Physiology Flashcards

1
Q

Which type of blood cell can come from either myeloid or lymphoid progenitor cells?

A

Dendritic cells

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2
Q

The common myeloid progenitor (CMP) cell can develop into the megakaryocyte erythroid progenitor (MEP)- what mature cells can these differentiate into?

A

Platelets or erythrocytes

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3
Q

The common myeloid progenitor (CMP) cell can develop into the granulocyte macrophage progenitor (GMP)- what mature cells can these differentiate into?

A

Granulocytes (neutrophils, basophils, eosinophils) and monocytes (macrophages)

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4
Q

Other than dendritic cells, what mature cells can common lymphoid progenitor cells differentiate into?

A

B cells, T cells or natural killer cells

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5
Q

At what stage in erythropoiesis is the nucleus lost?

A

Just before becoming a reticulocyte (late normoblast phase)

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6
Q

What do reticulocytes contain than mature erythrocytes do not?

A

RNA

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7
Q

Which cell is this describing: a segmented nucleus (polymorph) which has neutral staining granules?

A

Neutrophils

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8
Q

Which cell is this describing: a bi-lobed cells with bright orange/red granules?

A

Eosinophils

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9
Q

Which cell is this describing: contains large deep purple granules obscuring the nucleus?

A

Basophils

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10
Q

What chains is adult haemoglobin composed of?

A

2 x alpha and 2 x beta chains

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11
Q

What chains is foetal haemoglobin composed of?

A

2 x alpha and 2 x gamma chains

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12
Q

Which of the following does oxygen bind to: Fe2+ or Fe3+?

A

Fe2+

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13
Q

When hypoxia is sensed by the kidneys, what is produced in order to stimulate erythrocyte production?

A

Erythropoietin

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14
Q

Where does destruction of erythrocytes normally take place?

A

Spleen

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15
Q

When an erythrocyte is destroyed, a haem group is broken down into what two things?

A

Iron and bilirubin

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16
Q

In erythrocytes, glutathione reacts with hydrogen peroxide to form water and GSSG- what is the rate-limiting enzyme in this process?

A

Glucose-6-phosphate dehydrogenase

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17
Q

How is the majority of CO2 transported in the blood?

A

As bicarbonate

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18
Q

In what direction does foetal haemoglobin shift the oxygen-haemoglobin dissociation curve?

A

To the left

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19
Q

Shifting the oxygen-haemoglobin dissociation curve to the right suggests what?

A

There is less oxygen bound to haemoglobin, and more given to the tissues

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20
Q

Shifting the oxygen-haemoglobin dissociation curve to the left suggests what?

A

There is more oxygen bound to haemoglobin, and less given to the tissues

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21
Q

What must happen to the pH for the oxygen-haemoglobin dissociation curve to shift right?

A

Decreased

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22
Q

What must happen to the 2, 3-DPG for the oxygen-haemoglobin dissociation curve to shift right?

A

Increased

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23
Q

What must happen to the temperature for the oxygen-haemoglobin dissociation curve to right?

A

Increased

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24
Q

What must happen to the pH for the oxygen-haemoglobin dissociation curve to be shifted left?

A

Increased

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25
Q

What must happen to the 2, 3-DPG for the oxygen-haemoglobin dissociation curve to be shifted left?

A

Decreased

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26
Q

What must happen to the temperature for the oxygen-haemoglobin dissociation curve to be shifted left?

A

Decreased

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27
Q

How much iron is absorbed per day? Where is most iron absorbed?

A

1mg, mostly absorbed in the duodenum

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28
Q

Where can iron be taken to once it has been absorbed?

A

To the liver for storage or to the bone marrow to make haem

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29
Q

How much iron is lost per day?

A

1mg

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30
Q

What is iron bound to in the plasma?

A

Transferrin

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31
Q

What are some examples of drugs which may limit the absorption of iron?

A

PPIs and calcium supplements

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32
Q

What molecule is responsible for facilitating iron export from cells and passing it onto transferrin for transport elsewhere?

A

Ferroportin

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33
Q

What molecule is the major negative regulator of iron uptake, that works by degrading ferroportin so iron is effectively ‘trapped’ inside cells?

A

Hepcidin

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34
Q

If there is plentiful iron, what happens to the levels of hepcidin and ferroportin?

A

Increased hepcidin, decreased ferroportin

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35
Q

If there is iron deficiency, what happens to the levels of hepcidin and ferroportin?

A

Decreased hepcidin, increased ferroportin

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36
Q

Transferrin will only bind to iron in what state- Fe2+ or Fe3+?

A

Fe3+

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37
Q

If someone is in iron overload, what happens to transferrin saturation?

A

Increased

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38
Q

If someone is iron deficient, what happens to transferrin saturation?

A

Decreased

39
Q

What molecule is a spherical intracellular protein that stores many Fe3+ ions?

A

Ferritin

40
Q

Why is an increase in serum ferritin not specific for iron overload?

A

It is an acute phase protein

41
Q

What happens to the level of serum ferritin in iron deficiency?

A

Decreased

42
Q

What happens to the level of serum ferritin in iron overload?

A

Increased

43
Q

What is the lifespan of a red blood cell?

A

120 days

44
Q

What is the lifespan of a platelet?

A

7-10 days

45
Q

What is the lifespan of a neutrophil?

A

7-8 hours

46
Q

Which type of lymphocyte is responsible for mediating humoral immunity?

A

B cells

47
Q

Which type of lymphocyte is responsible for mediating cell mediated immunity?

A

T cells

48
Q

Which type of lymphocyte has anti-viral/anti-tumour properties?

A

Natural killer cells

49
Q

What are blast cells? Where are these located in adults?

A

Nucleated precursor cells located in the bone marrow of adults

50
Q

What is the name of the platelet precursor cell?

A

Megakaryocyte

51
Q

What is the name of the immediate erythrocyte precursor cell?

A

Reticulocyte

52
Q

What are myelocytes?

A

Nucleated precursor cells between neutrophils and blasts

53
Q

Embryonically, haemopoietic stem cells originate in which germ layer?

A

Mesoderm

54
Q

Where does haemopoiesis take place in adults?

A

In the bone marrow of the axial skeleton, pelvis and long bones

55
Q

What is the only lymphoid cell that can be recognised down a microscope?

A

Plasma cell

56
Q

What is the only investigation that can be used to differentiate between B, T and natural killer cells?

A

Immunophenotyping

57
Q

The presence of Howell-Jolly bodies suggests what pathology?

A

Hyposplenism

58
Q

What is meant by the term hypersplenism?

A

Splenomegaly, fall in one or more cellular components of blood, correction of cytopenias by splenectomy

59
Q

What is meant by primary haemostasis?

A

The formation of a platelet plug

60
Q

What is meant by secondary haemostasis?

A

The formation of a fibrin clot

61
Q

What is fibrinolysis?

A

The breaking down of a fibrin clot to avoid occlusion of a blood vessel

62
Q

Platelets are formed in the bone marrrow from which precursor cells?

A

Megakaryocytes

63
Q

When there is endothelial damage in a vessel, collagen is exposed and produces what factor, that platelets bind to?

A

Von-Willebrand’s factor

64
Q

The process of platelets sticking to exposed collagen via binding with Von Willlebrand’s factor is known as what?

A

Platelet adhesion

65
Q

The process of platelets which are already bound to exposed collagen producing chemicals to attract more platelets to the site of injury is known as what?

A

Platelet aggregation

66
Q

What is a vascular cause for failure of primary haemostasis?

A

Loss of collagen with ageing

67
Q

What are some platelet causes for failure of primary haemostasis?

A

Reduced number or reduced function of platelets

68
Q

What is the Von-Willebrand’s factor cause for failure of primary haemostasis?

A

Inherited low levels

69
Q

What is the most common cause of reduced function of platelets?

A

Anti-platelet and NSAID drugs

70
Q

What are some potential consequences of failure of primary haemostasis?

A

Spontaneous bruising/purpura, mucosal bleeding, intracranial/retinal haemorrhages

71
Q

What is the screening test for primary haemostasis function?

A

Platelet count

72
Q

What process starts the extrinsic pathway of the coagulation cascade?

A

Tissue factor activates factor VII

73
Q

In the common coagulation pathway, tissue factor and factor VII activate which other clotting factors?

A

V and X

74
Q

In the common coagulation pathway, factors V and X active which clotting factor to form what?

A

Prothrombin to form thrombin (factor II)

75
Q

In the common coagulation pathway, factor II (thrombin) is responsible for activating what clotting factor?

A

Fibrin (factor I)

76
Q

When thrombin (factor II) is first generated, what factors does it activate in order to amplify the process?

A

VIII, IX, XI and XII

77
Q

In the common coagulation pathway factors VIII, IX, XI and XII get reactivated by thrombin and work to activate which other clotting factors?

A

V and X

78
Q

Which clotting factors are involved in the intrinsic pathway and in what order do they activate each other?

A

XII - XI - IX - VIII

79
Q

Which electrolyte is a common co-factor in activating a lot of clotting factors in the coagulation cascade?

A

Calcium

80
Q

Is deficiency of a single clotting factor more likely to be inherited or acquired?

A

Inherited

81
Q

Is deficiency of multiple clotting factors more likely to be inherited or acquired?

A

Acquired

82
Q

Most clotting factors are produced where?

A

In the liver

83
Q

What is the best screening test to assess the function of the extrinsic pathway, i.e. tissue factor and factor VII?

A

Prothrombin time (PT)

84
Q

What is the best screening test to assess the function of the intrinsic pathway, i.e. factors VIII and IX?

A

Activated partial thromboplastin time (APTT)

85
Q

If all clotting factors are low, which will be increased- PT, APTT or both?

A

Both

86
Q

If only factors VIII or IX are low, which will be increased- PT, APTT or both?

A

APTT

87
Q

What molecule is responsible for converting fibrin into fibrin degradation products in fibrinolysis?

A

Plasmin

88
Q

How is plasmin formed?

A

Plasminogen is converted to plasmin via tissue plasminogen activator (tPA)

89
Q

Fibrin degradation products are measured in the lab as what?

A

D-dimers

90
Q

Which naturally occurring anticoagulant is responsible for turning off thrombin and some other clotting factors directly?

A

Anti-thrombin III

91
Q

Which naturally occurring anticoagulant is responsible for turning off factors V and VIII?

A

Protein C

92
Q

What is a co-factor that helps out protein C?

A

Protein S

93
Q

When haemostasis has been achieved, thrombin binds to thrombomodulin and this has what effect?

A

Activates protein C and switches off haemostasis