Oncology Patho Flashcards

1
Q

Cancer the number 1 cause of death in SG. True or false?

A

True.

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2
Q

What are the top 5 leading cancers for both genders in SG?

A

Female:
1. Breast
2. Colo-rectum
3. Corpus uteri
4. Lung
5. Ovary

Male:
1. Colo-rectum
2. Lung
3. Prostate
4. Lymphoid neoplasms
5. Liver

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3
Q

What is the most common cancer in males?

A

Prostate cancer

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4
Q

What is the most common cancer in females?

A

Breast cancer

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5
Q

What is a tumour?

A

Abnormal mass of tissue
The growth is autonomous, exceeds that of normal tissue and persists after cessation of the stimuli that initiated it.

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6
Q

What are the 2 types of tumours?

A

Benign & malignant

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7
Q

Histology of benign tumour vs malignant tumour:

A

Benign: typical of tissue of origin, few mitoses

Malignant: anaplastic, with abnormal cell size and shape, many mitoses

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8
Q

Growth rate of benign tumour vs malignant tumour:

A

Benign: slow
Malignant: fast

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9
Q

Localization of benign tumour vs malignant tumour:

A

Benign: strictly local, often encapsulated/no metastasis

Malignant: infiltrative/frequent metastasis

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10
Q

Recurrence after treatment of benign tumour vs malignant tumour:

A

Benign: Rare
Malignant: Common

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11
Q

Local invasion of benign tumour vs malignant tumour:

A

Benign: cohesive growth, capsule & basement membrane not touched

Malignant: poorly cohesive and infiltrative, capsule & basement membrane breached

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12
Q

Tumour necrosis of benign tumour vs malignant tumour:

A

Benign: Rare
Malignant: Common

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13
Q

Prognosis of benign tumour vs malignant tumour:

A

Benign: good, unless in critical area
Malignant: poor if untreated

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14
Q

What are the 4 phases of tumour development & growth?

A
  1. Transformation
  2. Growth of transformed cells
  3. Invasion of tumour cells into the surrounding tissues
  4. Metastasis of tumour cells to distant sites
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15
Q

What occurs in phase 1 (transformation) of tumour development for benign & malignant tumours?

A

Benign: mostly well differentiated, resemble the cell from which they originated

Malignant: transformation - ANAPLASIA!!
- nuclear and cellular pleoporphism (size & shape changes)
- abnormal nuclear morphology (hyperchromasia, high nuclear cytoplasmic ratio, chromatin clumping, prominent nucleoli)
- loss of polarity
- abundant mitoses

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16
Q

What is hypoplasia?

A

Fewer cells than what is deemed a normal amount (usually BENIGN) - underdevelopment of tissue

Shrinking of cells

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17
Q

What is hyperplasia?

A

Increased cell number, under control of normal proliferation regulatory mechanism

A result of external stimuli (trauma, pressure etc.)

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18
Q

What is neoplasia?

A

Similar to hyperplasia but denotes abnormal multiplication due to loss of normal proliferation regulation and absence of stimuli

AKA cells manifesting hyperplasia with atypia

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19
Q

What is dysplasia?

A

A change in the normal shape, size and organisation , usually a response to chronic irritation (eg. cigarette smoke or inflammation) within a tissue

NOT YET MALIGNANT: Changes are reversible if stimulus is removed, otherwise cells with become metaplastic

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20
Q

What is metaplasia?

A

A reversible change of one cell type to another. (NOT YET MALIGNANT)

eg. ciliated columnar epithelium of the respiratory surface becoming stratified squamous epithelium after prolonged irritation from smoking

Changes are reversible if the stimulus is removed, otherwise the cells become anaplastic

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21
Q

What is anaplasia?

A

A reversal in differentiation (dedifferentiation) OR loss of structural & functional differentiation of normal cells.

Not reversible, high grade malignant tumour, very poor prognosis

A characteristic of cancerous tumours (MALIGNANT)

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22
Q

What occurs in phase 2 (rate of growth) of tumour development?

A

Grading of the tumour by how differentiated the cells are.

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23
Q

What are the levels of differentiation?

A
  • Well differentiated neoplasm
  • Poorly differentiated neoplasm
  • Undifferentiated or “anaplastic” tumour
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24
Q

What will well differentiated neoplasm look like?

A

It will resemble mature cells of the tissue of origin.

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25
Q

What will poorly differentiated neoplasm look like?

A

Composed of primitive cells with little differentiation

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26
Q

What occurs in phase 3 (local invasion) of tumour development of benign tumours?

A

Benign: cohesive cells, have a rim of condensed connective tissue - capsule

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27
Q

What occurs in phase 3 (local invasion) of tumour development of malignant tumours

A

Malignant: invade locally
- detachment “loosening up” of the tumour cells from each other
- attachment to matrix components
- degradation of matrix components (eg. using collegenase)
- migration of tumour cells

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28
Q

What occurs in phase 4 (metastasis) of tumour development?

A

Unequivocal sign of malignancy
- Lymphatic
- Hematogenous
- Seeding of body cavities

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29
Q

What is the significance of nodal metastasis?

A

Prognostic is an important component of TNM staging system

T: Tumour
N: Nodes
M: Metastasis

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30
Q

T1N0M0 vs T4N1M1, what do these mean and which has a better prognosis?

A

T1 - small
T4 - large

N0 - no spread to regional lymph nodes
N1 - spread to regional lymph nodes

M0 - no metastasis
M1 - metastasised to other organs

T1N0M0 - stage I
T4N1M1 - stage IV

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31
Q

What are the steps of metastasis?

A
  1. Intravasation
    - tumour cells pass through basement membrane, penetrate a nearby artery/blood vessel
  2. Embolization
    - tumour cells get attached to e.g. a platelet, forms an embolus
  3. Adhesion
    - more platelets will gather and stick to the existing platelet embolus, this is called adhesion
  4. Extravasation
    - adhere to a cell wall and exit
  5. Metastatic Growth
    - tumour cells could go to another organ
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32
Q

What are the nomenclature for neoplasms (benign & malignant)?

A

Benign:
-oma (eg. lipoma, fibroma, osteoma etc.)

Malignant:
- carcinoma - epithelial cells (eg. squamous cell carcinoma, adenocarcinoma)
- sarcoma - mesenchymal cells (eg. liposarcoma, fibrosarcoma, osteosarcoma etc.)

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33
Q

What are the predisposing factors for cancer?

A
  • Age
  • Body Mass (obesity increases cancer risk by 50%)
  • Chronic inflammation
  • Precancerous conditions
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34
Q

What are common childhood cancers?

A
  • Leukemias & CNS neoplasms
  • Wilms tumour
  • Retinoblastoma
  • Bone and skeletal muscle tumours
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35
Q

Why are elderly predisposed to cancer?

A

Older persons have a greater propensity to develop neoplasms from lack of effective control mechanisms.

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36
Q

What are some precancerous conditions that predispose people to cancer?

A
  • Chronic ulcerative colitis
  • Atrophic gastritis of pernicious anemia
  • Leukoplakia of mucous membranes
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37
Q

What is the etiology of cancer?

A

90-95% Environmental factors
5-10% Genetic factors

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38
Q

What are the environmental factors that can lead to cancer?

A
  1. Chemicals
  2. UV light/ionizing radiation
  3. Viral infections
  4. Smoking and alcohol abuse
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39
Q

What are the genetic factors that can lead to cancer?

A

Familial cancer syndromes
- Early age at onset
- Multiple or bilateral tumours
- Two or more primary relative with the cancer

40
Q

What are some chemical carcinogens?

A

2-Naphthylamine (dyes, antioxidant)

Benzo[a]pyrene (coal tar, rooding, cigarette smoke)

Aflatoxin B (mycotoxin found in contaminated food)

Asbestos (thermal insulation, gaskets)

Vinyl chloride (plastics - PVC, co-polymers)

41
Q

What cancers can UV radiation cause?

A

Basal cell carcinoma (BCC), squamous cell carcinoma, malignant melanoma

42
Q

What cancers can ionizing radiation cause?

A

Hematopoetic and thyroid tumours in fallout victims

Basal cell carcinoma (BCC)s in therapeutic radiation

43
Q

What are the viral carcinogens and which cancers do they cause?

A

HPV -> squamous cell carcinoma (cervix)

EBV -> Burkitt lymphoma, nasopharyngeal carcinoma

HBV -> hepatocellular carcinoma

HTLV1 -> T cell malignancies

KSHV -> Kaposi sarcoma

44
Q

What are the 4 kinds of regulatory genes targeted in carcinogenesis?

A

Proto-oncogenes
Tumour suppressor genes
Genes that regulate apoptosis
Genes involved in DNA repair

45
Q

What are proto-oncogenes?

A

Normal genes whose proteins promote cell proliferation

Mutation leads to “gain-of-function”, proto-oncogene –> oncogene (leads to uncontrolled cell proliferation)

Normally “switched on” only for short periods in the cell cycle

46
Q

What are oncogenes?

A

Mutated proto-oncogenes (damaged by carcinogens)

  • Dominant genes
  • Function autonomously, causing unregulated growth
47
Q

State some examples of proto-oncogenes. (not tested)

A

RAS genes (rat sarcoma)
- most commonly mutated proto-oncogene (in 30% of all tumours)

MYC gene (myelocutomatosis)
- on chromosome 8
- implicated in Burkitt’s lymphoma

ABL gene (Abelson leukemia)
- on chromosome 9
- increases tyrose kinase activity (increases blood cell division)
- Philadelphia chromosome is formed when the ABL gene is translocated to chromosome 22

48
Q

What do tumour suppressor genes do?

A

Inhibit cellular proliferation, stimulate apoptosis

Promote DNA repair

Mutation leads to “loss-of-function” –> cannot stop abnormal cell growth

49
Q

State some examples of tumour suppressor genes.

A

RB gene
BRCA1, BRCA2 genes*
p53 gene

*BRCA1 and 2 screening (blood or oral cavity): when there is strong family history

If BRCA1 and 2 abnormal: indicates potential presence of cancer

50
Q

What is the RB gene?

A
  • First tumour suppresor gene to be discovered
  • Associated with retinoblastoma
  • Located on chromosome 13
  • Inactivated in HPV infections
  • Implicated in almost all cancers
51
Q

What is the p53 gene?

A
  • located at chromosome 17
  • activated when cell is stressed or injured
  • prevents cell div, repairs DNA, triggers apoptosis if DNA is irreparable

tumour suppression decreases when p53 is damanged

> 70% of cancers have mutated p53 (all CA breast, lung, colon)

51
Q

What are the BRCA1, BRCA2 genes?

A

BRCA1 located at chromosome 17, BRCA2 located at chromosome 13

  • Repair damaged DNA, destroy unrepairable cells
  • Implicated in 5-10% of CA breast, 50% of women with mutated genes will develop breast CA
  • Also increases risk of CA colon & CA prostate
52
Q

Describe what each staging in TNM means.

A

Tis - In situ, non-invasive
T1 - small, minimally invasive within primary organ site
T2 - larger, more invasive within primary organ site
T3 - larger and/or invasive beyond margins of primary organ site
T4 - very large and/or very invasive, spread to adjacent organs

N0 - no lymph node involvement
N1 - nearby lymph node involvement
N2 - regional lymph node involvement
N3 - more distant lymph node involvement

M0 - no metastasis
M1 - distant metastasis present

53
Q

Describe the grades of malignant neoplasms.

A

Grade I - well differentiated
Grade II - moderately differentiated
Grade III - poorly differentiated
Grade IV - nearly anaplastic

54
Q

What are the diagnostic methods for neoplasia?

A

History and physical exam
Radiography techniques
Laboratory analyses
Genetic testing
Cytology
Tissue biopsy & surgery
Autopsy

55
Q

What are the effects of tumours on the host?

A
  • Location -> ANATOMIC ENCROACHMENT
  • hormone production
  • bleeding, infection
  • acute symptoms (eg. rupture, infarction)
  • CACHEXIA
  • PARA-neoplastic syndromes
56
Q

What is cachexia?

A

Fat loss + Muscle loss
- TNF a (alpha)
- IL-1
- PIL (proteolysis inducing factor)

57
Q

What are para-neoplastic syndomes?

A

Not directly related to the spread of tumour or elaboration of hormones indigenous to the tissue of origin

Mediated by humoral factors (hormones or cytokines) excreted by tumor cells or by an immune response against the tumor

58
Q

What are some examples of para-neoplastic syndromes?

A

Skin:
- acanthosis nigricans (gastric/lung cancers)

Bone/joint/soft tissue:
- clubbing (lung cancer)

Vascular:
- trousseau (migratory thrombophlebitis) (pancreatic cancer)

Cushing syndrome/SIADH: (small cell CA lung)

59
Q

Definition of benign tumours

A

Non-cancerous growths that do not
invade nearby tissues or spread to other
parts of the body

60
Q

Definition of malignant tumours

A

Cancerous growths that invade
surrounding tissues and can metastasize
(spread) to distant sites

61
Q

Benign vs Malignant tumour

A

Benign:
- non cancerous, do not metastasise
- slow growing
- localised and encapsulated
- cells are well-differentiated, resemble normal cells
- may cause symptoms due to pressure on nearby structures, but asymptomatic
- management involves observation, surgical removal and regular monitoring (asymptomatic)

Malignant:
- cancerous, metastasise
- fast growing
- infiltrates surrounding tissues
- cells are poorly differentiated, often vary in shape and size
- can cause various symptoms depending on location and extent of spread
- management includes surgery, chemotherapy, radiation therapy, targeted therapy

62
Q

Examples of benign tumours

A

Lipoma (fat tissue)
Fibroma (connective tissue)
Adenoma (glandular tissue)
Hemangioma (blood vessels)
Neuroma (nerve tissue)
Chondroma (cartilage)
Osteoma (bone)
Meningioma (meninges)
Cysts
Myoma (muscle tissue)

63
Q

Examples of malignant tumours

A

Carcinoma (breast, lung, prostate)
Sarcoma (e.g. osteosarcoma, liposarcoma)
Melanoma (skin cancer)
Leukemia (blood cancer)

64
Q

What causes cancer?

A
  1. Environmental factors (90%)
    - exposure to chemicals, smokes, pollutants, viruses
  2. Genetic factors (10%)
    - e.g. colon cancer
65
Q

Process of tumour development and growth

A
  1. Transformation (cellular)
  2. Growth of transformed cells
  3. Invasion of tumour cells into surrounding tissues
  4. Metastasis of tumour cells to distant sites
66
Q

Process of tumour development - Growth of transformed cells

A

Differentiation refers to how closely tumor cells resemble the normal, mature cells of the tissue they originate from.

The less differentiated a neoplasm, the faster it grows.

Growth is also dependent upon the ability of the tumour to develop a blood supply.

67
Q

Process of tumour development - Invasion of tumour cells into surrounding tissues

A

Benign tumours: have a rim of condensed connective tissue (capsule) –> do not invade

Malignant tumours: invade locally
Process: DADM
1. Detachment (“loosening up”) of tumour cells from each other

  1. Attachment to matrix components (attach to basement membrane –> infiltrate)
  2. Degradation of matrix components e.g. using collagenase
  3. Migration of tumour cells
68
Q

Process of tumour development - Metastasis of tumour cells to distant sites

A

Medium of transport of tumour cells:
- lymphatic system (slower transport)
- blood
- seeding of body cavities (stomach cancer cells proliferate through stomach wall into peritoneum –> peritoneum fluid –> duodenum, etc.)

69
Q

Cancer is often the result of activation of ______ and the inactivation of _______ genes.

A

Activation of the oncogenes.

Inactivation of the proto-oncogenes.

70
Q

BRCA1, a human tumour suppressor gene is associated with _______

A. leukemia
B. neurofibroma
C. breast carcinoma
D. thyroid carcinoma

A

C. Breast cancer

Can also be ovarian cancer or prostate cancer.

71
Q

Which one of the following tumours would MOST commonly be treated with intraperitoneal chemotherapy?

A. Lung Cancer
B. Breast Cancer
C. Bladder Cancer
D. Ovarian Cancer

A

Ans: D Ovarian cancer

Ovarian cancer often metastasizes within the peritoneal cavity, making IP chemotherapy an effective method to deliver high concentrations of chemotherapy directly to the tumor-affected areas while minimizing systemic toxicity.

What are the organs in the peritoneum:
Stomach, small intestine, large intestine, liver, gall bladder, spleen

72
Q

The term ‘sarcoma’ denotes malignancy arising from:

A. blood vessels.
B. fibrous tissue.
C. adipose tissue.
D. gland epithelium.

A

B. Fibrous tissues

Epithelium: adenoma

73
Q

The goal of oncology treatment is to _______.

A. establish histological analysis for diagnosis
B. allow staging of the disease
C. considerably prolong life with best possible quality
D. prevent the formation of cancers

A

C

74
Q

Surgical decision of cancer treatment depends on ________.

A. anatomical location
B. pain and anxiety
C. physiological delayed wound healing
D. follow up treatments

A

A

75
Q

(Canvas onco quiz) Q1

Mr David, a 71-year-old man presented with Acute Myeloid Leukemia to the clinic. His Blood investigations revealed pancytopenia. Which one of the following is NOT CORRECT about the presenting complaints of the patient due to pancytopenia?

A. Bone pain over the sternum & hips
B. Intracranial haemorrhage
C. Bruises over skin
D. Repeated infections

A

A

76
Q

(Canvas onco quiz) Q2

Mr David, a 71-year-old man presented with Acute Myeloid Leukemia to the clinic. His Blood investigations revealed pancytopenia.What is the pathological basis of pancytopenia in the patient?

A. The abnormal blast cells infiltrate the bone marrow, preventing proliferation of normal cells.
B. Splenomegaly prevents the process of hemopoesis.
C. The blast cells destroy the normal blood cells in the peripheral blood stream
D. The liver stops producing the hemopoetic cells.

A

A

77
Q

(Canvas onco quiz) Q3

Mr David, a 71-year-old man presented with Acute Myeloid Leukemia to the clinic. His Blood investigations revealed pancytopenia. Which of the following signs/symptoms is not expected in the patient?

A. Chest pain
B. Pyrexia of unknown origin
C. Unexplained loss of weight
D. Cachexia

A

A

78
Q

(Canvas onco quiz) Q4

Which one of the following factors mentioned below is also considered one of the important predisposing factors for carcinogenesis?

A. retrovirus
B. bacteria
C. spores
D. All of the above

A

A

79
Q

(Canvas onco quiz) Q5

Which one of the following terms should be at highest risk of the malignant transformation of cells leading to Breast cancer?

A. Anaplasia
B. metaplasia
C. dysplasia
D. hyperplasia

A

A.

80
Q

(Canvas onco quiz) Q6

One of the modes of malignant metastasis is lymphatic spread. What is the significance of knowing the nodal metastasis under the TNM classification?

A. Patient prognosis.
B. Type of chemotherapy.
C. Duration of malignant growth.
D. Origin of tumour.

A

A.

81
Q

(Canvas onco quiz) Q7

Which one of the following malignant tumour has a mesenchymal origin?

A. acute myeloid leukemia
B. breast carcinoma
C. Squamous cell carcinoma
D. renal cell carcinoma

A

A

82
Q

(Canvas onco quiz) Q8

A sales representative is trying to promote a moisturising cream to you at a local pharmacy. According to her, the cream has properties which will prevent the ultraviolet (UV) rays’ penetration & prevent cancer. What type of cancer is the lady referring to?

A. Malignant melanoma.
B. rhabdomyoma
C. leiomyoma
D. liposarcoma

A

A.

83
Q

(Canvas onco quiz) Q9

A patient , aged 41, visits the gynaecology clinic. After examining her, the physician suspects cervical cancer. The nurse reviews the client’s history for risk factors for this disease. Which history finding is a risk factor for cervical cancer?

A. Infection with Human Papilloma virus at age 32
B. Pregnancy complicated with eclampsia at age 27
C. Onset of sporadic sexual activity at age 17
D. Spontaneous abortion at age 19

A

A.

84
Q

(Canvas onco quiz) Q10

Mary is 25-year-old. Her 2 older sisters were both diagnosed with breast cancer when they were 35-year-old. She should:

A. Consult an oncology-geneticist to consider BRCA gene testing
B. Consult a doctor and start receiving 2-yearly mammogram within the next 5 years
C. Receive 2-yearly breast MRI screening
D. Undergo prophylactic mastectomy to reduce her risk of getting breast cancer

A

A

85
Q

Breast cancer - Non-modifiable risk factors

A
  1. Gender: Women are much more likely
  2. Age: Risk increases with age, especially after age 50.
  3. Genetic Mutations: Inherited mutations in genes like BRCA1 and BRCA2 significantly increase breast cancer risk.
  4. Family History: Having close relatives with breast cancer increases risk, especially if they had it at a younger age.
  5. Personal History of Breast Cancer: A prior diagnosis increases the likelihood of developing it again, either in the same or the other breast.
  6. Race and Ethnicity: Caucasian women have a slightly higher risk than African American women
  7. Dense Breast Tissue: Women with denser breast tissue have a higher risk of breast cancer and may find it
    harder to detect on mammograms.
  8. Early Menstruation and Late Menopause: Starting menstruation before age 12 or entering menopause after age 55 slightly increases risk due to prolonged estrogen exposure.
  9. Previous Radiation Therapy: Exposure to radiation therapy in the chest area (often for other cancers) before age 30 increases risk.
86
Q

Breast cancer - Modifiable risk factors

A
  1. Alcohol
  2. Obesity and being overweight (especially after menopause)
  3. Physical inactivity
  4. Hormone Replacement Therapy (HRT): Use of combined estrogen and progesterone therapy after
    menopause increases risk.
  5. Reproductive Factors:
    * Not Having Children or Having Children Later in Life: Women who have no children or have their first child after age 30 may have a slightly increased risk.
  • Not Breastfeeding: Breastfeeding, especially for over a year, has been shown to reduce risk slightly, likely due to reduced lifetime exposure to estrogen.
  1. Use of Oral Contraceptives
  2. Diet and Lifestyle: Diets high in fat and low in fruits and vegetables may increase risk
87
Q

7 warning signs of cancer

A

“CAUTION”

C: Change in bowel or bladder habits
A: A sore that does not heal
U: Unusual bleeding or discharge
T: Thickening or lump in breast or elsewhere
I: Indigestion or difficulty swallowing
O: Obvious change in wart or mole
N: Nagging cough or hoarseness

88
Q

General presentation of cancer patients

A
  • Asthenia or Cancer-Related Fatigue (CRF)
  • Profound tiredness after usual or minimal effort
  • Anticipatory sensation of generalized weakness

3 mechanisms of CRF
* Direct tumor effects
* Tumor-induced by-products
* Accompanying factors e.g. anemia & chronic infection

89
Q

Specific presentation of breast cancer patients

A
  1. Breast lump or thickening: a palpable lump or thickening in breast or underarm area
  2. Change in breast shape or size
  3. Skin changes on breast: Dimpling or puckering like orange peel
  4. Redness or scaly skin
  5. Nipple changes: Nipple retraction or inversion
  6. Nipple discharge: Especially if bloody or occurs in only one breast
  7. Breast pain: If tumour is close to nerves
  8. Swollen lymph nodes
90
Q

Types of radiotherapy used for breast cancer

A
  1. External beam radiotherapy
  2. Bradytherapy (Internal radiation)
  3. Intraoperative radiotherapy (IORT)
91
Q

Oncology emergency in breast cancer - Structural obstruction (caused by space occupying tumour)

A
  • Superior vena cava syndrome
  • Pericardial tamponade
  • Spinal cord compression
  • Increased intracranial pressure
  • Urinary obstruction
  • Haemoptysis
  • Airway obstruction
92
Q

Oncology emergency in breast cancer - Metabolic or hormonal

A
  • Hypercalcemia
  • Inappropriate secretion of ADH (SIADH)
93
Q

Oncology emergency in breast cancer - Complications from treatment

A
  • Tumour lysis syndrome
  • Anaphylactic reaction to chemotherapy drug
  • Hemorrhagic cystitis
94
Q
A