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Medicine > Case 4 > Flashcards

Case 4 Flashcards

1
Q

What is a cell cycle?

A

The orderly sequence of events cell by which a cell duplicates its chromosomes and (sometimes) its other cell contents and divides into two.
*The period between two mitotic cell divisions

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2
Q

All cells have the same cell cycle

True/False?

A

False

The duration of the cell cycle varies from cell type to cell type

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3
Q

What is the definition of mitosis?

A

Separation of the duplicated chromosomes produced during S-Phase, division of the nucleus into two daughter nuclei.

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4
Q

What are all the stages of mitosis?

A 
Prophase
Prometaphase
Metaphase
Anaphase
Telophase
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5
Q

What is cytokinesis?

A

Division of the cell cytoplasm into two daughter cells

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6
Q

What do errors in the control of the cell cycle lead to?

A

Uncontrolled cell division - cancer

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7
Q

What does Cell Cycle Control System do?

A

Regulates and controls cell cycle

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8
Q

Describe the three checkpoints of the CCCS

A

1) Restriction point (Start) = Commitment to S-Phase
2) G2/M checkpoint = Commitment to mitosis
3) Metaphase-anaphase transition = Commitment to completion of mitosis

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9
Q

What are cyclin dependant kinases (Cdks)?

A

Enzymes which control phosphorylation of proteins in the cell cycle, regulating their activities.

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10
Q

Cdks work on their own. True/False?

A

False

They need to couple with Cyclin to be activated and work. (Hence ‘Cyclin dependant’)

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11
Q

What are Cyclins?

A

Proteins which bind to Cdks.

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12
Q

What are the four major Cyclins of the CCCS?

A
  • G1-cyclins (Cyclin D)
  • G1/S-cyclins (Cyclin E)
  • S-cyclins (Cyclin A)
  • M-cyclin (Cyclin B)
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13
Q

What does G1-cyclins (Cyclin D) do?

A

Initiates activities of G1/S Cdks in late G1 phase

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14
Q

What does G1/S-cyclins (Cyclin E) do?

A

Bind Cdks late in G1, G1/S cyclin-Cdk complexes promote progression through the restriction point.

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15
Q

What does S-cyclins (Cyclin A) do?

A

Bind Cdks after restriction point, S cyclin-Cdk complexes stimulate S-Phase and early mitotic events. Gets proteins ready in cell to progress into s phase and early mitosis.

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16
Q

What does M-cyclin (Cyclin B) do?

A

Bind Cdks during late G2 and M-phases M cyclin-Cdk complexes stimulate entry into M-phase

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17
Q

The concentration of cyclins is the same throughout the cell cycle. True/False?

A

False

They vary in concentration throughout

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18
Q

What are mitogens?

A

Extracellular signal molecules which stimulate cell division.

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19
Q

Give examples of mitogens

A
  • PDGF
  • fibroblast growth factor
  • erythropoietin
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20
Q

What are oncogenes?

A

Protein that stimulates cell growth, but is associated in malignant tissues and uncontrolled cell division.

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21
Q

What stimulates cell growth?

A

Growth factors

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22
Q

What stops a cell undergoing apoptosis/cell death?

A

Survival factors

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23
Q

Describe how mitogens are ‘amplified’ in the cell cycle

A

‘Amplification’ explains how the small signal is able to trigger many reactions in a ‘domino’ style.

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24
Q

What steps do mitogens trigger?

A
  • Mitogen binds to receptor on membrane
  • Ras activation and initiation of intracellular signalling pathway
  • MAP kinase is activated
  • Increase in Myc transcription
  • Transcription of G1 cyclins leads to increase in G1-Cdk activity
  • This activates G1/S cyclins and promotes progression towards S-Phase
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25
Q

What is checked at G1/S (Restriction Point)?

A
  • Is the environment favourable

- Is the DNA ready/good for replication

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26
Q

What is checked at G2/M Checkpoint

A
  • Is the environment favourable

- Has the DNA been replicated correctly

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27
Q

What is checked at Metaphase to anaphase transition?

A

-Is the environment favourable
-Has the DNA been replicated correctly and is it ready to be split
YES = Mitosis

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28
Q

What happens when DNA is damaged?

A

CDKI’s are activated

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29
Q

What are CDKI’s?

A

Inhibit the action of Cdks

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30
Q

Which CDKI’s inhibit Cyclin D complex?

A

p16, p15, p18, p19

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31
Q

Which CDKI’s inhibit Cyclin E, A and B complexes?

A

p21, p27, p57

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32
Q

What does p53 do?

A
  • Suppresses tumours and prevents uncontrolled growth
  • Pauses the cell cycle to stop damaged cells dividing
  • Can cause cell to undergo apoptosis
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33
Q

How does p53 act?

A

Indirectly inactivates G1/S-Cdks and S-Cdks

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34
Q

What stimulates p53 to pause cell cycle?

A
  • Excessive mitogenic induction
  • Cell stress
  • DNA damage
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35
Q

What can cause p53 to be lost from the body?

A
  • Human Papilloma Virus E6 (viral protein that targets p53)

- Mutation or deletion of p53

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36
Q

What is the danger of not having p53?

A

The cell cycle goes unchecked = lead to uncontrolled cell division.

  • p53 mutations or deletions present in 50% of detectable human cancers
  • anti-cancer drugs rely on p53 induced cell apoptosis
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37
Q

What is Replicative Cell Senescence?

A

Human fibroblasts have limited cell division (40-50 times)

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38
Q

What are telomeres?

A

Repetitive DNA sequences found at the end of chromosomes

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39
Q

How are telomeres involved in controlling cell division?

A
  • Number of telomere repeats controls the number of divisions a cell can make
  • With each division the telomere length becomes shorter
  • The cell recognises uncapped chromosome as damaged DNA – p53 mechanisms prevent further replication
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40
Q

Why can’t p53 act on cancer cells?

A

Cancer cells have telomerase, which keep the telomeres intact and allow them to keep dividing. The chromosomes do not become uncapped and recognised as ‘damaged’.

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41
Q

What are the two main phases of the cell cycle?

A
  • Interphase

- M-phase

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42
Q

What are the steps in interphase?

A

G1
S-Phase (12 hours)
G2

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43
Q

What are the steps in M-phase?

A

Mitosis (1 hour)

Cytokinesis

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44
Q

How long does a cell cycle range from?

A

18-24 hours

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45
Q

What is G0?

A

A prolonged G1 phase. Usually small cells like neurones do not move past this phase. These cells are terminally differentiated under G0 - function, but do not grow.

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46
Q

What factors affect G1?

A

Extracellular signals, nutrient availability, temperature

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47
Q

What is G1 phase?

A

Major phase of cell growth
In-between M and S-phases
*If conditions are favourable, then cell cycle will pass Restriction Point
*Can take longer if the conditions are not favourable

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48
Q

What happens during the S phase?

A

DNA Synthesis.
Replication of genetic material (chromosomes) prior to division
*Approx 12 hours in typical mammalian cell

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49
Q

What happens during G2 phase?

A

Successful completion of S-phase
Period of rapid cell growth/protein synthesis in preparation for M phase
The purpose of this phase is not completely clear - method of cell size control?
G2/M checkpoint triggers early stages of mitosis
*G2 Not present in some cancers (G2 important in cell division control)

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50
Q

What is M phase?

A

Mitotic phase/ Mitosis

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51
Q

Give descriptions of each stage of mitosis

A

Prophase - sister chromatids condense, mitotic spindles that have replicated move apart
Prometaphase - nuclear envelope breaks down, spindle microtubules attach to kinetochores, movement begins.
Metaphase - chromosomes align at the equator, midway between spindle poles, kinetochore microtubules attach sister chromatids to opposite poles of the spindle.
Anaphase - Chromatids seperate and are pulled towards spindle pole, chromosome segregation
Telophase - daughter chromosomes reach poles and new nuclear envelope forms formation of two nuclei, end of mitosis, cytoplasm division begins with formation of contractile ring
Cytokinesis - final division of the cell

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52
Q

Describe the molecular structure of haemoglobin

A

Quaternary structure

Four polypeptide chains (4 subunits, each with 1 haem group)

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53
Q

What kind of polypeptide chains does haemoglobin have in foetal stage? (Hb foetal)

A

2 alpha

2 gamma

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54
Q

What kind of polypeptide chains does an adult haemoglobin have? (Hb A1 or Hb A2)
*which is more common?

A 
Hb A1 - 2 alpha
             2 beta
Hb A2 - 2 alpha
              2 delta
*Hb A1
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55
Q

How does haemoglobin react to oxygen?

A

20 amino acids hold the harm group (iron)
The haem group associates with O2 in the presence of it
The binding to O2 is reversible

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56
Q

What does Dalton’s law suggest about haemoglobin binding to oxygen?

A

High partial pressure of O2 = High affinity

Low partial pressure of O2 = Low affinity

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57
Q

Where is the amino acid, histidine, found in a protein?

A

Alpha helix

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58
Q

What does histidine do?

A

Is associated with iron and is the location for O2 binding

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59
Q

Why is it important that Hb has a low affinity for O2 in the presence of low partial pressure of O2?

A

A low partial pressure of O2 means there is little O2 available, therefore the tissues require O2. Hb will have a lower affinity for O2 and dissociate from O2, supplying the tissues that need it.

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60
Q

Name the conditions which decrease the affinity of O2/ binding of O2 to Hb

A
  • Increase in temp (happens during exercise)
  • Decrease in pH (CO2 decreases pH)
  • 2-DPG increase
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61
Q

Why do we tend to avoid reaching low levels of O2 dissociation?

A

Body has a large capacity of Hb, which reduce in anaemia so the body is able to compensate for it.

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62
Q

Why is CO dangerous?

A

CO binds to Hb but doesn’t let go (Hb has a higher affinity for CO than O2)
Too much CO results in no available Hb to carry oxygen

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63
Q

Name the conditions which increase the affinity of O2/ binding of O2 to Hb

A
  • Temperature decrease
  • pH increase (alkaline)
  • 2-3 DPG decreases
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64
Q

CO2 and 2-3DPG increase temperature. True/False?

A

True

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65
Q

How does low pH lead to Hb releasing O2?

A

-Lower pH
-Change in Hb shape/conformation
-Lower O2 affinity
= O2 release

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66
Q

Write the equation for Hb when pH decreases

A

Hb(O2)4 + 2H+ <> Hb(H)2 + 2O2

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67
Q

Write the equation for Hb in the presence of increased CO2

A

(O2)4Hb-NH3+ + CO2 <> (O2)3Hb-NH3-COO- + O2 + 2H+

*See O2 released and replaced with CO2

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68
Q

How does CO2 decrease pH?

A

Releases two protons (H+)

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69
Q

What is 2-3DPG?

A

A product of glycolysis, interacts with amino acids on beta chains and stops Hb-O2 interaction = O2 released

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70
Q

Describe the feedback mechanism to hypoxia involving 2-3 DPG

A

-Low pO2 in tissues
-Increase in Glycolysis
-Increase in 2-3 DPG
= Increase in O2 release

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71
Q

What is hypoxia?

A

Decreased O2 to tissues

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72
Q

Why does high altitude affect the availability of O2?

A

There is a decreased atmospheric pressure at high altitudes, so gas exchange in the lungs is more difficult to drive.

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73
Q

How does the body adapt to high altitudes?

A
  • Increase in glycolysis
  • Increase in 2-3 DPG production
  • Increased O2 release
  • Hormone erythropoietin triggers RBC production
  • Increase in RBC
  • Increase in Hb
  • Increase in breathing depth and rate
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74
Q

Describe the relationship between temperature and Hb saturation

A

At higher temperatures, less Hb is saturated, but can carry more O2. Compared to Hb in lower temperatures - they are more saturated, but carry less O2.

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75
Q

How is CO2 carried in the body?

A
  1. Dissolved in the plasma (5% in the artery, 10% in the veins)
  2. As bicarbonate (90% in artery, 60% in veins)
  3. Bound to Hb, making carbamino Hb (5% in the artery, 30% in veins)
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76
Q

Describe the journey of CO2 after its made from tissues

A
  • Tissue makes CO2
  • CO2 diffuses out
  • Some CO2 dissolves in plasma
  • Rest of CO2 enters RBC
  • Some CO2 dissolves in RBC
  • Rest react with H2O and make H+ and HCO3- (catalysed by Carbonic Anhydrous enzyme) this is carbonate.
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77
Q

How does bicarbonate help the cell’s gradient?

A
  • Bicarbonate diffuses out of the cell down a concentration gradient
  • This electrical imbalance means CL- diffuses into the cell
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78
Q

How does bicarbonate help with CO2 removal?

A
  • Bicarbonate enters lungs
  • High O2 partial pressure in alveoli
  • This O2 binds to Hb
  • H+ leaves Hb
  • H+ reacts with bicarbonate
  • Breaks down into water and CO2
  • CO2 is breathed out
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79
Q

Write the reaction for bicarbonate in the lungs

A

HCO3- + H+ > H2CO3 > H20 + CO2

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80
Q

What are the principles of cancer surveillance?

A
  • Case definition
  • Cases identified through a variety of sources
  • Systematic collection of data for cases
  • Analysis of data and summary statistics
  • Feedback to providers and distribution of information to those who require it for action
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81
Q

How is information collected and used in surveillance?

A
  • Ongoing systematic collection
  • Collation (bringing information together)
  • Analysis and interpretation of data
  • Dissemination of information in order that action may be taken.
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82
Q

What is cancer surveillance for? (Why is it useful)

A

Use it for…

  • provides a quantitative portrait of cancer and its determinants in a defined population
  • measurement of cancer incidence (new cases)
  • morbidity (people living with cancer)
  • survival and mortality for persons with cancer
  • tells us where we are in the effort to reduce the cancer burden
  • generates the observations that form the basis for cancer research and interventions for cancer prevention and control
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83
Q

What does cancer surveillance assess?

A
  • genetic predisposition (genetic characteristic which influences the possible phenotypic development of an individual organism within a species or population under the influence of environmental conditions)
  • environmental and behavioural risk factors
  • screening practices
  • quality of care from prevention through to end of life care.
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84
Q

What is cancer registration?

A
  • Patient diagnosed with cancer/condition that may lead to cancer information
  • Passed on to the National Cancer Registration and Analysis service.
  • Info taken includes patient name, address, sex, date of birth, type and nature of cancer
  • This is then linked to other sources of routine data (health service data and survey) to provide a comprehensive picture
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85
Q

What are the components of blood?

A
  • Red blood cells – Erythrocytes
  • White blood cells – Leukocytes
  • Platelets – Thrombocytes (blood clotting)
  • Extracellular fluid – Plasma, blood is a fluid
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86
Q

What is the function of RBC’s/Erythrocytes, and what features help them do this?

A
  • Carry oxygen
  • small and flat to allow diffusion
  • packed with Hb
  • no nucleus, few organelles
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87
Q

What is the function of White blood cells/Leukocytes?

A

Various roles in immune system:

  • Phagocytosis
  • Produce antibodies
  • Destroying infected cells (t-killer)
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88
Q

What is the function of Platelets/ Thrombocytes?

A

Involved in blood clotting

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89
Q

RBC’s only live for 90 days. True/False?

A

False

They live for 120 days (don’t produce own proteins to live longer)

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90
Q

What are the types of white blood cells?

A
  • Monocyte
  • Lymphocyte
  • Neutrophil
  • Basophil
  • Eosinophil
91
Q

What are the features of platelets/Thrombocytes?

A

Fragment of a cell called a ‘megakaryocyte’

Membrane bound bodies, no nuclei

92
Q

What are the features/components of blood plasma?

A
  • Whole blood minus cells and platelets
  • Straw’ coloured
  • Dissolved gases
  • Electrolytes
  • Dissolved substances (glucose, urea, vitamins…)
93
Q

Why are there electrolytes in blood plasma?

A

To maintain osmotic balance

94
Q

Where is the spleen found?

A

Left Hypochondrium/ Hypochondriac

95
Q

What is the function of the spleen?

A
  • Lymphoid organ: involved in immune response
  • Remove old erythrocytes into red pulp, recycle these later
  • Screen for pathogens - White pulp
  • Stores platelets
96
Q

What are types of plasma proteins?

A
  • Globulins
  • Albumin
  • Fibrinogen
97
Q

What are the types of Globulins and what are they used for?

A 
a1 – various, glycoproteins
a2 – various, prothrombin (coagulation), erythropoietin
b1 – transport 
lipid carrier proteins eg LDL
carrier some vitamins, metals etc.
g – Immunoglubulins
98
Q

What is Albumin used for?

A
  • 80% controls oncotic pressure

- Transports substances eg, drugs, hormones, fatty acids

99
Q

What is Fibrinogen used for?

A

Blood clotting

100
Q

What is Oncotic pressure?

A

Proportion of osmotic pressure due to proteins (only dissolved proteins)

101
Q

What is Oncotic pressure/Colloid Osmotic Pressure?

A

Proportion of osmotic pressure due to proteins (only dissolved proteins)

102
Q

What is Osmotic pressure?

A

The pressure due to ALL dissolved particles (includes electrolytes)

103
Q

What is the proportion of Osmotic pressure that is Oncotic pressure?

A

0.5% (80% of this is from Albumin)

104
Q

How do proteins in the blood draw water in capillaries?

A
  • Proteins are too big to pass through endothelial walls
  • Proteins remain dissolved in blood
  • Reduce the water potential of the capillaries
  • Results in oncotic pressure and water being drawn in
105
Q

How do proteins in the blood draw water in capillaries?

A
  • Proteins are too big to pass through endothelial walls
  • Proteins remain dissolved in blood
  • Proteins are usually negatively charged
  • Attracts positive ions/cations
  • Reduce the water potential of the capillaries
  • Results in oncotic pressure and water being drawn in
106
Q

Small molecules are able to pass through endothelial walls. Why is this?

A

Blood capillary is leaky – endothelium doesn’t have tight junctions so molecules can easily pass across

107
Q

What is the Gibbs-Donnan effect?

A
  • Dissolved proteins result in water being drawn into capillaries
  • However, capillaries don’t swell up and burst because hydrostatic pressure is competing against oncotic pressure (heart beating, increase pressure in blood, force water out of capillaries).
108
Q

Hydrostatic pressure draws water into capillaries. True/False?

A

False

Hydrostatic pressure pushes water out

109
Q

Oncotic pressure draws water back into capillaries. True/False?

A

True

110
Q

Hydrostatic pressure remains the same in the arteries and veins. True/False?

A

False
Hydrostatic pressure is high in the arteries, so there is a lot of fluid loss in the capillaries. It then decreases until it reaches the venules, resulting in fluid being drawn back in.

111
Q

Oncotic pressure fluctuates in the arteries and venules. True/False?

A

False
It remains the same throughout to balance out hydrostatic pressure.
*Interstitial oncotic pressure rises slightly towards venous end as fluid absorbed

112
Q

Is all the fluid pushed out the arterial end reabsorbed in the venous end?

A

In reality, no

113
Q

What happens if there is increased hydrostatic pressure?

happens during heart failure

A
  • INCREASED Hydrostatic pressure at venous end
  • pushing a lot fluid out, not taking enough back
  • Gain of fluid
114
Q

Why might right sided heart failure result in oedema?

A

-Right sided heart failure = in pooling of blood in the right atrium and vena cava
- Less/ inhibition of venous return to the heart increases hydrostatic pressure
- More fluid lost from capillaries, build up in body
=Oedema

115
Q

How does nephrosis affect oncotic pressure?

A

-Nephrosis is kidney disease (so tubules are being damaged)
-Kidney’s cannot function properly and do not filter properly = proteins escape out of tubules
-Less protein in plasma
-Decreased oncotic pressure
-Less gain of fluid
-Loss of fluid > Gain of fluid
=oedema

116
Q

What is oedema?

A

Swelling that occurs from too much interstitial fluid

117
Q

What is the role of the lymphatic system?

A
  • Removing waste products and interstitial fluid
  • Draining and immune system
  • Requires muscle movement
118
Q

What are some examples of oedema that are not serious?

A
  • Minor Oedema (from standing long periods for on long flights)
  • Localised Oedema (following removal lymph nodes – lost drainage system)
119
Q

What is the oedema that happens as a result of the immune system?

A

Immune cells (eg mast cells) release chemical mediators
eg, histamine
Increase capillary permeability
Localised swelling

Problems with immune system:
Angioedema – swelling from release of fluid in localised space
Anaphylaxis

120
Q

What are the two blood groups we need to know?

A

ABO

Rhesus

121
Q

What defines the ABO blood groups?

A

-ABO antigens
These are short sugar chains and can be attached to lipids (glycolipids) or proteins (glycoproteins)
They are synthesised by enzymes – glycosyltransferases
Different versions of enzymes lead to different sugar chains

122
Q

Which blood group is a universal donor?

A

Type O

123
Q

Which blood group is a universal acceptor?

A

Type AB

124
Q

Which antigen does Rhesus type blood have?

A

Antigen D

125
Q

What is the danger of having Rhesus type blood?

A

Can be problematic in pregnancy and result in Haemolytic disease of the newborn

126
Q

What is Haemolytic anaemia?

A

Increased destruction of red blood cells.

127
Q

How do we treat haemolytic anaemia?

A

Removal of the spleen (reduces rate RBC’s are destroyed) followed by life-long penicillin prophylaxis is necessary.
*Folic acid may be necessary prophylactically (preventive measure)

128
Q

When does Anaemia of chronic disease occur?

A

In response to chronic infection, chronic inflammatory processes or malignancy.

129
Q

What is the result of Anaemia of chronic disease?

A

Intestinal iron absorption is reduced. However, iron storage in macrophages and liver cells is increased. Serum iron is reduced but ferritin, the protein that stores iron, is normal or elevated

130
Q

How should you treat Anaemia of chronic disease?

A

Treat the underlying disorder - if caused by renal disease try treating with an erythropoietin.
Iron therapy is not appropriate as the underlying problem is impaired iron utilisation and not deficiency.

131
Q

What causes Pernicious anaemia?

A

Deficiency of vitamin B12

132
Q

How should Pernicious anaemia be treated?

A

Treat with Hydroxocobalamin 1000 micrograms IM to a total of 5-6mg over 3 weeks followed by 1000 micrograms every 3 months. Hydroxocobalamin is an injectable form of vitamin B12 that is given by intramuscular injection if there are problems with providing oral vitamin B12 such as poor absorption.
Alternatively, Vit B12 2mg PO per day as 1-2% absorbed orally. However, compliance may be a problem in elderly patients.

133
Q

What are the side affects of treatment for Pernicious anaemia?

A

Side effects may include hypokalaemia, and iron deficiency may occur over the first few weeks

134
Q

How is Folic acid acid deficiency treated?

A

5 mg folic acid daily for 4 months and treat the underlying cause.

135
Q

How is iron deficiency anaemia treated?

A

Treat underlying cause and treat with iron replacement therapy in the form of oral iron, ferrous sulphate 200 mg 2-3 times per day, absorbed best when patient is fasting.
Monitor Hb level and reticulocyte count, an Hb increase of 1g/dL per week would be expected during treatment. It may take up to 6 months of treatment to replenish iron stores.

136
Q

What are the adverse affects of iron replacement therapy and how do we prevent them?

A

Adverse effects include nausea, vomiting, constipation. If adverse effects are troublesome combine with food and/or reduce dose. Interaction with drugs such as tetracyclines reduces drug absorption.

137
Q

Why do patients with sickle cell disease experience pain?

A

Due to the blockage of small blood vessels by the sickled red blood cells.

138
Q

How is sickle cell disease treated?

A

Treat with Hydroxycarbamide to help reduce painful episodes. Hydroxycarbamide (also known as hydroxyurea) is a chemotherapy drug used to treat sickle cell anaemia. It works by raising the levels of fetal haemoglobin (Hbf) which protects against sickling in red blood cells.
Also give morphine/diamorphine to control pain. Treat with folic acid if there are signs of haemolysis.

139
Q

What is Thalassaemia?

A

Group of inherited conditions associated with abnormal haemoglobin

140
Q

How is Thalassaemia treated?

A

Treat with long-term folic acid supplements. Regular blood transfusions may be required every 4-6 weeks
Severe thalassaemia - likely to require regular red cell transfusions
Less severe forms - only require more intermittent transfusions

141
Q

What are the risks of blood transfusions?

A

Lead to iron overload or haemosiderosis and require iron chelation (removal of excess iron through drugs) by desferrioxamine.

142
Q

What is aplastic anaemia?

A

Damage to the bone marrow resulting in deficiency of blood cell production from haematopoietic stem cells. This results in a deficiency of red blood cells, white blood cells and platelets.

143
Q

How is aplastic anaemia treated?

A

Treated with blood and platelet transfusions.

144
Q

What is a papilloma?

A

A benign epithelial tumor growing in an exophytic direction (outwardly projecting) in a nipple-like fashion

145
Q

What is a carcinoma?

A

A benign tumor arising in glandular tissue such as the mucosa of stomach, small intestine, and colon, in which tumor cells form glands or gland like structures, growing in an exophytic direction

146
Q

What is an adenoma?

A

A tumor arising in the epithelial tissue of the skin or the lining of the internal organs, such as the liver, lungs, kidneys etc. Papilloma/Adenomas become carcinomas when their growth changes to an endophytic direction (inward / downward projecting

147
Q

What is a sarcoma?

A

A tumor arising in connective or other non-epithelial tissue, such as blood vessels, nerves, bones, muscles, deep skin tissues, and cartilage

148
Q

How does cancer happen?

A
  • DNA Damaging Stimulant / Spontaneous DNA Replication Error
  • Genetic Alterations (Mutations in DNA or Epigenetic Changes)
  • Uncontrolled cell proliferation
  • Cells divide at a faster rate; not co-ordinated with surrounding tissue
149
Q

What is a tumour?

A
  • ‘new growth’ of cancer
  • Abnormal mass of cells/ tissue, the growth of which exceeds and is uncoordinated with that of the normal tissue
  • Seen as ‘swelling’
  • Different types of tumours
  • Advanced description: An abnormal mass of cells resulting from the loss of normal control of cell growth and/or differentiation, triggered by stepwise accumulation of multiple genetic alterations affecting a single cell and its clonal progeny
150
Q

What does clonality mean?

A

Derived from a single cell and genetically identical

151
Q

Why are tumours harmful?

A
  • Interfere with the adjacent cellular function at the originating site
  • Tumour cells create a necrotic environment (killing healthy cells by creating toxins)
  • Compression (physically get in the way), occlude blood vessels, lymph nodes
  • Complete colonization (no healthy cells left) – no function of that cell
  • Advance stages, they can interfere with functions of distant organs
152
Q

Describe the phases of neoplasia

A
  1. Cell is mutated
  2. Hyperplasia: increased cell division but cells look and act ‘normal’ (Reversible)
  3. Dysplasia: pre-cancer -‘atypical hyperplasia’ increased cell division, cells look abnormal (different to hyperplasia) Growth is dependent upon initial stimulus and the acquisition of new driver mutations (Reversible)
  4. Neoplasia: uncontrolled cellular proliferation, abnormal cell structure and function. Growth is independent of the initial stimulus and without the need for new mutations (Irreversible)
  5. Carcinoma in situ: neoplastic cells remain growing and contained within their originating site / cell layer (e.g. epithelial layer) and have not invaded through the basement membrane
  6. Intraepithelial neoplasia: synonymous with Carinoma in situ. Also a term used to describe the interface/boundary between non-invasive and invasive neoplasms
  7. Invasion - Refers to the direct extension and penetration bycancercells into neighbouring tissues by crossing their originating sites basement membrane
  8. Metastasis - The development of a secondary neoplastic growth in a distance tissue / organ
153
Q

What does staging of cancer refer to?

A

Anatomical

The size of a cellular mass and how far it has spread from where it originated

154
Q

What are all the stages of cancer?

A 
Stage 0 = Carcinoma in Situ, contained
Stage 1 = Localised 
Stage 2 = Locally Invasive 
Stage 3 =  Local Spread to lymph nodes 
Stage 4 = Metastasised
155
Q

What does grading of cancer refer to?

A

Histological
Appearance of the cancer cells
Microscopic and Macroscopic degree of differentiation of the cancer

156
Q

What are the grades of cancer?

A

Grade 1 = Nearly normal cell. Small, uniform glands
Grade 2 = Some abnormal cells. More space between glands.
Grade 3 = Many abnormal cells. Emergence of Carcinoma In situ
Grade 4 = Very few normal cells left. Many irregular masses of cells
Grade 5 = Completely abnormal cells. Lack of glands

157
Q

Colonic adenoma and carcinoma are both epithelial derived growths, just direction changed. True/False?

A

True

158
Q

What is metastasis?

A

Development of secondary malignant growths at a distance from a primary site of cancer.

159
Q

What is the result of a neoplasm becoming malignant?

A

Cancer

160
Q

What is the difference between benign and malignant?

A

Benign - condition, tumor, or growth that is not cancerous. Does not spread or invade.
Malignant - tumor or growth as cancerous

161
Q

What name is given to the process of normal cells becoming cancer cells?

A

Transformation/carcinogenesis/oncogenesis/ tumorigenesis

162
Q

What are the classic hallmarks of cancer, and how do they happen?

A
  1. Sustaining self-sufficient proliferation:
    -Need to uncontrollably and uncoordinatedly
    -Tumour cells activate proteins and signaling pathways
    -Liberate them from the need for external growth stimulation (growth factors)
    = self reliantly entering and moving through the stages of the cell cycle
  2. Resisting cell death:
    - Tumour cells are characteristically able to bypass Apoptosis
    -Apoptosis is programmed cell death (cell suicide), mechanism which programmes cells to die when damaged
  3. Insensitivity to anti-growth signals:
    -Need grow uncontrollably and uncoordinatedly
    -Tumour cells inactivate proteins and signaling pathways that suppress cell cycle progression
    = cells can progress through the cell cycle unchecked.
    4.Enabling replicative immortality:
    -Non-tumour cells die after certain number of divisions to the protect effect of reduced telomere length following DNA replication.
    -Tumour cells escape this limit by activating the enzyme telomerase
    -Replace telomere length lost during DNA replication = capable of indefinite growth and division (immortality).
  4. Activation of invasion and metastasis:
    -Need to invade and metastases to other sites within the body
    -Tumour cells activate multiple proteins and signaling pathways
    -Degrade the basement membrane
    = Migrate and survive “unattached” in the blood and colonise new tissue environments.
  5. Inducing Angiogenesis (process that creates new blood vessels):
    -Need tumours to continue to grow in size
    -Require supply of oxygen and nutrients.
    -Tumour cells active proteins and signaling pathways
    -Growth and infiltration of new blood vessels
    = cells receive a continual supply of oxygen and other nutrients.
163
Q

What are the emerging hallmarks of cancer?

A
  1. Avoiding immune destruction – cancer cells hide from immune system. Treatment to be seen by immune system.
  2. Deregulated cellular energetics – cancer cells are hypoxic (not enough O2). Leads to anaerobic respiration
164
Q

What are the enabling hallmarks of cancer?

A
  1. Tumour promoting inflammation

2. Genome instability and mutation – drive patients to get cancer

165
Q

Mutations in which two genes lead to neoplasia?

A

Oncogenes

Tumour suppressor genes

166
Q

What are oncogenes?

A

A mutated/activated gene which contributes positively to neoplasia, usually by promoting autonomous cell proliferation
Dominant acting – Driver Gene e.g. Kinase called Raf
Activated by inappropriate expression or structural alteration
Have maternal and paternal copy of gene – only need one copy to be mutated to cause cancer.

167
Q

What are Proto-oncogenes/cellular oncogenes?

A

Unaltered (non-mutated) cellular counterpart of an oncogene

168
Q

What is B-Raf Kinase?

A

Checks cell is okay before replication during G1 checkpoint

169
Q

Describe what happens to B-Raf Kinase during normal cell cycle

A

-B-Raf Kinase is inactive, its active site is hidden
-Growth Factor Signal will open and expose active site
-B-Raf Kinase is activated and exposed
-ATP on active site
gives phosphate group to transcription factor
-Turns on transcription factor
= genes translated which allow cells to move through cell cycle
=transcription and translation of G1 checkpoint proteins made

170
Q

What happens when someone has a V600E mutation?

A
  • B-Rafe Kinase does not fold back and always has active exposed
  • It is always active regardless of growth signal
  • Transcription factors are hyperphosphorylated = always turned on
  • Always making new cells
171
Q

What is a viral-oncogene?

A

Virally encoded protein which contributes positively to neoplasia e.g. E6 / E7 in the HPV16 virus

172
Q

What is a tumour-suppressor gene?

A

A gene which normally functions in a manner which inhibits neoplasia, usually by suppressing cell proliferation. Inactivated during oncogenesis.
Recessively acting – Requires both alleles of a gene to be altered (both copies have to be mutated)
Inactivated by structural alteration or deletion
E.g. p53 - checks cell before division

173
Q

Describe the differences between oncogenes and tumour suppressor genes?

A

Oncogenes: Promotes cell growth / division
Gain of Function
Car Accelerator
One Hit - Only require one copy to be mutated
Tumour suppressor: Prevents cell growth / division
Loss of Function
(Broken) Car Brakes
Two Hit – Requires both gene copies to be mutated

174
Q

What is a DNA mutation?

A

A change in the DNA base sequence

175
Q

What are the types of DNA mutations?

A
  • Germ Line DNA mutations (present at birth)

- Somatic (acquired after conception) DNA mutations (vast majority of cancer)

176
Q

How does Germ Line DNA mutation occur?

A

Variations in constitutional (germline) genetics influence our risk of developing cancer, so some families are “cancer prone”.
Key examples are BRAC1 and BRAC2, these can’t repair DNA effectively = more likely to get extra mutations.

177
Q

How does Somatic cancer occur?

A

Exposure to:
Carginogens: any substance, radionuclide, or radiation that promotestransformation/carcinogenesis/oncogenesis/tumorigenesis
Oncogenic Viruses: Viruses which encode Viral-oncogenes

178
Q

What do carcinogenic initiators do?

A

Mutagenic and promote DNA mutations = cause mutations

179
Q

What do carcinogenic promoters do?

A

Non-mutagenic, act by stimulating cell division – the original mutant population increases, increasing the likelihood of further mutations.

180
Q

Carcinogens can only be initiators or promoters. They cannot be both. True/False?

A

False

Complete carcinogens can be both

181
Q

Describe how direct damage to DNA by chemical carcinogens leads to cancer

A

-Mistakes happen when DNA is “imperfectly” repaired
-DNA break – Single and Double stranded
-Crosslinking (stick to each other) – DNA/DNA or DNA/Proteins
-Intercalation – carcinogen binding directly to DNA between minor and major grooves, distorting shape
-Enzymes involved in cell repair are mutated, can’t repair, only through imperfect measures
= inability of cells to create identical copy when being repaired leads to mutations

182
Q

Describe how chemical carcinogens affect epigenetic regulation?

A
  • Methylation and Acetylation cause genes to be turn on/off
  • Alter gene expression
  • Do not mutate the primary DNA sequence
  • Activation of oncogenes and inactivation of tumor suppressor genes
183
Q

How does UV rays cause damage?

A

UV Directly Damages DNA:

  • DNA/DNA Crosslinking
  • Thymidine Dimer – T nucleotides which make up DNA, dimerise and make kinks = difficult to read and replicate

UV Indirectly Damages DNA:
Free radials mediate
Oxidative DNA damage

184
Q

Why are UV rays dangerous?

A

UV light causes carcinogenesis, promotes mutation and directly damages DNA

185
Q

What is Human Papilloma Virus, and why is it dangerous?

A

Viral Oncogene

Induce neoplasms of cervix in infected woman – Latency 5 - 15 years

186
Q

What are low risk forms of viral oncogenes?

A

Cervical squamous cell papilloma (warts)

187
Q

What are high risk forms of viral oncogenes?

A

Cervical squamous cell carcinoma, papilloma which have converted rate of growth endophytically

188
Q

Which viral oncoproteins does HPV present, and what do they do?

A

E6 – inhibits tumour suppressor, p53 (Guardian of the genome)
E7 – inhibits tumour suppressor Retinoblastoma (pRb) – (G1 checkpoint regulator)

189
Q

What measures have been put in place to stop the complications of HPV?

A

HPV testing being incorporated into cervical screening program
HPV vaccination now introduced for girls 12-18y

190
Q

What is the danger of not having E6 and E7?

A

Cells can progress through G1 checkpoint without being detected, usually p53 would induce apoptosis. No E6 to stop cell proliferation. E6 and E7 build in new mutations – drive tumour forward, leading to invasion and metastasis.

191
Q

What are the features of a benign tumour?

A 
Growth Rate - Slow
Resemblance to normal tissue - similar, preservation of glands
Nuclear morphology - near normal
Invasion - none, just grow into space
Direction of growth - often exophytic
Necrosis - rare
Border - circumscribed / encapsulated
192
Q

What are the features of a malignant tumour?

A

Growth Rate - Fast, Increased proliferation
Resemblance to normal tissue - Variable but poor. Loss of mucus production
Nuclear morphology - Enlarged nuclear : cytoplasmic ratio. As tumours become more malignant, nucleus becomes larger and irregular.
Invasion - yes, growing into tissues like muscle wall.
Direction of growth - often endophytic
Necrosis - common
Border - poorly defined/ irregular

193
Q

Which groups of people are more likely to develop cancer?

A

Older people

People from lower socio economic group

194
Q

What is Burkitt Lymphoma?

A

Burkitt Lymphoma – B cell lymphoma, associated with EBV and malaria, endemic in central Africa

195
Q

What is Ewing sarcoma?

A

Ewing sarcoma – ulcerating cancer of the bone

196
Q

What is Hodgkin lymphoma?

A

Hodgkin lymphoma – malignant lymphoma characterized by reed-Sternberg cells

197
Q

What is Kaposi Sarcoma?

A

Kaposi Sarcoma – vascular endothelium neoplasm, related to HIV (immune system is damaged, cancer can survive) and jewish populations living in eastern Europe

198
Q

What are blastomas and what types are there?

A

Derived from blasts
Tumour of childhood
Retinoblastoma – right eye retina is white in photos
Nehproblastoma
Neuroblastoma - most common solid organ tumour in children at 26% (less common than leukaemia)
Hepatoblastoma
Blasts - incompletely differentiated cells

199
Q

What are endocrine tumours and what types are there?

A

Affects cells where hormones are released
Neuroendocrine’ or ‘APUDomas’
Specific hormones:
Gastrinoma & Zollinger Ellison syndrome = peptic ulcers
Inuslinoma = hypoglacaemia
Medullary carcinoma of the thyroid gland = calcitonin (reduces bloods calcium)
Carcinoid = appendix > small bowel, small amounts serotonin + prostaglandins, mets to lymph nodes and liver cause serotonin syndrome (sweating, tachycardia)
MEN = (multiple endocrine neoplasia syndrome)

200
Q

What are harmatomas?

A

Not a true neoplasm
Grow with patient
Often cause anxiety when found on scans
Doesn’t cause harm

201
Q

What are cysts?

A

A fluid filled space lined by epithelium

202
Q

What types of cysts are there?

A

Not all are neoplastic, but can cause diagnostic uncertainty and can produce similar local effects (compression)

Neoplastic – cystadenoma, cystadenocarcinoma, teratoma
Congenital – brachial cyst, thyroglossal cyst – usually due to failure of an embryological space to close
Parasitic – hyatid cysts (Echinococcus granulosus) caused by parasites
Retention – epidermoid (implantation of epidermis into the dermis, usually due to trauma) and pilar cysts (hair follicle cysts filled with wet keratin)

203
Q

What defines a cancer as malignant rather than benign?

A

It is their spread of cancers which defines them as malignant rather than benign. It is also this spread which is responsible for the majority of their negative clinical effects including death.

204
Q

What is the general route of growth for cancer?

A

Detachment and local invasion
Metastases
Routes of metastases

205
Q

Describe all the routes of metastases

A

-Haematogenous spread is usually to the liver, lung, bones or brain (large blood supplies, follow venous system). Interestingly skeletal muscle and spleen get very few (have large blood supplies)
-Tumours usually spread down the afferent lymphatic channels, in lymph drainage. They tend to start in the periphery of the node and then grow inward. This leads to a larger and firmer node but clinically this should be taken with caution as they may be reactive. This can then cause blockages to flow and oedema.
-Transcoelomic refers to pleural, pericardial or peritoneal spread. This is often made easier by effusions in the various spaces which are directly caused by the tumours.
Bowel cancer through blood, pain in abdomen

206
Q

What is Prognostication and what are its principles?

A

Grading and staging of cancer
Principles:
Examples – evidence based prognostics, guides treatment options (know surgery is likely to work), patient has actual idea on survival rate, communication (just give stage and grade number to colleagues).

207
Q

What are Prognostic indices?

A 
Tumour type
Level of differentiation
Molecular features
Tumour location
Extent of spread
208
Q

Why do grading and staging?

A

Evidence based prognostics – higher numbers = worse prognosis
Guides treatment options
Good to know
Communication

209
Q

How is typing of tumours decided?

A

Usually determined from histology, e.g.
glands = adenocarcinoma
Keratin = squamous cell carcinoma
Anaplastic cannot be differentiated as the cells are so immature.
*some use molecular analysis or macroscopic appearance

210
Q

What is the difference between grading and staging?

A

Grading is histological, based on
Biopsies
Staging is anatomical, based on
Scans

211
Q

What is used to determine grading?

A 
Degree of differentiation
Mitotic activity
Nuclear size
Hyperchromasia
Differentiation

Nuclear size is usually expressed as a ratio (look at the size of the nucleus)
Hyperchromasia = darkly staining nucleus = increased DNA content

Exact process varies by tumour type and location.
Due to the heterogeneity of tumours this tends to look at the most poorly differentiated area – as this area is likely to be the most aggressive

212
Q

Describe the grading system

A 
Colorectal example
GX – cannot be identified, not enough info
G1 – well differentiated
G2 – moderately differentiated
G3 – poorly differentiated
G4 – undifferentiated, could be any one
213
Q

Name all the staging systems

A

TNM
Duke’s
Stage 0-IV
Terminology

214
Q

What is TNM staging?

A

T = tumour size
TX, unaccessible
T0, no cancer present
Tis, in situ, tumour has potential to be cancerous
T1-4, varies from tissue to tissue, 1 = small, 4 = large
Colon cancer example – T1 = invasion into the submucosa, T2 = invasion into the muscalaris propria, T3 = invasion into subserosa, T4a = into visceral peritoneum, T4b = attached to other organs / structures

N = nodal involvement
NX
N0
N1 – 1 lymphnode
N2 – group of lymphnodes

M = metastases
M0
M1

215
Q

What is Duke’s staging?

A 
Staging for bowel cancer only
Duke’s A – invasion into bowel muscle
Duke’s B – invasion through the bowel wall
Duke’s C – local lymph node involvement
Duke’s D – hepatic metastases present
216
Q

What are other forms of staging?

A

Stage 0 – carcinoma in situ
Stage I, II and III – local growth and spread
Stage IV – distant metastases

In situ
Localized
Regional
Distant

217
Q

What are the signs and symptoms of anaemia?

A 
Lack of oxygen transport to peripheral tissues
Symptoms: Fatigue
Lethargy
Breathlessness in severe anaemia, decreased capacity to carry oxygen
Palpitations (chest pain)
Fainting
Signs: Pallor
Tachycardia (fast heart rate)
Tachypnoea (fast breathing)
Hypotensio
218
Q

What is the difference between a sign and a symptom?

A

Sign is a patient complaint

Symptom is a mental/physical indicator of the disease

219
Q

What is Haematocrit (%)?

A

% of blood volume occupied by red cells

220
Q

How does the blood counter measure Haemoglobin g/L and MCV: mean cell volume fL?

A

Haemoglobin g/L
Blood counter lyses blood and measures haemoglobin by spectroscopy
MCV: mean cell volume fL
Blood counter measures directly

221
Q

What is needed to make RBCs?

A 
Haemoglobin:
iron – lots to make Hb
heme – a ‘cofactor’ binds iron
globin genes – protein
DNA synthesis (proliferation, cell division to make many RBC from stem cell)
Thymidine  (GCAT) – not enough of this, not enough RBC’s made (not enough cell division)
B12 and folate
A normal bone marrow
222
Q

Describe the production RBCs

A

-Stem cell
-Expansion of Hb starts
-Cell proliferation & DNA synthesis:
B12 and folate
-Committed progenitors, BFU-E then
CFU-E
-Precursors
-Differentiation when Hb made
-Haemoglobin synthesis: Iron and globin
-Mature cells

223
Q

What happens in B12 and folate deficiency?

A
  • DNA cannot replicate
  • Cytoplasm increases ‘waiting for nucleus’
  • Megaloblasts accumulate, tries to mature and divide but can’t = delayed nuclear maturation causes megaloblastic anaemia
  • Large red cells created - macrocytosis
224
Q

What happens in globin abnormality and iron deficiency?

A
  • Hb can’t form
  • Nucleus divides before adequate Hb synthesized
  • Small pale red cells created - microcytosis

Medicine (11 decks)

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