone marrow (Of all bones), liver, spleen

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5
Q

Where are blood cells produced in young animals?

A

Bone marrow (Of all bones)

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6
Q

Where are blood cells produced in adult animals?

A

Bone marrow of long bones (Red marrow)

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7
Q

What type of cell can lymphoid stem cells produce?

A

Lymphocyte

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8
Q

What type of cells can myeloid stem cells produce?

A

Erythrocyte, neutrophil, monocyte, eosinophil, basophil, and megakaryocyte (Then turns into platelets)

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9
Q

What are the main functions of erythrocytes?

A

Provide O2 to tissues via hemoglobin and remove CO2 from tissues (As carbonic acid or carbamino acids)

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10
Q

What percentage of marrow cells make RBCs?

A

25%

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11
Q

What is the hemoglobin content of most mammals (Excluding lactating cows and cold blooded horses)?

A

13-15 g/dl

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12
Q

What is the name of the complex formed when CO binds to hemoglobin?

A

Carbonmonoxyhemoglobin

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13
Q

How can the production of methemoglobin be reversed?

A

With NADH and methemoglobin reductase

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14
Q

Why does fetal Hb have a higher affinity for O2 than adult Hb?

A

To promote maternal-fetal O2 transfer

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15
Q

What proportion of erythrocytes are in peripheral circulation?

A

Less than half

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16
Q

What proportion of non-circulating erythrocytes are stored in the spleen?

A

1/3

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17
Q

How are erythrocytes removed from circulation?

A

Intravascular hemolysis (Aged cells lyse, Hb dimerizes and binds to haptoglobin, digested by mononuclear phagocytic or macrophage system (MPS)) or extravascular hemolysis (Directly engulfed by MPS)

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18
Q

Where is the mononuclear phagocytic or macrophage system (MPS) located?

A

Domestic animals: Red bone marrow, humans: Spleen, birds and some other species: Liver

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19
Q

What are the requirements for erythropoiesis?

A

Lipids, amino acids, carbohydrates, iron (Hb production), folic acid (DNA/RNA synthesis), and Vitamin B12 (DNA production/maturation of erythrocytes)

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20
Q

How is erythropoiesis regulated?

A

Erythropoietin: Stimulated when decreased O2 to kidney, then stimulates RBC production in bone marrow

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21
Q

What is MCV and how is it calculated?

A

Mean Corpuscular Volume: (PCV x 10)/# erythrocytes per ul x 10-6

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22
Q

What is MCH and how is it calculated?

A

Mean Corpuscular Hemoglobin content: (Hb in g/dl x 10)/# erythrocytes per ul x 10-6

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23
Q

What is MCHC and how is it calculated?

A

Mean Corpuscular Hemoglobin Concentration: (Hb in g/dl x 100)/(PCV in dl/dl)

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24
Q

What are three types of anemia?

A

Hemolytic, hemorrhagic, hypoproliferative (Non-regenerative)

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25
Q

How does hemorrhagic anemia occur and what are some causes?

A

Blood loss due to trauma, coagulation disorders, parasites, or GI lesions

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26
Q

How does hypoproliferative (Non-regenerative) anemia occur and what are some causes?

A

Decrease in erythropoietin due to dietary deficiencies (Folic acid, vit. B12, iron), desetruction of bone marrow, or bracken poisoning

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27
Q

How does hemolytic anemia occur and what are some causes?

A

Destruction of erythrocytes due to blood parasites, bacterial infection, chemicals, drugs, poisonous plants/venoms, or autoimmune disorders

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28
Q

Which blood type is considered the universal donor?

A

O

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29
Q

Which blood type can only receive its own blood type?

A

O

30
Q

Which blood type are the majority of non-pedigree cats?

A

A

31
Q

Explain how a blood transfusion in dogs could result in a significant antibody production and possible transfusion reaction.

A

There are barely any naturally occurring antibodies against DEA 1.1 and somewhat 1.2, so giving DEA 1.1 the first time will most likely be fine. But because both of these blood types are highly antigenic, the body may produce antibodies against them and therefore a second transfusion of DEA 1.1 or 1.2 may cause a large reaction.

32
Q

What three stages allow hemostasis to be achieved?

A

Vascular response, formation of platelet plug, coagulation to form clot

33
Q

What vascular response occurs in response to endothelial damage?

A

Constriction of smooth muscle

34
Q

How are platelet plugs formed?

A

Damage to collagen in the endothelial lining causes activated platelets to signal arachadonic acid to activate thromboxane A. Thromboxane A causes aggregate platelets to become active and bind to Von Willebrand factors on the internal epithelial surface, creating a clot.

35
Q

How are platelets stopped from clotting?

A

Once the damaged collagen is no longer exposed, arachadonic acid converts prostaglandin 1 into prostacyclin, which is a aggregate platelet inhibitor.

36
Q

In the final common pathway of blood coagulation, what three products are formed?

A

Thrombin (From prothrombin), loose fibrin (From fibrinogen), and Active Factor XIII (From Inactive Factor XIII)

37
Q

What does loose fibrin become in the final common pathway of blood coagulation?

A

Stabilized fibrin

38
Q

What is required but not limiting in the coagulation pathway?

A

Ca+2

39
Q

Which two mechanisms act on Factors V and VIII in the coagulation pathway to prevent thrombin from being produced?

A

PGI2 and activated protein C

40
Q

What acts on thrombin to prevent it from changing fibrinogen to loose fibers?

A

Antithrombin III with heparin

41
Q

What extrinsic factor triggers the coagulation pathway?

A

Tissue factor

42
Q

What is the purpose of tissue plasminogen activator (t-PA)?

A

Turns plasminogen to plasmin, which is an enzyme that breaks down fibrin in clots

43
Q

How does aspirin work on the coagulation pathway?

A

Prevents COX and therefore thromboxane A2, which prevents platelets from aggregating and clots from forming.

44
Q

Name some Ca+2 chelating agents that prevent coagulation.

A

Citrate, oxalate fluoride salts, EDTA

45
Q

What diagnostic tests can be done to assess hemostasis?

A

Bleeding time (Time between cut and platelet plug formation, tests platelets and vasculature), whole blood clotting time (Time for 1mL blood to clot, tests coagulation cascade), one stage prothrombin test (Plasma, tissue, Ca+2 incubation to test extrinsic and common coagulation pathway), and activated partial prothrombin test (Plasma activated with phospholipid and Ca+2 to test intrinsic and common coagulation pathway)

46
Q

What is von Willebrand Disease?

A

An autosomal deficiency in von Willebrand factor that prevents platelets from aggregating

47
Q

What does a deficiency in Factor VIII cause?

A

Hemophilia A, lack of clotting that could lead to excessive and/or internal bleeding, hematomas, sudden death, sex-linked recessive

48
Q

What causes Hemophilia B?

A

Factor IX deficiency, prevents clotting, same clinical signs as Hemophilia A

49
Q

Do enzymes shift the substrate:product equilibrium?

A

No

50
Q

How do enzymes affect activation energy?

A

They lower activation energy in order to increase the rate of reaction

51
Q

How do enzymes affect the transition state of the reaction?

A

They stabilize the transition state

52
Q

What is the fastest enzyme in the body?

A

Carbonic anhydrase

53
Q

How does pH affect an enzyme’s rate of reaction?

A

pH affects the charge on the enzyme/substrate, therefore affecting the bonds of each. It also affects the charge on the R groups of amino acids.

54
Q

How does temperature affect enzyme activity?

A

Affects 3D structure, causes denatuation and decrease of activity at non-optimal levels

55
Q

What are coenzymes and where do they come from?

A

Aid enzymes in their reaction, NAD+ (From vit. B3), FAD and FMN (From riboflavin), and other vitamins

56
Q

What are enzyme cofactors?

A

Usually metal ions (Ca+2, Fe+2, Cu+2, Mn+2) that help stabilize a substrate in the enzyme binding site

57
Q

How does EDTA prevent blood clotting?

A

It chelates metal so that substrates cannot bind to an enzyme, including enzymes involved in the coagulation pathway.

58
Q

How can enzyme/substrate complexes be visualized?

A

Electron Microscopy

59
Q

Where is the saturation effect shown (Catalyzed/Uncatalyzed reactions)?

A

Shown in catalyzed reactions, not shown in uncatalyzed reactions

60
Q

What is Km and how do you find it?

A

[Substrate] when the rate of reaction is half of the maximum value, find V1/2 and follow to the curve, then follow down to x-axis. Km is also an indicator of enzyme affinity for the substrate and how stable the reaction is, dissociation constant

61
Q

What does a low Km indicate?

A

Low [Substrate] at V1/2, meaning enzyme has a high affinity for substrate

62
Q

What does a high Km indicate?

A

High [Substrate] at V1/2, meaning enzyme has a low affinity for substrate

63
Q

What is the equation for V in Michaelis-Menten kinetics?

A

V = Vmax x ([S]/([S] + Km))

64
Q

What is the equation to turn a Michaelis-Menten curve into a Lineweaver-Burke plot?

A

1/V = (1/Vmax) + (Km/(Vmax[S]))

65
Q

Are competitive and non-competitive enzyme inhibitors reversible or non-reversible?

A

Reversible

66
Q

Where do competitive enzyme inhibitors bind?

A

In the binding site of the enzyme, inhibiting the substrate from binding. Decreases rate of reaction but can still reach maximum saturation by adding a lot of substrate, increased Km

67
Q

How can enzymes be negatively regulated?

A

The product of a reaction can become a competitive inhibitor for the same reaction

68
Q

How does ethanol save cats from ethylene glycol poisoning?

A

Ethanol competes with ethylene glycol and therefore inhibits its binding to enzymes

69
Q

Where do non-competitive enzyme inhibitors bind?

A

At a site away from the enzyme binding site which causes a conformational change of the enzyme, preventing the substrate from binding. Decreases rate of reaction, will NOT reach maximum saturation, same Km

70
Q

Do allosteric enzymes follow Michaelis-Menten kinetics?

A

No

71
Q

What do activators and inhibitors do to allosteric enzymes?

A

Activators bind to R form and increase affinity for substrate, inhibitors bind to T form and decrease affinity for substrate

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