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MOD Flashcards

0
Q

List the 5 macroscopic features of acute inflammation

A 
Calor - heat
Rubor - red
Tumor - swollen
Dolor - pain
Loss of function
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1
Q

List some common causes of acute inflammation

A 
Microbial infections
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis
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2
Q

What is the purpose of acute inflammation?

A

To limit tissue damage

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3
Q

What are the steps in acute inflammation?

A

Vasodilation, gaps in endothelium form, exudation, margination (neutrophils adhere to endothelium) and emigration (neutrophils migrate through membrane). Neutrophils move there by chemotaxis. Macrophages and lymphocytes behave similarly to neutrophils

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4
Q

List some chemical mediators and what they do

A

Histamine and prostaglandins - increase vascular permeability and vasodilation
Leukotrienes - emigration of leukocyte

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5
Q

What do neutrophils do in acute inflammation?

A

Phagocytise microorganisms then fuse the phagosomes with lysosomes to destroy them. They can also release metabolites/enzymes which causes damage to tissue

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6
Q

What are some symptoms of acute inflammation?

A

Decreased appetite, raised heart rate, altered sleep pattern, fever and shock

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7
Q

What are the possible outcomes to acute inflammation?

A

Resolution
Continued acute inflammation and chronic inflammation
Chronic inflammation
Death

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8
Q

How might resolution of acute inflammation be achieved?

A

The chemical mediators all have short half lives so may degrade or inactivate or be diluted. This means the changes are reversed (neutrophils stop marginating, vessels return to normal, exudate drains and fibrin degrades) and damaged tissue regenerates

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9
Q

What are some potential complications of acute inflammation?

A

Swelling could block tubes - in GI
Exudate could compress organs - cardiac tamponade
Excessive fluid could be lost
Pain/loss of function

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10
Q

Give some examples of acute inflammation

A

Skin blister, abscess and pericarditis

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11
Q

Give some inherited disorders of acute inflammation

A

Alpha 1 anti trypsin deficiency
Hereditary angio-oedema
Chronic granulomatous disease
Defect in neutrophil function/number

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12
Q

Explain Hereditary angio-oedema and how it is treated

A

The C1 inhibitor is deficient. As well as C1, C1 inhibitor also inhibits bradykinin, a peptide which increases permeability and therefore causes a build up of fluid and oedema. Treat with a C1 inhibitor infusion or fresh frozen plasma

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13
Q

Explain alpha 1 anti trypsin deficiency

A

Alpha 1 antitrypsin inhibits trypsin. Trypsin activates elastase which will break down lung and liver tissue causing emphysema and liver sclerosis

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14
Q

Explain chronic granulomatous disease

A

A recessive sex linked condition which stops the body from making ROS so certain bacteria can’t be killed and therefore they are contained in granulomatous

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15
Q

What is an abscess?

A

In solid tissues. Exudate forces tissue apart. Liquefaction necrosis in the centre. Can cause high pressure and therefore pain. Can damage nearby tissue

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16
Q

How can chronic inflammation arise?

A

Take over from acute inflammation if the damage is severe
Arise de novo - autoimmune, certain infections, chronic low level irritation
Alongside acute inflammation

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17
Q

What are the effects of chronic inflammation?

A

Fibrosis
Impaired function
Atrophy
Stimulation of immune response

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18
Q

List the cells involved in chronic inflammation

A

Macrophages, lymphocytes, eosinophils, fibroblasts, myofibroblasts, and giant cells formed by fused macrophages such as langerhans, foreign body type and touton giant cells

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19
Q

What to macrophages do in chronic inflammation?

A

Phagocytosis, processing and presentation of antigen, synthesis and release of cytokines, complement components, clotting factors and proteases

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20
Q

What do lymphocytes do in chronic inflammation?

A

B - differentiation into plasma cells to produce antibodies

T - involved in control and cytotoxic function

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21
Q

When will eosinophils appear in chronic inflammation?

A

Allergic reactions, parasitic infection and certain tumours

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22
Q

Give two clinical examples of chronic inflammation with fibrosis

A

Chronic cholecystitis
Gastric ulceration
(Liver cirrhosis)

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23
Q

Give 2 clinical examples of chronic inflammation with impaired function

A

Ulcerative colitis
Crohn’s disease
(Liver cirrhosis)

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24
Q

Explain chronic cholecystitis and how it is treated

A

Repeated obstruction of the gall bladder by gallstones causes repeated acute inflammation which will lead to chronic inflammation and fibrosis of the gall bladder wall. Treat by removing gall bladder

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25
Q

What is gastric ulceration, what are possible causes and how is it treated?

A

Acute gastritis - due to alcohol/drugs
Chronic gastritis - due to helicobacter pylori
Ulceration occurs due to an imbalance between acid production and mucosal defences
Treat helicobacter pylori with proton pump inhibitors (omeprazole) and 2 antibiotics (amoxicillin/clarithromycin)

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26
Q

What is liver cirrhosis, some possible causes and how is it treated?

A

Chronic inflammation of the liver with fibrosis. This leads to disorganisation of architecture and attempted regeneration.
Causes: alcohol, hep b/c, immunological, drugs, toxins and fatty liver disease
Treatment: modify lifestyle to prevent further damage or liver transplant

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27
Q

What are granulomas?

A

These form when the immune system can’t eliminate something and therefore act to wall it off

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28
Q

What are some possible causes of granulomatous diseases?

A 
Mycobacterium - TB, leprosy
Syphilis
Some fungi
Sarcoidosis
Crohn's disease
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29
Q

Explain tuberculosis

A

The mycobacterium causing TB don’t actually do any damage to the cells themselves but as they can’t be removed the persistent induction of cell mediated immunity (granulomas) causes the damage.

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30
Q

Define haemostasis

A

The body’s response to stop bleeding and the loss of blood

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31
Q

What is required for successful haemostasis?

A

Vessels - constrict to limit blood loss
Platelets - adhere to walls and each other to form a platelet plug
Coagulation system - clotting cascade
Fibrinolytic mechanisms - break down fibrin after

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32
Q

How does fibrinolysis occur and what drugs can be given to do so?

A

Plasminogen is activated and becomes plasmin which breaks down the fibrin.
Streptokinase

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33
Q

Define thrombosis

A

The formation of a solid mass of blood within the circulatory system

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34
Q

What makes thrombi more likely to form?

A

Virchow’s triad:
Change in blood flow - stagnant/turbulent blood
Change in vessel wall - atheroma, injury or inflammation
Change in blood components - smokers or pregnancy

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35
Q

What are the differences between arterial and venous thrombi?

A 
Arterial/Venous
Pale/deep red
Granular/soft
Lines of Zahn/gelatinous
Lower cell content/higher cell content
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36
Q

What are the potential outcomes to a thrombus and briefly explain each one?

A

Lysis - complete dissolution of thrombus
Propagation - thrombus moves along blood stream
Organisation - in growth of fibroblasts and capillaries
Recanalisation - incomplete blood flow reestablishment by channels forming in thrombus
Embolism - thrombus breaks off, moves through blood stream and lodges elsewhere

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37
Q

What are the differences between the effects of arterial and venous thrombi?

A

Arterial - ischaemia and infarction

Venous - ischaemia, infarction, oedema and congestion

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38
Q

Define embolism

A

The blockage of a blood vessel by a solid liquid or gas at a site distant from its origin

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39
Q

What are some types of embolism?

A

Thrombo-emboli (90%), air, nitrogen (the bends), amniotic fluid, medical equipment and tumour cells

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40
Q

Where would the following embolisms end up if they formed in: systemic veins?
Heart?
Carotid arteries?
Abdominal aorta?

A

Lungs
Arteries
Brain
Legs

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41
Q

Outline the differences in the severity of pulmonary embolisms including symptoms

A

Massive - if over 60% blood flow blocked it is rapidly fatal
Major - shortness of breath, cough and blood in sputum
Minor - asymptomatic or shortness of breath
Recurrent - pulmonary hypertension

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42
Q

What makes a deep vein thrombus more likely to form?

A

Immobility, post operation, post partum, oral contraceptive, burns and cardiac failure

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43
Q

How do you treat deep vein thrombosis?

A

Intravenous Heparin

Oral Warfarin

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44
Q 
How might the following emboli form:
Fat?
Cerebral?
Iatrogenic?
Nitrogen?
A

Long bone fracture breaks up adipose tissue
Atrial fibrillation
Medical equipment (air injection)
Nitrogen - bubbles form from decompression

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45
Q

What is Disseminated Intravascular Coagulation?

A

Lots of small clots form in the body which uses up the clotting factors so can cause haemorrhaging

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46
Q

Explain haemophilia

A

X linked recessive from a nonsense mutation
Two types - A: factor VIII deficient B: factor IV deficient
Causes haemorrhaging

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47
Q

What is thrombocytopenia?

A

Low platelet count due to: low rate of production, high rate of destruction or they’re being sequestered. Usually an accompanying bone marrow dysfunction

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48
Q

What are some causes of cell injury?

A

Trauma, chemicals, drugs, electrical, heat, immunological, hypoxia, radiation, cold, toxins and microorganisms

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49
Q

What are the reversible changes of hypoxia and how do they occur?

A

Lack of oxygen means oxidative phosphorylation can’t take place. This means anaerobic respiration takes place so there’s a build up of lactic acid and pH decreases. The lack of ATP means that Na pumps don’t work so no Na gradient can be made and therefore Na builds up in the cell, bringing water in as well causing swelling. Ribosomes detach

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50
Q

What are the different types of hypoxia?

A

Hypoxaemic - e.g. High altitude
Anaemic - e.g. CO poisoning, iron deficiency anaemia
Ischaemic - e.g. Ischaemia
Histiocytic - e.g. Cyanide

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51
Q

What are the irreversible changes in hypoxia?

A

Cytosolic calcium concentration massively increases because the sodium calcium exchanger is reversed. Enzymes are activated

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52
Q

Define hypoxia

A

Hypoxia is reduced O2

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53
Q

What are the reversible, microscopic structural changes in cell death?

A

Swelling, chromatin clumping, autophagy, ribosome dispersal and blebs

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54
Q

What are the irreversible, structural changes in cell death?

A

Pyknosis (nucleus shrinks), karryohexis (nucleus fragments), karryolysis (nucleus dissolves), membrane defects, lysosomes rupture and ER lysis

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55
Q

Define apoptosis?

A

Controlled cell death that is energy dependent

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56
Q

Define necrosis?

A

The morphological changes after cell death

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57
Q

What is oncosis?

A

The changes in a cell prior to cell death

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58
Q

What are the possible types of necrosis?

A

Liquefactive - enzyme release > protein denaturation. Infections
Coagulative - protein denaturation > enzyme release. Infarcts.
Caseous - between liquefactive and coagulative. Occurs in TB
Fat - occurs in adipose tissue

59
Q

What is gangrene? What are the differences between the two types?

A

Grossly visible cell necrosis.
Wet - liquefactive
Dry - coagulative

60
Q

What are the two types of infarct and where do they occur?

A

White infarct - kidney, heart and spleen

Red infarct - bowel or lungs

61
Q

Outline the mechanism of apoptosis

A

Initiation is triggered by intrinsic (mitochondrial) and extrinsic pathway which activates proteases. Execution is done by caspases which cleave proteins breaking up the cytoskeleton and degrade DNA. Degradation is when the cell breaks into small fragments which are phagocytosis by nearby cells

62
Q

What is an atheroma?

A

Accumulation of intracellular and extra cellular lipids in the intima and media of large and medium arteries

63
Q

What are the similarities and differences between atherosclerosis and arteriosclerosis?

A

They bit cause the thickening and hardening of arterial walls however atherosclerosis is due to an atheroma whereas arteriosclerosis is a result of hypertension or diabetes

64
Q

Describe the macroscopic appearance of atheroma

A

Fatty streak - yellow and raised
Simple plaque - yellow/white, raised, widely distributed and irregular outline
Complicated plaque - thrombosis, haemorrhage into plaque, calcification and aneurysm formation

65
Q

What are the early and late microscopic changes in an atheroma?

A

Early - smooth muscle proliferates, accumulation of foam cells and extra cellular lipids
Late - fibrosis, necrosis and cholesterol clefts

66
Q

What could the effect of atherosclerosis in a coronary artery be?

A

Cause ischaemic heart disease causing death, myocardial infarction, angina, arrhythmia and cardiac failure

67
Q

What is a symptom of peripheral vascular disease?

A

Intermittent claudication - pain in legs after walking short distances. Will get better on stopping but worse again and quicker upon restarting

68
Q

List some risk factors for atheroma

A 
Age
Gender - women protected before menopause
Hyperlipidaemia
Smoking 
Hypertension
Diabetes
Alcohol >5 units a day
Infection - chlamydia/ helicobacter pylori
Obesity
Stress
69
Q

How can you prevent atheroma?

A

Modify lifestyle - stop smoking and change diet

Temperature hyperlipidaemia, diabetes and LDL level

70
Q

Define fibrous repair

A

Replacement of functional tissue by scar tissue

71
Q

What are the key components of fibrous repair?

A

Cell migration - inflammatory cells, endothelial cells and myo/fibroblasts
Angiogenesis
Extra cellular matrix

72
Q

Outline the process of angiogenesis

A

Proteolysis of the basement membrane, endothelial cells migrate there by chemotaxis, proliferate, mature and then undergo tubular remodelling. Periendothelial cells are recruited

73
Q

What does the extra cellular matrix do?

A

Support and anchor cell, separate into compartments, sequester growth factors, allow communication between cells and cell migration

74
Q

Outline fibrous repair

A

Inflammatory cells infiltrate, blood clot forms, clot replaced by granulation tissue, angiogenesis, myo/fibroblasts migrate and produce ECM, cells then decrease in number, myofibroblasts contract the wound and collagen increases

75
Q

How are cells recruited in angiogenesis?

A

Chemotaxis (inflammatory cells) and cytokines (angio and pro-fibro cytokines)

76
Q

Define regeneration

A

Replacement of dead/damaged cells by functional, differentiated cells derived from stem cells

77
Q

Name the 3 types of stem cell and an example of each type

A

Unipotent - epithelia
Multipotent - haematopoietic
Totipotent - embryonic stem cells

78
Q

What are differences between labile, stable and permanent cells and give examples?

A

Labile - G1-M-G1. Rapid proliferation. Epithelial and haemopoietic cells
Stable - in G0 normally but can still, slowly regenerate. Hepatocytes and osteoblasts
Permanent - always in G0 and can’t regenerate. Neurones and cardiac myocytes

79
Q

How is proliferation stimulated?

A

Growth factors and when contact is lost with the basement membrane

80
Q

When does healing occur by primary intention and secondary intention?

A

Healing an incised wound with apposed edges

Healing a large wound with unapposed edges

81
Q

What are the differences in healing by primary and secondary outcomes?

A

Primary: smaller scar, less contraction, quicker

82
Q

Name some local factors that affect cell repair

A

Type, size, location, apposition, lack of movement, blood supply, infection, foreign material, radiation

83
Q

Name some general factors affecting repair

A

Age, drugs, dietary deficiencies, general state of health (e.g. Diabetes)

84
Q

How does a peripheral nerve regenerate?

A

Wallerian degeneration

The proximal end degenerates and the distal end proliferates

85
Q

What is the order of the cell cycle and what is the most important checkpoint?

A

G1 - cell grows. Near the end is the most important checkpoint R, where passage beyond is governed by phosphorylation of pRb
S - DNA replicates
G2 - cell prepares to divide
M - cell division by mitosis

86
Q

Define hyperplasia and give physiological and pathological examples

A

Increase in tissue or organ size due to increased cell numbers
Can only occur in labile or stable cells
Physiological - proliferative endometrium or bone marrow at altitude
Pathological - thyroid goitre

87
Q

Define hypertrophy and give pathological and physiological examples

A

Increase in tissue or organ size due to increased cell size
Physiological - skeletal muscle or pregnant uterus (hyperplasia as well)
Pathological - ventricular cardiac muscle hypertrophy or bladder smooth muscle hypertrophy

88
Q

Define atrophy and give pathological and physiological examples

A

Shrinkage of tissue or organ size due to decrease in cell size and/or number of cells
Physiological - ovarian atrophy in post menopausal women
Pathological - muscle atrophy (denervation) or cerebral atrophy (Alzheimer’s)

89
Q

Define metaplasia and give an example

A

Reversible change of a differentiated cell type to another
Usually an adaptive change in epithelia
Smoker - pseudostratified ciliated become squamous as it is more robust
Can be a prelude to cancer/dysplasia

90
Q

Define aplasia and hypoplasia

A

Aplasia - complete failure of a specific tissue or organ to develop
Hypoplasia - incomplete development of a tissue or organ

91
Q

Define dysplasia

A

Abnormal maturation of cells within a tissue (reversible and can be pre-neoplastic)

92
Q

Define a benign neoplasm a malignant neoplasm

A

An abnormal growth of cells that persists after the initial stimulus is removed
A malignant neoplasm is an abnormal growth of cells that persists after the initial stimulus is removed and invades surrounding tissue with potential to spread to distant sites

93
Q

What is a tumour?

A

Any clinically detectable lump or swelling. A neoplasm is just one type of tumour

94
Q

What is a cancer?

A

Any malignant neoplasm

95
Q

Define metastasis

A

A malignant neoplasm that has spread from its original site to a new contiguous site. The original location is the primary site and the new location is the secondary site

96
Q

What are the visible (microscopically and macroscopically) differences between benign and malignant neoplasms?

A

Benign - remain confined to site of origin, have a pushing outer margin and are well differentiated
Malignant - have the potential to metastasise, an irregular outer margin and shape which may show areas of necrosis or ulceration and range from well to poorly differentiated

97
Q

How do poorly differentiated tissues differ from well differentiated ones?

A

More poorly differentiated are given a higher grade and can indicate a poorer survival rate.
More poorly differentiated have: increasing nuclear size, nuclear hyperchromasia, more mitotically figures, a higher nucleus to cytoplasm ratio and more variation in size and shape of cells/nuclei

98
Q

What causes neoplasm formation?

A

Accumulated mutations in somatic cells (gremlins cells get a head start)
Initiators - mutagens
Promoters - cause cell proliferation
In combination you get an extended monoclonal population of mutant cells. The neoplasm will emerge via a process called progression where further mutations accumulate

99
Q

What is the evidence that neoplasms are monoclonal?

A

Monoclonal means a single founding cell
There are 2 types of the X-linked gene for G6PD in heterozygous women but 1 is inactivated (lyonisation) leaving a patchwork of both types in normal tissue. Neoplastic tissue has just one type

100
Q

What are the main kinds of genetic alteration leading to neoplasms?

A

Proto-oncogenes become abnormally activated = oncogenes

Tumour suppressor genes become inactivated

101
Q

How are neoplasms named?

A 
Benign= -oma
Malignant= -carcinoma
102
Q

How are neoplasms in the following cells types named: smooth muscle, fibrous tissue, bone, cartilage, fat, nerve, nerve sheath and glial cells?

A 
Leiomyo-
Fibro-
Osteo-
Chondro-
Lipo-
Neurofibro-
Neurolemmo-
Glioma/malignant glioma
103
Q

What are the different types of: lymphoma, leukaemia, germ line and epithelial neoplasm?

A

Hodgkin’s disease and non hodgkins
Testis - malignant teratoma/seminoma
Ovary - benign teratoma = dermoid cyst
Stratified squamous - squamous papilloma/carinoma
Transitional - transitional cell papilloma/carcinoma
Glandular - adenoma/adenocarcinoma

104
Q

What are blastomas?

A

Cancer, usually in children, from immature precursor cells

105
Q

What is the difference between in-situ and invasive neoplasms?

A

In-situ - no invasion of epithelial basement membrane

Invasive - penetrate basement membrane

106
Q

Why are malignant neoplasms more lethal?

A

They can metastasise which increases the tumour burden

107
Q

What is the process of metastasis?

A

Grow and invade primary site
Enter a transport system and then lodge at a secondary site
Grow at secondary site into a new tumour (colonisation)
All the time avoiding destruction by immune system

108
Q

What alterations occur in malignant neoplasms to allow them to metastasise?

A

Altered adhesion by changing E-Cadherin and integrin
Increase proteolysis so can degrade a membrane - MMP
Increase motility by changing the actin skeleton

109
Q

What comprises the cancer niche?

A

Stroma, fibroblasts, endothelial and inflammatory cells

110
Q

What G-protein does most cancerous signalling occur via?

A

Rho

111
Q

What are the possible transport systems?

A

Blood vessels
Lymphatic vessels
Coelomic spaces “transcoelomic”

112
Q

What can happen once the neoplasm reaches the secondary site?

A

Can grow by extravasation (leave vessel) and then colonisation
Die
Don’t grow but remain as a micrometastases which gives a disease free appearance known as dormancy

113
Q

What determines the secondary site?

A

Regional drainage and the “seed and soil” effect

114
Q

Where are the likely secondary sites for a malignant neoplasm that spread via the lymphatics, coelom or blood?

A

Regional lymph node
Elsewhere in coelomic space
Lung and liver as these are the first capillary bed most will encounter

115
Q

How do carcinomas usually travel? How do sarcomas usually travel and usually where to?

A

Lymphatics

Blood - lung, bone, liver, brain

116
Q

What are the most likely primary sites for a neoplasm in the bone?

A

Breast, bronchus, kidney, thyroid, prostate

117
Q

What is meant by the different neoplasm personalities?

A

More or less likely to metastasise
More - small cell bronchial carcinoma
Less - basal cell carcinoma

118
Q

What are huge possible effects of a neoplasm?

A

Local effects - destroy tissue, ulceration, compression, block tubes
Systemic - increase burden (reduce appetite, lose weight, immunosuppresion, thrombus formation) produce hormones

119
Q

What is likely to happen if you have a benign neoplasm of a gland and why?

A

As they are well differentiated they will produce the hormones e.g.
Thyroid - thyroxine

120
Q

Define carcinogenesis

A

Causes of cancer

121
Q

How are causes of cancer grouped?

A

Intrinsic - age/sex/heredity

Extrinsic - environment/lifestyle

122
Q

What are some lifestyle changes that increase risk of cancer?

A

Smoking, drinking, high BMI

123
Q

What do we know about carcinogens from chemicals?

A

Long delay between exposure and cancer onset
Risk dependent of dosage
There can be organ specificity

124
Q

What are the types of carcinogens?

A

Initiators - mutagens
Promoters - cause excess proliferation
Pro-carcinogens - need cytochrome p450 to become carcinogen
Complete carcinogen - initiator + promoter

125
Q

What are the types of radiation and how do they cause cancer?

A

UV light -skin
Ionising - x-rays, nuclear radiation (alpha, beta, gamma)
Damage DNA directly or through generation of free radicals

126
Q

How can infection cause cancer?

A

Damage genes that control growth - HPV
Chronic tissue injury leading to excess proliferation - H.pylori
Reduce immunity leading to carcinogenic infections - HIV

127
Q

Explain the two hit theory

A

A cancer may need to mutations to develop. Some cancers have a genetic link so there is already one hit and only need one of millions of cells to get a second mutation

128
Q

How many alleles must mutate for tumour suppressor and proto-oncogenes? Give an example of each

A

2 - Rb

1 - RAS

129
Q

What is Xeroderma Pigmentosum?

A

Autosomal recessive condition. Faulty NER. Person is sensitive to UV damage and therefore skin cancer

130
Q

What is the adenoma-carcinoma sequence? What is this also known as?

A

Multiple mutations are required
Adenoma–>carcinoma–>metastatic carcinoma
More mutations for each stage (possibly up to 10)
Progression

131
Q

What are the 6 hallmark features of cancer mutations?

A 
Self sufficient growth signals
Resistance to growth stop signals
Cell can divide infinitely 
Angiogenesis
Resist apoptosis
Invade and produce metastases (malignant)
132
Q

What are the 4 most common cancers and what percentage of all cancers do they approximately make up?

A

Breast, lung, prostate, bowel

50%

133
Q

What are the best and worst survival rates for cancer?

A

Testis - 98%
Breast - 87%
Lung - 10%
Pancreas - 3%

134
Q

What makes a favourable outcome against cancer more likely?

A

Age, health, tumour site and type, grade, staging, treatment

135
Q

Explain the universal staging method for cancer

A

TNM
T - size of primary tumour
N - metastasis to regional nodes
M - distant metastatic spread

136
Q

What staging is used for lymphoma?

A 
Ann Arbor
I) 1 node
II) 2 nodes on same side of diaphragm
III) a node on each side of diaphragm
IV) into an organ
137
Q

What is the staging for colorectal cancer?

A 
Duke
A) invasion but not through bowel wall
B) invasion through the bowel wall
C) involvement of lymphatics
D) metastasis
138
Q

What is the grading for breast cancer?

A

Bloom-Richardson

Tubules, nuclear variation and mitoses

139
Q

What are the orders that cancer treatment can be given?

A 
Curative treatment (surgery) --> adjuvant (eliminate sub clinical disease)
Neodjuvant (reduce size of tumour before removal) --> curative
140
Q

Explain radiotherapy

A

Use frequent small doses of ionising radiation such as X-rays to damage the DNA triggering apoptosis from cell checkpoints

141
Q

What are possible chemotherapy targets?

A

Antimetabolites
Cross link DNA stopping it replicating
Inhibit DNA synthesis
Block micro tubule assembly (spindle formation in mitosis)

142
Q

Explain a hormone therapy

A

Tamoxifen - bind to oestrogen receptors to treat hormone receptor positive breast cancer

143
Q

What are some tumour markers and why are they used?

A

HCG - testicular
AFP - testicular/liver
See if a cancer is recurring and how effective treatment is

144
Q

What are some problems with cancer screening?

A

Lead time bias
Length bias
Over diagnosis

ESA 2 (4 decks)

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