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ESA 2 > MOD 6-9 > Flashcards

MOD 6-9 Flashcards

0
Q

Describe the alterations to DNA which cause neoplasm

A

Initiators and promoters needed resulting in monoclonal growth which, through progression, accumulates more mutations.

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1
Q

What is pleomorphism?

A

More mitosis figures and increasing variation in size and shape of cells - seen in malignant neoplasm.

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2
Q

What is lyonisation?

A

One x is randomly inactivated during early embryogenesis

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3
Q

Distinguish between in situ and invasive malignancy

A

In situ- no invasion through basment membrane

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4
Q

What is an adenoma?

A

Benign, glandular origin, epithelioial

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5
Q

What is a papilloma?

A

Benign tumour which projects out wards

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6
Q

What is a carcinoma?

A

Malignant tumour of epithelial cells

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7
Q

What is a sarcoma

A

Malignant, stromal cells

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8
Q

What is the most crucial check point in the cell cycle

A

The restriction (r) point towards the end of G1

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9
Q

How is the cell cycle controlled?

A

Check points at the end of each growth phase.
Levels of cyclins regulate processes and control transitions between stages as well as the speed. They act by binding to CDks to form active kinases.

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10
Q

What is the difference between regeneration and reconstruction?

A

Regeneration is more cells. Reconstruction is the replacement of a lost part of the body e.g. Babies fingers.

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11
Q

How does the body increase the rate of cell proliferation?

A

Growth factors e.g. Epidermal growth factor.
Binds to receptors which triggers gene transcription. Shortens cell cycle and takes stable cells out of G0. Also affects differentiation, activation, angiogenesis, locomotion ect.

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12
Q

What type of cells does hypertrophy occur?

A

Mainly permanent but may occur in any

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13
Q

What causes hypertrophy (generally)?

A

Functional demand or hormone stimulation

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14
Q

Physiological examples of hypertrophy

A

Skeletal muscle, pregnant uterus, compensatory e.g. Removing a kidney.

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15
Q

Pathological examples of hypertrophy

A

Ventricular hypertrophy, bladder outlet obstruction-SM hypertrophy.

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16
Q

Give examples of physiological hyperplasia

A

Endometrium under influence of oestrogen. Bone marrow produces erythrocytes in response to hypoxia.

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17
Q

Give pathological examples of hyperplasia

A

Goitre and eczema

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18
Q

Give pathological examples of atrophy

A

Osteoporosis, tissues around a tumour due to ischemia, loss of blood supply, cerebral atrophy in Alzheimer’s, loss of nutrients, loss of innervation to muscle, persistent injury - polymyositis (inflammation of muscle), aging

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19
Q

Give a physiological example of atrophy, what can this be called?

A

Ovarian atrophy in post menopausal women (technically involution - programmed cell shrinkage) thymus

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20
Q

What is hypoplasia?

A

Underdevelopment of an organ or tissue in the embryonic stage due to inadequate number of cells.
It is congenital - not the opposite of hyper.

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21
Q

What is the difference between aplasia and hypoplasia?

A

Aplasia is the complete failure of an organ or tissue to develop, hypo is partial.
Aplasia is also used to describe an organ whose cells nolonger proliferate e.g. Bone marrow.

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22
Q

What is metaplasia

A

Reversible changes of one cell type to another.
Not across germ layers.
Fully differentiated in response to stress.
May lead to cancer

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23
Q

Give examples of pathological metaplasia

A

Smoking epithelium changed to stratified (bronchial).

Gastric glandular columnar epithelium instead of stratified squamous with persistent acid reflux.

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24
Q

What is atresia?

A

When a hole doesn’t open

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25
Q

Define an atheroma

A

The accumulation of intra and extracellular lipid in the intima and media of large and medium sized arteries.

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26
Q

Define atherosclerosis

A

Thickening and hardening of arterial walls due to An atheroma

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27
Q

What is arteriosclerosis

A

Thickening of arterial walls due to DM or hypertension.

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28
Q

Describe the macroscopic appearance of an atheroma

A

Starts as fatty streak - lipid deposits in intima, slightly raised.
Then becomes a simple plaque - deposits are more widespread with an irregular outline, enlarge and coalesce.
Can become a complicated plaque which involves thrombosis, haemorrhage into plaque, calcification or aneurysm.

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29
Q

Describe the early and later changes in the microscopic appearance of an atheroma.

A

Early - SM cells proliferate and foam cells accumulate, extracellular lipid.

Late- cholesterol deposits and clefts(in tissue too), possibly inflammatory cells, fibrosis, necrosis.

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30
Q

Describe the unifying hypothesis

A

Endothelial damage due to high LDL, toxins e.g. Cigarette smoke, haemodynamic stress, herpertension.

Damage causes platelet adhesion, PDGF release, SMC proliferation and migration, monocyte migration to intima, insulation of lipid, oxidised and taken up by SM cells and macrophages.

SMC produce matrix material.

Foam cells secrete cytokines causing further SMC stimulation and recruitment of other inflammatory cells.

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31
Q

Discuss the risk factors for atherosclerosis

A 
Pre menopausal women are protected.
Age
Smoking
DM - double risk
Alcohol over 5 units
Hypertension
Hyperlipideamias
Infection e.g. Chlamydia
Exercise
Oral contraceptive
Stress
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32
Q

Effects of an atheroma in the brain

A

Cerebral ischemia
Transient ischemic attack
Cerebral infarction/ stroke
Multi-infarction dementia.

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33
Q

Effects of an atheroma on mesenteric arteries

A

Mal absorption, ischemic colitis, intestinal infarction, anneurysm due to high pressure

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34
Q

What is haemostasis?

A

Stopping of blood flow

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35
Q

What does successful haemostasis depend on?

A

Vessel wall
Platelets
Coagulation system
Fibrinolytic system

36
Q

What initiates the intrinsic and extrinsic pathways?

A 
Extrinsic = external trauma
Intrinsic = internal e.g. Damage to endothelium.
37
Q

Describe tests that determine blood clotting

A

FBC
Bleeding time - small cut (should take 3-8 minutes)
General blood clotting tests where factors are added to a blood sample to see how long it takes to clot compared with a normal sample. Different factors/activators are added to work out which factors are low/absent.

38
Q

Why is such fine control needed over the coagulation system?

A

1ml of blood contains enough thrombin to convert all of the fibrinogen into fibrin.

39
Q

Discuss the regulation of the coagulation system

A

Thrombin activates other factors by positive feedback.

Thrombin inhibitors:
Anti thrombin III
A1 anti trypsin
A2 macro globulin
Protein C/S
40
Q

Which fibrin inhibitors may be deficient due to inherited mutations?

A

Anti thrombin III

Protein C/S

41
Q

Describe the main components of fibrinolysis

A

Streptokinase and t-PA (tissue plasminogen activator) both activate plasminogen to plasmin which can break down fibrin

42
Q

What is a thrombus

A

The formation of a solid mass of blood within the circulatory system during life.

43
Q

Discuss causes in blood components that may lead to thrombus formation

A

Smoking, pregnancy.

44
Q

Describe the difference between arterial and venous thrombi

A

Venous are deep red, soft, gelatinous and have. High cell content.
Arterial are pale, granular, have lines of zahn and a lower cell content.

45
Q

What does the damage of a thrombus fully concluding a vessel depend on?

A

Collateral circulation

46
Q

What can a venous thrombus lead to?

A

Congestion oedema.

If tissue pressure due to oedema> arterial pressure then ischemia and infarction.

47
Q

Discuss the possible outcomes of thrombosis

A

Lysis - fibrinolytic system breaks down the thrombus
Propagation - thrombus continues to grow proximally in veins and distally in arteries.
Organisation - fibroblasts and capillaries grow into thrombus (reparative) but lumen is still obstructed.
Recanalisation - channels form from reorganisation of thrombus which restores blood flow partially.
Embolism - dislodges and travels to a distant site.

48
Q

Define embolism

A

Blockage of a blood vessel by a solid, liquid (e.g. Amniotic fluid) or gas at a site distant from its origin

49
Q

Decribe the types of PE

A

Massive - 60% reduction to blood flow- fatal.
Major - medium sized vessels blocked, shortness of breath, cough, blood stained sputum.
Minor - small blood vessels blocked, normally asymptomatic
Recurrent - pulmonary hypertension

50
Q

Describe the causes of DVT

A 
Immobility
Severe burns
Post op
Pregnancy- post partum
Disseminated cancer.
51
Q

Shat could cause fat embolism?

A

Fractures of long bones.

Causes rash, shortness of breath and confusion

52
Q

How may you get a nitrogen embolism

A

Rapid decompression elf. The bends.

53
Q

Give one gain of function G protein mutation and one loss of function.

A

Loss is retinitis pigmentosa, mutation in rhodopsin.

Gain is familial male precocious puberty, mutation in LH receptor so it is always active

54
Q

Define metastasis and invasion

A

Metastasis- a malignant neoplasm growing at a secondary site

Invasion - the spreading of malignant cells into surrounding tissue.

55
Q

Describe process by which a tissue metastisises including any alterations to the cell

A

Grows through basement membrane, and invades into transport system, lodges at distant site.

Epithelial to mesenchyme transition EMT

Altered adhesion: Change in integrins which bind the cells to stromal cells. Changes to E cadherin for binding to other cancerous/ epithelial cells.
Produces proteolytic enzymes to degrade basement membrane and invade e.g. MMP, matrix metalloproteinases.
Motility - changes in actin steucture and integrins that signal to other cells via small G proteins such as the Rho family.

56
Q

What is transcoelomic spread?

A

Spread of cancer through being in the same cavity.

57
Q

What is extravasation

A

Malignant cells coming out of a vessel

58
Q

Where do carcinomas and sarcomas normally spread

A

Carcinomas via lymph first then blood. Sarcomas via blood.
Lung, bone, liver and brain are common sites for blood Bourne metastasis.

Bone metastasis normally come from BBKTP - brain, breast, kidney, thyroid and prostate

59
Q

A cancer that metastisises quickly and one that doesn’t

A

Small cell bronchial carcinoma does, basal cell carcinoma does not,

60
Q

Describe systemic and local effects of cancer (benign only has local)

A

Local effects: compression of tubes, compression of other cells, ulceration, bleeding, destruction of normal tissue

Systemic effects: loss of apetite, hormone secretion e.c.t. ACTH in small cell bronchial carcinoma and ptrh squamous cell carcinoma, malaise, immunosupression, skin problems, abnormal pigmentation, fever, clubbing, myositis.

61
Q

What are paraneoplastic syndromes?

A

Systemic effects of cancer e.g. Hormone effects, tumour burden and immune response

62
Q

Give some intrinsic and extrinsic host factors for cancer and 5 main causes

A

Intrinsic- genetics, age, sex, hormone levels
Extrinsic - environment
Obesity, low f&v, smoking, lack of exercise and alcohol

63
Q

Lessons learned from 2 napthylamine

A

Dose dependent- as dose increase so does risk - need long exposure. Organ specificity e.g. Bladder. Delay between exposure and disease.

64
Q

What is needed for cancer from chemicals?

A

Initiators at start followed by constant promotors. Initiators cause mutations and promotors cause prolonged proliferation.

65
Q

Give examples of some common carcinogens

A 
Aromatic amines e.g. 2 nap
Polycyclic aromatic hydrocarbons
Alkylating agents
Natural chemicals e.g. Aflatoxin B1 in asbestos
N-nitroso compounds
66
Q

Define pro carcinogens and complete carcinogens

A 
Pro= are converted in liver to carcinogen by cytochrome P450
Complete= initiator and promotor
67
Q

Normal exposure to ionising radiation

A

UV and radon. Can alter bases, cause chromosomes to split and cause free radical damage.

68
Q

How may infections cause cancer. HPC and hepatitis.

A

Alter genes that control cell growth. Cause chronic injury resulting in regeneration which acts as a promoter (e.g. Hep B/C and helicobacter pylori). Some viruses e.g. HPV inhibit p53 and pRB by expressing proteins such as E6/7.
HIV lowers immunity for other carcinogens to enter.

69
Q

Example of 2 hit theory

A

Retinoblastomas - can inherit- dominant pattern

70
Q

What is needed to enhance tumour growth

A

One POG activated

Both TSG mutated

71
Q

What does the OG RAS do? Also rs

A

Via G protein signals for cell to push past restriction point and keep dividing unchecked.
RS does opposite so is a TSG.

72
Q

Give diseases in which there is a defect in DNA excision repair, DNA mismatch repair and brac1/2 genes which fix chromosome breaks.

A

Xeroderma pigmentosum is excision results in skin cancer.
Hereditary non-polyposis colon cancer (HNPCC) is mismatch repair.
Familial breast carcinoma is brac1/2 leading to breast cancer

73
Q

What is progression?

A

Accumulation of mutations (required for malignancy) after initiation and promotors. May arise from an adenoma-carcinoma sequence.

82
Q

Difference between tumour grading and staging

A

Staging is overall burden

Grading is differentiation

83
Q

Describe a universal form of staging?

A 
TNM
T- size 1-4
N- nodes traveled to 0-2
Metastasis 0-1
These can be converted to stages, often any metastasis means stage IV (highest)
84
Q

Describe a staging system for lymphoma

A

Ann Arbor.
I - single rode region
2- multiple node regions on one side of diaphragm
3 - both sides of diaphragm
4- disseminated involvement of one or more organs e.g. Bone or lung.

85
Q

Uses of hormone therapy

A

Tamoxifen antagonise selective oestrogen receptor modulators (SERM) this prevents oestrogen from binding. Androgen blockade is used to treat prostate cancer.

86
Q

Describe the uses or herceptin and imatinib

A

Herceptin blocks the HER2 receptor which is present in a quarter of Breast cancers.
Imatinib blocks the protein produced by the Philadelphia chromosome where an oncogene is formed in a translocation which can lead to chronic myeloid leukaemia.

87
Q

Name some common tumour markers

A

Human chorionic gonadotropin in testicular cancer.
Alpha fetoprotein in hepatocellular carcinoma
Prostate specific antigen
CA-125 in ovarian cancer.
Carcino-embryonic antigen in GI tract tumours

88
Q

Describe the basis for radiotherapy

A

Breaks chromosomes, interferes with mitosis or triggers apoptosis. Produces radicals.
More effective in doses due to the fact that healthy tissue can repair e.g. Restriction points but cancerous tissue cannot.

89
Q

Describe agents used in chemotherapy

A

Anti metabolites
Alkylating agents and platinum based drugs
Antibiotics (effect DNA or it’s synthesis)
Plant derived drugs.

90
Q

Describe a staging for colorectal carcinoma

A 
Dukes' staging
Dukes' A = invasion into but not through bowel
B - invasion through bowel wall
C- involvement of lymph nodes
D- metastasis e.g. Liver.
91
Q

Grading for prostate?

A

Gleason- looks at gland spacing

92
Q

Grading for squamous cell and colorectal

A

G1-4 depending on differntiation

93
Q

Grading for breast cancer?

A

Bloom-Richardson

Differentiation, mitosis figures and nuclear variation, tubular arrangement.

94
Q

Difference between adjuvant and neoadjuvant?

A

Adjuvant - treatment after surgery to decrease risk.

Neoadjuvant- try to shrink tumour prior to surgery.

99
Q

4 main types of cancer

A

Bowl, breast, lung (deadly) and prostate 40-50k

ESA 2 (9 decks)

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