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Form and Function > Hematology > Flashcards

Hematology Flashcards

1
Q

Electrolytes on chem panel?

A

Sodium, potassium, chloride

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2
Q

pH indicators on chem panel?

A

Bicarbonate, anion gap

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3
Q

Kidney function indicators on chem panel?

A

Urea, creatinine

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4
Q

Indicators of metabolic status on chem panel?

A

Glucose, cholesterol

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5
Q

Liver function indicators on chem panel?

A

Bilirubin, alk phos, GGT, ALT, GLDH

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6
Q

Muscle enzyme on chem panel?

A

CK

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7
Q

Three most common proteins in blood plasma?

A

Albumins, globulins, fibrinogen

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8
Q

Site of synthesis of plasma proteins?

A

Liver, lymphatics, mucosal tissue

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9
Q

Sites of turnover for plasma proteins?

A

Liver, tissues, mononuclear phagocytes

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10
Q

Two main factors affecting blood plasma protein levels?

A

Liver function and dietary protein deficiency

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11
Q

Value in bloodwork which estimates plasma protein levels?

A

Specific gravity (refractometry)

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12
Q

Three main visible abnormalities in blood plasma?

A

Icterus (yellow), lipemia (white/cloudy), hemolysis (red)

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13
Q

Difference between hematocrit and PCV?

A

Hematocrit is a proportion of RBC volume, PCV is the height of the RBC column in spun blood

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14
Q

Factors contributing to normal variation in RBC numbers?

A

Species, breed, age, excitement, exercise, pregnancy/lactation/estrus, altitude

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15
Q

Factors contributing to abnormal variation in RBC numbers?

A

Anemia, dehydration, erythrocytosis

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16
Q

Which molecules determine an individual’s blood type?

A

Surface glycoproteins

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17
Q

Cytoskeleton element responsible for RBC shape?

A

Spectrin

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18
Q

Which species have nucleated RBCs?

A

Amphibians, reptiles, birds

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19
Q

Normal shape of RBCs?

A

Biconcave disc

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20
Q

Functions of RBC shape?

A

Increase SA:V, allow RBCs to fold/bend

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21
Q

Name for abnormally shaped RBC?

A

Poikilocyte

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22
Q

How is gas concentration represented in blood?

A

Partial pressure

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23
Q

What % of oxygen in blood is bound to hemoglobin?

A

98.5%

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24
Q

Chemical structure of hemoglobin?

A

4 subunits (globins), each with one heme group bound to ferrous iron (Fe2+)

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25
Q

Hemoglobin found in muscle?

A

Myoglobin - one polypeptide chain with one heme group

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26
Q

Structure of heme group in deoxygenated state?

A

Non-planar (dark red)

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27
Q

Structure of heme group in oxygenated state?

A

Planar (bright red)

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28
Q

Definition of cooperative binding?

A

When oxygen binds to one Hb subunit, it increases the oxygen binding affinity of other subunits

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29
Q

Chemical group causing change in heme structure during oxygen binding?

A

Histidine residue (pulled towards heme)

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30
Q

Maximum saturation of oxygen in blood with hemoglobin?

A

20ml O2 per 100ml blood

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31
Q

Define Bohr Effect

A

Right-shift of oxygen disassociation curve to maximize oxygen delivery to tissues with high oxygen demand

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32
Q

Mechanisms by which oxygen disassociation can be increased?

A

Increased acidity, CO2, temperature, BPG

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33
Q

Mechanism of CO toxicity in blood?

A

Hemoglobin affinity is 220x higher for CO than O2 - inhibits oxygen delivery to tissues

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34
Q

Define methemoglobinemia

A

Oxidization of iron in heme group from ferrous (2+) to ferric (3+), which cannot bind O2. Caused by nitrites, chlorates, some antibiotics, acetaminophen, topical anesthetics.

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35
Q

How is hematocrit calculated in a CBC?

A

HCT = RBC x MCV

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36
Q

What is MCHC?

A

Mean corpuscular hemoglobin concentration (average concentration of hemoglobin in a given volume of RBC, often in g/L)

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37
Q

What is MCH?

A

Mean corpuscular hemoglobin (average amount of hemoglobin per individual RBC, often in picograms)

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38
Q

Two mechanisms by which RBCs/Hgb increases CO2 transport?

A

Conversion of CO2 to bicarbonate by carbonic anhydrase, and counter-transportation of bicarbonate with chloride, allowing more conversion

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39
Q

Define the Haldane effect

A

Oxygenated hemoglobin has deprotonated histidine, and deoxygenation of hemoglobin results in histidine protonation

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40
Q

Relationship between Haldane effect and oxygen binding?

A

Transport of bicarbonate out of RBCs results in increased proton concentrations in RBCs, resulting in increased protonation of histidine, increasing oxygen disassociation

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41
Q

Relationship between Haldane effect and CO2 transport?

A

Oxygen disassociation causes protonation of histidine, deacidifying RBCs and allowing for increased blood carrying capacity for CO2

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42
Q

Location of hematopoiesis in young vs. adult animals?

A

Young animals: tibia and femur
Adult animals: vertebrae, sternum, ribs

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43
Q

Hormone involved in regulating erythropoiesis?

A

Erythropoietin

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44
Q

6 stages of erythrocyte development?

A

Rubriblast, prorubricyte, rubricyte, metarubricyte, polychromatic erythrocyte, mature erythrocyte

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45
Q

Stage of erythrocyte development with maximum hemoglobin production?

A

Rubricyte

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46
Q

5 main steps of hemoglobin synthesis?

A

2 succinyl-CoA + 2 glycine –> pyrrole

4 pyrrole –> protoporphyrin IX

Protoporphyrin IX + Fe2+ –> heme

Heme + polypeptide –> hemoglobin chain

2 a + 2 B chains –> hemoglobin

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47
Q

Mechanism for iron uptake for use in hemoglobin?

A

Slow absorption in small intestine, bound to transferrin as a Fe-transferrin complex in blood to rubricytes, where it is endocytosed and delivered to mitochondria

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48
Q

Main characteristics of metarubricytes?

A

Mitosis stops, hemoglobin production nears completion, nucleus condenses and is expelled at the end of this stage

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49
Q

What differentiates polychromatophilic erythrocytes from mature erythrocytes?

A

Polychromic staining due to residual ribosomal RNA

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50
Q

Which species never releases immature erythrocytes?

A

Horses

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51
Q

Another term for polychromatophilic erythrocytes?

A

Reticulocytes

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52
Q

Location of erythropoietin synthesis?

A

Kidneys

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53
Q

Important nutritional factors for erythropoiesis?

A

Iron for hemoglobin production

B9 (folic acid) and B12 for DNA synthesis

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54
Q

Describe morphology of degenerating RBCs

A

Without a nucleus or capacity for protein synthesis, RBCs cannot repair themselves. Damage to membrane allows water to enter, causing RBCs to lose their biconcave shape and become spherical

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55
Q

What is MPS?

A

Mononuclear phagocytic system - responsible for targeting abnormally-shaped RBCs for destruction

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56
Q

Primary site of RBC filtering?

A

Spleen

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57
Q

How does spleen physically filter RBCs?

A

Spherocytes are larger and get physically trapped in the spleen where they can be targeted by macrophages

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58
Q

Where does biliruben come from?

A

When RBC is broken down, heme is released and further broken down to release porphyrin, which is converted to biliruben

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59
Q

What does the “retics” value in a CBC indicate?

A

Measured in cases of anemia: high retics indicates regenerative anemia, low retics indicates nonregenerative anemia

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60
Q

What is RPI?

A

Measured in dogs; adjust retics count relative to degree of anemia. Not commonly performed anymore

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61
Q

Unique feature of camelid RBCs?

A

Ovoid shape

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62
Q

Definition of Rouleaux and species in which it is normal?

A

Coin-like stacking of RBCs on a blood slide. Can be normal in horses in cats, but can indicate disease in other patients. Can also be an artifact of poor slide preparation.

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63
Q

What does hypochromia of RBCs indicate?

A

Iron deficiency

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64
Q

What do microcytic RBCs indicate?

A

Iron deficiency anemia

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65
Q

What do macrocytic RBCs indicate?

A

Increased polychromatophilic reticulocytes

66
Q

What are ghost cells?

A

Red blood cells leached of hemoglobin; indicate intravascular hemolysis

67
Q

What does a high number of spherocytes typically indicate?

A

IMHA

68
Q

What do eccentrocytes/Heinz bodies look like and what do they typically indicate?

A

Asymmetric RBCs - often indicate onion toxicity

69
Q

What are the sources of reactive oxygen species in RBCs?

A

Endogenous: Oxygen transport

Exogenous: Exposure to drugs, toxins, etc.

70
Q

What does hemoglobin become when damaged by reactive oxygen species?

A

Methemoglobin

71
Q

Antioxidant defense mechanism in RBC?

A

Pentose phosphate pathway catalyzed by G-6-P dehydrogenase

72
Q

What are Heinz bodies?

A

Aggregates of denatured hemoglobin

73
Q

What are eccentrocytes?

A

RBCs which have undergone lipid peroxidation

74
Q

What is the role of selenium in RBCs?

A

Essential co-factor for the pentose phosphate pathway to prevent oxidative damage in RBCs

75
Q

Three main causes of low RBC count?

A

Hemolytic, hemorrhagic, dyshemopoietic

76
Q

What does hyperchromia of RBCs indicate?

A

Nothing - only ever due to an issue with CBC

77
Q

Types of erythrocytosis?

A

Relative - due to dehydration, fluid redistribution, or splenic contraction in horses

Absolute - Primary (erythropoiesis independent of erythropoietin (rare)) or secondary (increased erythropoietin due to hypoxia or renal disease)

78
Q

Which WBC types are included under the category of “agranulocytes” in a CBC?

A

Lymphocytes and monocytes

79
Q

6 main stages of granulopoiesis?

A

Myeloblast, promyelocyte, myelocyte, metamyelocyte, band cell, mature granulocyte

80
Q

Role of promyelocyte stage in granulopoiesis?

A

Make lysosomal hydrolases - azurophilic granules common to all granulocytes

81
Q

Role of myelocyte stage in granulopoiesis?

A

Production of molecules for cell type-specific granules

82
Q

Characteristics of metamyelocyte stage in granulopoiesis?

A

Round nucleus, azurophilic and cell-specific granules both present in high abundance. Reduced Golgi

83
Q

What do bands indicate on a CBC?

A

High number of immature granulocytes (typically neutrophils) - Left shift, indicates inflammation

84
Q

Primary role of neutrophils?

A

Rapid response to inflammation/infection. Phagocytosis

85
Q

Primary role of eosinophils?

A

Response to parasitic infections

86
Q

Primary role of basophils?

A

Response to ticks and roundworms, involvement in allergic reactions

87
Q

Is there a storage pool of monocytes in the bone marrow?

A

No

88
Q

Progenitor cell of platelets?

A

Megakaryocyte

89
Q

Two most abundant WBC types in all species?

A

Neutrophils and lymphocytes

90
Q

Main cytoplasmic contents of platelets?

A

Actin/myosin, ER and Golgi, mitochondria

91
Q

Histological characteristics of rubriblast/prorubricyte?

A

Dark blue staining, little cytoplasm

92
Q

Histological characteristics of rubricytes?

A

Round nucleus, basophilic cytoplasm

93
Q

Histological characteristics of metarubricytes?

A

Round nucleus, more condensed and eosinophilic cytoplasm

94
Q

Two main pools of mature neutrophils in the body?

A

Circulating (large vessels) and marginating (microcirculation)

95
Q

Effect of stress hormones (e.g. cortisol) on neutrophil levels?

A

Decrease (inhibits growth factors and cytokines) - hence why corticosteroids can be used as anti-inflammatory medication

96
Q

Effect of epinephrine on leukocyte numbers?

A

Increased due to leukocytes being flushed out of marginating pool and into circulating pool. Neutrophilia/lymphocytosis without left shift.

97
Q

Clinical signs of inflammation?

A

Heat, pain, swelling, redness, loss of function

98
Q

Possible CBC changes due to mild inflammation?

A

Slightly elevated WBC count, upper normal neutrophil count

99
Q

Possible CBC changes due to moderate inflammation?

A

Leukocytosis, neutrophilia with left shift

100
Q

Possible CBC changes due to severe inflammation?

A

Marked leukocytosis with neutrophilia. Could also present as leukopenia and neutropenia due to increased tissue consumption. Pronounced left shift present regardless.

101
Q

Possible CBC changes due to chronic inflammation?

A

Mild to moderate leukocytosis, monocytosis with possible plasma cells noted. Could also present with leukopenia

102
Q

4 main stages of inflammation (as related to blood vessels)

A
  1. Local vasodilation
  2. Increased capillary permeability leading to fluid leakage
  3. Granulocyte and monocyte migration into tissue
  4. Clot formation due to fibrinogen leakage into tissue space
103
Q

Action of kinins?

A

Promote vasodilation, increase permeability, contribute to pain sensation

104
Q

Action of complement system?

A

Pathogen lysis via membrane attack complex, and opsonization for phagocytosis

105
Q

Action of acute phase proteins (C-reactive protein)?

A

Marks dead or dying cells to activate complement. Used as a diagnostic marker for inflammation

106
Q

Describe how a leukocyte would go about exiting blood vessels and entering tissues?

A

Rolling facilitated by selectin ligands on leukocyte and selectins on endothelium. Adhesion facilitated by integrins on leukocyte and integrin receptors on endothelium. Diapedesis between endothelial cells

107
Q

What could eosinophilia indicate?

A

Parasitic infection, allergic reaction in horses and dogs

108
Q

What could basophilia indicate?

A

Uncommon. Could indicate hypersensitivity and chronic inflammatory states

109
Q

What could monocytosis indicate?

A

Prolonged inflammatory response

110
Q

What is a granuloma?

A

Collection of immune cells which form to wall off an infection

111
Q

Transit time of neutrophils from stem cell to granulocyte in circulation?

A

7-10 days

112
Q

Half life of circulating neutrophil?

A

6-10 hours

113
Q

Blood proteins increased by inflammation?

A

Growth factors (G-CSF) and cytokines (IL-1, IL-6). Possibly also antimicrobial peptides

114
Q

Possible CBC changes caused by granuloma formation?

A

Pronounced neutrophilia with left shift (due to increased production and inhibited consumption due to wall)

115
Q

What is the main mechanism involved in the transition from hemostasis to fibrinolysis?

A

Thrombin inhibits its own production, so gradually stops inhibiting fibrinolysis.

116
Q

Examples of conditions caused by excess hemostasis?

A

Deep vein thrombosis, stroke, myocardial infarction, embolism

117
Q

Condition caused by a lack of hemostasis?

A

Hemorrhage, petechia

118
Q

Two main processes during primary hemostasis?

A

Vasoconstriction and platelet plug formation

119
Q

Main process during secondary hemostasis?

A

Clot formation

120
Q

Proteins involved in platelet plug formation?

A

von Willebrand Factor, subendothelial matrix proteins (collagen), integrin/non-integrin receptors on platelets

121
Q

Factors involved in promoting platelet plug formation?

A

Thrombin, collagen, thromboxane, ADP

122
Q

Factors involved in inhibiting platelet plug formation?

A

Nitric oxide, prostaglandin, ADPase

123
Q

Sequence of events in platelet plug formation?

A

Capture, adhesion, activation, plug formation

124
Q

Secondary sites of thrombopoiesis?

A

Spleen, lung

125
Q

Define endomitosis

A

Division of chromosomes without nuclear division (relevant in megakaryocytes, which can be up to 64N)

126
Q

Approximate number of platelets produced per megakaryocytes?

A

1000-5000

127
Q

Hormone involved in platelet production?

A

Thrombopoietin; produced in liver. Negative feedback mechanism via TPO sequesteration by platelets

128
Q

Effect of corticosteroids on platelet levels?

A

Causes thrombocytosis

129
Q

Where does vWf come from?

A

Weibel palade bodies in endothelial cells. Release induced by thrombin

130
Q

When is collagen-tethered vWf necessary for platelet adhesion?

A

Blood vessels with high shear rates

131
Q

Which cell surface factors on platelets are bound to vWf/collagen?

A

Non-integrin receptors

132
Q

Cell surface changes to platelets when activated?

A

Granule release (vWf, fibrinogen, factors V/XIII, ADP, serotonin, calcium), membrane metabolism to synthesize eicosanoids, membrane flipping, fibrinogen receptor activation (integrin), increased cell SA

133
Q

Primary ion required for hemostasis?

A

Calcium

134
Q

What is a thrombus?

A

A grouping of platelets held together by fibrinogen bound to fibrinogen receptors

135
Q

Steps of clot stabilization (after platelet plug formation)

A

Fibrinogen linking adjacent platelets activated by thrombin to form fibrin, then fibrin stabilizing factor (XIII) causes adjacent fibrin molecules to cross-link

136
Q

How is an activated coagulation factor indicated?

A

With an “a” after the roman numeral

137
Q

What is coagulation factor I?

A

Fibrinogen

138
Q

What is coagulation factor II?

A

Prothrombin

139
Q

What is coagulation factor IV?

A

Ionized calcium

140
Q

What does coagulation factor Xa do?

A

Converts prothrombin to thrombin

141
Q

What does thrombin do?

A

Converts fibrinogen to fibrin

142
Q

What does coagulation factor XIII do?

A

Cross-links fibrin

143
Q

Describe initiation phase of coagulation?

A

Damaged endothelium exposes tissue factor, which forms a complex with factor VIIa, activating factor X, generating a small amount of thrombin

144
Q

What is coagulation factor III?

A

Tissue factor

145
Q

Describe amplification phase of coagulation?

A

Thrombin causes membrane flipping, enables assembling of clotting factor complexes and activates these factors

146
Q

Describe propagation phase of coagulation?

A

Coagulation complexes on platelet surfaces causes production of a large amount of factor Xa, leading to robust fibrin formation via thrombin activation

147
Q

Two main pathways for clot formation

A

Intrinsic (initiates clotting independent of tissues) and extrinsic (tissue-dependent clotting)

148
Q

What does antithrombin do?

A

Binds free thrombin in circulation, preventing new clot formation beyond injury site

149
Q

How does fibrin inhibit clotting?

A

Binds thrombin, reducing its ability to produce more fibrin from fibrinogen

150
Q

What does plasmin do?

A

Degrades fibrin fibers, procoagulants (fibrinogen, prothrombin, Factors X/VIII/XII)

151
Q

Which factors regulate conversion of plasminogen to plasmin?

A

Tissue plasmin activator and urokinase upregulate, plasmin activator inhibitor and a2-antiplasmin downregulate

152
Q

What does heparin do?

A

Amplifies the effect of antithrombin when bound to it

153
Q

Natural anticoagulant features of endothelium?

A

Vessel wall smoothness, glycocalyx barrier repels clotting factors, production of thrombin inhibitors and vasodilators (nitric oxide, prostacyclin)

154
Q

What is the most common class of oral anticoagulant drugs?

A

Factor Xa inhibitors

155
Q

How do anticoagulant rodenticides inhibit clotting?

A

Inhibiting vitamin K (reduces production of clotting factors VII, IX, X), which prevents carboxylation needed to bind calcium

156
Q

What are examples of diseases which can reduce blood clotting?

A

von Willebrand disease, vitamin K deficiency (can include GI disease impairing absorption, and liver disease

157
Q

How do clinical signs differ between disorders of primary and secondary hemostasis?

A

Disorders of primary hemostasis likely result in petechia, hematochezia, hematuria, epistaxis. Disorders of secondary hemostasis are more likely to result in widespread bleeding (hematomas, etc.)

158
Q

What is DIC&F?

A

Disseminated intravascular coagulation and fibrinolysis. Excessive and simultaneous clotting and bleeding - typically occurs shortly before death and secondary to conditions such as sepsis, trauma

159
Q

What is BMBT (bloodwork value)?

A

Buccal mucosal bleeding time - a measure of how long it takes for a platelet plug to form after a superficial vessel is cut

160
Q

What is ACT?

A

Activated coagulation time. Evaluates the function of the intrinsic clotting pathway

161
Q

What is PTT?

A

Partial thromboplastin time. Measures intrinsic/common pathway

162
Q

What is PT?

A

Prothrombin time. Tests extrinsic and common pathway

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