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Semester 2 > MoD Session 9 > Flashcards

MoD Session 9 Flashcards

0
Q

Why is cancer said to be ‘in remission’ rather than ‘cured’ when a primary tumour is removed?

A

Any remaining micrometastases can spread and develop

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1
Q

What are the most lethal features of malignant neoplasm?

A

Invasion

Metastasis

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2
Q

What increases tumour burden?

A

Extra cells increasing metabolic demand

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3
Q

How does metastasis take place?

A

Tumour cells grow and invade at primary site
Enter transport system and lodge at secondary site
Grow at secondary site to form a new tumour

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4
Q

What must occur before a new metastasis is formed?

A

Colonisation

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5
Q

How does the body try to prevent metastasis?

A

Immune attack at each stage

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6
Q

If a cell can carry out some but not all of the steps of metastasis, will it metastasise?

A

Nope

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7
Q

What type of tumour has been used mainly to study metastasis?

A

Carcinomas

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8
Q

How does cancer in the peritoneal cavity cause uncomfortable breathing?

A

Exudate (ascites) splits abdomen

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9
Q

To prevent splitting of the abdomen in cancer in the peritoneal cavity a shunt is used to allow the ascite fluid into a great vein. How does what you expect to see in the lungs compare with what is actually seen?

A

Expect lots of metastases but actually very few, if any, are seen

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10
Q

How is adhesion between malignant cells altered in carcinoma invasion?

A

Decreased E-Catherine expression

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11
Q

How is adhesion altered between malignant cells and stromal proteins in carcinoma invasion?

A

Changes in integrin expression

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12
Q

What does altering the integrin expression in carcinoma cells cause?

A

Actin production so the cell can fan out

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13
Q

How does integrin act as a signalling molecule?

A

Via G-proteins such as those in the Rho family

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14
Q

What is carried out by fibroblasts which allows stromal proteolysis?

A

Altered expression of Matrix Metalloproteinases (MMPs)

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15
Q

What must occur in stromal proteolysis for the carcinoma cells to invade surrounding tissue?

A

Degrade basement membrane and stroma

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16
Q

How are changes in motility achieved in invasion of carcinoma cells?

A

Changes in the actin cytoskeleton

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17
Q

What do altered adhesion, stromal proteolysis and motility cause the carcinoma cell phenotype to more closely resemble?

A

Mesenchyme

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18
Q

What is epithelial-to-mesenchyme transition (EMT)?

A

Three changes seen in carcinoma invasion which cause the carcinoma cell phenotype to resemble mesenchyme more closely than epithelia

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19
Q

What do malignant cells take advantage of?

A

Nearby non-neoplastic cells

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20
Q

What is the cancer niche?

A

Inflammatory cells
Endothelial cells
Fibroblasts
Stroma

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21
Q

What provides growth factor and proteases to malignant cells?

A

Normal cells

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22
Q

What can malignant cells enter to be transported to distant sites?

A

BV
Lymphatic vessels
Fluid in body cavities

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23
Q

What is transcoelemic spread?

A

Spread of malignant cells via pleura, peritoneal, pericardial, or brain ventricles fluid

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24
Q

What precedes colonisation at a secondary site?

A

Extravasation

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25
Q

Why do many malignant cells that lodge at secondary sites not create clinically detectable tumours?

A

They die or fail to grow

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26
Q

How many cells are present in a micrometastasis?

A

10-15

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27
Q

What is tumour dormancy?

A

When an apparently disease-free person harbours many micrometastases

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28
Q

What can cause tumour dormancy?

A

Hostile secondary site
Decreased angiogenesis
Immune attack

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29
Q

What causes relapse even after an apparent cure?

A

Micrometastasis growth

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30
Q

Why do transplant patients have a higher risk of melanoma?

A

Transplant organs can harbour micrometastases which grow in the receipient as they are immunosuppressed

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31
Q

Which system probably has a prominent role in melanoma?

A

Immune system

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32
Q

What does the site of a predictable secondary tumour depend on?

A

Regional drainage of blood, lymph or coelomic fluid

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33
Q

Where would you expect to see a secondary tumour if spread is via the blood?

A

Next capillary bed encountered - lungs or liver

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34
Q

Where would you expect to see a secondary tumour if spread of malignancy is via lymph?

A

Regional lymph node

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35
Q

Where would you expect to find secondary tumours spread by coelomic fluid?

A

Elsewhere in the coelomic space/adjacent organs

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36
Q

Where is a common site of metastatic deposits?

A

Pouch of Douglas

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37
Q

What is the unpredictable spread of secondary tumours also known as?

A

Seed and soil

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38
Q

What determines unpredictable, distant site of secondary tumour?

A

Interaction b/w malignant cells and nice at secondary site

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39
Q

What is a common pathway of ‘seed and soil’ secondary tumour site location?

A

Bronchial to adrenal

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40
Q

How do carcinomas typically spread?

A

Into draining lymph nodes and blood-borne to distant sites

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41
Q

What distant sites do carcinomas typically spread to?

A

Lung
Bone
Liver
Brain

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42
Q

Define osteolytic.

A

Decrease in bone mass

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43
Q

What type of malignant neoplasm typically causes osteosclerotic bone metastases?

A

Pancreatic

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44
Q

Define osteosclerotic.

A

Decrease in bone mass

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45
Q

Which neoplasms most frequently spread to bone?

A 
Breast
Bronchus
Kidney
Thyroid
Prostate
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46
Q

Give an example of a malignant neoplasm that metastasises very early in its course.

A

Small cell bronchial carcinoma

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47
Q

Does basal cell carcinoma of the skin metastasise?

A

No, almost never

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48
Q

Why is basal cell carcinoma of the skin considered malignant even though it almost never metastasises?

A

Has aggressive, invasive growth instead

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49
Q

What increases the risk of metastasis?

A

Cell number in the primary neoplasm

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50
Q

What is the basis of cancer staging?

A

Cell number in the primary neoplasm

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51
Q

What are the local effects of a neoplasm due to?

A

Primary or secondary neoplasm itself

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52
Q

What are local effects of neoplasm?

A

Direct invasion and destruction of normal tissue
Ulceration at surface causing bleeding and potential perforation
Compression of adjacent structures
Blocking of tubes and orifices

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53
Q

How do mediastinum tumours present as an emergency?

A

Occlude SVC

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54
Q

How does a tumour lead to a stricture?

A

Tumour in wall –> contractures –> stricture

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55
Q

What causes systemic effects of neoplasm?

A

Increased tumour burden increasing metabolism

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56
Q

What causes massive protein loss by entry into a catabolic state in neoplasm?

A

Secreted hormone and cytokines

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57
Q

What effects can neoplasm have on appetite and weight?

A

Decrease

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58
Q

What is cachexia?

A

Wasting syndrome

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59
Q

What systemic effects other than massive protein loss are seen in neoplasm?

A

Malaise
Immunosuppression
Thrombosis

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60
Q

What local effect of neoplasm can cause immunosupression?

A

Direct bone marrow destruction

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61
Q

What happens to platelets as a result of the systemic effects of neoplasm?

A

They become more sticky

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62
Q

What will a thyroid adenoma secrete which would cause systemic effects due to the neoplasm?

A

Thyroxine

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63
Q

How can malignant tumours such as bronchial small cell carcinoma cause Cushing’s or hyponatreamia?

A

Secretion of ACTH or ADH

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64
Q

How can bronchial squamous cell carcinoma cause hypercalcaemia?

A

Secretion of PTH-like hormone

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65
Q

How can a local effect of neoplasm cause hypercalcaemia?

A

Direct destruction of bone

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66
Q

Name some miscellaneous systemic effects of neoplasm whose link to neoplasm is poorly understood.

A 
Neuropathic so affecting brain and peripheral nerves
Pruritis
Abnormal pigmentation
Fever
Finger clubbing
Myositis
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67
Q

What cells other than tumour cells invade?

A

Trophoblast invades uterine wall

Leucocytes invade tissues during inflammation

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68
Q

Why are hyaline cartilage and arterial walls rarely invaded by malignant tissue?

A

Malignant tissue tends to produce collagenase but not elastase so the elastin present in these tissues is not broken down

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69
Q

Why may happen if tumour cells reach a serosal surface?

A

Fall into it causing seeding

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70
Q

What proportion of patients have microscopic metastases by the time a diagnosis of cancer is made?

A

> 50%

71
Q

What is the most common portal of entry of tumour cells into the bloodstream?

A

Capillaries and veins

72
Q

How do renal cell carcinomas invade the right heart?

A

Tumour cells enter the large renal vein and grow within it as a continuous root through the IVC into the right heart

73
Q

What shape do metastases tend to be?

A

Spherical

74
Q

How are metastases described on chest X-Ray?

A 
Single = coin lesion
Multiple = cannon balls
75
Q

Where do tumours in organs drained by the portal system metastasise primarily to?

A

Liver

76
Q

What acts as filters and receives 20-25% of cardiac output yet develops far fewer metastases than the smaller adrenal glands?

A

Kidneys

77
Q

What tumours favour metastasising to the ovaries?

A

GI tumours

78
Q

What are bilateral metastatic tumours of the ovaries called?

A

Kruckenberg tumours

79
Q

How are some metastases to the vertebrae explained?

A

Presence of a system of veins in and around the spine - vertebral venous plexus

80
Q

What method of spread is favoured by carcinomas?

A

Via lymphatics

81
Q

How do malignant cells spread via the lymphatics?

A

Penetrate w/out destroying endothelium –> float to next lymph node –> settle in peripheral sinus –> grow

82
Q

What is peau d’orange?

A

Slightly oedematous and puckering of the skin due to lymphatic obstruction common in carcinomas of the breast

83
Q

Why may lymph nodes downstream from a tumour swell but not be metastatic?

A

Secondary to antigens and irritating material that leach out from the tumour especially if it is necrotic, ulcerated or infected causing hyperplasia

84
Q

Why do ascites develop?

A

Possibly secondary to factors produced by tumours causing fluid leakage from peritoneal membrane
Possibly secondary to fluid leaking from the surface of malignancy

85
Q

How can seeding in the CSF occur?

A

With tumours of the CNS

86
Q

Why is implantation on epithelial surfaces rare?

A

They are inhospitable, covered in mucus, cornfield cells and bacteria

87
Q

What is a more histiologically atypical tumour more likely to do?

A

Invade and metastasise

88
Q

Where does basal cell carcinoma appear?

A

Skin exposed to sunlight, especially the face

89
Q

Why do tumours of the CNS rarely produce metastases for the rest of the body?

A

They are in a closed space so often kill before visceral metastases are detected

90
Q

Can implantation of tumour cells along a needle track after biopsy occur?

A

Yes but it is rare

91
Q

What must a metastatic cell escape in the blood in order to metastasise?

A 
Antibodies
Complement
Macrophages
Killer cells
Toxic oxygen concentration
Blood clotting
92
Q

What must a tumour cell do once it has reached a vessel small enough to be embolised during spread via the blood?

A

Survive impact and mechanical squeeze

93
Q

How do tumour cells penetrate BV?

A

Reverse diapedesis

94
Q

Where is it most likely that tumour cells enter the bloodstream?

A

Vessels of the tumour itself rather than preformed surrounding vessels

95
Q

How do tumour cells attach to basement membrane when entering a vessel with endothelial lining and basement membrane?

A

Laminin receptors

96
Q

What can tumour cells become coated in within the blood which can help the metastatic process?

A

Platelets

97
Q

Why is the mechanical impact of embolism fatal to many tumour cells?

A

They are larger and less deformable than WBCs

98
Q

What is the possible explanation for why capillaries in the heart and skeletal muscle are rarely metastasised?

A

Bio mechanical trauma is too great due to squeezing with heart beat or muscular contraction

99
Q

What is organ selection in metastasis?

A

Selection because they drain the blood of the primary tumour e.g. colon–> liver
Selection due to seed or soil properties

100
Q

What are fistulae?

A

Abnormal communications between two distinct tissues e.g. B/w bladder and rectum

101
Q

What is paraneoplastic syndrome?

A

Symptom complexes that accompany tumours and concern distant targets whether the mechanisms be hormonal, toxic, immunologic or unknown

102
Q

What happens to paraneoplastic syndrome is the tumour is removed or destroyed?

A

It usually disappears

103
Q

What may be the first sign of a hidden tumour and can help follow the regression or recurrence of a tumour?

A

Paraneoplastic syndrome

104
Q

What are the most common offenders in ectopic hormone secretion?

A

Lung carcinomas

105
Q

What can renal cell carcinomas produce that results in high haematocrit and symptoms related to high blood viscosity?

A

Erythropoietin

106
Q

Why is a hypercoaguable state seen in 90-95% of cancer patients?

A

Platelets activated by tumour products e.g. ADP

Tumours secrete procoagulents

107
Q

What is Trosseau’s syndrome?

A

Migratory thrombophlebitis where bouts of thrombophlebitis are seen in multiple locations without an apparent predisposing factor

108
Q

Which types of cancer is Trousseau’s syndrome often seen in?

A

Pancreatic
Lung
Stomach

109
Q

What is acanthosis nigricans?

A

Symmetric, brown, warty hyper pigmentation w/hyperkeratosis of the axilla and other flexural areas

110
Q

What is the possible cause of acanthosis nigricans?

A

Transforming growth factor alpha

111
Q

What does more than 50% of acanthosis nigricans occur in association with?

A

Internal malignancy - esp. GI carcinoma

112
Q

What produces tumour necrosis factor which results in cachexia caused by tumour?

A

Macrophages

113
Q

What causes changes in sense of taste in neoplasm?

A

Tumour

114
Q

What is tumour lysis syndrome?

A

Extensive, acute necrosis of a tumour that is v. sensitive to X-Rays or chemotherapy which can cause life-threatening release of toxic amounts of potassium and uric acid

115
Q

What is often seen in Burkitt’s lymphoma?

A

Tumour lysis syndrome

116
Q

What limits tumour lysis syndrome to 5-7 days?

A

Wave of cell death ends

117
Q

How does cancer kill?

A 
Infection - cancer and its treatment are anti inflammatory
Haemorrhage and thromboembolic phenomena
Cachexia
Respiratory failure
Renal failure
118
Q

What molecules are carcinogenic with a delay of 5-30 years?

A

Aromatic amines

119
Q

Why are carcinogenic molecules described as electrophilic reactants?

A

They have relatively electron deficient sites which make them seek nucleophilic sites such as amine groups

120
Q

How are nucleophilic groups relatively abundant in a cell?

A

As DNA, RNA and proteins

121
Q

What happens to carcinogens in the body?

A

They are activated into an electrophilic state

122
Q

What are procarcinogens?

A

Inactive carcinogens

123
Q

Why does each carcinogen always affect the same organ?

A

Due to their need for modification before they are effective

124
Q

What may the organ selectivity of carcinogens depend on?

A

Presence, absence or balance of enzymes that activate procarcinogens

125
Q

Is alcohol carcinogenic?

A

Not directly but causes liver cirrhosis and liver nodules may become neoplastic

126
Q

Where does alcohol increase risk of cancer for?

A 
Mouth
Pharynx
Larynx
Oesophagus
Lung
Rectum
Breast
127
Q

What two things interact to increase the risk of oesophageal cancer?

A

Alcohol and tobacco

128
Q

What is the principal theory to explain gastric cancer?

A

Based on nitrosamine formation in the stomach

129
Q

Where can nitrosamines come from?

A

Tobacco smoke

Sodium nitrite prescursor used as a food additive in cured meat and fish

130
Q

What inhibits the production of nitrosamines from nitrites?

A

Adding ascorbic acid/increasing the amount of fruit and vegetables in the diet

131
Q

What is produced by Aspergillus flavus which grows on grain stored in warm and humid conditions that is a very potent carcinogen?

A

Aflatoxin B1

132
Q

What is a major factor in the high incidence of liver cancer in Africa and Asia and appear in conjunction with hepatitis B?

A

Aflatoxin B1

133
Q

What dietary agents inhibit mutations and tumour formation?

A

Fibre
Vitamin A
Vitamin C
Certain seeds

134
Q

How does obesity cause an increased risk of endometrial cancer?

A

Adipose tissue converts androgens to oestrogens

135
Q

What type of cancer can the contraceptive pill cause?

A

Liver adenomas

136
Q

What protects against breast cancer?

A

Early first pregnancy and bearing a child at all

137
Q

What are approximately 10% of breast cancers due to?

A

Genetic predisposition often associated w/BRCA1 and BRCA2

138
Q

How does asbestos cause cancer?

A

Fibres inhaled and produce fibrosis and malignant tumours of mesothelium of the pleura, pericardium and peritoneum

139
Q

What acts synergistically with cigarette smoke to cause cancer?

A

Asbestos

140
Q

What is involved in carcinogensis by ionising radiation?

A

Free radicals

141
Q

What is given to women during pregnancy to stop bleeding and can cause adenocarcinoma of the vagina in the daughters of treated women?

A

Diethylstillboestrol

142
Q

What are the only two types of radiation that are carcinogenic?

A

Ultraviolet

Ionising

143
Q

How do UV rays behave as complete carcinogens on repeated exposure?

A

Damage DNA strands by forming dimers and cross-links

144
Q

How many exposures of ionising radiation are needed to cause cancer?

A

One

145
Q

What genetic predisposition can individuals be born with which increases their risk of developing cancer?

A

Mutation in one allele so they only need one more ‘hit’ to cause a cancer that is caused by mutations of both alleles of a gene

146
Q

Which are the most sensitive cells to radiation injury causing shortened cell survival?

A

Bone marrow
Intestinal epithelial
(Both have high mitotic rates)

147
Q

Which common worldwide tumour is the only one to be virus induced?

A

Hepatocellular carcinoma

148
Q

Where does schistosoma cause cancer in humans?

A

Bladder

149
Q

How do retroviruses work?

A

Transduce cellular genes and turn them into cancer genes

150
Q

What unique enzyme do retroviruses possess?

A

Reverse transcriptase

151
Q

Why are viral copies of transduced cellular genes not perfect?

A

Reverse transcriptase is a highly error-prone mechanism

152
Q

What are proto-oncogenes?

A

Normal genes with important growth-related functions in a cell’s normal activity

153
Q

About how many oncogenes are known to exist?

A

70

154
Q

What is one-step oncogenesis?

A

Where the oncogene acts alone

155
Q

Which DNA viruses can cause neoplasm?

A

Hep B
HPV
EBV
Molluscum contagiosum (forms benign molluscum bodies)

156
Q

Which retrovirus can cause leukaemia and lymphoma?

A

Human T-cell leukaemia virus

157
Q

How does Burkitt’s lymphoma usually present?

A

Large mass in the upper or lower jaw

158
Q

What is the most common cause of infectious mononucleosis?

A

Epstein Barr virus

159
Q

What does Epstein Barr virus do?

A

Parasitises B lymphocytes

Parasitises epithelium of upper pharynx

160
Q

What does the distribution of Burkitt’s lymphoma in Africa coincide with?

A

Distribution of malaria

161
Q

What do all Burkitt’s lymphomas show?

A

Chromosome translocations known to activate the oncogene c-myc

162
Q

What does nasopharyngeal carcinoma always contain?

A

DNA of the EBV

163
Q

How do DNA viruses produce tumours?

A

Carry genes that transform cells

Act indirectly by depressing genes that normally inhibit cell growth

164
Q

What are RNA oncogene viruses also called?

A

Acute transforming proteins

165
Q

How quickly can RNA oncogene viruses produce a leukaemia?

A

In a matter of days or weeks

166
Q

Describe human T-cell lymphocytic virus-I.

A

A relative of the AIDS virus

Like HIV it affects helper lymphocytes (T4+)

167
Q

What two types of neoplastic associations does the AIDS virus have?

A

Tumours related to immunosupression

Kaposi’s sarcoma

168
Q

How does Kaposi’s sarcoma appear?

A

Bluish-red plaques or nodules on skin and mucosae seen in multiple locations due to multi centric origin not metastasis causing widespread involvement of internal organs

169
Q

What is the likely cell of origin in Kaposi’s sarcoma?

A

Endothelium

170
Q

How can Helicobacter pylori cause stomach cancer?

A

Causes chronic gastritis therefore may cause cancer due to chronic stimulus to regenerate

171
Q

What are liver flukes?

A

Parasites that live in bile ducts causing hyperplasia and sometimes cholangiocarcinoma

172
Q

How do Schistosoma haematobium cause cancer?

A

Larvae burrow into skin from infected water –> enter bloodstream and travel to liver where they mature into adult flukes –> migrate and breed in bladder –> constant regeneration of bladder epithelium –> squamous cell carcinoma of the bladder

173
Q

How is water contaminated by Schistosoma haematobium?

A

Human host eliminates eggs in urine where they can enter the water supply

174
Q

What happens to the eggs of Schistosoma Haematobium once they have been eliminated in the urine?

A

Hatch into miracidia and enter snail host which releases larvae into the water

Semester 2 (45 decks)

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