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HAP > WEEK 2 (PART 1) > Flashcards

WEEK 2 (PART 1) Flashcards

1
Q

What are the main stages of new blood cell production (haematopoiesis)?

A
  • Cellular proliferation * Differentiation from stem cell to mature cell * Cell morphological changes specific to each cell type * Functional maturation of cells * Cell death
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2
Q

Where does haematopoiesis begin in the embryo?

A

Blood islands of the yolk sac (mesoblastic period)

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3
Q

When does the mesoblastic period occur and what is its primary function?

A

19-20 days of gestation, mainly red blood cell production (erythropoiesis)

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4
Q

When and where does the hepatic period of haematopoiesis begin?

A

5th-6th week of gestation, fetal liver

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5
Q

What cell type is minimally produced in the fetal liver?

A

Leukocytes

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6
Q

When do the spleen, thymus, and lymph nodes become involved in haematopoiesis?

A

Around the same time the fetal liver starts (5th-6th week)

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7
Q

When and where does the myeloid period of haematopoiesis begin?

A

5th month of gestation, bone marrow

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8
Q

When does the bone marrow become the sole site of blood cell production (under healthy conditions)?

A

3 weeks after birth

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9
Q

What is extramedullary haematopoiesis?

A

Blood cell production in liver and spleen (outside bone marrow) due to bone marrow dysfunction

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10
Q

Why might the spleen and liver resume blood cell production in adults?

A

When bone marrow cannot meet the body’s demands due to pathology

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11
Q

How does the capacity for extramedullary haematopoiesis change with age?

A

Decreases with age as bone marrow matures

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12
Q

What happens to red bone marrow as we age?

A

Replaced by yellow (fatty, inactive) bone marrow

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13
Q

Where are the active sites of haematopoiesis located in adult bones?

A

Pelvis, vertebrae, ribs, sternum, skull, and proximal ends of long bones

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14
Q

Can yellow bone marrow become active again?

A

Yes, it can be reactivated to become red marrow

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15
Q

What are the main components of bone marrow?

A
  • Blood vessels * Nerves * Blood cells (differentiated and undifferentiated) * Niche cells (supporting blood cell development) * Bone stromal cells * Venous sinusoids (specialized for blood cell release)
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16
Q

What is the main function of erythrocytes (red blood cells)?

A

Oxygen delivery to tissues

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17
Q

Where do erythrocytes originate from?

A

Colony-forming unit stem cells

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18
Q

What are the early precursors to erythrocytes called?

A

Erythroid progenitor cells

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19
Q

Where do erythrocytes mature?

A

Bone marrow

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20
Q

What is the first nucleated stage of erythrocyte development?

A

Proerythroblast

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21
Q

What does a proerythroblast produce?

A

Hemoglobin and other proteins (using ribosomes)

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22
Q

What is the next stage of development after a proerythroblast?

A

Reticulocyte (immature red blood cell)

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23
Q

What is a key feature of a mature erythrocyte?

A

Lacks a nucleus (anuclear)

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24
Q

What is the shape of a mature erythrocyte?

A

Biconcave disc

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25
Q

How does the shape of an erythrocyte help with its function?

A

Allows it to deform and squeeze through narrow capillaries

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26
Q

What benefit does the biconcave shape provide for gas exchange?

A

Increases surface area to volume ratio, maximizing gas diffusion

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27
Q

What is the function of hemoglobin (Hb) in red blood cells?

A

Carries oxygen

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28
Q

What is the basic structure of a hemoglobin molecule?

A
  • Two pairs of polypeptide chains (globins) * Four iron-containing complexes (hemes)
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29
Q

How do different types of hemoglobin vary?

A

Primarily in the type of polypeptide chains (alpha, beta, gamma, delta, epsilon, or zeta)

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30
Q

What is the most common type of hemoglobin in adults?

A

Hemoglobin A (HbA)

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31
Q

What are the polypeptide chains in Hemoglobin A?

A

Two alpha (α) and two beta (β) chains (α2β2)

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32
Q

What is a fetal type of hemoglobin with high oxygen binding affinity?

A

Hemoglobin F (HbF)

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33
Q

What are the polypeptide chains in Hemoglobin F?

A

Two alpha (α) and two gamma (γ) chains (α2γ2)

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34
Q

How does carbon monoxide (CO) affect hemoglobin?

A

It competes with oxygen for binding sites on the iron ion, but with a stronger affinity

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35
Q

What is the main factor controlling erythropoiesis (red blood cell production)?

A

Feedback loop involving erythropoietin (EPO)

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36
Q

What stimulates EPO production?

A

Low blood oxygen levels (anemia, high altitude)

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37
Q

How does the body sense low blood oxygen?

A

Chemoreceptors in the carotid body and aortic arch signal the brain

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38
Q

Where is EPO produced?

A

Primarily by kidneys, with some from the liver

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39
Q

What is the target of EPO in the bone marrow?

A

Niche and hematopoietic stem cells (HSCs)

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40
Q

What is the primary function of EPO?

A

Stimulates proliferation and differentiation of red blood cell precursors

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41
Q

Why is erythropoiesis a high-energy process?

A

RBCs need energy to maintain cell membrane and keep hemoglobin in its reduced state for oxygen binding

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42
Q

What are the two vulnerable sites in hemoglobin for oxidation?

A

Iron atom in the heme ring and sulfhydryl groups on the globin chain

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43
Q

What happens when the iron atom in hemoglobin is oxidized?

A

It forms methemoglobin, which cannot carry oxygen

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44
Q

What is the main energy source for red blood cells?

A

Glucose

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45
Q

How do red blood cells generate energy since they lack mitochondria?

A
  • Embden-Meyerhof Pathway (anaerobic): converts glucose to lactate for ATP production * Hexose monophosphate shunt (oxidative pathway): generates NADPH to maintain reduced state of hemoglobin
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46
Q

What is the lifespan of a red blood cell?

A

Approximately 120 days

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47
Q

Where are red blood cells destroyed?

A

Reticuloendothelial system (spleen being the major site)

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48
Q

What is a potential consequence of a splenectomy (spleen removal)?

A

Reduced ability to destroy old red blood cells and fight encapsulated bacteria

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49
Q

What are leukocytes (WBCs)?

A

Nucleated blood cells involved in immune defense

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50
Q

Where are leukocytes found?

A
  • Bone marrow * Peripheral blood * Tissues (spend most of their time here)
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51
Q

How many main types of leukocytes are there?

A

5: neutrophils, basophils, eosinophils, monocytes, and lymphocytes

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52
Q

How are leukocytes classified based on granularity?

A
  • Granulocytes (have visible granules): neutrophils, eosinophils, basophils * Non-granulocytes (no visible granules): monocytes, lymphocytes
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53
Q

How are leukocytes classified based on nuclear shape (when mature)?

A
  • Polymorphonuclear cells (multi-lobed nucleus): neutrophils, eosinophils, basophils * Mononuclear cells (single nucleus): monocytes, lymphocytes
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54
Q

What are neutrophils?

A

Most common type of leukocyte (white blood cell)

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55
Q

Where are neutrophils found?

A

Peripheral blood

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56
Q

What is the lifespan of a neutrophil?

A

9-10 days

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57
Q

What are the stages of neutrophil development?

A

Myeloblast, promyelocyte, myelocyte, metamyelocyte, band, segmented

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58
Q

How do neutrophils leave the bloodstream?

A

Diapedesis (passing between endothelial cells)

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59
Q

What is a main function of neutrophils?

A

Protecting against infection through phagocytosis

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60
Q

What is the significance of band forms in blood tests?

A

Presence of band forms suggests acute inflammation

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61
Q

What is the main energy source for neutrophils?

A

Anaerobic glycolysis (like red blood cells)

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62
Q

What are the steps of phagocytosis by neutrophils?

A
  1. Motility: Induced by chemotaxis from injured tissue
  2. Recognition: Binding to antibodies and complement proteins (opsonins) on foreign particles
  3. Ingestion: Fusion of the neutrophil with the foreign particle to form a phagosome
  4. Degranulation: Release of digestive enzymes from neutrophil granules into the phagosome
  5. Killing: Production of toxic metabolites (superoxide anion and hydrogen peroxide) to kill the ingested particle
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63
Q

What are eosinophils?

A

A type of leukocyte (white blood cell)

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64
Q

Where are eosinophils drawn to?

A

Sites of allergic reactions (hypersensitivity)

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65
Q

How do eosinophils help fight parasites?

A

They can damage the larval stage of parasitic worms.

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66
Q

What is the lifespan of an eosinophil?

A

Only 18 hours

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67
Q

What is the main energy source for eosinophils?

A

Glycolysis (like neutrophils)

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68
Q

What do eosinophil granules contain?

A
  • Hydrolytic enzymes for digestion * Peroxidase (an enzyme in higher concentration than in neutrophils)
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69
Q

What are basophils?

A

The least common type of leukocyte (white blood cell)

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70
Q

Where are basophils formed?

A

Bone marrow

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71
Q

Where do basophils migrate?

A

Tissues

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72
Q

How are basophils similar to mast cells?

A

They share some resemblance but are distinct cell types

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73
Q

What is the lifespan of a basophil?

A

Short (similar to eosinophils)

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74
Q

What potential role do basophils play?

A

Managing parasitic infections

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75
Q

Where are basophils recruited to?

A

Sites of allergic reactions

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76
Q

What do basophils secrete during allergic reactions (similar to mast cells)?

A

Histamine

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77
Q

What molecule triggers degranulation (release of contents) in basophils during allergic reactions?

A

IgE (same as mast cells)

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78
Q

Examples of conditions where basophils are involved:

A
  • Bronchial asthma * Urticaria (hives) * Allergic rhinitis * Anaphylaxis
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79
Q

What is the main function of monocytes?

A

Phagocytosis

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80
Q

What other immune system roles do monocytes play?

A

Cellular and humoral immunity

81
Q

What happens to monocytes when they migrate from blood to tissues?

A

They become macrophages

82
Q

What is the main energy source for monocytes?

A

Aerobic glycolysis (for phagocytosis)

83
Q

What is the main energy source for macrophages?

A

Anaerobic glycolysis

84
Q

What do mature monocytes contain to aid phagocytosis?

A

Lysosomal enzymes

85
Q

What conditions can cause monocytosis (increased monocytes in blood)?

A
  • Similar conditions that cause neutrophilia * Tuberculosis * Subacute bacterial endocarditis * Syphilis * Glucocorticoid administration * Overwhelming infections
86
Q

Can monocytosis be benign or malignant?

A

Yes, it can be reactive (benign) or malignant

87
Q

Where do lymphocytes originate?

A

Primary lymphoid organs (bone marrow, thymus)

88
Q

What is the fate of mature lymphocytes?

A

Proliferation, differentiation, function, then apoptosis (programmed cell death)

89
Q

Where do lymphocytes mature further and learn self-tolerance?

A

Secondary lymphoid organs (lymph nodes, spleen, tonsils, Peyer’s patches)

90
Q

What is the main function of lymphocytes?

A

Immune response: antigen recognition and controlled immune response generation

91
Q

What are the main types of lymphocytes?

A
  • B cells * T cells * Natural Killer (NK) cells
92
Q

How are lymphocytes different?

A

Maturation process, cell markers, response to stimulation (though similar in morphology)

93
Q

Can lymphocytes move between blood and tissues?

A

Yes

94
Q

Is lymphocyte development dependent on antigens?

A

No, lymphopoiesis is continuous

95
Q

What happens to lymphocytes in secondary lymphoid organs?

A

They are educated to not attack self-antigens and become immunocompetent upon antigen encounter

96
Q

What are some infectious causes of lymphocytosis?

A
  • Epstein-Barr virus (infectious mononucleosis) * Cytomegalovirus infection * Bordetella pertussis (whooping cough) * Toxoplasmosis
97
Q

What are some malignant causes of lymphocytosis?

A
  • Chronic lymphocytic leukemia * Acute lymphoblastic leukemia
98
Q

What can cause transient lymphopenia (low lymphocyte count) and neutropenia (low neutrophil count)?

A

Measles, mumps, chickenpox (followed by lymphocytosis as part of the immune response)

99
Q

How are platelets formed?

A

The exact process is not fully understood, but they are fragments of cytoplasm from megakaryocytes (which develop from hematopoietic stem cells).

100
Q

What is the shape and size of a platelet?

A

Flat disc, 1-2 microns in diameter

101
Q

What is a key feature of platelets?

A

They lack a nucleus but have a complex surface

102
Q

Where are platelets normally found?

A

Circulating in the blood

103
Q

What happens to platelets when there is an injury?

A

They change shape, interact with the damaged blood vessel lining, and form a plug to stop bleeding.

104
Q

What are some functions of platelets?

A
  • Adhere to the injured vessel wall * Aggregate (clump together) * Swell to form a seal * Secrete compounds that help form a blood clot
105
Q

What is the first response to a blood vessel injury (A)?

A

Vasoconstriction (blood vessel narrowing) to reduce blood flow at the injury site.

106
Q

What causes vasoconstriction (A)?

A

Local neurohumoral factors released at the injury site.

107
Q

How do platelets form a plug (B)?

A
  • Platelets adhere to exposed tissue using von Willebrand factor (vWF). * Platelets become activated, change shape, and release granules. * Released ADP and thromboxane A2 (TxA2) cause further platelet aggregation (clumping).
108
Q

What is the main component of the primary hemostatic plug (B)?

A

Aggregated platelets.

109
Q

What triggers the coagulation cascade (C)?

A

Tissue factor and platelet phospholipids after platelet activation.

110
Q

What is the role of the coagulation cascade (C)?

A

To form fibrin, a protein mesh that strengthens the clot.

111
Q

How does fibrin strengthen the clot (C)?

A

Fibrin polymerizes (forms strands) around platelets, creating a stronger barrier.

112
Q

What are some counterregulatory mechanisms that limit clot formation (D)?

A
  • Tissue-type plasminogen activator (t-PA) breaks down clots. * Thrombomodulin on endothelial cells inhibits the coagulation cascade.
113
Q

What is the difference between primary and secondary hemostasis?

A
  • Primary hemostasis involves platelets forming a plug. * Secondary hemostasis involves the coagulation cascade forming a fibrin clot.
114
Q

Do primary and secondary hemostasis occur sequentially?

A

No, they overlap functionally.

115
Q

What happens when a blood sample is centrifuged?

A

It separates into layers based on component density.

116
Q

What is the composition of the bottom layer (red)?

A

Erythrocytes (red blood cells).

117
Q

What is the name of the middle layer (white)?

A

Buffy coat.

118
Q

What is in the buffy coat?

A

Leukocytes (white blood cells) and platelets.

119
Q

What is the composition of the top layer (yellowish liquid)?

A

Plasma.

120
Q

Why might FBE results vary slightly between labs?

A

Different regions, instruments, or methods can be used.

121
Q

What are the typical components measured in a full blood examination (FBE)?

A
  • Hemoglobin concentration * Erythrocyte count (number of red blood cells) * Leukocyte count (number of white blood cells) * Platelet count * Differential white blood cell count (estimates of major leukocyte types)
122
Q

What is the normal hemoglobin reference range for men (g/L)?

A

135 – 175 g/L

123
Q

What is the normal hemoglobin reference range for women (g/L)?

A

115 – 155 g/L

124
Q

What is the main function of hemoglobin?

A

Binds and transports oxygen to tissues throughout the body.

125
Q

What can happen if a person has low hemoglobin (anemia)?

A

Tissues may not receive enough oxygen to function properly.

126
Q

What is a potential cause of low hemoglobin?

A

Iron deficiency in the diet

127
Q

What does red blood cell count estimate?

A

The number of red blood cells in circulation

128
Q

Typical red blood cell count in adults (million cells/microliter):

A
  • Men: 5.4 million * Women: 4.8 million (slightly lower due to physical and physiological differences)
129
Q

What is the lifespan of a red blood cell?

A

Approximately 120 days

130
Q

Where are red blood cells destroyed?

A

Primarily by the spleen

131
Q

What is PCV (packed cell volume) or Hct (hematocrit)?

A

The proportion of red blood cells in whole blood.

132
Q

What can affect PCV/Hct levels (other than red blood cell count)?

A

Fluid intake: * Dehydration can increase PCV/Hct. * Overhydration can decrease PCV/Hct.

133
Q

What does MCV measure?

A

The average volume or size of red blood cells (erythrocytes).

134
Q

Why is the biconcave shape of erythrocytes important?

A
  • Allows them to squeeze through narrow capillaries. * Slows them down in capillaries for efficient oxygen and carbon dioxide exchange.
135
Q

How does MCV change with erythrocyte age?

A

Young erythrocytes tend to be slightly larger than older ones due to aging and deformation.

136
Q

What can a decreased MCV indicate?

A

Iron deficiency anemia (smaller red blood cells).

137
Q

What can an increased MCV indicate?

A

Megaloblastic anemia caused by deficiencies in vitamin B12 or folate (larger red blood cells due to problems with DNA synthesis).

138
Q

What does MCH represent?

A

The average amount of hemoglobin in one red blood cell.

139
Q

What factors influence MCH?

A
  • Mean cell volume (MCV) * Iron availability for hemoglobin formation
140
Q

How does MCV influence MCH?

A

Larger erythrocytes (higher MCV) tend to have more hemoglobin.

141
Q

How does iron deficiency affect MCH?

A

Less iron can lead to less hemoglobin per red blood cell (lower MCH).

142
Q

How is MCHC calculated?

A

Hemoglobin level divided by PCV

143
Q

What does MCHC represent?

A

The average concentration of hemoglobin within a red blood cell.

144
Q

How is MCHC different from MCH?

A

MCHC considers the size of red blood cells (unlike MCH).

145
Q

What does reticulocyte count measure?

A

The number of immature red blood cells (reticulocytes) in circulation.

146
Q

Are reticulocytes normally seen in healthy adults?

A

Rarely.

147
Q

What can a high reticulocyte count indicate?

A
  • Increased red blood cell production due to conditions like anemia. * Certain blood cancers (leukemias).
148
Q

Where are red blood cells produced?

A

Bone marrow.

149
Q

What is the process of red blood cell production called?

A

Erythropoiesis.

150
Q

What hormone stimulates erythropoiesis?

A

Erythropoietin.

151
Q

Where is erythropoietin produced?

A

Primarily in the kidneys.

152
Q

How do kidneys regulate erythropoietin production?

A
  • Oxygen sensors in the kidneys detect blood oxygen levels. * Low blood oxygen levels trigger increased erythropoietin production.
153
Q

How can anemia be classified?

A

By cause (etiology) and red blood cell appearance (morphology).

154
Q

What is the main consequence of anemia?

A

Reduced oxygen delivery to tissues (tissue hypoxia).

155
Q

How does the body compensate for anemia?

A
  • Increased cardiac output (heart pumps more blood). * Increased erythropoietin (EPO) production to stimulate red blood cell production.
156
Q

What are some clinical signs of severe anemia?

A
  • Pale skin (pallor) due to less hemoglobin carrying oxygen. * Leg cramps. * Dizziness. * Breathlessness. * Fatigue. * In extreme cases: coma and death.
157
Q

Normal WBC count in adults (per microliter)?

A

5,000-10,000

158
Q

What does an elevated WBC count often indicate?

A

Inflammation or infection

159
Q

What can a decreased WBC count indicate?

A
  • Decreased production in bone marrow * Increased destruction of WBCs
160
Q

What are leukemias?

A

Cancers of the white blood cells or their precursors in the bone marrow.

161
Q

How can leukemias be classified (generally)?

A

Malignant (cancerous) vs. non-malignant WBC abnormalities

162
Q

Example of a cause of neutrophilia (increased neutrophils)?

A

Leukemia

163
Q

What are some causes of neutrophilia?

A
  • Infection * Inflammation * Malignancy
164
Q

What is a sign of acute (sudden) or chronic neutrophilia?

A

Increased presence of band forms (immature neutrophils)

165
Q

What factors can influence the severity of neutrophilia?

A
  • Patient age and health * Invading organism type
166
Q

What is neutropenia?

A

A condition with a lower than normal white blood cell count specifically for neutrophils (cells that fight bacteria).

167
Q

What are the two main types of neutropenia?

A
  • Acquired (developed later in life) * Inherited (present from birth)
168
Q

What can cause acquired neutropenia?

A
  • Chemical toxicity (e.g., from medications) * Bone marrow problems (e.g., tumors) * Nutritional deficiencies * Increased neutrophil destruction (e.g., from infections) * Neutrophil sequestration (cells trapped in organs like the spleen)
169
Q

What causes inherited neutropenia?

A

Very rare genetic defects in stem cell development

170
Q

What is an example of a malignant cause of neutropenia?

A

Mutations or chromosomal abnormalities in leukemias (e.g., chronic myelogenous leukemia)

171
Q

What causes eosinophilia? (High eosinophils)

A
  • Inherited (very rare) * Reactive (caused by allergic reactions, parasitic infections) * Malignant (leukemia)
172
Q

What causes eosinopenia? (Low eosinophils)

A
  • May be difficult to detect due to low baseline levels * Associated with ACTH administration (if adrenal function is normal)
173
Q

What causes basophilia (High basophils)

A

Hypersensitivity reactions

174
Q

What causes basopenia? (Low basophils)

A
  • Stress * Hyperthyroidism * Increased glucocorticoids
175
Q

What are platelets?

A

Platelet = fragment of cytoplasm from megakaryocytes (bone marrow cells). Not true cells themselves.

176
Q

Size and resting shape of platelets?

A

2-3 micrometers, lens-shaped (inactive).

177
Q

What happens to platelets during blood vessel injury?

A
  • Become round and develop projections. * Stick to injured area (endothelial cells/collagen fibers). * Change shape to facilitate clumping (platelet aggregation).
178
Q

What is the function of platelet aggregation?

A

Form a multi-layered plug to stop bleeding.

179
Q

Where are platelets produced?

A

Bone marrow, from megakaryocytes (each makes 1,000-3,000 platelets).

180
Q

What do platelet granules contain?

A

Components affecting the shape and behavior of other platelets and cells during bleeding.

181
Q

How is platelet production regulated?

A

By thrombopoietin (produced by the liver).

182
Q

What is thrombocytopenia?

A

Low platelet count.

183
Q

How can thrombocytopenia be treated (sometimes)?

A

Synthetic thrombopoietin to stimulate platelet production.

184
Q

Typical lifespan of a platelet?

A

Around 10 days.

185
Q

What does mean platelet volume (MPV) measure?

A

Average size of platelets in a blood sample.

186
Q

What can an increased presence of large platelets suggest?

A
  • Premature platelet death. * Bone marrow compensating by making more platelets.
187
Q

Why can transfused red blood cells cause an immune reaction?

A

The recipient’s immune system may recognize donor red blood cells as foreign.

188
Q

How does blood grouping prevent transfusion reactions?

A

Blood groups identify compatible blood types to avoid immune attack on transfused cells.

189
Q

What are the most common blood groups?

A

A, B, AB, and O

190
Q

What antibodies are present in type A blood?

A

Anti-B antibodies

191
Q

What can happen if type A blood receives type B blood?

A

Anti-B antibodies in type A blood attack type B transfused red blood cells.

192
Q

What is special about type O blood?

A
  • Has anti-A and anti-B antibodies. * Can be transfused to anyone (universal donor). * Does not have A or B antigens on red blood cells.
193
Q

Who can receive type AB blood?

A

Anyone (universal recipient) due to the absence of anti-A and anti-B antibodies.

194
Q

Who can donate blood to someone with type AB blood?

A

Anyone (A, B, AB, or O) because type AB blood has both A and B antigens.

195
Q

What is the Rh blood group system?

A

Another important blood group system besides ABO.

196
Q

What is the most important Rh antigen?

A

Rh(D)

197
Q

Rh positive vs. Rh negative:

A
  • Rh positive: Has Rh(D) antigen on red blood cells. * Rh negative: Does not have Rh(D) antigen.
198
Q

Example: Blood type A negative

A

A group antigens present, but Rh(D) antigen absent.

HAP (12 decks)

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