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BOD > Blood > Flashcards

Blood Flashcards

1
Q

What are B12/folate coenzymes for?

A

Thymidine and folate polyglutamate

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2
Q

Why are erythoblasts and released RBCs enlarged in megaloblastic anaemia?

A

Continue to make RNA and protein

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3
Q

In which anaemia do cells vary in size and shape?

A

Megaloblastic

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4
Q

What happens to nuclei in megaloblastic anaemia?

A

Hypersegmented nuclei

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5
Q

What happens to gut epithelium nuclei in megaloblastic anaemia?

A

Enlarged

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6
Q

What happens to iron in megaloblastic anaemia?

A

Can’t be utilised and is deposited in organs

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7
Q

Why is there an IF deficiency during pernicious anaemia?

A

Autoimmune gastric mucosa destruction

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8
Q

What conversion is B12 needed for?

A

Methyl-tetrahydrofolate to tetrahydrofolate conversion

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9
Q

What does B12 bind to in the stomach?

A

Haptocorrin

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10
Q

Where is haptocorrin produced?

A

Salivary glands

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11
Q

Where is the haptocorrin digested?

A

Pancreas

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12
Q

Where is IF produced?

A

Parietal cells

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13
Q

What is the IF receptor called?

A

Cubilin

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14
Q

What does IF bind to when it is taken to the portal blood?

A

Transcobalamin

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15
Q

Where is B12 stored?

A

Liver

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16
Q

Where is folate absorbed from?

A

Proximal small intestine and jejunum

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17
Q

How many days of foalte reserves are there?

A

100

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18
Q

What diseases cause folate malabsorption?

A

Small bowel disease

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19
Q

What causes hypoplastic anaemia?

A

Reduced cellularity of marrow

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20
Q

Which part of the body regulates iron absorption?

A

Duodenum

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21
Q

What is iron usually bound to?

A

Ferritin

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22
Q

What is ferritin converted to if iron levels are high?

A

Haemosiderin

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23
Q

Why are iron deficient people more susceptible to ROS?

A

Catalases

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24
Q

What is produced to prevent iron absorption if levels are high?

A

Hepcidin

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25
Q

What are RBCs like in iron deficiency anaemia?

A

Microcytic, hypochromic, poikilocytosis

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26
Q

What happens to erythropoiesis during haeolytic anaemia?

A

Increased

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27
Q

What happens to extra-medullary haematopoiesis in haemolytic anaemia?

A

Increases

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28
Q

Which kind of anaemia causes splenomegaly?

A

Haemolytic

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29
Q

Which kind of anaemia causes hereditary spherocytosis?

A

Haemolytic anaemia

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30
Q

Which enzyme deficiency can cause haemolytic anaemia?

A

Pyruvate kinases

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31
Q

What happens to the number of reticulocytes in blood during haemolytic anaemia?

A

Increases

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32
Q

Where is the point mutation in sickle cell?

A

Beta globin

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33
Q

What is the amino acid change in HbS?

A

HbA has beta globin 6 Glu to Val

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34
Q

When do heterozygotes get cell distortion?

A

If oxygen decrease is severe

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35
Q

What happens to globin levels in thallassaemia?

A

Decreases

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36
Q

What happens to RBCs in thallassaemia?

A

Microcytic and hypochromic

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37
Q

What happens to the other chain during thallassaemia?

A

Relative excess, precipitates as inclusion

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38
Q

What happens to erythroblasts during thallassaemia?

A

Destroyed

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39
Q

How many copies of the gene are deleted in alpha thallassaemia?

A

1-4

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40
Q

Which chromosome is the alpha globin on?

A

16

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41
Q

Which chains are the most soluble?

A

Beta/gamma

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42
Q

What happens following just one alpha deletion?

A

Silent

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43
Q

What happens during two alpha deletions?

A

Alpha thallassaemia

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44
Q

What happens during three alpha deletions?

A

HbH (beta 4) disease

45
Q

What happens during 4 alpha deletions?

A

Hb Bart’s disease (gamma 4)

46
Q

What is loss of a beta chain called?

A

Beta0

47
Q

Which is inadequate beta synthesis called?

A

Beta+

48
Q

Where is the beta gene?

A

Chromosome 11

49
Q

What is beta thallassaemia major?

A

B0/B0 or B+/B+ or B0/B+

50
Q

What is beta thallassaemia minor?

A

B0/B or B+/B

51
Q

What haemoglobinopathy causes perpendicular skull bone?

A

Beta thallassaemia

52
Q

Which thallassaemia causes iron overload?

A

Beta

53
Q

Which haemoglobinopathy causes compensatory HbF/HbA2?

A

Beta thallassaemia

54
Q

Subunits of HbF?

A

alpha 2 gamma 2

55
Q

Subunits of HbA2?

A

alpha 2 delta 2

56
Q

What is pancytopenia?

A

Reduced RBCs, platelets and granulocytes

57
Q

What happens to the erthyroblast nucleus?

A

Shrinks and is extruded

58
Q

Does a reticulocyte have a nucleus?

A

No

59
Q

What happens to the rRNA in a reticulocyte?

A

Forms meshwork

60
Q

What is a megaloblast?

A

Enlarged RBC precursor

61
Q

What is a macrocyte?

A

Enlarged RBC

62
Q

What is anisocytosis?

A

Different sized RBCs

63
Q

What is poikilocytosis?

A

Different shapes of RBCs

64
Q

What is the word for a pale RBC?

A

Hypochromic

65
Q

What is erythropoiesis?

A

RBC production

66
Q

What is haematopoiesis?

A

Blood cell and platelet production in bone marrow

67
Q

What does a price Jones curve show?

A

cells against diameter

68
Q

Which kind of enzyme is factor XII?

A

Endopeptidase

69
Q

Do microparticle promote thrombus formation?

A

Yes

70
Q

Which method do macrophages usually take up lipid by?

A

Scavenger

71
Q

What condition predisposes to aortic aneurysm?

A

Atherosclerosis

72
Q

What does thrombomodulin inhibit?

A

Thrombin generation

73
Q

How long folate reserves are there?

A

5 years

74
Q

What does antithrombin do?

A

Binds and inactivates thrombin

75
Q

What does TFPI do?

A

Blocks factor X inactivation

76
Q

What clears thrombin-antithrombin complexes?

A

Liver

77
Q

What can thrombin activate in the presence of thrombomodulin?

A

Protein C

78
Q

Which factors does protein C inactivate?

A

V and VIII

79
Q

Another name for TF?

A

Thromboplastin

80
Q

Virchow’s triad?

A

Vessel wall, blood flow, constituents

81
Q

Genetic deficiencies causing blood clots?

A

Antithrombin III or protein C

82
Q

What do Lines of Zahn contain to make them dark?

A

Erythrocytes

83
Q

Structure of venous thrombus?

A

Pale head, long red tail

84
Q

Lifespan of endothelial cells?

A

Over 5 years, rarely divide

85
Q

What are inherited atherosclerosis risk factors?

A

CRP, 5-lipoxygenase

86
Q

What protects pre-menopausal females from atherosclerosis?

A

Oestrogens

87
Q

Which infection can predispose to atherosclerosis?

A

Chlamydia

88
Q

In which cells is LDL receptor pathway active?

A

Hepatocytes

89
Q

What happens to mice deficient in apoE or the LDL receptor?

A

Advanced atherosclerosis

90
Q

What happens to mice deficient in scavenger receptors SR-A or CD36 or the enzyme ACAT?

A

Reduced atherosclerosis

91
Q

What does high LDL concs cause?

A

Toxicity

92
Q

What does low LDL concs cause?

A

Angiogenesis

93
Q

Which chemokines and mitogens are expressed in atherosclerosis?

A

MCP-1, IL1 and Il8, M-CSF

94
Q

Which cytokines activate endothelial cells?

A

IL1, TNFa, VEGF

95
Q

WHich clotting protein does oxidised LDLs inhibit?

A

Plasminogen

96
Q

What does fibrous cap contain?

A

Collagen, smooth muscle, macrophages, T lymphocytes

97
Q

What does lipid core contain?

A

Foam cells, necrotic debris, extracellular lipid

98
Q

What does cap shoulder contain?

A

Foam cells, smooth muscle cells, T lymphocytes, angiogenesis

99
Q

Which tissues may attempt regeneration after infarction?

A

Liver

100
Q

Is organisation or regeneration performed after infarction?

A

Organisation

101
Q

What happens to infracts in the brain?

A

Liquefactive necrosis - form cyst surrounded by glial cells

102
Q

Which two mechanisms cause ischaemic reperfusion injury?

A

Fresh mediators of cell injury, initiation of acute inflammation

103
Q

RBC lifespan?

A

120 days

104
Q

Where is B12 absorbed?

A

Terminal ileum

105
Q

How many years of B12 storage do humans have?

A

5 years

106
Q

Which changes cause the HbS to aggregate and polymerise?

A

Dehydration, infection, decrease O2, decreased pH

107
Q

Why does HbS decrease malaria risk?

A

Increased clearance

108
Q

Which globin chains are more soluble?

A

Beta and gamma

109
Q

Which thalassaemia is more severe?

A

Beta

BOD (7 decks)

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