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ESA 2 > Haematology > Flashcards

Haematology Flashcards

1
Q

Where are RBC, platelets and most of the WBC produced?

A

Bone marrow

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2
Q

Who has more extensive bone marrow ?

A

Infants

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3
Q

In adulthood bone marrow is limited to predominantly where?

A 
Pelvis
Sternim
Skull
Ribs
Vertebrae
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4
Q

What controls haematopoeisis?

A

Hormones and cytokines

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5
Q

How do hormones and cytokines control haemopoiesis?

A

Alter gene expression, altering how a stem cell divides

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6
Q

For a haemopoetic stem cell to become an erythrocytes what must it first differentiate into

A

Myeloid progenitor

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7
Q

What system removes faulty cells (rbc)

A

Reticuloendothelial system (RES)

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8
Q

What is the main organ that disposed of faulty blood cells

A

Spleen

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9
Q

What does the mean cell volume help us differentiate between?

A

Microcytic, normocytic and macrocytic disorders.

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10
Q

How long is a red cells life?

A

120 days

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11
Q

In what state do rbc carry haemoglobin (the iron)

A

Ferrous state

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12
Q

Why do red cells need to generate atp

A

To maintain membrane and osmotic equilibrium

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13
Q

What shape are RBC

A

Biconcave

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14
Q

Why are RBC biconcave

A

It allows them to passage through microcirculation

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15
Q

A change in rbc shape often results in what?

A

Lysis

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16
Q

What are some RBC shape changes ?

A

Spherocytes, speculated, sickle

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17
Q

Haemaglobin is what structure?

A

Tetramer of 2 pairs of globin chains

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18
Q

What states can haemaglobin be in?

A

T and R

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19
Q

Where are the globin genes located?

A

Chromosome 11 and 16

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20
Q

What is important about globin gene expresion and age?

A

Different expression at different ages

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21
Q

When do we switch rom foetal to adult haemaglobin?

A

3-6months

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22
Q

What is the purpose of globin in relation to haem?

A

Protect haem from oxidation keeping it ferous.

Promotes variation in affinity

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23
Q

When RBC are broken down what is the fate of globin, haem and the iron?

A

Globin broken down into aminos and reformed
Iron retained from haem
Wate haem into billivurdin

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24
Q

What colour is billivurdin?

A

Green

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25
Q

What is haem broken down into (fully)

A

First billivurdin
Then billirubin
Then stercobillin in faeces or urobillnogen in urine

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26
Q

What organ controls erythropoeises?

A

Kidney

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27
Q

What does the kidney do if reduced pO2 is detected in the interstitial peritubular of the kidney?

A

EPO is produced

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28
Q

What does EPO stimulate?

A

Maturation and release of RBC from marrow

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29
Q

How is the release of EPO regulated?

A

A raise in pO2 reduced EPO production

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30
Q

Why is kidney damage associated with anaemia?

A

Reduced EPO production

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31
Q

What 2 metabolic pathways do RBC use to generate ATP?

A

Glycolysis (glucose to Lactate)

Pentode phosphate pathway

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32
Q

What are some key roles of iron?

A

Transport and store oxygen
Integral part of many enzymes
Collagen formation
Neurotransmitter production

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33
Q

What mechanism do we have to excrete iron?

A

We dont!

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34
Q

How do we excrete iron from the body?

A

Bleeding
Loss of skin and hair
Can’t actively excrete

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35
Q

What is the consequence of low or high iron?

A

Anaemia if low

Dangerous deposition if high

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36
Q

Iron in the body is in what 2 forms?

A

Available or stored

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37
Q

What examples of available iron in the body are there?

A

Haemoglobin
Myoglobin
Tissue iron (enzyme)
Transported iron (serum iron)

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38
Q

What are some examples of stored iron in the body

A

Ferritin
Haemosiderin
Macrophage iron

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39
Q

When does the iron status (required) increase in life?

A

Pregnancy

Children

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40
Q

Where does 80% of active iron come from?

A

Recycling

Not from gut absorption

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41
Q

What is an iron macrophage?

A

One that eats an old senescent red blood ell mostly splenic macrophages and kupfer cells of the liver

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42
Q

Where is 85% of stored iron located?

A

As ferritin in hepatocytes

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43
Q

How much iron enters and leaves the body in a day?

A

1-2g

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44
Q

What is the best source of iron intake?

A

Haem sources

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45
Q

How much iron do we need in our diet in a day?

A

10-15mg

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46
Q

Why is haem intake of iron better than non haem?

A

Haem enters as fe2+ ferrous

Non haem enters as Fe3+ feriric

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47
Q

What has to happen to ferric iron before it can enter the body?

A

It has to be reduced

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48
Q

What does fe2+ bind to to enter cells (where)

A

Divalent metal transporter 1 in apical cells of duodenum and upper jejunum

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49
Q

How does iron get transported out of the apical cells of duodenum

A

Ferroportin

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50
Q

What is required for iron to enter a cell, such as a RBC?

A

Iron transferrin complex

Binds to transferrin receptor

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51
Q

What is essential in enhancing absorbtion of non haem iron?

What suggestion does this lead to when talking iron supplements

A

Ascorbic acid

Take with OJ not with cuppa (antacid)

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52
Q

How do we regulate how much iron we absorb?

A

Hepcidin

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53
Q

What does hepcidin do?

A

Binds to ferroportin and stops iron absorbtion

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54
Q

Where is hepcidin transported from?

A

LIver and kidneys

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55
Q

What leads to Hepcidin synthesis ? What leads to decreased hepcidin?

A

Iron overload increases synthesis

High EPO activity decreases it

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56
Q

What’s the most common nutritional disorder

A

Iron defficency

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57
Q

Is iron defficency a diagnosis?

A

No its a symptom

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58
Q

What are the 3 root causes of iron defficeny

A 
Poor intake
Physiological loss (period)
Pathological loss
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59
Q

What are some symptoms of iron defficent anaemia

A

Tiredness, reduced ex tolerance. Pale (reduced o2 carrying)

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60
Q

What are some signs of iron defficent anaemia

A

Tachycardia, increased RR, pallor

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61
Q

In iron defficent anaemia what is the HB content? What do the cells look like?

A

Hypochromic, low HB , look pale

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62
Q

What size are rbc in iron defficent anaemia?

A

Microcytic (small mcv)

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63
Q

What changes other than microcytic and hypochromic are there in iron defficent anaemia?

A

Change in shape
Low serum ferritin
Low reticulocyte haemoglobin content

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64
Q

What do reduced ferritin level indicate?

A

Iron defficent anaemia?

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65
Q

Can you rule out iron defficent anaemia with normal ferritin? Why

A

No

Ferritin raised with inflammation, liver disease, alcoholism

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66
Q

What marker is used to test for functional iron defficent anaemia? When can this not be used?

A

CHR

Thalassaemia

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67
Q

How would you treat iron defficent anaemia?

A

Diet, oral iron, IM injection, IV iron.

Transfusion if cardiac comprimise likely

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68
Q

Why is excess iron dangerous?

A

Causes damage to lipid membranes and proteins

Deposited in tissues

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69
Q

What ca reduced iron produce that are dangerous?

A

Reactive hydroxyl and lipid radicals

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70
Q

What disease is associated with excess iron ?

A

Haemochromatosis

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71
Q

What does haemochromatosis damage?

A

End organs

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72
Q

What secondary diseases can haemochromatosis lead to

A

Liver cirrhosis
Diabetes
Cardiomyopathy
Arthropathy

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73
Q

Haemochromatosis is due to a mutation in what?

A

HFE gene

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74
Q

What’s anaemia?

A

Inability to deliver enough oxygen to tissue due to decreased RBC or decreased haem

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75
Q

The spleen is where?

A

Left upper quadrant

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76
Q

The process of making red blood cells is known as what?

A

Eryhtropoesis

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77
Q

If erythropoeisis is reduced or not effective what is it known as?

A

Dyserythropoiesis

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78
Q

Why does chemo induce anemia?

A

The bone marrow can become empty meaning it cant respond to EPO

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79
Q

What does a marrow infiltrate do to cause anemia

A

Decreases the number of haematopoetic cells

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80
Q

What happens in anaemia of chronic disease?

A

The iron stored in bone marrow isn’t released, this reduces red blood cell lifespan and the marrow has a lack of response to EPO

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81
Q

In anaemia of chronic disease what size RBC are seen?

A

It can be microcytic, normocytic or macrocytic

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82
Q

What clinical clue can be seen in anaemia of chronic disease?

A

Raised CRP and ferritin

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83
Q

What is myelodysplastic syndrome?

A

Production of abnormal clones of marrow cells

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84
Q

In myelodysplastic syndrome what kind of anaemia develops? And why

A

Red cells are defective and large- macrocytic

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85
Q

How is diagnosis of myelodyslplastic syndrome made?

A

Microscopy of blood and bone marrow cells

Often genetic change at chromosomes in marrow cells

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86
Q

What develops in a high proportion of myelodysplastic syndrome cases?

A

Acute Leukaemia

Pancytopenia

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87
Q

What is the treatment of myelodysplastic syndrome?

A

Chronic transfusion

Occcasionaly chemo followed by stem cell transplant

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88
Q

A defficency in what building blocks of dna synthesis leads to anaemia?

A

Vit b12

Folate

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89
Q

What is seen in terms of red cells in b12 and folate defficencies and why?

A

Large red cel precursors with inappropriately large nuclei and chromatin
This is because nuclear maturation and cell division lags behind cytoplasmic development

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90
Q

What anemia do you get with b12 or folate deficency

A

Macrocytic

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91
Q

What happens to b12 in the stomach

A

Combined with intrinsic factor produced by patietal cells

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92
Q

B12 bound to intrinsic factor in the ileum does what?

A

B12 is absorbed and the intrinsic factor destroyed

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93
Q

In portal blood what is b12 bound too?

A

Transcoblamin

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94
Q

A deficency is vit b12 can be the result of what?

4

A

Poor diet eg vegan
Intrinsic factor- pernicious anaemia
IF-B12 complex- disease of ileum eg crohns
Transcobalmin deficent

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95
Q

Where does folate absorbtion occur

A

Duodenum and jejunum

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96
Q

What is dietary folate converted to

A

MethylTHF

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97
Q

When are we physiologically more likely to develop folate deficency

A

Pregnancy

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98
Q

A defficency in folate can occur due to what 4 things?

A

Folate defficent due to diet or increased use (haemolytic anemia, skin disease etc)
Duodenum/jejunum absobrtion issue
MethylTHF issue- some drugs inhibit this eg methotrexate
Urinary loss- liver and heart disease

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99
Q

What’s a pancytopenia

A

Low rbc, low platelets, low wbc

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100
Q

The peripheral blood fill in folate or b12 defficency shows what?

A

Macrocytic red cells with hypersegmented neutrophils

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101
Q

What is b12 defficency associated with that folate isn’t/

A

Focal demyelination

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102
Q

What is thalassaemia ?

A

Reduced rate of synthesis of normal alpha or beta globin genes

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103
Q

What is sick cell disease

A

Synthesis of abnormal haemoglobin

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104
Q

What mutation causes sickle

A

Point mutation
Valine for glutamic acid
Position 6 beta gene

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105
Q

What is a sickle cell crisis?

A

A vaso-occlusive episode that leads to organ damage.

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106
Q

What is the life cycle of a sickle cell like?

A

It’s a reversibly sickled erythrocytes but repeated cycles of deoxigantion cause irreversible sickle

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107
Q

What do irreversibly sickled cells do?

A

They have increased adherence to endothelium

They can cause thrombosis.

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108
Q

What kind of RBC are seen in thalassaemia?

A

Hypochromic

Microcytic

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109
Q

Why are thalassaemia cells hypochromic?

A

Decreased haem

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110
Q

How does the body try and compensate with the anaemia induced by thalassaemia?

A

Extramedullary haemopoeisis -results in splenomegally

Stimulation of EPO

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111
Q

What’s a major cause of death in thalassaemia patients? Why does it happen?

A

Iron overload- excessive dietary absorbtion as ineffective haematopoeisis is occurring

112
Q

What are some heriditeray conditions associated with red cell membranes

A

Hereditary spherocytosis

Hereditary eliptocytosis

113
Q

What are target cells?

A

Red cells that have abnormal haemaglobin

114
Q

What are some acquired causes of red cell membrane disruption/

A

Mechanical damage- heart valves, vasculitis, DIC
Heat damage
Osmotic change in drowning

115
Q

What are some well known deficiencies in metabolism that can result in red cell metabolism issues?

A

Glucose 6 phosphate dehydrogenase deficency G6PD

Pyruvate kinase defficency

116
Q

If there is no issue with the bone marrow- erythropoesis or haemaglobin synthesis, no issue with the red blood cells structure or metabolism and no issue with the RES, then why could someone have anaemia? What kind of anaemia would it be?

A

Loss of blood- gastric ulcer, gastric cancer, excessive menstruation, bladder cancer
Microcytic due to excess iron loss

117
Q

What is haemolytic anaemia

A

Increased red cell destruction causing anaemia

118
Q

What are some key lab features of excessive red cell removed by the RES

A 
Increased reticulocytes (marrow trying to compensate)
Raised billirubin (haem breakdown)
Raised LDH (enzyme red cells are rich in)
119
Q

Myelofibrosis causes anaemia how? Hint multifactorial

A

There is decreased Erythropoeisis as marrow fibrotic

The spleen grows to compensate but also breaks down more red cells (RES)

120
Q

Thalassamia causes anaemia multifactorally, how so?

A

Ineffective haemoglobin synthesis
Poor structure
Increased removal

121
Q

If there is an appropriate reticulocytes response but no evidence of haemolysis what should you look for?

A

Evidence of bleeding

122
Q

When working out what kind of anaemia it is. If the reticulcytes are low/normal levels. What would you look at next?

123
Q

What do myeloproliferative disorders involve?

A

Dysregulation at the multipotent haematopoetic stem cell

124
Q

What is polycythaemia Vera (PV)

A

Neoplasm where too many red cells are produced

125
Q

What is the diagnostic criteria for polycythaemia Vera?

A

High haematocrit

126
Q

What is erythrocytosis?

A

Increase in conc of RBC

127
Q

If a patient doesn’t have a primary reason to have increased red cell mass (PV) what is a secondary cause likely driven by?

A

EPO production

128
Q

What is physiologically appropriate EPO production ?

A

When there is central hypoxia- chronic lung disease, altitude training
When there is renal hypoxia- renal artery disease

129
Q

What are examples of pathological production of EPO

A

Hepatocellular carcinoa, renal cancer, meningionma, uterine leimyomas

130
Q

If EPO production isn’t pathological or a physiological response, what could it be?

A

Injected. Will cause polycythaemia

131
Q

What is used to manage PV

132
Q

What does the spleen consist of?

A

Red pulp and white pulp

133
Q

What is red pulp? Spleen

A

Sinuses lined by endothelial macrophages and cords

134
Q

What is white pulp?

A

Structure similar to lymphoid follicles

135
Q

Where does blood enter the spleen from?

A

Via the splenic artery

136
Q

What cells pass through what parts of the spleen?

A

White cells and plasma through white pulp

Red cells through red pulp

137
Q

What are 4 functions of the adult spleen?

A

Sequestering and phagocytosis
Blood pooling
Extramedullary haemopoiesis
Immunological function

138
Q

What pools in the spleen and why?

A

Platelets and red cells for rapid mobilisation during bleeding

139
Q

When does extramedullary haemopoiesis occur?

A

During haematological stress or if marrow fails

140
Q

What proliferates in extramedullary haemopoiesis?

A

Pluripotent stem cells

141
Q

What is the immunological function of the spleen?/ what does it have

A

25% of T cells and 15% of B cells in spleen

142
Q

Where should you begin to palpate for the spleen? What are you feeling for?
When does the spleen edge move towards you?

A

Right iliac fossa
Feel for splenic notch
Spleen edge moves towards you on inspiration

143
Q

Why would the spleen grow in splenomegally?

A 
Back pressure
Over working red or white pulp
Extramedullary haemopoiesis
Cancer infiltrate
Other infiltrate (eg sarcoidosis)
144
Q

What kind of back pressure would cause splenomegally?

A

Portal hypertension in liver disease

145
Q

Why would you get splenomegally with chronic lymphocytic leukaemia?

A

Expanded white pulp, infiltrated

146
Q

What can cause a massive splenomegally?

A

Chronic myeloid leukaemia
Myelofibrosis
Chronic malaria
Schistosomiasis

147
Q

What size splenomegally would liver cirrhosis with portal hypertension cause?

148
Q

What size splenomegally would endocarditis cause?

149
Q

What can occur in hypersplenism?

A

Pancytenia or thrombocytopenia due to pooling of blood

150
Q

What’s the risk in splenomegally

A

Rupture as not protected by rib cage

151
Q

Asides from rupture leading to haematoma what is another complication of splenomegally?

A

Infarction

152
Q

What is hyposplenism?

A

Lack of functioning splenic tissue

153
Q

What are some causes of hyposplenism?

A

Splenectomy
Sickle cell isease
Coeliac

154
Q

What do blood films demonstrate in hyposplenism?

A

Howell jolly bodies

155
Q

What are Howell jolly bodies?

A

Dna remenants

156
Q

A hypospleic patient is at risk of what?
From what in particualr?
What examples?

A

Sepsis
Encapsulated orgnanisms
Pneumococcus, haemophilus influenza, meningococcus

157
Q

What is cytopenia

A

Reduction in the number of blood cells, can take many forms

158
Q

What is a low red cell count known as?

159
Q

What is a low white blood count known as?

A

Leucopenia

160
Q

What is a low neutrophil count known as?

A

Neutropenia

161
Q

What is a low platelet count known as?

A

Thrombocytopenia

162
Q

What is a low RBC, WBC and platelet count known as?

A

Pancytopenia

163
Q

If it is a cytosine or a philia, what is it?

A

An increase in the number of blood cells

164
Q

What is a high red cell count known as

A

Erythrocytosis

165
Q

What is a high white blood cell count known as

A

Leucocytosis

166
Q

What is a high neutrophil count known as

A

Neutrophilia

167
Q

What is a high lymphocyte count know as

A

Lymphocytosis

168
Q

What is a high platelet count known as ?

A

Thrmbocytosis

169
Q

What’s the commonest white cell

A

Neutrophil

170
Q

How many segments does a neutrophil have?

171
Q

How long do neutrophils lasts?

172
Q

Who is the first responder phagocyte

A

Neutrophil

173
Q

What hormone controls neutrophil maturation?

174
Q

What effect does G-CSF have?

A

Increase production of neutrophils
Decrease time to release mature cells from bone marrow
Enhances chemotaxis
Enhances phagocytosis

175
Q

If we need more neutrophils in a patient with neutropenia what can we do?

A

Administer recombinant GCSF

176
Q

What are some causes of neutrophilia?

A 
Infection
Acute inflammation
Tissue damage
Cancer
Smoking
Myeloproliferative disease 
Acute haemorrhage
177
Q

What range is the neutrophil count in a neutropenic? When does it become severe neutropenia?

A

1.5x10^9

Severe if less than 0.5

178
Q

What are the 3 causes (generally) of increased removal/use of neutrophils to induce neutropenia?

A

Immune destruction
Sepsis
Splenic pooling

179
Q

What can reduce the production of neutrophils inducing neutropenia

A 
B12/folate defficent
Aplastic anaemia (empty marrow)
Infiltration of marrow
Radiation
Drugs (chemo, antibiotics, anti epileptics...)
Viral infection (common)
Congenital cause
180
Q

What are some consequences of neutropenia

A

Life threatening bacterial infection
Life threatening fungal infection
Mucousal ulceration

181
Q

What do monocytes respond to?

A

Inflammation and antigenic stimuli

182
Q

What to monocytes differentiate into?

What do there lysosomes contain?

A

Macrophages

Lysozyme, complement, interleukins, arachnoid acid, CSF

183
Q

When do we see monocytosis?

A

Chronic infection
Chronic inflammatory condition
Carcinoma
Myeloproliferative disorders/leukaemias

184
Q

How long are eosinophils in circulation? What is there lifespan

A

3-8 hours in circulation

8-12 day lifespan

185
Q

What are eosinophils responsible for dealing with specifically?

186
Q

What do eosinophils mediate?

A

Allergic response

Hypersensitivity reactions

187
Q

Eosinohils migrate where?

A

To epithelial surfaces

188
Q

What do eosinophils granules contain?

A

Arginine, phospholipid, enzymes

189
Q

When is eosinophilia seen?

A

Allergic diseases like asthma, eczema
Drug hypersensitivity
Parasitic infection

Hodgkin lymphoma
Certain leukaemias

190
Q

When are basophils active?

A

Allergic reactions and inflammatory conditions

191
Q

What do basophils granules contain?

A

Histamine, heparin, hyaluronic acid

192
Q

When is basophilia seen?

A

Immediate hypersensitivity
Ulcerative colitis
RA

193
Q

What do basophils look like?

A

Blackberrys

194
Q

Where do lymphocytes originate?

A

Bone marrow

195
Q

What lymphocyte is part of the humoral immune?

196
Q

What lympcyte produces antibodies

197
Q

What lympcyte would a cd4 be?

198
Q

What cell is the lymphocyte of cellular immunity?

199
Q

What lymphocyte is know for cell mediated cytotoxicity

200
Q

When is a reactive lymphocytosis seen?

A

Viral infections
Bacterial infection
Stress- eg MI
Post splenectomy

201
Q

When is a lymphoproliferative lymphocytosis seen?

A

Chronic lymphocytic leukaemia
T or NK leukaemia
Lymphoma

202
Q

What are 3 reasons that cause pancytopenia through increased removal

A

Splenic pooling hypersplenism
Haemophagocytosis
Immune destruction

203
Q

What can be underlying causes for a pancytopenia due to reduced production?

A 
B12/ folate defficent
Marrow fibrosis/infiltrate
Radiation
Drugs
Virus- EBV, viral Hepatitis, HIV, CMV
204
Q

What is aplastic anaemia

A

Pancytopenia with a hypocellular bone marrow in the abscence of abnormal filtrate or fibrosis

205
Q

What can haematological malignancies cause?

A

Pancytopenia

206
Q

What are symptoms of pancytopenia?

A

Symptoms of anaemia- fatigue, dizzy chest pain etc
+
Symptoms of thrombocytopenia- bleeding, brushing etc
+
symptoms of neutropenia- infection, ulcers etc
+
Symptoms of underlying cause

207
Q

What are some sources of haematopoetic stem cells

A

Bone marrow aspitarate
Leucopheresis- stem cells mobilised into blood by GCSF
Umbilical cord stem cells

208
Q

When does haemopoeises begin in the embryonic liver?

A

Week 5-8 of gestation

209
Q

What factors alter the lineage pathway a differentiating progenitor cell takes?

A

Transcription factors, hormones, interactions with non haemopoetic cell types

210
Q

How many major lineages arise from the haemopoietic stem cell?

211
Q

What kind of nuclei do platelets have?

A

They have no nucleui

212
Q

What is megakaryocyte formation driven by?

A

Thrombopoietin TPO

213
Q

What kind of cell is a megakaryocyte?

A

Polyploid- several copies of each chromosome

214
Q

What are the granulocytes?

A

Basophils, neutrophils, eosinophils

215
Q

What do granulocytes arise from?

A

Myeloblast cells

216
Q

What can monocytes differentiate into?

A

Macrophages or dendritic cells

217
Q

The development of B lymphocytes commences where?

A

Fatal liver and bone marrow

218
Q

What happens to the immunoglobulin genes of B lymphocytes in development

A

Genes rearracnce to produce antibodies with wide array of variation

219
Q

Where to T lymphocytes arise from and then mature

A

Arise from fetal liver mature in thymus

220
Q

What commits progenitor cells to erythroid lineage?

A

Transcription factors GATA1, FOG1, PU1

221
Q

Once the progenitor cell has been committed to erythroid lineage what drives it ?

A

EPO from kidneys

222
Q

How does EPO work?

A

Inhibits apoptosis of colony forming units of ertyhroid cell line.

223
Q

What do reticulocytes do once in the bloodstream

A

Extrude ruminants of organelles- mitochondria and ribosomes

224
Q

What is a diagnostic estimate of EPO level?

A

Reticulocytes count

225
Q

Why are red blood cells particularly succeptibe to oxidative damage

A

Lack nuclei, cant replace damaged proteins

226
Q

What cells make up the RES system

A

Kupffer (liver)
Microglia (CNS)
Re pulp macrophage (Spleen)
Langerhans (skin and mucosa)

227
Q

What does the shape of RBC allow them to have as a properties

A

Optimal laminar flow

228
Q

What proteins of the erythrocytes lipid bilayer are particulary important

A

Spectrin, ankyrin, band 3, protein 4.2

229
Q

What conditions are associated with gene mutations in spectrum, ankyrin, band 3 or protein 4.2

A

Alter rbc cell membrane eg hereditary spherocytosis

230
Q

How much of the RBC cell volume is haemoglobin?

231
Q

What does 2,3 BPG do to oxygen afffinity in rbc

A

Decreases it

232
Q

A fall in ph or increase in co2 does what to rbc affinity

A

Decrease (Bohr)

233
Q

Ferric iron is reduced to ferrous iron by what

A

Duodenal cytochrome b reductase

234
Q

Iron within enterocytes can either be what

A

Stored as ferritin

Transported via ferroportin

235
Q

Hepcidin binds directly to what? It also inhibits transcription of what

A

Ferroportin

DMT1 gene

236
Q

What does the normal haemoglobin range vary on?

A

Age, sex, ethnicity

237
Q

How does the body adjust to a slow anaemia

A

Increase stroke volume, increase conc of 23bpg

238
Q

How is an initial iron defficency overcome

A

Mobilisation of iron from stores

239
Q

In anaemia of chronic disease what happens to macrophage activity

A

It’s increased

240
Q

In anaemia of chronic disease what is happening to hepcidin?

A

Cytokines IL-6 increases production resulting in less iron absorbtion

241
Q

What’s folate converted into? What’s its purpose

A

Tetrahydrofolate

It’s a one carbon carrier, needed for synthesis of base thymidine

242
Q

Folate defficency in pregnancy can result in what

A

Neural tube defect

243
Q

Vit b12 can only be obtained from what

A

Animal origin food

244
Q

Where is half the dietary b12 taken up

245
Q

If b12 stores are high how long before its depleted

246
Q

What is functional folate defficent

A

Lack of b12 traps folate in stable methyl state

247
Q

What is G6PDH the rate limiting enzyme in?

A

Pentose phosphate pathway

248
Q

Myeloproliferative neoplasms are cursed by what

A

Mutation in the gene coding for tyrosine kinase Janus kinase

249
Q

In post cases what is PV driven by?

A

Oncogenes mutations that activate jack-stat pathway

250
Q

What does white pulp do

A

Synthesised antibodies and removes antibody coated bacteria and blood cells

251
Q

Howel jolly bodies are an indicator of what

A

Reduced splenic function

252
Q

What colour do basophils stain

253
Q

What colour do eosinophils stain

254
Q

What colour do neutrophils stain

255
Q

Eisoniphils nuclues are..

256
Q

When do basophils release histamine and heparin

A

Following binding of IGE to surface receptor

257
Q

How is increased EPO stimulated?

A

Reduced pO2 in the intersitital peritubular of the kidney

258
Q

Iron is either available or stored, what are some forms of available iron? And what are some forms of stored iron? Are the stored irons soluble or insoluble?

A

Available: haemoglobin, myoglobin, tissue iron (enzymes), transported serum iron
Stored: ferritin (soluble) haemosiderin and macrophage iron (insoluble)

259
Q

Stored iron is mostly ferritin or haemosiderin, what is it mostly stored as?

A

Ferritin (95%) haemosiderin (5%)

260
Q

Where Is iron absorbtion occuring?
What channel is needed for Fe2+ to be absorbed?
What converts Fe3+ to Fe2+ for absorbtion?

A

Duodenum and jejunum
DMT1
Enzyme DcytB, ferrireductase, citric acid can form complexes to increase absorbtion of Fe3+

261
Q

How is haem converted to Fe2+ in the enterocyte?

What is the fate of Fe2+ within the enterocyte?

A

Haem oxidase converts him to fe2+ form
Fe2+ stored as ferritin in fe3+ state
Exported from cell via ferroportin

262
Q

What 3 effects does hepcidin have to decrease iron absorbtion?

A

Degrades ferroportin
Inhibits transcription of DMT1
Inhibits release of stored iron from macrophages

263
Q

Once Fe2+ is bound to transferrin in the blood where does it go? What competes with it? What inherited disorder results in iron overload due to changes with this syste?

A

Can bind to transferrin receptors eg on red blood cells
HFE competes with these receptors
Hereditary haemochromatosis is an error in the gene for HFE

264
Q

How is hepcidin release controlled?

A

High EPO reduces its expression

High iron increases its expression

265
Q

What are 2 tests for iron defficency

A

Ferritin- also an acute phase protein

CHR- reticulocyte haemoglobin content (would also be low in thalassaemia

266
Q

A 32 year old man presents worried about the fact his dad died of heart attack at a young age
You do labs to look for what

A

Total cholesterol
Serum Traicyglycerol
Serum lipoprotein profile and check blood glucose for diabetes

267
Q

What is hyperlipoproteinaemias?

A

Any condition where after 12 hour fast the plasma cholesterol and/or plasma triglyceride is raised

268
Q

A man who’s dad died early of a heart attack and has labs indicating high serum holesterol and increased LDL is likely to have what hyperlipoproteinaemia?

A

Familial hypercholeseramia

269
Q

What are the 2 pathways in which tissues obtain the cholesterol they need?

A
  1. Direct synthesis via HMG coa

2. Cells can obtain via receptor mediated endocyots of LDL

270
Q

What’s a well known statin?

And a well known bile sewquestant?

A

Atorvastatin

Cholestyramine

271
Q

Why are serum iron levels not reliable indicators of iron defficency?

A

Diurnal variation in levels

272
Q

What vitamin defficency would cause a sideroblsatic anaemia

273
Q

What ferritin level indicates iron defficency?

What excludes it?

A

Low serum ferritin indicates it

High or normal doesnt exclude it

274
Q

Where are blister cells commonly seen on blood film

A

G6PDH defficency

275
Q

How does anaemia of chronic disease result in anaemia with a high ferritin and a high CRP

A

Chronic inflammation causes high levels of IL 6 which stimulates hepcidin which causes ferroportin to go back into cell and also for macrophage stores not to be released. The RBC doesnt get the iron and therfore has short lifespan leading to anaemia. But body iron levels are high

276
Q

How does myelodysplastic syndrome lead to anaemia or pancytopenia

A

Abnormal clones of marrow stem cells are produced. These produce macrocytic cells that get prematurely destroyed inducing anaemia

ESA 2 (10 decks)

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