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First Semester: Physiology 1 > Lecture 17: Blood 4 and Hemostasis 1 > Flashcards

Lecture 17: Blood 4 and Hemostasis 1 Flashcards

1
Q

Anemia

A

A reduction below normal in the O2 carrying capacity of blood and is characterized by a low hematocrit

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2
Q

Hematocrit

A

The percentage of total blood volume occupied by erythrocytes

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3
Q

Hematocrit is often reported as the

A

volume of packed RBC

PCV (packed cell volume)

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4
Q

Hematocrit is lower in anemia because

A

of too few circulating erythrocytes

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5
Q

Three ways anemia can be brought about

A
  1. Decreased rate of erythropoiesis
  2. Excessive loss of erythrocytes
  3. Deficiency in the hemoglobin content of erythrocytes
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6
Q

6 Categories of anemia

A
  1. Nutritional
  2. Pernicious
  3. Aplastic
  4. Renal
  5. Hemorrhagic
  6. Hemolytic
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7
Q

Nutritional anemia

A

Caused by dietary deficiency of a factor needed for erythropoiesis

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8
Q

Nutritional anemia example: Iron deficiency

A

Occurs when not enough iron is available for hemoglobin synthesis due to an iron deficient diet or poor iron absorption from the digestive tract
The usual number of RBC are produces but they contain less hemoglobin than usual and transport less O2

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9
Q

Nutritional anemia example: folic-acid deficiency

A

Folic acid is critical for stem cell division and maturation of erythrocytes, so deficiency causes fewer RBC formed and they are very fragile
Anemia is due to the production of fewer RBC and the early demise due to fragility

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10
Q

Pernicious anemia

A

Caused by an inability to absorb adequate amounts of V B12 from digestive tract

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11
Q

B12 is essential for

A

Proliferation and development of RBC and only when it is combined with intrinsic factor can it be absorbed by the intestinal tract by special support mechanisms

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12
Q

Intrinsic factor

A

Secreted by lining of stomach or pancreatic cells
When it is deficient, B12 isn’t sufficiently absorbed from the intestinal tract resulting in impairment of RBC production, leading to anemia

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13
Q

Aplastic anemia

A

-Caused by failure of the bone marrow to produce adequate number of RBC, even though everything needed for erythropoiesis is available

Destructive process may selectively reduce the RBC output by the bone marrow.

Severity depends on extent of erythropoietic tissue damage and can be fatal

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14
Q

In aplastic anemia, reduced erythropoietic activity can be caused by destruction of red bone marrow by:

A
  1. Toxic chemicals
  2. Radiation exposure
  3. Invasion of marrow by cancer cells
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15
Q

Renal anemia

A
  1. May be a consequence of renal disease
  2. Since erythropoietin from the kidneys is the primary stimulus for promoting erythropoiesis, inadequate EPO as a result of kidney disease causes insufficient RBC production and anemia
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16
Q

Hemorrhagic anemia

A

Caused by loss of substantial quantities of blood

Anemia is present until the lost cells are replaced

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17
Q

Hemolytic anemia

A

Caused by rupture of excessive numbers of circulating erythrocites

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18
Q

Example of hemolytic anemia: Immunohemolytic Disease of the Newborn

A
  • May occur in animals including horses and cats
  • Similar to the Rh factor in humans
  • Occurs when parents have different blood types and the offspring inherits father’s blood type
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19
Q

Immohemolytic disease of the newborn in horses

A
  • Sensitization of mare to foal’s blood type occurs during parturition
  • Mare produces antibodies against foal’s BT and transfers these antigens through her milk as foal nurses
  • Her antibodies destroy offspring’s RBC
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20
Q

Two types of hemolytic anemia in dogs

A
  1. Primary - Autoimmune hemolytic anemia (immune mediated hemolytic anemia)
    - Body attacks own RBC
    - Cause is unknown
  2. Secondary
    - Caused by parasite or toxin
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21
Q

Viscosity of blood depends mostly on

A

concentration of RBC

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22
Q

In anemia, viscosity decreases, leading to

A

decreased resistance to blood flow in the peripheral vessels -> increased venous return -> increased work load on the heart -> cardiac hypertrophy due to volume overload -> heart failure

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23
Q

Polycythemia

A

excess of circulating RBC and an elevated hematocrit

24
Q

Two types of polycythmia

A

Primary

Secondary

25
Q

Primary polycythemia

A
  • Caused by tumor-like condition of the bone marrow in which erythropoiesis proceeds at an excessive uncontrolled rate
  • Extra O2 carrying capacity is not beneficial because O2 delivery is more adequate with normal RBC numbers
26
Q

Primary Polycythemia adverse effects

A
  • Excessive # of RBC increase the viscosity of blood up to 5-7x which reduces o2 delivery to tissues
  • Increases total peripheral resistance, elevating blood pressure, and increase heart work load, and causes cardiac hypertrophy due to pressure overload
27
Q

Secondary polycythemia is also called

A

physiological polycythemia

28
Q

Secondary polycythemia

A
  • EPO induced adaptive mechanism to improve O2 carrying capacity of blood in response to a prolonged reduction in O2 delivery to tissues
  • Occurs in high altitudes where there is less O2
  • Occurs with chronic lung disease and heart disease
29
Q

Hematocrit in secondary polycythemia is usually _____ than that of primary polycythemia

A

lower
The rbc count usually rises about 30% above normal, causing increased viscosity -> pressure overloading of the heart -> cardiac hypertrophy

30
Q

An elevated hematocrit can occur when body loses fluid but not _______, such as in diarrhea

A

erythrocytes

dehydration

31
Q

Relative polycythemia

A
  • Dehydration
  • Normal number of erythrocytes but in a higher concentration due to less plasma
  • Blood viscosity increases, leading to sluggish blood flow
32
Q

The life span of erythrocytes is dependent on

A
  • species

- It has no nucleus so it is not able to replace the enzymes it needs for metabolism

33
Q

Erythrocytes are able to use some _____ as a source of energy

A

glucose

34
Q

Erythrocyte aging and degradation

A
  • Proteins go through a process of degradation and cannot be replaced
  • This causes leaky cell membranes
  • Aged cells pass through capillaries of spleen, liver, and bone marrow, and their leaky membranes rupture
  • Cellular remnants are engulfed by resident phagocytic macrophages
35
Q

Are platelets whole cells?

A

Nope

36
Q

Thrombocytopoiesis means

A

platelet production

37
Q

Platelet production occurs where?

A

In the bone marrow

38
Q

Normal bone marrow contains giant cells called _____ that give rise to platelets

A

megakaryocytes

39
Q

Upon maturing, megakaryotcytes

A
  • Shed cytoplasm in small membrane-enclosed packets which enter the circulation as platelets
  • It will gradually lose all cytoplasm, shedding about 4000 platelets before nucleus is engulfed by macrophages
40
Q

What hormone influences megakaryocyte maturation and platelet formation?

A

Thrombopoietin

41
Q

Thrombopoietin (TPO) is also called

A

Thrombocyte-stimulating factor

42
Q

Where is thrombopoietin produced?

A

The kidneys

43
Q

Thrombopoietin

A

A peptide hormone that accelerates platelet formation and stimulates the production of megakaryocytes resulting in a rapid increase in platelets

44
Q

Platelets remain functional for an average of ____ days

A

10

45
Q

Do platelets leave the blood?

A

Nope

46
Q

At any given time, about 1/3 of total platelets are

A

In storage in the spleen
These can be released into circulation by sympathetically induced splenic contraction in times of need (ex. bleeding from a vessel occurs)

47
Q

The vascular clotting system includes (3)

A
  • Plasma proteins
  • Tissues of circulatory network
  • Platelets
48
Q

Three functions of platelets

A
  1. Transport chemicals important to clotting process
  2. Formation of a temporary platelet plug that can slow the rate of blood loss while clotting occurs at the walls of damaged blood vessels
  3. Active contraction after clot formation has occured
49
Q

How/why do platelets actively contract after clot formation has occurred?

A
  • Contain filaments of actin and myosin

- Contraction of platelets shrinks the clot and reduces the size of the break in the vessel wall

50
Q

Hemostasis

A

The arrest of bleeding from a broken blood vessel and establishes a framework for tissue repair

51
Q

Although hemostasis is a series of steps, it is more like a

A

chain reaction

52
Q

Three major steps are involved in hemostasis

A
  1. Vascular spasm
  2. Platelet plug formation
  3. Clotting (coagulation) phase
53
Q

Vascular spasm stage of hemostasis

A
  • Cutting the wall of a blood vessel triggers contraction in the smooth muscle fibers in the vessel wall
  • Contraction produces a local vascular spasm that decreases the diameter of the vessel at the site of the injury
  • Constriction slows blood flow through the defect and thus minimizes blood loss
54
Q

During vascular spasm phase, what changes occur in the endothelium at the injury?

A
  • Endothelial cells contract and expose underlying basement membrane to the bloodstream
  • Endothelial cells begin releasing chemical factors
  • Endothelial cell membranes become sticky and in small blood vessels, endothelial cells on the opposite sides of the blood vessels may stick together which further seals off the damaged vessel
55
Q

Endothelin

A
  • Example of chemical factor released by endothelial cells during vascular phase
  • Stimulates smooth muscle contraction
  • Stimulates the division of endothelial cells, smooth muscle cells, and fibroblasts to accelerate the repair process
56
Q

Are physical measures alone enough to completely prevent blood loss during vascular stage?

A

Nope, but important in minimizing blood flow until other hemostatic measures are able to plug up defect

First Semester: Physiology 1 (34 decks)

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