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Biomed2 > Oncology > Flashcards

Oncology Flashcards

1
Q

Onco =

A

Tumour

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2
Q

Neoplasm =

A

New growth
Mass of tissue growing faster & uncontrolled manner

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3
Q

Tumour =

A

‘Swelling’
Now mass / growth of tissue
Either benign or malignant

No longer responds to normal growth factors, faster & uncontrolled

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4
Q

Benign =

A

Non-cancerous growth

Still excesseive but no metastasis
Grows slowly
Non life-threatening but can damage due to compression of space

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5
Q

Malignant =

A

Cancerous growth

Excesseive & uncontrolled & faster
Metastasise, often systemic & life-threatening
Undifferentiated, non-functional cells with varied shape&size nuclei, not encapsulated/loosely bound

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6
Q

Why is oncology so important & prevalent

A

Second leading cause of death in works - 9 million a year
Predicted to double by 2030

Most common causes: lung, liver, colorectal, stomach & breast

More developed countries have higher cancer rates - emphasising link to environment, lifestyle, diet, meds, drugs

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7
Q

Mitosis is

A

Growth & repair of somatic cells

All cells differentiated & specialised
Some cells so much they cannot undergo mitosis

Mitosis - how malignant tumours grow

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8
Q

Meiosis is

A

Growth & reproduction of sex cells (gametes)

Differentiated & specialised

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9
Q

How do malignant tumours grow

A

Via mitosis

Uncontrollable manner, loses specialised function & become disorganised

Cell architecture key to observe in suspected neoplastic growth

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10
Q

% of cases of inherited cancer

A

5-10%

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11
Q

What is cancer

A

A result of genetic mutations
Result of an UNDERLYING CAUSE - which ultimately promote mutations of multiple genes

Essential to explore interaction of patients genes with environment

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12
Q

What is a proto-oncogene

A

A gene that Causes mitosis
Growth of a tissue

Inactivated by
Tumour suppression genes

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13
Q

What is an oncogene

A

Tumour suppresion genes & proto-oncogenes mutations = New genes that cause overproduction of growth factors & increased cell division uncontrolled
(Divide uncontrolled & rapid)

Malignant cells can only grow 1-2mm3 without a blood supply

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14
Q

What is angiogenesis

A

Angio = vessel

Manufacture more blood vessels to creat a blood supply

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15
Q

What environment promotes cancerous cell growth

A
  1. Acidic environment
  2. Anaerobic environment
  3. Glucose rich
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16
Q

What are malignant cells dependent upon

A

Glucose for their own metabolism
Have many more glucose receptors on their membrane

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17
Q

What is contact inhibition

A

Proteins produced by normal cells that prevent cells dividing beyond available space

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18
Q

What process do cancerous cells lose

A

Contact inhibition
Causing uncontrolled growth

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19
Q

What is a mutation

A

Change in genetic information

Disruption to DNA sequence/number/“recipe”

Promoting abnormal growth

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20
Q

What is a mutagen

A

Agent that changes genetic information
& disrupt normal growth
Such as:

Environmental hazards
Chemicals (environmental, household, drugs, vaccines)
Radiation (x-rays, microwave, mobiles)
Viruses
Inflammation
Defective immunity
Stress/trauma

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21
Q

What is a carcingogen

A

Any cancer causing agent

Nitrosamines, heavy metals, asbestos, X-rays, UV-rays

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22
Q

What is carcinogenesis

A

The process by which normal cells are transformed into cancer cells
5-10% inherited genetic defects
90-95% attributed to environment & lifestyle

Some tumours can take 20-40 years

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23
Q

Environmental & lifestyle cancer risk factors

A
  • 5-10% genetic predisposition
  • chronic inflammation
  • chronic stress
  • chronic immunodeficiency
  • radiation
  • smoking
  • GIT dysfunction, liver & intestines
  • drugs & cosmetics
  • vit D deficiencies & thyroid disorders (requires iodine)
  • sexual behaviour
  • excessive sunlight exposure
  • metal toxins
  • vax ingredients
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24
Q

What gene represents breast cancer susceptibility

A

BRCA

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25
Q

Why are parabens harmful

A

Have been found in breast tumours, can also mimic oestrogen hormone leading to oestrogen-driven cancers

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26
Q

Why can chronic stress increase cancer risk

A

Suppress immune system
Increase cortisol & sympathetic NS
Anaerobic environment forms which leads to acidity

MHC-I antigen illustrates if damaged cell inside

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27
Q

What virus has been linked to cervical cancer

A

HPV
Human papilloma virus

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28
Q

How does obesity increase cancer risk

A

Excess body fat changes hormone metabolism&raquo_space; higher oestrogen&raquo_space; drives oestrogen+ thmours

Breast cancer is linked to post-menopausal women

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29
Q

Dietary risk factors for cancer

A
  • pro-inflammatory
  • red meats, charcoal/smoked/burnt
  • n-nitroso compounds in cured meats
  • excess alcohol
  • low fibre diet
  • refined sugars
  • dairy
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30
Q

What are acrymalides

A

Carcinogenic compounds produced by burning food

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31
Q

Why is dairy increase cancer risk

A

Pro-inflamm
Contains IGFs that promote tumour growth
Hormones added - is an endocrine disruptor

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32
Q

What is grading of tumours

A

Measure of degree of tumour cell differentiation/abnormality

Grade 1: similar to original cells, differentiated & specialised (benign)

Grade 4: undifferentiated/many abnormal cell sizes & shapes

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33
Q

What is cancer staging

A

Classification of malignant tumours extent
Helps to identify treatment approaches, disease progression & prognosis

34
Q

Cancer stages 0-4

A

0: pre-cancerous
1: cancer limited to tissue origin
2: limited local spread of cancer cells
3: extensive local & regional spread
4: distant metastasis

35
Q

What is TNM cancer staging

A

Tumour, Node, Metastases

T(1-4): size of primary tumour
N(0-3): degree of lymph node involvement
M(0-1): metastases

X = cannot be assessed

36
Q

Local effects of cancer

A
  • Damages ‘space’ occupies
  • Can compress blood vessels leading necrosis of surrounding tissues & eventually its own leading to calcification (seen in Xray)
  • metastasise
  • pain occurs as later symptom by pressure or inflammation
  • obstruction can occur in tubes/ducts
  • tissue ulceration/inflammation may produce infection (especially in immunocompromised chemo/radiotherapy)
37
Q

Systemic effects of cancer

A
  • weight loss & cachexia (but can still have strong appetite)
  • anaemia
  • infection (pneumonia)
  • para-neoplastic syndromes (secondary site symptoms)
38
Q

Eg of para-neoplastic syndrome

A

Lung cancer tumour cells may produce ACTH (orother hormones) leading to cushing’s syndrome (excess cortisol)

39
Q

Metastasis =

A

Spread of a malignant tumour usually via blood or lymph
Producing secondary tumours

40
Q

Common sites of metastasis

A

Bone, liver, lung & brain
Due to rich blood supply

41
Q

Key cancer presentation red flags

A

Anaemia, fatigue
Unexplained weight loss & cachexia
Night sweats
Unusual bleeding/discharge
Persistent indigestion/heartburn
Dysphagia
Change in bowel habits
Solid lump
Persistent cough/hoarseness
Swollen lymph nodes

42
Q

Types of diagnostic testing for cancer

A
  1. Blood tests
  2. Tumour markers
  3. Imaging
  4. Biopsies
43
Q

What is CEA

A

A glycoprotein tumour marker present within normal mucosal cells

Can be elevated in certain types of cancer, especially colorectal cancer
& ulcerative colitis, pancreatitis, liver cirrhosis

44
Q

What is PSA tumour marker

A

Protein produced by prostatic cells
Present in small quantities in serum

May be elevated in presence of prostate cancer & other prostate disorders
Assists diagnosis & monitoring of tumour progression & metastasis but can produce false positives

45
Q

What is hCG tumour marker

A

Should only be produced during pregnancy, males do not produce

Tests for cancer in testes, pancreas, pituitary, placenta

46
Q

What is M2-PK tumour marker

A

Not organ-specific so can present in many types

Stool levels being investigated as a screening method for colorectal tumours

47
Q

What is CA-125

A

Protein elevated in many cases ovarian cancer
Blood test ranges less than 35 U/mL

48
Q

What is CA 15-3

A

Elevated in breast cancer
Blood ranges less than 30 U/mL

49
Q

Main forms of allopathic cancer treatment

A

Combination or single
- surgery
- chemotherapy
- radiation

Aimed at removing/suppressing not treating cause - cancers often return !

50
Q

What is palliative treatment

A

Care focuses on reducing symptoms severity rather than ‘curing’
Seen in late stages, preventing complications is vital
Focuses on quality of life!

51
Q

Mastectomy =

A

Removal of breast

52
Q

Prostatectomy =

A

Removal of the prostate gland with a very high rate of side effects!

53
Q

Orchiectomy =

A

Removal of testes

54
Q

What is fractionation

A

Dividing a dose of radiotherapy for cancer patients

55
Q

What cells does radiotherapy target

A

Affects cells which divide most rapidly (both cancerous & healthy)
Causes loss of reproduction & induces apoptosis

56
Q

External beam radiotherapy

A

Beams generated outside patient to target specific area

57
Q

Internal beam radiotherapy aka brachytherapy

A

Probe inserted into body & releases within body cavity
Eg cervical or colorectal

58
Q

System beam radiotherapy

A

Radioactive material enters body to reach cells all over body (very harmful)

59
Q

What is chemotherapy

A

Chemical agents that enter the bloodstream & are destructive to malignant cells

Target rapidly dividing cells (cannot distinguish between normal & cancer)
Interfere with protein synthesis & DNA replication

Different drug combinations for different cancers

60
Q

Radiotherapy & chemo adverse effects

A
  • bone marrow depression = immunocompromised
  • diarrhoea, bleeding, vomiting, nausea
  • hair loss
  • sterility
  • organ damage & cancer (chemo)
61
Q

What hormones are used for cancer treatment

A
  • Oestrogens or anti-androgen drugs for prostate cancer
  • tamoxifen to block oestrogen receptors = side effects (induces menopause)
  • glucocorticosteroids (in lymphomas)
62
Q

Type of biologic response modifiers for cancer treatment

A

Interferon

63
Q

Analgesics for cancer treatment

A

opioid analgesics such as morphine (acts on CNS) to assist with symptomatic management (common in palliative)

64
Q

Cancer prognosis

A

“Cure” for cancer is defined by orthodox medicine as a 5 year survival without reoccurrence
Cancer reoccurrence after this period is common

Several periods of remission can occur before cancer becomes terminal

65
Q

Carcinomas =

A

Cancers which form in epithelial tissue lining
Skin, mouth, nose, throat, respiratory tract, lung, breast, prostate, stomach, intestines

66
Q

Sarcomas =

A

Cancers which develop in connective tissue
Bone, cartilage, muscles, tendons

67
Q

Leukaemias

A

Cancers which evolve in blood & bone marrow

Abnormal leukocytes produced travel throughout the bloodstream
Do NOT form solid tumours, but invade other cells

68
Q

Lung cancer risks

A

Peak incidence between 60-70, men 3:1
90% due to smoking
Frequently follows COPD
Most commonly follows secondary tumour eg colorectal, osteosarcoma, prostate

Low prognosis 15%

69
Q

Colorectal cancer risks

A
  • Common >50yrs & developed countries
  • Strong link with diet high in meat -(processed, smoked, excess salt), low fibre, lack of vitamin D
  • Polyps
  • Family history

Secondary complications of liver due to portal vein

70
Q

Benign breast masses vs malignant

A

(90% benign)

Benign = pain/tenderness/mobile/smooth/regular borders

Malignant = asymptomatic, painless, unilateral fixed lump, overlying skin changes i.e dimpling, asymmetry of breasts, inverted & discharging nipple, enlarged lymph nodes

71
Q

Breast cancer hormones roles

A

Breast cancer cells contain receptors that hormones or other proteins bind to & promote tumour growth

  • receptors are most commonly for oestrogen (80% cases oestrogen dominant) as it builds & grows tissue
  • progesterone receptors (65%)
  • epidermal growth factor receptors (20%)
  • tumour with no receptor types ‘triple negative’ more lethal (15%)
72
Q

Breast cancer risk factors

A
  • high oestrogen exposure increases risk i.e endogenous (excess formed within body) or exogenous (from outside eg contraceptive pill)
  • longer reproductive life leading to higher oestrogen exposure
  • BPA mimics oestrogen
  • aluminium & parabens in antiperspirants (both been found in tumours)
  • IGF1 in dairy
  • BRCA 1&2 gene mutations - consider environment that promotes risk (only 5% total cases)
73
Q

How does breast cancer thermography work

A

Safer & more effective to detect earlier changes
Cancer cells divide undergoing angiogenesis aka growing new blood vessels for own blood supply which gives off detectable heat

74
Q

Ovarian cancer risks

A
  • high oestrogen exposure (as in breast cancer risks)
  • family history
  • BRCA 1&2 gene mutations
  • infertility/never birthed
  • poor lifestyle: exercise, obesity, smokers
  • diet rich in animal fats
  • common >40
  • most LETHAL gynaelogical malignancy
  • talcum powder between legs
75
Q

Cervical cancer risks

A
  • persistent HPV infection (16+18 cause 70% cases)
  • sexual behaviour (multiple partners)
  • smoking, COCP
  • most common cancer in young women 25-35
  • 20% of all female cancers
76
Q

What is malignant seeding in ovarian cancer

A

Spreading along peritoneum & can cause secondary cancer in bowel/colorectal

77
Q

Gastric cancer risks

A
  • diet rich in salted, pickled & smoked foods (N-nitroso compounds)
  • male, smoking, age >55
  • H pylori infection
  • low fruit & veg
  • highest rates in eastern asia (korea & japan)
78
Q

Oesophageal cancer risks

A
  • chronic irritation, alcohol, smoking
  • GORD & Barretts oesophagus

(75% be obstructed before syMptoms present)

79
Q

Pancreatic cancer risks

A
  • poorly understood disease
  • most arise from exocrine cells
  • less common endocrine Islet cells (pancreatic neuroendocrine tumour): presents as glucose intolerance & insulin problems
  • age >40, family history (germ line defects in 5-10%)
  • smoking
  • other health condition (diabetes, chronic pancreatitis, H pylori)
80
Q

Prostate cancer risks

A

Obesity
High meat consumption (chargrilled), dairy, saturated fays, refined sugars
Increasing age >50yrs
Sexual abstinence

81
Q

Bladder cancer risks

A
  • Smoking (amines/hydrocarbons = carcinogens pooling in the bladder & inducing mutations)
  • Chronic cystitis
  • increasing age (70-80)

(Painless haematuria = red flag!)

82
Q

Testicular cancer risks

A

Most common in young men 15-35
Higher risk if undescended testes & family history

Biomed2 (9 decks)

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