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Year 1 Medicine Newcastle > Case 4 > Flashcards

Case 4 Flashcards

1
Q

What are the 4 main components of blood

A

RBCs- erythrocytes
White blood cells- leukocytes
Platelets- thrombocytes
Fluid-plasma

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2
Q

What is the haematocrit

A

The proportion of the blood that is taken up by red blood cells

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3
Q

What is the erythrocyte sedimentation rate

A

The rate at which RBCs settle in a tube under the forces of gravity

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4
Q

With anaemia, is the erythrocyte sedimentation rate greater or smaller

A

Greater

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5
Q

How wide is an erythrocyte

A

6-8mm

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6
Q

How long does an average erythrocyte live

A

120 days

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7
Q

How long do platelets last in the circulation

A

7-14 days

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8
Q

What is the proteins role in the plasma (5)

A 
Reserve supply of amino acids 
Carriers for other molecules 
Act as buffers
Help blood to coagulate 
Oncotic pressure
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9
Q

What are globulins

A

Proteins in the blood plasma that transport lipid and vitamins with some being immunoglobins

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10
Q

What is albumin

A

A negatively charged protein making up 60% of the blood

Has a role in maintaining oncotic pressure and transporting substances

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11
Q

How does oncotic pressure vary as you go along a capillary bed

A

It stays the same (slight raise towards venous end as fluid volume decreases)

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12
Q

What are electrolytes role in the blood

A

They maintain osmotic balance

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13
Q

What other substances are in the blood beyond proteins, electrolytes and blood cells

A 
Glucose for energy
Amino acids for protein synthesis
Hormones
Dissolved gases
Vitamins and minerals 
Urea and uric acid
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14
Q

How does hydrostatic pressure vary as you go through a capillary

A

It decreases

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15
Q

How can heart effect hydrostatic pressure in a capillary why

A

There may be increased hydrostatic pressure at the venous end as there is a back up in the system which may result in less fluid going back into the capillary at this end

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16
Q

How can nephrosis alter oncotic pressure

A

This may decrease it as there will be decreased albumin synthesis

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17
Q

What visible symptoms caused by a change in increased hydrostatic or reduced oncotic pressure result in

A

An oedema

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18
Q

How can a compromised immune system result in an oedema

A

Localised oedema can occur upon the removal of a lymph node
The immune system may also form an oedema on injury to allow an influx of chemical mediators into the site of injury to fight off any potential infection

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19
Q

Where is the spleen situated

A

In the left hypochondrium

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20
Q

What arteries supply the spleen

A

The splenic artery and vein

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21
Q

What is the function of white pulp in the spleen

A

It is part of the immune system and is mainly made up of white blood cells

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22
Q

What is the function of red pulp in the spleen

A

It is made up of connective tissue and filters the blood for antigens, microorganisms and defective red blood cells

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23
Q

What are the main key functions of the spleen

A 
It's a lymphoid organ for the immune system 
Removes old erythrocytes in the red pulp
Screens for pathogens in the white pulp
Stores platelets 
Stores iron
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24
Q

Where are antigens found on erythrocytes and what are they

A

The surface attached to glycolipids or glycoproteins

they are short sugar chains

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25
Q

What synthesises antigens

A

glycosyltransferases- different types lead to different antigens

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26
Q

Why is blood group O considered a ‘universal donor’

A

Because it contains no antigens on it’s surface

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27
Q

What blood can patients with blood type A and blood type B receive

A

Group A or O however A is preferable

Same idea however with B

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28
Q

What blood groups can blood group AB receive

A

All blood groups as it contains antigen A and B on its surface so won’t react when transfused

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29
Q

What antibodies are present in blood type AB

A

There are no antibodies present

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30
Q

What complication does giving the wrong blood type lead to

A

Haemolytic disease

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31
Q

What percentage of the population are rhesus positive

A

85%

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32
Q

How can complications arise in pregnancy if the father and mother have differing blood types and how can this be combatted

A

If the mother and father have conflicting rhesus types this may lead to haemolytic disease of the newborn
This can be prevented by giving an injection that neutralises antigens the mother produces that may attack the foetus’ blood

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33
Q

What does the suffix poiesis refer to

A

making of a substance

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34
Q

What is granulopoiesis

A

The making of WBCs

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35
Q

What are granulocytes

A

neutrophils, eoisinophils and basophils

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36
Q

What are mononuclear cells

A

Monocytes and lymphocytes

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37
Q

What is the site of primitive haematopoiesis

A

The yolk sac

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38
Q

Where is the major site of haematopoiesis

A

The bone marrow however this retracts with age and is replaced by fat

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39
Q

Where, beyond the bone marrow, can the body naturally make blood cells

A

Peripheral blood stem cells

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40
Q

What procedure can occur to transfer many stem cells into the peripheral blood cells of adults

A

Using an umbilical cord

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41
Q

What are committed progenitors

A

These are stem cells that are going to become a specific cell and this path cannot be altered

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42
Q

What are precursors

A

These are cells that have lost the ability to make any other cells and look almost exactly like the mature cell they are about to develop into

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43
Q

What is the lineage-primed model of haematopoiesis

A

Stem cells tend to differentiate in a certain way and have their path set out for them, if the environment is altered in a certain way this path may be changed however if not then they will differentiate to form the cell they intended

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44
Q

Whta defines a stem cell

A

They are self renewing so can copy themselves indefinitely

They are pluripotent so can differentiate into many different cell types

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45
Q

What results in a stem cell differentiating from the bone marrow

A

If one of the daughter cells the stem cell produces becomes unattached from its specific niche within the bone marrow

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46
Q

What controls stem cell differentiation

A

Transcription factors control the expression of specific genes
Growth factors act as extrinsic factors that influence cell fate

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47
Q

What specific transcription factors dictate RBC differentiation and leukocyte differentiation

A

GATA 1 forms an erythrocyte and PU. 1 tends towards a leukocyte

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48
Q

How are the transcription factors in stem cells regulated

A

Through positive feedback loops

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49
Q

If there is a slight imbalance of one specific transcription factors between daughter cells of stem cells what occurs

A

The daughter cell with greater levels of this transcription factor will continue to produce more and the one with less will have that transcription factor inhibited

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50
Q

What is EPO

A

Erythropoietin is the colony stimulating factor for erythrocytes

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51
Q

What is G-CSF

A

Granulocyte colony stimulating factor

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52
Q

What is TPO

A

thrombopoietin

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53
Q

When would EPO be clinically treated to combat disease

A

Renal failure, bone marrow failure and may help blood shortages

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54
Q

When would G-CSF be administered clinically

A

After chemo or for stem cell mobilisation

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55
Q

Where is erythropoietin produced and how is it regulated

A

The kidneys

Dependent on the amount of oxygen in the body

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56
Q

What are reticulocytes

A

immature red blood cells

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57
Q

When does reticulocytosis occur

A

When there is a sudden need for RBCs such as extreme bleeding or haemolysis

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58
Q

What four stresses drive the production of G-CSF

A

Infection
Inflammation
Immunity
Infarction

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59
Q

What does the activation of high levels of G-CSF result in

A

Progenitor expansion
Toxic granules
Left shift (mobilisation of immature cells)

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60
Q

What are the four components of the mononuclear phagocyte system

A

Blood monocytes
Mobile tissue macrophages
Fixed tissue macrophages
Dendritic cells

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61
Q

What are the roles of macrophages (6)

A 
Developing blood, brain and bone 
Storing iron 
Clearing debris
Detecting pathogens 
Priming immunity 
Immune response
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62
Q

How is the mononuclear phagocyte system important in disease and infection

A

There are specialised macrophages in each part of the body to deal with and pathogens coming in to that specific part

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63
Q

How does the state of haem change upon the binding of oxygen

A

The haem goes from a ‘tense’ to a ‘relaxed’ state and this allows further O2 to bind as it increases its affinity to O2

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64
Q

How does p.p. affect oxygen release by haem

A

The lower the p.p. the mroe oxygen is given off

Therefore organs that require a lot of oxygen have low p.p.

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65
Q

How does an increase in temp. decrease in pH or increase in 2-3 DPG levels affect the oxygen dissociation curve

A

It shifts it to the right

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66
Q

What is 2-3 DPG

A

A product of glycolysis

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67
Q

Why is a tissue affected by a shift in the oxygen haemoglobin dissociation curve but an alveolus isnt

A

Because a tissue is usually at 5-7kPa whereas an alveolus is at 14kPa so it is barely affected

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68
Q

What do metabolically active tissues give off that results in a shift of the oxygen haemoglobin curve to the right and why does this assist them

A

Very active metabolic tissues require a lot of oxygen they give off heat due to metabolic processes and this shifts the curve to the right
As a result oxygen dissociates from haemoglobin more readily and the affinity of oxygen for Hb is reduced

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69
Q

How is pH linked to the Bohr effect

A

A lower pH occurs due to an increase in CO2 in the bloodstream due to respiratory acidosis
This shifts the oxygen haemoglobin curve to the right alongside an increase in the presence of CO2

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70
Q

How does 2-3 DPG result in a shift to the right of the oxygen haemoglobin curve

A

It interacts with amino acids on beta chains and this destabilises the interaction of Hb with O2

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71
Q

How does altitude affect 2-3DPG

A

Higher altitudes increase 2-3DPG production so more oxygen goes to the tissues

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72
Q

What are the three main forms of CO2 carriage in the bloodstream

A

Dissolved in the plasma
Bicarbonate
Bound to haemoglobin

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73
Q

How does carbonic anhydrase promote the Bohr effect

A

Carbonic anhydrase catalyses the reaction CO2 + H2O -> HCO3- + H+
This H+ can bind with haemoglobin instead of some oxygen which decreases Hb affinity for oxygen

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74
Q

What does carbon dioxide form when combined with haemoglobin

A

Carbaminohaemoglobin

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75
Q

What groups are mainly affected by sickle cell disease

A

Those of African, Caribbean, Middle Eastern and Indian descent

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76
Q

What are the three main types of sickle cell anaemia and what are their genotypes

A

Sickle cell anaemia (HbSS)
Sickle haemoglobin-C disease (HbSC)
Sickle beta Thalassemia

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77
Q

What is the inheritance pattern in sickle cell anaemia

A

Autosomal recessive

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78
Q

How does sickle haemoglobin C disease affect a patient

A

Similar symptoms to sickle cell however less anaemia in general

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79
Q

Where is the mutation in the haemoglobin in sickle cell anaemia

A

On the beta globin chain

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80
Q

What is the nature of the mutation that codes for HbS

A

A single base substitution on the sixth codon of the beta-chain gene

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81
Q

How does the HbS mutation result in a sickle shaped RBC

A

It forms polymers under deoxy conditions so the erythrocyte distorts and collapses in on itself
This occurs when it is cold, infection, hypoxia and exercise but if these episodes reccur then the cells amy become irreversibly sickled

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82
Q

What is the disadvantage of the sickle cell RBCs

A

They are stickier and less flexible than normal RBCs so can form clusters and get stuck, blocking and damaging blood vessels

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83
Q

What is a sickle cell crisis

A

This is the clustering of sickle cells in blood vessels and is characterised by harsh pain

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84
Q

What is the lifespan of a sickle cell

A

around 17 days

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85
Q

How does Sickle cell anaemia present

A

Usually in early childhood
Variable severity
Half the sufferers experience sickle cell crisis with most having a few each year
Anaemia and infection common
Chronic manifestations can be seen by ischaemia and infarction due to blocking of blood vessels by sickle cells

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86
Q

Why do children in general not present with sickle cell in the first 6 months

A

They are protected by elevated levels of HbF

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87
Q

How can FBC and blood film indicate sickle cell disease

A

They will present with a high percentage of reticulocytes and then sickled RBCs

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88
Q

What does the sickle solubility test do but what is it’s limitation

A

This exposes RBCs to a deoxygenating agent that gives a cloudy appearance in the presence of HbS
however it doesn’t differentiate between sickle cell disease and sickle trait

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89
Q

How can you confirm sickle cell disease after a positive sickle solubility test

A

You can analyse with electrophoresis or high-performance liquid chromatography

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90
Q

What is the only curative treatment of sickle cell disease

A

Bone marrow transplant

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91
Q

What is dactylitis, a symptom of sickle cell disease

A

This is hand and foot swelling, mainly in infants

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92
Q

What is an aplastic crisis

A

When the body doesn’t produce enough new RBCs to replace the old ones

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93
Q

How can sickle cell anaemia affect the eyes

A

Vision loss or even blindness may occur when sickle cells become blocked in the retina so sufferers should have their eyes checked

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94
Q

What is spherocytosis

A

The presence of sphere shape RBCs instead of bioconcave discs

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95
Q

What causes spherocytosis

A

Genetic or various forms of haemolytic anaemia

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96
Q

What is the pattern of inheritance of spherocytosis

A

It is autosomal dominant

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97
Q

What is the defect cause that leads to the spherical shaped blood cells in spherocytosis

A

A defect in one or more of the coupling proteins that connect the cytoskeleton and lipid bilayer membrane
This means the lipid bilayer isn’t supported by the cytoskeleton

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98
Q

What consequences can arise as a result of spherocytosis

A

This results in a smaller surface area for gas exchange and less efficient oxygen transportation

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99
Q

What occurs in the spleen to spherocytes

A

These cells are often caught in there and promote phagocytosis by splenic macrophages leading to extravascular haemolysis, shortened lifespan and subsequent anaemia

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100
Q

How may spherocytosis be discovered if not found in early life

A

This may be of an incidental finding of haemolysis, haemolytic anaemia or spherocytes on the blood smear

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101
Q

What is the life expectancy of sickle cell disease

A

40-60 years

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102
Q

What is the life expectancy of those suffering from spherocytosis

A

Generally normal

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103
Q

What are qualitative abnormalities with globin chains

A

Structual variations to the Hb molecule

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104
Q

What are quantitative abnormalities to the Hb chain

A

There is a quantitative decrease in the production of alpha or beta globin chains
Chains are structurally normal
Known as Thalassemias

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105
Q

What is alpha thalassemia

A

A reduction in alpha globin chain synthesis

106
Q

What is beta thalassemia

A

A reduction in beta globin chain synthesis

107
Q

How many types of alpha thalassemias are there and how are they dictated

A

There are 4 different types characterised by the mutation of a number of alpha globin genes on each chromosome as there are four different genes that can be affected

108
Q

How does a single deletion of an alpha globin allele affect sufferers

A

Hardly, asymptomatic

109
Q

How does a two gene alpha globin gene deletion affect sufferers of alpha thalassemia

A

Very rarely majorly however they may present with mild hypochromic anaemia

110
Q

How does a three gene deletion on the alpha globin allele affect sufferers

A

This leaves one normal gene and therefore excess beta globin chains form HbH

111
Q

How does HbH affect an RBC

A

It which has a high affinity for oxygen which results in the RBCs being ineffective at delivering oxygen to hypoxic tissues
It also is prone to oxidation which results in intracellular occlusions that may promote haemolysis

112
Q

What does a four gene deletion fo the alpha globin gene result in

A

Severe lack of HbF- extremely important in gestation
Gamma chains take place and form gamma tetrameters which cannot deliver oxygen as their affinity of O2 is too high
Baby is stillborn and has hydrops fetalis- full body oedema

113
Q

How can you diagnose alpha thalassemia

A

Complete blood count and blood smear

Haemoglobin analysis such as electrophoresis determines what type is present

114
Q

How is beta thalassemia inherited normally

A

In the autosomal recessive manor

115
Q

What classifies patients who have beta thalassemia intermedia from major

A

If they are transfusion dependent (major) or not (intermedia)

116
Q

Why are newborns asymtomatic despite having the beta thalassemia genotype

A

Because they have HbF as their major haemoglobin source

117
Q

What occurs in beta thalassemia major to the RBCs

A

The unpaired alpha chains may precipitate to form inclusions
This leads to anaemia and inefficient erythropoiesis due to earlier breakdown by the spleen and apoptosis of inclusions

118
Q

What are the symptoms of beta thalassemia major

A

Abdominal swelling
Bony deformities due to erythroid hyperplasia
Palor and jaundice
Exercise intolerance

119
Q

How can you diagnose beta thalassemia

A

The complete blood count and peripheral blood smear

120
Q

How can you cure beta thalassemia

A

If identified early you can do a stem cell transplant

121
Q

What is the most common form of anaemia in the Uk

A

Iron deficiency anaemia

122
Q

What causes iron deficiency anaemia

A 
Pregnancy or child growth spurts
Heavy menstrual periods 
Poor absorption of iron 
Bleeding from the gut 
Eating a poor or restricted diet
123
Q

What are causes of anaemia beyond iron deficiency

A

Lack of vitamin B12 and folic acid
RBC problems
Bone marrow problems
RA and chronic kidney disease

124
Q

How do you treat iron deficiency anaemia

A

Oral iron salts (100-200mg) given daily

Folic acid and iron for pregnant women

125
Q

What can you administer if the patient can’t take oral iron

A

Parenteral iron

126
Q

What dose of folic acid should be taken daily for adults suffering with anaemia

A

5mg

127
Q

What drug can be taken for those with pernicious anaemia

A

Hydroxocobalamin

128
Q

Should you ever take hydroxocobalamin daily

A

No

129
Q

What side effects does hydroxocobalamin generally cause

A 
Diarhhoea
dizziness
headache
Hot flush
Nausea
130
Q

What forms of anaemia result in microcytic anaemia

A

Iron deficiency anaemia

Anaemia due to chronic infection

131
Q

What forms of anaemia result in megaloblastic anaemia

A

Folic acid deficiency

Vitamin B12 deficiency

132
Q

What form of anaemia results in normocytic anaemia

A

Anaemia due to bone marrow or renal failure

133
Q

What is the normal daily requirement of iron

A

5mg in men
15mg growing children and menstruation
2-10x more in pregnant women

134
Q

What B vitamin is folic acid

A

B9

135
Q

Where can you find folic acid in your diet

A

Leafy green vegetables and folic acid preparations

136
Q

What can a lack of folic acid in pregnancy cause

A

Neural tube defects

137
Q

What is the role of vitamin B12 in the body

A

Normal DNA synthesis
Haematopoiesis
Maintenance of myelin in the nervous system

138
Q

Where does absorption of vitamin B12 occur

A

The terminal ileum

139
Q

What drugs can be administered to control the differentiation of pluripotent stem cells

A

Haemopoietic factors such as erythropoietin and colony stimulating factors

140
Q

How are haematopoietic factors administered

A

Intravenously

141
Q

What are examples of erythropoietin haematopoietic factors

A

Epoietin and darbepoetin

142
Q

What is an example of a granulocyte-macrophage-CSF

A

Sargramostim

143
Q

What are common side effects to erythropoietins

A

Flu-like symptoms
iron deficiency
increased blood viscosity

144
Q

What are common side effects to leukocyte stimulating factors

A

Fever and chills
Rash
GI effect
Bone pain

145
Q

What are examples of G-CSFs given clinically

A

end in -grastim

146
Q

What does Oprelvekin stimulate the production of

A

Megakaryocyte

Thrombopoiesis

147
Q

If there is too high levels of abnormal HbS what drug can be taken and what is its mode of action

A

Hydroxycarbamide acts to inhibit synthesis of HbS

148
Q

What is a tumour

A

An abnormal mass of tissue that the growth of it is uncoordinated and exceeds natural tissue size

149
Q

What is a papilloma

A

A benign epithelial tumour that grows exophytically

150
Q

What is an adenoma

A

A benign tumour that arises in glandular tissue

151
Q

What is a carcinoma

A

A malignant tumour that arises in the epithelial tissue of the skin or internal organs

152
Q

What is a sarcoma

A

A malignant tumour arising in connective or non-epithelial tissue

153
Q

What is dysplasia

A

A pre-cancerous increased cell division that results in abnormal looking cells and is reversible

154
Q

What is neoplasia

A

Uncontrolled cell proliferation resulting in an abnormal cell structure and function and is irreversible

155
Q

What is a carcinoma in situ

A

Neoplastic cells remain growing and contained within their original site and haven’t invaded the basement membrane

156
Q

What is intraepithelial neoplasia

A

This describes the difference between invasive and non-invasive neoplasms

157
Q

What is metastasis

A

The development of secondary neoplastic growths in non-neighbouring tissues

158
Q

How are cancers staged and what does each stage represent

A 
Stage 0: carcinoma in situ 
Stage 1: localised 
Stage 2: locally invasive
Stage 3: Local spread to lymph nodes 
Stage 4: metastasised
159
Q

What is the grading of cancer and what does each grade mean

A

1: nearly normal cells
2: Some abnormal cells
3: many abnormal cells
4: very few normal cells
5: completely abnormal cells

160
Q

What is the transformation of cells with neoplasia

A

The changes that normal cells undergo as they become malignant

161
Q

What is clonality

A

When multiple cells are derived from a single cell and are genetically identical

162
Q

What is a carcinogen

A

Any substance that promotes transformation of a cell

163
Q

What are the two types of carcinogens

A

Initiators: mutagenic and promote DNA mutations
Promoters: Non-mutagenic and act by stimulating cell division to increase the mutant population

164
Q

What is an oncogene

A

This is a mutated gene that contributes to drive neoplasia

165
Q

What is a proto-oncogene

A

an unaltered cellular counterpart of an oncogene

166
Q

What is a viral oncogene

A

A virally encoded protein that contributes positively to neoplasia

167
Q

What is a tumour-suppressor gene

A

a gene involved in regulating cell growth and division that is usually inactivated by cancers

168
Q

Why does a mutation in a gene responsible for regulating the cell cycle mean further mutations of this cell are likely

A

Because the cell is dividing much more rapidly and replicating DNA at a faster rate, increasing the chance of mutations
Eventually the mutations will result in the cell dividing in an uncontrollable way that results in a clonal cellular mass

169
Q

Why are tumour cells damaging

A

They don’t perform their original function

170
Q

How can tumour cells interfere with adjacent cells

A

They can release toxins to create a necrotic environment
They compress organs and neighbouring organs
They can result in complete colonisation

171
Q

What is hyperplasia

A

Increased cell division but cells look and act normal

172
Q

What are post-mitotic cells

A

These are cells that have left the cell cycle and don’t know how to divide

173
Q

What occurs in the G1 phase of the cell cycle

A

Increasing in size and number of organelles

174
Q

What is the S phase of the cell cycle

A

Where the DNA is replicated

175
Q

What is the G2 phase of the cell cycle

A

Where the cell grows and prepares for mitosis

Checks if the DNA has been replicated correctly

176
Q

What occurs in the M phase of the cell cycle

A

the division of the cell to form two new cells

177
Q

What are the stages of mitosis and what occurs at each one

A

Prophase: chromosomes condense to become more compact
Prometaphase: chromosomes organise themselves within the cell and nuclear membrane breaks down
Metaphase: chromosomes align
Anaphase: the chromosomes are pulled to either pole
Telophase: the nuclear membrane reforms around each daughter cell

178
Q

What pulls the chromosomes apart from the centromeres

A

The mitotic spindle

179
Q

Where are the 4 checkpoints of the cell cycle

A

The point between G1>S
In S-phase
G2>M checkpoint
The metaphase to anaphase transition

180
Q

What does the G1/S checkpoint check

A

If the environment is favourable and in a growth stable environment

181
Q

What does the S phase checkpoint check for

A

Problems with DNA replication

182
Q

What does the G2/M phase checkpoint check for

A

If the DNA has been replicated correctly and if the environment is favourable for mitosis

183
Q

What does the metaphase-anaphase checkpoint check for

A

If the spindle is correct and that the chromosomes are aligned in an optimal way to divide

184
Q

What enzymes drive the cell cycle

A

Cyclin dependent kinases

185
Q

What proteins activate Cdks and how

A

Cyclins are needed to form complexes with the Cdks to activate them

186
Q

How do cyclin-Cdk complexes trigger events in the cell cycle

A

They phosphorylate target proteins

187
Q

In G1 what cyclin binds to what CDKs

A

Cyclin D to CDK 4 and then 6

188
Q

What cyclin binds at the end of G1 to what cyclin

A

Cyclin E to CDK 2

189
Q

What cyclin binds to what CDK at the end of S phase

A

Cyclin A to CDK2

190
Q

What cyclin binds to what CDK during G2

A

Cyclin A to CDK 1

191
Q

What cyclin binds to what CDK during M phase

A

Cyclin B binds to CDK1

192
Q

What occurs if the correct cyclin isn’t present

A

The cell will not have the right enzymatic reaction to go through the cell cycle

193
Q

What activates the transcription and binding of cyclins to CDKs

A

The binding of growth factors to the CSM
This activates a MAP kinase signalling cascade
This activates transcription that codes for cyclins

194
Q

What proteins can inhibit the cell cycle

A

INK4 or Cip/Kip

195
Q

What are mitogens

A

Growth factors that stimulate cell division

196
Q

Why is P53 referred to as the guardian of the genome

A

Because it acts as an inhibitor of the cell cycle

197
Q

What is an example of a tumour suppressor gene

A

P53

198
Q

When is P53 active

A 
If there are:
errors in mitosis 
DNA damage 
Cell stress 
Oncogene activation 
Excessive mitogenic pressure
199
Q

Why aren’t telomeres effective in cancer cells

A

cancer cells can continue to divide even if the telomeres are too short

200
Q

What is the first step of cancer cell production

A

A carcinogen initiates a cell through initiation

201
Q

What occurs after initiation of a cancer cell

A

a genetic change occurs to form a pre-neoplastic that then undergoes a genetic change to form a malignant cell

202
Q

What can genetic mutations in cancerous cells lead to

A 
Loss of function 
Silencing tumour suppressors 
Expression of oncogenes 
Loss of sensitivity to growth inhibition factors 
Evasion of cell death 
Limitless replication potential
203
Q

Why can there be a selection of tumour cells in a patient

A

Because they may be undergoing different selection pressures

204
Q

Why may chemo not kill all the cancerous cells

A

Some may adapt to the selection pressure of chemo and not be killed from it

205
Q

Why is a cancer relapse harder to treat

A

Because the cells have undergone chemo and may be more resistant to it as they have survived and can then multiply

206
Q

What are the 6 hallmarks of a cancerous cell

A 
Self stimulus to growth 
Evading growth suppressors 
Resisting cell death 
Replicative immortality 
Angiogensis (own blood supply)
Invasion and metastasis
207
Q

What are the two types of mutations that cause cancer cells

A 
Somatic mutation (carcinogens or oncogene viruses)
Germ line (inherited)
208
Q

How can direct DNA damage cause mistakes in the DNA

A

There may be imperfect repairing of the DNA

209
Q

What can a carcinogen do to DNA

A

directly damage DNA crosslinking
Mutate DNA bases
Produce free radicals that damage the DNA

210
Q

What are examples of viral oncoproteins that inhibit tumour suppressor genes

A

E6 inhibits P53

E7 inhibits retinoblastoma

211
Q

How do oncogenes promote constant cell division

A

When active they phosphorylate target proteins that allow continuation through the cell cycle

212
Q

What are the clear differences between malignant and benign cells

A

Malignant don’t really look like normal tissue
They grow endophytically
Have an enlarged nuclear:cytoplasm ratio
Fast growth rate
Poorly defined border

213
Q

What is the key difference with regards to invasion between benign and malignant tumours

A

Invasion through the basement membrane

214
Q

How does the differentiation of tissues vary with benign and malignant tumours

A

benign tumours are well differentiated and malignant are not

215
Q

What is anapalstic tissue

A

Tissue destroyed by tumour so much so that it doesn’t represent the original tissue

216
Q

How do the levels of necrosis vary between benign and malignant tumours

A

There is a much higher level of necrosis in malignant tumours due to high cell turnover and replication

217
Q

What is an adenocarcinoma

A

A malignant tumour in the glandular tissue

218
Q

What is Burkitt’s lymphoma

A

A cancer of B cells that affects the lymphatics system

219
Q

What is Ewing’s sarcoma

A

An ulcerating cancer of the bone

220
Q

What is Hodgkin’s lymphoma

A

A certain type of lymphoma that is characterised by the presence of Reed-Sternberg that are cells that contain more than one nucleus

221
Q

What are blastomas

A

Tumours of the blast cells

222
Q

What are harmatomas

A

These affect connective tissue and cause cells in the connective tissue to grow larger as the patient grows
They don’t cause any symptoms but appear as tumours on scans

223
Q

What is the most common symptom of endocrine tumours

A

Excessive hormone production

224
Q

What is a cyst

A

A fluid filled space that is lined by epithelium

225
Q

What is a teratoma

A

A tumour of an egg cell or sperm cell

226
Q

What are cells bound to each other by normally

A

Adhesion molecules

227
Q

How can malignant cells separate from surrounding cells

A

They lose expression of adhesion molecules

228
Q

How do malignant cells break down connective tissue

A

They secrete proteolytic enzymes

229
Q

How do malignant epithelial cells produce mobility in order to spread and move more effectively

A

They produce enzymes usually produced by the more mobile mesenchymal cells

230
Q

What is contact inhibition and how does it apply to malignant cancer cells

A

This is that if a moving cell bumps into another cell it will stop moving through contact inhibition
Malignant cells don’t have movement inhibition so keep moving

231
Q

What are secondary tumours

A

These are metastases located in distant organs from the primary cancer

232
Q

Why are metastases more aggressive than primary tumours

A

Because for a malignant cell to spread around the body it has to undergo many mutations

233
Q

What are the three main ways malignant cells can spread

A

Haematogenously
Lymphatically
Transcoelemic

234
Q

Why may you feel enlarged lymph nodes in metastatic cancer

A

Because some malignant cells may congregate in the lymph nodes

235
Q

What is the transcoelomic route of metastatic spread

A

This is through the cavities of the body:

The pleural, pericardial or peritoneal cavities

236
Q

What determines the grading of a cancer

A

Mitotic activity
Nuclear size
Hyperchromasia (how dark the nucleus appears)

237
Q

What does TNM staging look at

A

tumour size, nodal involvement and metastases

238
Q

What is the Duke’s staging used for

A

Colorectal cancers

239
Q

What is public health

A

The science and art of promoting health and preventing disease by organised efforts of society

240
Q

What is primary intervention

A

Reducing the risk of disease in areas

241
Q

What is secondary intervention

A

Identifying and managing diseases early

242
Q

What is tertiary intervention

A

Preventing chronic or disabling effect of chronic disease

243
Q

What is screening

A

Identifying healthy people who may be at risk of a condition and offering them information, further tests and appropriate treatment to reduce the risk of complications

244
Q

What are the potential weaknesses of screening

A

False negatives and positives
People getting the all clear on their unhealthy lifestyles
Over diagnosis of disease
Health inequalities may increase

245
Q

What are the main cancer screening tests offered by the NHS

A

Bowel cancer screening
Breast cancer
Cervical cancer

246
Q

What are the main non-cancer screening tests offered by the NHS

A 
Diabetic eye 
Fetal anomaly (structural)
Infectious diseases in pregnancy 
Newborn and infant physical examination 
Newborn blood spot (heel prick)
Newborn hearing 
Sickle cell and thalassemia
247
Q

What are the three main categories of screening

A

Proactive, targeted screening
Voluntary
Opportunistic- e.g. attending the GP and screening for cholesetrol

248
Q

What are the 4 criteria for screening

A

The disease
The test
Sensitivity
Specificity

249
Q

What criteria must the disease fulfil in order for it to be satisfactory for screening

A

It should be a serious, frequent disease
Its history should be understood It should be treatable
There should be a long period between when it’s detected and when treatment becomes no longer effective

250
Q

What criteria must the screening test fulfil in order to be satisfactory

A

It must be valid, simple and cheap, safe, acceptable and reliable

251
Q

What is sensitivity

A

The ability to test correctly those who have the disease

252
Q

What is specificity

A

The ability to test correctly those who have the disease

253
Q

How should the program be apparent to combat disease

A

There must be evidence it’s reducing disease
The opportunity cost must not outweigh it Participants must be able to make an informed choice about participating
Quality assessed by the SQAS

254
Q

What occurs in the bowel cancer screening program

A

FIT testing- end of test is dipped into a single bowel motion
gFOB testing where two samples are collected from three separate bowel movements
There may be heavy bleeding or perforations in rare cases

255
Q

What are the principles of cancer surveillance

A

There must be a clear definition of the case
The cases can be identified through various sources
There must be a systematic collection of data for cases
The data and summary statistics must be analysed

256
Q

What are the risk factors of bowel cancer

A 
Age>50
Previous CRC
Strong family history of CRC
Longstanding IBD
Inherited symptoms 
Type 2 diabetes 
Unhealthy lifestyle
257
Q

What are symptoms of bowel cancer

A 
Maybe none 
Often iron deficiency 
Rectal bleeding 
Change in bowel habit 
Pain
258
Q

Where does foregut pain present

A

On the left side

259
Q

Where does hind and mid gut pain present

A

Higher up than the foregut on the right side

260
Q

At what point can a bowel cancer not be removed by endoscopy

A

When it reaches the muscle layer

261
Q

What does a positive bowel cancer screening test lead to

A

A colonoscopy

Year 1 Medicine Newcastle (8 decks)

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