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Nur 1142 Patho > Hematology > Flashcards

Hematology Flashcards

1
Q

Blood is made of what percentage of water?

A

92% water and 8% dissolved substances (solutes)

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2
Q

What percentage is plasma?

A

50-55%

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3
Q

Whole blood is percentage by volume

A

Plasma 55%
Formed elements 45%

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4
Q

Plasma is made up of what volume of blood?

A

50-55% of blood volume of which 90% is water and 10% solute

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5
Q

Whole blood is made of ?

A

Plasma 55% of total blood
Buffy coat ( leukocytes & plasma) <1%
Erythrocytes 45%

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6
Q

50% of cells in blood is what?

A

Erythrocytes- RBC
Leukocytes- WBC
Platelet - Thrombocytes

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7
Q

List the plasma proteins

A

Albumin - most abundant-57%
Globulins
Clotting factors- (fibrinogen)

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8
Q

Buffy coat is made up of what?

A
  1. Platelets

2 Leukocytes - neutrophils, lymphocytes, monocytes, eosinophils and basophils

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9
Q

Which is the most abundant leukocyte

A

Neutrophils

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10
Q

What’s the function of blood!

A

Respiratory gas exchange
Transport of nutrients and waste
Themoregulation
Hemostasis
Immunity
Regulate cell function, osmotic pressure and pH

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11
Q

Plasma is made up of what?

A

Water, electrolytes and gases.
Proteins which are; albumin, globulins, fibrinogen, additional immune mediators and clotting factors

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12
Q

What is the function of plasma protein albumin

A

Albumin is most abundant protein

**Function*
works to maintain colloidal osmotic pressure within circulatory system

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13
Q

What’s the function of blood protein globulin(alpha, beta and gamma globulins

A

Gamma globulin is immunoglobulin- antibodies

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14
Q

Function of fibrinogen

A

Protein that converts to fibrin and is necessary for clot formation

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15
Q

Erythrocytes- RBC

A

Most prevalent blood cell in peripheral blood
Function:
1. Tissue oxygenation, contain Hgb
2. has compensatory capability.ie can increase number in anoxic environment

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16
Q

What the classification of leukocytes?

A

Granulocyte and agranulocyte

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17
Q

Examples of granulocyte are

A

Neutrophils
Basophils
Eosinophils

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18
Q

Examples of agranulocytes are

A

Lymphocytes and monocytes

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19
Q

What are platelets(thrombocytes)?

A

Platelets are cellular fragments stemming from the megakaryocytrs in bone marrow

Function:
Important for clotting

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20
Q

RBC originate from?

A

Myeloid stem cells

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21
Q

Granulocyte originates from where?

A

Myeloid stem cells to
myeloblast to
granulocyte ( neutrophil, basophils and eosinophils)

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22
Q

Cytokines

A

Small proteins important for cell signalling

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23
Q

What are the classifications of cytokines?

A

Autocrine action: have effects on cells that secrete them

Paracrine action: have effects on surrounding cells

Endocrine action: may also act on far away cells

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24
Q

What function of cytokines

A

Play role in inflammation, pain sepsis

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25
Q

Erythropoietin EPO

A

Red blood cell production

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26
Q

Eosinophils

A

Nucleus sometimes in 2 pieces

Has bright red granules in cytoplasm

Function:
Control inflammation, phagocytosis, defence agains parasites, allergic reaction

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27
Q

What are functions of eosinophils

A

Control inflammation
Phagocytosis
Defence against parasites
Allergic reaction

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28
Q

Basophil characteristics

A

Has bright blue granule in cell protoplasm

Function;
Allergic reaction
Parasites

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29
Q

Basophil function

A

Inflammation
Allergic reaction

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30
Q

Neutrophils characteristics

A

Nucleus is segmented
Main component of pus

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31
Q

Function of neutrophils

A

For response to infection and inflammation. Phagocytosis

Increase in number is indication of infection

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32
Q

Characteristics of platelet

A

Derived from megakaryocytes

Circulate in inactive state

Activate the clotting cascade

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33
Q

Where do platelet originate from

A

Megakaryocytes

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34
Q

RBC is made up of what?

A

4 heme and 4 polypeptide

4 iron atoms

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35
Q

Function of RBC?

A

Deliver O2

Remove CO2

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36
Q

RBC production and EPO

A

Low O2 stimulate kidney to produce erythropoietin EPO.
EPO induce bone marrow to produce RBC

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37
Q

In what form do platelet circulate

A

Inactive form

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38
Q

Neutrophil is important for what?

A

Acute response to infection and inflammation

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39
Q

What cells are seen in leukaemia?

A

Increase in immature WBC because immature cells are pushed out too quickly

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40
Q

In immunosuppressives individuals what do you find

A

Low neutrophil count

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41
Q

EPO is what?

A

Cytokine produced in kidney

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42
Q

Why should they be on high alert for those receiving erythropoietin? By cancer pt

A

It can lead to emboli and thrombus formation

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43
Q

EPO in oncology caused what?

A

Produced adverse reaction such as pulmonary emboli, thrombus and increased relapse in solid tumor

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44
Q

What is the use of EPO

A

Use to decrease transfusion in palliative patients

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45
Q

EPO uses?

A

To treat anemia related to kidney dysfunction

To anemia due to chemotherapy

For performance enhancement in athletes

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46
Q

Systolic murmur/he is murmur/flow murmur occurring due to what?

A

Anemia because increased blood flow over heart valves

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47
Q

Physical signs of anemia are?

A

Pale skin and mucus membranes is important in diagnosis if anemia is severe- <80

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48
Q

In elderly and individual with CAD what are some signs present in severe anaemia that are signs of CHF

A

Distended neck vein, tachycardia, right upper quadrant abdominal tenderness, hepatomegaly

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49
Q

Neurological findings (Paresthesia, balance problem, stocking-glove neuropathy and confusion can be found in which patient?

A

Vitamin B12 deficiency patients

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50
Q

IDA anemia what are the lab findings

A

Microcytic,
Hypochromic
Ferritin low

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51
Q

Treatment of IDA

A

Increase iron in diet
Ferrous gluconate, sulphate or fumerate
(Give with vit C)

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52
Q

AE related to IDA treatment and response

A

Adverse effect(AE):
Nausea + constipation
IV allergic reaction

Response:
start slow, go slow
Laxatives
Increase dietary fibre

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53
Q

B12 anemia lab findings

A

Macrocyclic, normocromic

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54
Q

Cause of B12 anemia is what?

A

Malabsorption due to lack of intrinsic factor

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55
Q

Treatment of B12 deficiency

A

Oral B12 or IM

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56
Q

AE related treatment

A

Headache, joint pain, dizziness, cold symptoms

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57
Q

Folate deficit lab finding

A

Macrocytic normocromic

Serum folate test not normally performed by if done it’s low serum folate

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58
Q

Treatment of folate deficiency

A

Oral folic acid

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59
Q

AE related to folate deficiency treatment

A

Nausea, loss of appetite, confusion, irritability, allery

60
Q

Thalassemia anemia lab findings

A

Microcytic hypochromic

61
Q

Treatment of thalassmia

A

Regular transfusions with h chelation therapy to reduce iron overload

62
Q

What’s the AE related to thalassemia treatment?

A

Iron overload

Response: chelation therapy to prevent iron overload

63
Q

Anaemia of chronic disease lab findings

A

Normocytic normocromic

64
Q

What is hemostasis

A

Arrest bleeding

65
Q

What are the 3 systems involved in hemostasis?

A

Platelet factors

Platelets

Vasculature

66
Q

Coagulation factors circulate in what forms?

A

Inactive forms and require enzyme cleavage to become active

67
Q

What are the 4 major events in hemostasis?

A

Vasoconstriction and plug formation

Activation of coagulation factors and inhibition of thrombin

Fibrin clot formation and stablilization

Prevention of further coagulation and clot breakdown

68
Q

What’s the process of platelet plug formation?

A

Vasoconstriction
Adhesion
Aggregation

69
Q

Activation of coagulation factors and initiation of thrombin involves what?

A

Initiation of coagulation
Amplification phase
Propagation phase

70
Q

What happens in primary hemostasis?

A

Injury to vessels exposes subendothlium (collagen) results in
Vasoconstriction of smooth muscles

Adhesion as a result of vWF which act as glue causingAggregation of platelet

Platelet aggregate as a result of fibrinogen and forms a platelets plug

Platelet aggregate perpetuate the phospholipid surface that activates coagulation factor

71
Q

What is D dimer

A

A major product of fibrin degradation

72
Q

When is d dimer test use and for what?

A

When coagulopathy is suspected- e.g DVT

73
Q

Secondary hemostasis involves what?

A

Initiation:
TF release from injured cells and monocytes
TF and factor VIIa activated IX and X to generate thrombin
Amplification:
Thrombin activates factor V to factor Va, factor VIII to VIIIa and more platelet and Factor XI to XIa
Propagation:
More factor Xa is produced when TF/FVIIa complex activated FIX resulting in FIXa which along with FVIIIa cuausinf more X to convert to Xa
Xa and Va with Ca and phospholipids form prothrombinase complex conveying FII (prothrombin to thrombin FIIa)

74
Q

Fibrin clot formation and stabilization

A

Thrombin convert fibrinogen to fibrin to form stronger clot
Thrombin activated XIII with cross link fibrin monomers to stabilize it further

75
Q

Inhibition of coagulation

A

Thrombin binds to membrane receptor to activate protein C, activated protein C (APC),
APC combine with Protein S, to slow down factor Va and VIII a which slows the process
Thrombin becomes inactivated
Anti thrombin further inhibit thrombin

76
Q

Fibrinolysis

A

T-PA convert plasminogen to plasmin which breaks down fibrins and it shows up as D dimer in test

77
Q

What is anti thrombin

A

Glycoprotein synthesized in liver

Circulate in blood

Half life 2-3 days

Natural anti- coagulant

Inhibits activation of factors thrombin(factor IIa), factor Xa and to lesser extent factor XIa and Factor IX.

Heparin significantly increase the inhibition rate

78
Q

What are the 3 factors that increase risk of thrombosis ( Virchow’s triad)

A

Flow stasis
Endothelial damage
Hypercoagulable state

79
Q

How does flow stasis impact thrombosis?

A

Flow stasis occur in immobile individual e.g bedrest, long trip on airplane smoke is because of the increase blood viscosity and in chronic illness such as multiple myeloma

80
Q

Epithelial damage in virchow’s triad of increase risk of thrombosis

A

Epithelial damage causes platelets to aggregate. People living with cancer and chronic disease has increased risk of theombosis

81
Q

Hypercoagulable state

A

Individual with high platelet count Antos with specific cancer, are prone coagulopathy

82
Q

Replacing iron in some with high ferritin could cause what?

A

Iron overload

83
Q

Most common anemia is what?

A

Iron deficiency anemia

84
Q

Most common anaemia in older adult is what?

A

Anemia is chronic diasese

85
Q

Treatment of IDA

A

Oral Ferrous sulphate, ferrous gluconate and ferrous fumerate

86
Q

What’s the commonest IDA treatment in older adult?

A

Ferrous fumerate due to less side effect

87
Q

Side effects of oral iron

A

Constipation- to mitigate start slow and go slow. E.g once a day and later update to 1-2x/ day

88
Q

If oral iron is not enough what do you do?

A

Perenteral iron
E.g venfer or Iron dextran(risk of anaphylaxis but not very common)

89
Q

IDA is what type of anemia?

A

Microcytic homochromic anemia

90
Q

B12 and folate deficiency is what type of anemia

A

Macrocytic anemia

91
Q

Treatment of B12 and folate deficiency?

A

B12- cobalamin oral or injection
Folic acid form that

92
Q

B12 1000mcg orally is use to treat what?

A

Help improve B12 deficiency in individuals that have B12 deficiency not related to pernicious anemao

93
Q

Folate deficiency -anemia in pregnancy

A

Replace folate to prevent neural tube defect in fetus

94
Q

If one has Macrocytic anemia how do you treat?

A

Check if it’s B12 or folate
If you replace flolate and it’s B12 deficiency, it can mask B12 deficiency and B12 deficiency untreated can cause neurological problems

95
Q

Treating folate when someone has B12 deficiency?

A

The Macrocytic nature of the problem will go away but B12 deficiency is not addressed. Can cause neurological consequences

96
Q

ASA

A

Has fallen out of favour
Used by client who cannot take other anticoagulant
E.g atrial fibrillation

97
Q

ASA is used for what?

A

People with thrombotic stroke as secondary prevention

98
Q

Can ASA be used in children

A

Not without the advice of Pediatric hematolgist

99
Q

What mode of action of warfarin?

A

Inhibit enzyme needed to activate vit K

100
Q

What are the disadvantages of warfarin?

A

Need frequent INR monitoring
Interact with many medications
Dose adjust based on INR
INR target 2-3

101
Q

Heparin is given how

A

IV or SQ

102
Q

Heparin and LMW Heparin are what?

A

Antithrombin activators

103
Q

What do you use to monitor heparin

A

PTT or anti 10a assay
1/2 life is 60-90mins

104
Q

To reverse effect of heparin what do you do?

A

Discontinue 4hrs before planned surgery

For urgent revasal antidote is Protamine

105
Q

What’s the antidote for heparin

A

Protamine

106
Q

LMW heparin

A

Indirect anticoagulants

Inhibits 10a and 2a

Administered sq

They don’t require monitoring

If needing to monitor use anti 10

1/2 life 3-6hrs

Renal my cleared

D/c 10-12 hrs before procedure

No antidote

107
Q

Properties of heparin

A

Polysaccharide chain
Does not cross membrane (safe in pregnancy and Breast feeding)

108
Q

How does heparin compare to warfarin

A

Heparin has rapid onset where is warfarin has slow onset

109
Q

Does LMW heparin require PTT monitoring

A

No.
Only fractionated heparin need PTT

110
Q

Difference between heparin and LMW Heparin

A

LMW heparin has shorter molecules

Inactivate 10a

Where as heparin inactivate 10a & thrombin

111
Q

What is an example of direct thrombin inhibitors?

A

Diabigitran- for treating stroke related nonvalvular aerial fib and prophylactic treatment of veinous embolism
1/2 life 15hrs
Contraindicated in patient with eGFR <30

112
Q

Diabigitran is contraindicated in which population?

A

Pt with eGFR <30

+ pregnancy

113
Q

What is the dose of Diabigitran?

A

150mg BID

114
Q

What are the need to know about Diabigitran therapy

A

Contraindicated in eGFR <30

SE: dyspepsia and gastritis

Do not give with P- glycoprotein (ketoconazole) quinidine (cause bleeding)

115
Q

Antidote for Diabigitran

A

Idracuzimuba

116
Q

Antidote for Diabigitran

A

Idarucizumab

117
Q

Antidote for Diabigitran

A

Idarucizumab 5g IV bolus

118
Q

What’s and example of factor 10a inhibitor

A

Rivtoxaban, apixaban and edoxaban

119
Q

Direct factor Xa (10a) inhibitor ( Riviroxaban, apixaban and edoxaban)

A

Advantage:
1. fix dose

  1. No INR
  2. Low risk bleed

Disadvantage
1 unsafe in pregnancy

  1. Accumulate in p glycoproteins inhibitor ( ketoconazole) and CYP3A4

Apixaban effectiveness decreased by st John wort

120
Q

Special consideration in Direct doctor Xa inhibitors (Apixaban and Riviroxaban)

A

Stop 1-2 day before procedure

121
Q

Antidote to direct factor Xa inhibitors (Riviroxaban apixaban

A

Andexa

122
Q

Cytokine - colony stimulating factor
G-CSG and GM-CSF are use where and for what?

A

In oncology to stimulate WBC, for neutropenic patient at risk for infection

GCSF to stimulate partial blood stem cells. Use for transplant

123
Q

What are the side effects of G CSF and GM-CSF

A

Aches and pain in large bones

Flu like symptoms

WBC will be elevated in CBC

124
Q

EPO is used where

A

In renal failure clients dialysis

Was used in oncology but has adverse effect- increase viscosity of blood causes thrombosis like events
Early relapse

125
Q

MCV <80 means what

A

Microcytic

126
Q

If MCV is normal?

A

Normocytic

127
Q

If MCV is >100

A

Macrocytic

128
Q

When looking at CBC what do you look at first

A

Hgb
WBC
Platelets
Looking for abnormalities

129
Q

Decreased hemoglobin you look at what

A

MCV- volume of cell

130
Q

MCHC mean corpuscular hemoglobin concentration tell what?

A

Tells colour of cells

131
Q

List iron deficiencies that have microcytic RBC

A

IDA- most common anemia

Hemaglobinopathy - thalassemia

Anemia of chronic disease

Lead poisoning

132
Q

Anemia has d chronic Disease

A

Can be microcytic but usually Normocytic

133
Q

IDA

A

Defective synthesis of Hgb resulting in smaller that normal cells (microcytic) which contain reduce Amon cell of Hgb (hyoochromic)

134
Q

Symptoms of IDA

A

Fatigue
Dyspnea
Pica
Pallor- pale conjunctivia
Taste disturbance
Restless leg syndrome
Headache dizziness

135
Q

Other symptoms

A

Glossitis- inflammation of tongue
Angular stomatitis-cracks at mouth connects
Koilonychia- spoon shaped nail

136
Q

Sickle cell disease

A

Sickle cell shape which decrease survival of cell
Coagulatanopathy

137
Q

Test for sickle cell

A

CBC
High to normal MCV with mild anemia
Sickle cell in blood film
Sicledex- screening test
Hemoglobin electrophoresis
Hemolytic anemia workup

138
Q

Thalassemia mechanism of deficency

A

Alpha- Thalassemia (alpha globin chain synthesis defect

Beta - Thalassemia (insufficient or absent production of beta globin chain)

139
Q

Types of Thalassemia

A

Thalassemia minor (trait) mike asymptomatic microcytic anemia

Thalassemia intermedia

Thalassemia major-develop at early age(before 1yr) results in sever anemia

Lab: CBC anemia with low MCV, normal ferritin
Nucleated RBC film

140
Q

Anemia of chronic disease

A

2nd most common anemia

Decrease RBC production by bone marrow

141
Q

What are the causes if anemia or chronic disease

A

Cancer
CKD
Liver churros is
Hepatitis B &C
Auto immune (SLE and RA)
Infection (HIV/AIDS, osteomyelitis and endocarditis)
DM
Heart failure

142
Q

Lab work for anemia of chronic disease

A

CBC
Mild anemia (Hgb 100-110g/L with normal MCV)
Low reticukocyte
Normal or high ferritin
Low serum iron/TICB/ soluble transferrin receptor
Increased CPR or ESR

143
Q

Anemia of chronic disease is more common in which age group

A

Older adults

144
Q

Why is inflammation a marker in anemia of chronic disease

A

It’s thought that the inflammation is responsible for the degradation of the RBC

145
Q

Lead poison

A

Rare, found in children

Hypochromic microcytix anemia

Lead interfere with heme, causing RBC destruction and a decrease in Hgb

Dx: serum lead levels

146
Q

Further diagnosis of iron deficiency anemia

A

Serum ferritin- diagnostic test of choice for IDA
( low level)

Serum iron level

147
Q

What’s the test of choice to diagnosing Iron deficiency anemia?

A

Serum ferritin

Nur 1142 Patho (15 decks)

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