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Animal Body Systems & Cases > Blood > Flashcards

Blood Flashcards

1
Q

What are the two portions that make up blood

A
  1. Plasma
  2. Corpusculated portion (blood cells)
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2
Q

Where does hematopoiesis occur in neonates and juveniles

A

The bone marrow of long bones

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3
Q

Where does hematopoiesis occur in adults

A

The bone marrow of flat bones and the ends of long bones

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4
Q

What are 3 essential components needed for hematopoiesis to occur

A
  1. Stem cell pool
  2. Hematopoietic inductive microenvironment
  3. Hematopoietic cytokines
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5
Q

What is the earliest recognizable erythroid precursor

A

Rubriblast

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6
Q

Which stage of erythrocyte precursor can no longer undergo division

A

Metarubricyte

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7
Q

List 3 changes that occur as erythrocyte precursors mature

A
  1. Decrease in cell size
  2. Increasing proportion of the cell occupied by cytoplasm
  3. Decreased cytoplasmic basophilia
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8
Q

Which stage of erythrocyte precursor loses its nucleus

A

Reticulocyte (one stage before a mature RBC)

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9
Q

Where is erythropoietin produced

A

By the peritubular interstitial cells of the kidney

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10
Q

What physiological trigger causes EPO release

A

Low levels of oxygen in the blood

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11
Q

List 3 major functions of EPO

A
  1. Proliferation of committed erythroid cells
  2. Increase in hemoglobin synthesis
  3. Increase erythroid cell maturation rate
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12
Q

What are the 3 major functions of erythrocytes

A
  1. Transport oxygen
  2. Transport carbon dioxide
  3. Buffer hydrogen ions
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13
Q

What pathway do RBCs use to get most of their energy

A

Embden-Meyerhof pathway (anaerobic)

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14
Q

What is the role of NADH in RBC metabolism

A

It maintains iron in a reduced state (Fe2+) and glutathione in a reduced state

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15
Q

What are the 2 side pathways of RBC metabolism and what are their functions

A
  1. DPG shunt (modulate the affinity of hemoglobin for oxygen)
  2. Pentose phosphate pathway (generates more NADH)
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16
Q

What molecule controls the rate of iron absorption

A

Hepcidin

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17
Q

How is iron transported in the blood

A

It is bound to transferrin

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18
Q

Where is iron stored as ferritin

A

In tissues or plasma

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19
Q

Where is iron stored as haemosiderin

A

In tissues only

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20
Q

Explain the route that iron takes from the intestine to being incorporated into an RBC

A

Iron goes into the enterocyte and then is absorbed into the blood (rate of which is controlled by hepcidin). In the blood it is bound to transferrin. In red cell precursors, the iron will release from transferrin and incorporate into heme, which will become part of the hemoglobin molecule

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21
Q

How many oxygen molecules can be carried on hemoglobin

A

4

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22
Q

What can happen as a by-product of oxygen reacting with hemoglobin to make oxyhemoglobin

A

The iron in the hemoglobin can oxidize into the ferric state (Fe3+) and form methemoglobin and free oxygen

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23
Q

What is needed for the reaction to revert methemoglobin to function hemoglobin

A
  1. Cytochrome-b5-reductase
  2. NADH (from RBC metabolism)
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24
Q

Which two forms of oxidative injury to RBCs are irreversible

A
  1. Oxidative denaturation of Hb to form Heinz bodies
  2. Oxidative injury to membrane proteins
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25
Q

Which form of oxidative injury to RBCs are cats highly susceptible to

A

Hb oxidative denaturation to form Heinz bodies

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26
Q

What is the life span of a RBC in: horses & cows, dogs, and cat

A

Horses & cows: 150 days
Dogs: 100 days
Cats: 70 days

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27
Q

Hb in mammals should be ___ of the total hemoatocrit

A

1/3

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28
Q

What is the term for increased PCV, RBC and Hb, and what is the reason for this to happen

A

Erythrocytosis
Due to dehydration or increase EPO production

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29
Q

What influence does increased reticulocytes have on laboratory diagnostics

A

Increased MCV and decrease MCHC

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30
Q

Where does hematopoiesis occur in fetuses

A

The liver and spleen

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31
Q

How much of the body’s iron is stored in hemoglobin

A

50-70%

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32
Q

Describe the sigmoid oxygen dissociation curve

A

The % saturation of Hb with oxygen plotted against the partial pressure of oxygen (it looks like a hill)

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33
Q

What are the 3 classes of granulocytes

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
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34
Q

What are the 2 classes of mononuclear cells

A
  1. Lymphocytes
  2. Monocytes
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35
Q

____ have more neutrophils, where as ___ have more lymphocytes

A

Dogs, cats and horse have more neutrophils
Ruminants and rodents have more lymphocytes

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36
Q

What is the role of glutathione (GSH)

A

Protecting Hb and other red cell components against oxidative injury

37
Q

The majority of lymphocyte production occurs ___, whereas the majority of granulocyte production occurs ___

A

Lymphocyte: spleen, lymph nodes and GALT
Granulocytes: bone marrow

38
Q

What are the 3 major pools of neutrophils precursors in the bone marrow

A
  1. Mitotic pool
  2. Maturation pool
  3. Storage pool
39
Q

Dogs, pigs and cats have a __ neutrophil storage pool

A

Large

40
Q

What are the 2 main storage pools of neutrophils in the blood

A
  1. Marginal (neutrophils adhered to the endothelium)
  2. Circulating (neutrophils that are free flowing)
41
Q

In which animal is the marginal: circulating neutrophil pool ratio 3:1

A

Cats

42
Q

Define “left shift”

A

When there is an increase in circulating band neutrophils (immature neutrophils)

43
Q

What are ‘toxic changes’ and what are they represented by

A

Toxic changes are morphological abnormalities of the cytoplasm of neutrophils
They are represented by:
1. Increased cytoplasmic basophilia
2. Dohle bodies (aggregates of rough ER)
3. Foamy cytoplasm
4. Toxic granules

44
Q

List the causes of neutrophilia

A
  1. Catecholamine mediated stress
  2. Corticosteroid induced
  3. Inflammation
45
Q

List the causes of neutropenia

A
  1. Acute severe inflammation
  2. Endotoxemia
  3. Reduced production in bone marrow
  4. Increased peripheral destruction
46
Q

Define ‘degenerative left shift’

A

When the absolute number of immature neutrophils exceeds the absolute number of segmented neutrophils

47
Q

Which cause of neutrophilia will also cause a left shift

A

Inflammation

48
Q

In which species is inflammatory neutropenia more common

A

Ruminants and horses

49
Q

List the causes of lymphocytosis

A
  1. Catecholamine-mediated stress
  2. Age/young animals
  3. Chronic inflammation
  4. Endocrine disorders
  5. Lymphoid neoplasia
50
Q

List the causes of lymphopenia

A
  1. Corticosteroid-induced
  2. Acute inflammation
  3. Excess loss
  4. Congenital/acquired
  5. Lymphoma
51
Q

List the causes of monocytosis

A
  1. Inflammation
  2. Corticosteroid-mediated
52
Q

List the causes of eosinophilia

A
  1. Hypersensitivity/allergic disorders
  2. Parasitism
  3. Idiopathic conditions
  4. Paraneoplastic syndrome
53
Q

List the causes of eosinopenia

A
  1. Cortico-steroid induced
54
Q

Describe the mechanism of acute severe inflammation neutropenia

A

The rate of migration of neutrophils into the tissues exceeds the rate at which they can be released from the bone marrow

55
Q

Describe the mechanism of endotoxemia neutropenia

A

Endotoxins cause a rapid shift of neutrophils from the circulating to marginal pools by promoting adhesion to endothelial cells

56
Q

Describe the mechanism of catecholamine mediated stress neutrophilia

A

Catecholamines increase blood flow and cause a shift from marginal to circulating pool

57
Q

Describe the mechanism of corticosteroid induced neutrophilia

A

Increase release of neutrophils from bone marrow stores, cause a shift from marginal to circulating pool and increase life span of neutrophils in the blood

58
Q

Describe the mechanism of inflammatory neutrophilia

A

Cytokines cause the release of pre-formed neutrophils from the bone marrow and increase production in the bone marrow

59
Q

Describe the appearance of reactive lymphocytes

A

Larger than a regular lymphocyte with deeply blue (basophilic) cytoplasm and a mature chromatin pattern

60
Q

Describe the mechanism of corticosteroid induced lymphopenia

A

Increased migration of lymphocytes to lymphoid tissues and decreased efflux from lymph nodes

61
Q

Describe the mechanism of acute inflammatory lymphopenia

A

Increased migration to inflamed tissues, homing of lymphocytes in lymphoid tissue and decreased movement of lymphocytes from lymph nodes

62
Q

Describe the mechanism of catecholamine mediated stress lymphocytosis

A

Redistribution of lymphocytes from the spleen, more common in cats and foals

63
Q

Describe the mechanism of chronic inflammatory lymphocytosis

A

Increased lymphopoiesis in response to chronic antigenic stimulation

64
Q

Which endocrine disorder is most likely to cause lymphocytosis in cats

A

Hyperthyroidism

65
Q

Which endocrine disorder is most likely to cause lymphocytosis in dogs

A

Hyperadrenocorticism

66
Q

What can be a result of overactive haemostasis

A

The formation of thrombi that block blood vessels, resulting in ischaemia

67
Q

Why does hemostasis not occur in steady state conditions

A

The intact endothelium prevents circulating platelets and clotting factors from interacting with procoagulant proteins in the ECM by synthesizing anticoagulant factors

68
Q

What are the two phases of primary hemostasis

A

Vascular and platelet phase

69
Q

List 2 anticoagulant factors

A

Nitric oxide and prostaglandin E2

70
Q

List 3 factors that activate the endothelium to start producing procoagulant facotrs

A
  1. Direct injury
  2. Infectious agents
  3. Oxidative injury
71
Q

What is the main growth factor that regulates the production of platelets

A

Thrombopoietin

72
Q

Describe what happens in the vascular phase of primary hemostasis

A

Following injury to a blood vessel, vasoconstriction by contraction of smooth muscle reduces blood loss
This is cause by neural reflexes and endothelin

73
Q

What is von Willebrand factor

A

A substance found in plasma and the sub-endothelium that binds platelets, forming a bridge between sub-endothelial collagen and platelet receptors

74
Q

List 2 things that happen to platelets following platelet activation

A
  1. Undergo a shape change (create projections of the cell membrane)
  2. Release their granular content (coagulation factors)
75
Q

What stimulates recruitment and aggregation of platelets following platelet activation

A

ADP and thromboxane A2 (produced by platelets)

76
Q

How does the endothelium restrict the formation of the platelet plug to the site of injury

A

It secretes NO and PGI2 in response to the substances that platelets release, which inactivate anticoagulant factors

77
Q

Where are coagulation factors produced

A

The liver

78
Q

Which coagulation factors are vitamin K dependent

A

Factor II, Factor VII, Factor IX, Factor X

79
Q

Which electrolyte is required for nearly all reactions in the coagulation cascade

A

Calcium

80
Q

List 2 things that strengthen the platelet plug formed during primary homeostasis

A
  1. Fibrin
  2. Contraction of the platelet cytoskeleton
81
Q

What is the final product of the coagulation cascade

A

Cross-linked fibrin

82
Q

What initiates the coagulation cascade

A

The exposure of tissue factor, expressed on sub-endothelial cells such as fibroblasts and smooth muscle cells

83
Q

Describe how the intrinsic pathway of coagulation is activated from the extrinsic pathway

A

The small amount of thrombin generated from the extrinsic pathway amplifies its production by activation factor XI in the intrinsic pathway

84
Q

List the intermediates of the common pathway of the coagulation cascade, from thrombin to cross-linked fibrin

A

Thrombin -> fibrinogen -> fibrin -> cross-linked fibrin

85
Q

What activates tertiary hemostasis (fibrinolysis)

A

Tissue plasminogen activator (tPA)

86
Q

What is the role of tissue plasminogen activator

A

It cleaves plasminogen in the plasma to plasmin so it can cleave fibrinogen and fibrin

87
Q

What helps maintain the dissolution of a platelet plug/thrombus at an appropriate rate

A

Free plasmin is inactivated by alpha-2 plasmin inhibitor

88
Q

What is the relationship between the kallikrein-kinin system and the coagulation cascade

A

When factor XII from the intrinsic pathway of coagulation is activated, it converts prekallikrein to kallikrein, which then converts HMWK to bradykinin, causing vasodilation, increased vascular permeability and stimulates an inflammatory response

Animal Body Systems & Cases (10 decks)

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