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Anatomical pathology > NEOPLASIA > Flashcards

NEOPLASIA Flashcards

1
Q

neoplasia

A

NEOPLASIA – means “new growth”.
• TUMOUR – a term previously applied to a swelling caused by inflammation. The nonneoplastic meaning has vanished and TUMOUR=NEOPLASM in current medical
practice.

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2
Q

neoplasm in eras(definitions)

A

NEOPLASMPre-molecular Era:
• An abnormal mass of tissue, the growth of which exceeds and is
uncoordinated with that of normal tissue, and persists in the
same excessive manner after the cessation of the stimulus
which evoked the change.

Modern Era:
• Disorder of cell growth triggered by a series of acquired
mutations affecting a single cell and its clonal progeny

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3
Q

oncology

A
  • Study of tumours or neoplasms.
  • More oriented towards treatment of neoplasia
  • BENIGN NEOPLASMS
  • Gross and microscopic appearance appears ‘innocent’.
  • Remains localised; cannot spread to other sites.
  • Amenable to surgical removal; patient generally survives
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4
Q

malignant neoplasm

A

MALIGNANT NEOPLASMS
 Capable of invasive and destructive growth.
 Can metastasise (i.e. spread to distant sites).

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5
Q

hermatoma

A

Malformation comprising cells which are resident in the organ, but demonstrate
disorganised growth.

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6
Q

dysplasia

A

• Literally means “disordered growth.”
• Encountered principally in epithelia and is characterized by a
constellation of changes that include a loss in the uniformity of the
individual cells as well as a loss in their architectural orientation

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7
Q

differentiation

A

• Degree to which tumour cells histologically resemble the cell or tissue
of origin.
• Well-differentiated tumour cells look more like normal cells; tend to
grow and spread more slowly than poorly differentiated or
undifferentiated tumour cells.
• Differentiation is used in tumour grading systems for malignant
tumours.

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8
Q

anaplasia

A

• Lacking differentiation
• A tumour that defies accurate classification is designated as
anaplastic and such tumours are always malignant.

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9
Q

invasion

A

• The tendency of tumour cells to breach their basement membrane,
spread beyond the layer of tissue in which they developed growing
into surrounding, healthy tissues.
• Also called infiltration.

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10
Q

tumour nomeclature

A

The specific name of an individual tumour invariably ends in the suffix
‘-oma’.
• Relics of this suffix’s former wider usage remain, as in ‘granuloma’
(an inflammatory aggregate of epithelioid macrophages),
‘tuberculoma’ (the caseating lesion of tuberculosis), ‘atheroma’ (lipidrich intimal deposits in arteries), and ‘mycetoma’ (a fungal mass
populating a lung cavity) and ‘haematoma’ (mass of coagulated
blood), these are not neoplasms.

• NB: Tumour previously denoted just any abnormal swelling.

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11
Q

histogenic classification

A

• Histogenesis – the specific cell of origin of an individual tumor, determined
by histological examination and specifies the tumour type. This is
incorporated into the tumor name e.g. squamous cell carcinoma

  1. From epithelial cells
  2. From connective tissue
  3. From lymphoid and hematopoietic organs
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12
Q

epithelial tumours

A

• Named histogenetically according to their specific epithelial type and
behaviourally as benign or malignant.

• Benign epithelial tumours are either:
• papillomas- tumour of non-glandular or non-secretory epithelium such
as transitional epithelium or stratified squamous epithelium.
• adenomas- tumour of glandular or secretory epithelium.

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13
Q

malignant tumour

A

alignant epithelial tumours are always called carcinomas.

• Carcinomas of non-glandular epithelium are always prefixed by the
name of the epithelial cell type e.g. squamous cell carcinoma and
transitional cell carcinoma.

• Malignant tumours of glandular epithelium are always called
“adenocarcinomas’’

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14
Q

RENAL CELL CARCINOMA

A

Typical crosssection of yellowish, spherical neoplasm in one pole of the kidney.

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15
Q

Adenocarcinoma

A

Adeno-Glandular epithelium

carcinoma-Malignant epithelial neoplasm

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16
Q

mesenchymal neoplasm

A 
Benign
Smooth Muscle-Leiomyoma
Skeletal Muscle-Rhabdomyoma 
Fat-Lipoma 
Cartilage-Chondroma 
Blood vessels-Hemangioma
Bone-Osteosarcoma
Malignant
Smooth muscle- Leiomyosarcoma
Fat-Liposarcoma
skeletal  muscle-Rhabdomyosarcoma
cartilage-Chondrosarcoma
blood vessels- Angiosarcoma
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17
Q

HAEMATOLYMPHOID NEOPLASMS

A

benign
N/A

Malignant
Hematopoietic cells- Leukemia
Lymphoid cells - Lymphoma

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18
Q

MIXED TUMOURS (usually derived from 1 germ cell layer)

A

benign
Salivary gland-Pleomorphic adenoma

Malignant
salivary gland- malignant mixed
tumour of salivary gland origin
Renal anlage - Wilms tumour

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19
Q

Germ cell neoplasms

A 
Cell of Origin Benign Malignant
benign
Germ cell- Mature Teratoma Dermoid cyst 
Malignant 
germ cell : 1 malignant Teratoma
2.Teratocarcinoma
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20
Q

Embryonal tumours (blastoma)

A

• Usually in those below 5 years of age, resembles embryonic form of
organ it arises from.

Malignant

Kidney- Nephroblastoma
Liver- Hepatoblastoma
Eye -Retinoblastoma
Adrenal -Neuroblastoma

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21
Q

BEHAVIOURAL CLASSIFICATION

A
  • Benign

* Malignant

22
Q

Benign Neoplasms

A

• Non-invasive and remains localised.
• Slow growth rate.
• Close histological resemblance to parent tissue.
• Clinical Features
• Pressure on adjacent tissue (meningiomas → epilepsy).
• Obstruction of the flow of fluid (duct obstruction).
• Production of hormone (benign thyroid tumour -thyrotoxicosis).
• Transformation into malignant neoplasm (adenomatous polyp to
adenocarcinoma).
• Anxiety (fear that lesion may be something more sinister).

23
Q

Malignant Neoplasms

A
  • Relatively rapid growth rate.
  • Variable histological resemblance to the parent tissue.
  • Poorly circumscribed.
  • Invasive growth.
  • Encroach on & destroy adjacent tissues.
  • Central necrosis (outgrow blood supply).
  • Metastasize
24
Q

DIFFERENCES BETWEEN BENIGN AND MALIGNANT NEOPLASMS

A

Benign
Differentiation/Anaplasia: Well-differentiated (anaplastic)
Rate of Growth: Progressive and slow;May regress; Mitotic figures rare and normal
Local Invasion: Usually circumscribed and encapsulated
Metastasis: Absent

Malignant
differentiation/Anaplasia: Less well differentiated or completely undifferentiated
rate of growth: Erratic, but generally rapid; Mitotic figures may be numerous and abnormal
Local invasion: Poorly circumscribed and locally invasive
Metastasis: Frequent

25
Q

Eponymously named(after people) tumours

A
  • Hodgkin’s lymphoma
  • Burkitt’s lymphoma
  • Kaposi’s sarcoma
  • Ewing’s sarcoma
26
Q

Metastasis

A

Metastasis
• Tumour implants discontinuous with the primary tumour.
• Hallmark of malignancy.
• Almost all malignant tumours can metastasise.
• More likely to metastasise - more aggressive, rapidly growing larger

27
Q

Pathways of Metastasis

A

1.Lymphatic
• Carcinomas
• Lymph nodes become enlarged

2.Haematogenous
• Sarcomas
• Some carcinomas

• Sites include:(Lung,Liver,Bone &Brain)

3.Transcoelomic spread
• Peritoneal, pleural and pericardial cavities are common sites of this
type of metastasis.
• This results in an effusion of fluid into the cavity.
• The fluid is rich in protein and may contain fibrin.
• Fluid also contains neoplastic cells causing the effusion

28
Q

Paraneoplastic effects

A

• Symptom complex in patients with malignant neoplasms which cannot
be explained by local growth or distant spread of the neoplasm or by
elaboration of hormones indigenous to the tissue from which the
tumour arose.
• May represent earliest manifestation of an occult neoplasm.
• May cause significant morbidity / mortality.
• May mimic metastatic disease and confound treatment.

29
Q

Environmental factors of neoplasm

A
  • Established environmental factors affecting cancer risk:
  • Infectious agents – e.g. HPV
  • Smoking – mouth , lung, pharynx , larynx
  • Alcohol consumption – oropharynx, esophagus, hepatocellular ca
  • Diet – variation in diets colorectal ( common in developed world)
  • Obesity -52-62% higher death rates from cancer
  • Reproductive history
  • Environmental carcinogens- UV, smog, arsenic from well water ,asbestos
30
Q

age that is affected by neoplasm

A

ge
• Most carcinomas occur later in life >55 years
• Notable cause of death in individuals less than 15 years
of age in first world countries

31
Q

Acquired predisposing conditions

A
  • Chronic inflammatory conditions – IBD , cholecystitis , cholangitis, hepatitis.
  • Precursor lesions – Barrett’s esophagus ( gastric and colonic metaplasia of esophageal mucosa), endometrial hyperplasia, squamous metaplasia of bronchial mucosa (in response to smoking )
  • Immunodeficiency states – high risk from oncogenic viruses.
32
Q

Epidemiology of neoplasm

A
  • Genetic predisposition.

* Interactions between environmental and inherited factors.

33
Q

Carcinogenesis

A

“Creation of cancer”
• Process by which normal cells are transformed into neoplastic/cancer cells.
• Characterized by a progression of changes on cellular or genetic level.
• Genetic alterations are fundamental to the carcinogenic process.
• Multistep hypothesis: a series / accumulation of mutations leads to neoplastic
transformation

34
Q

carcinogen

A

carcinogen: environmental agent participating in the causation of tumours.
carcinogenic : cancer causing
oncogenic : tumour causing
• Attack the DNA of the cell to produce mutations.

35
Q

classes of carcinogen

A

• Chemicals

  • Microbes:
  • Viruses
  • Bacteria
  • Fungi
  • Parasites
  • Radiation - ionising and non-ionising
  • Miscellaneous -Exogenous hormones
36
Q

CHEMICAL CARCINOGENS

A
  • Most act directly requiring no metabolic conversion.
  • Enzymatic conversion usually in the liver.
  • There are no common structural formulas to predict carcinogenic risk.
37
Q

Microbial Carcinogens

A
  • Bacteria - e.g. Helicobacter pylori
  • Fungi - e.g. Aspergillus flavus
  • Viruses - e.g. Human papillomavirus (HPV)
  • Parasites - e.g. Schistosoma haematobium
38
Q

H pylori

A

• A microscopic image from gastric mucosa. The superficial aspect on the epithelial cells show bacteria in keeping Helicobacter pylori.

  • H. Pylori is implicated in
  • Gastritis
  • chronic peptic ulcer disease .
  • gastric adenocarcinoma
  • gastric lymphoma
39
Q

Fungi

A
  • Toxins produced by fungi = mycotoxins.
  • Aflatoxins produced by Aspergillus flavus.
  • Linked to hepatocellular carcinoma in Africa and China.
  • Aflatoxin and HBV collaborate to produce hepatocellular carcinoma.
40
Q

Bacteria

Helicobacter pylori

A

• Major cause for gastritis and peptic ulceration
• Implicated in gastric lymphomas and adenocarcinomas
• Pathogenesis: multifactorial. chronic inflammation,
reparative gastric cell proliferation.

41
Q

Parasites

A

• Schistosoma haematobium is strongly implicated in bladder cancer.
• Urothelium → squamous metaplasia → squamous cell carcinoma
(SCC).
• Liver flukes Clonorchis sinensis and Opisthorchis viverrini are
implicated in adenocarcinoma of the bile ducts (cholangiocarcinoma).

42
Q

Ionizing radiation

A

UV light – skin cancer.
• Ionising radiation:
• Skin cancer
• Leukaemia
• Mining of radioactive uranium – lung cancer
• Ultraviolet (UV) Light
• Skin cancers more common on parts of body exposed to sunlight
• More common in fair skinned (melanin is protective)
• High risk for basal cell carcinoma and malignant melanoma

  • Increased risk:
  • Albinos
  • Xerodermapigmentosum (XP)
  • XP – congenital deficiency of DNA repair enzymes
43
Q

effect of ionization radiation

A
  • Carcinogenic effects of radiation are long term.
  • More immediate dose-related acute effects:
  • Skin erythema
  • Bone marrow aplasia
  • Tissues sensitive to carcinogenic effects:
  • Thyroid
  • Breast
  • Bone
  • Haematopoietic
44
Q

tumour caused by ultraviolet rays

A

Squamous cell carcinoma Basal cell carcinoma Melanoma

UVB responsible for induction of cutaneous cancers
UVC a potent mutagen

45
Q

Tumour caused by ionising radiation

A

Carcinomas of the breast, colon, thyroid, bone, haematopoietic
and lung Causes chromosome
breakage, translocations and less commonly point mutations

46
Q

Miscellaneous

A

• Hormones:
• Exogenous oestrogen linked to promote formation of mammary and endometrial
carcinomas.
• Weak association between breast carcinoma and oestrogen-containing oral
contraceptives.

  • Asbestos fibres:
  • Mesothelioma
  • Carcinoma of the lung
  • Metals (e.g. nickel):
  • Risk of carcinoma of the mucosa lining the nasal cavities and of the lung
47
Q

Host Factors in Carcinogenesis

A

• Race

• Age:
Incidence of cancer increases with age.

• Gender:
Example: Breast cancer is more common in females; probably due to the greater
mammary epithelial volume and oestrogen-promoting effects.

  • Diet:
  • May contain procarcinogens or carcinogens.
  • May lack protective factors.
  • Low fibre increases intestinal transit time and exposure to carcinogens.

• Inherited predisposition:

  • Four classes of genes are principal targets of cancer causing mutations:
  • Growth promoting proto-oncogenes.
  • Growth inhibiting tumour suppressor genes.
  • Genes regulating programmed cell death (apoptosis).
  • Genes involved in DNA repair.
48
Q

Cellular and Molecular Events in Carcinogenesis

A
  • Multistep theory:
  • Initiation: Genetic defect that gives transformed cell its neoplastic potential.
  • Promotion: Stimulation of clonal proliferation of the initiated transformed cell.
  • Progression: Process culminating in malignant behaviour.

• Genetic mechanisms in carcinogenesis:
• Expression of telomerase to avoid replication senescence.
• Loss or inactivation of recessive tumour suppressor gene function.
• Enhanced or abnormal expression of dominant oncogenes to self-stimulate
cellular replication.

49
Q

Grading and Staging of Tumours

A

Grading
• Determined by cytologic appearance.
• Based on the idea that behaviour and differentiation are related
such that poorly differentiated tumours have more aggressive
behaviour.

Staging
• Determined by surgical exploration or imaging.
• Based on size, local and regional lymph node spread, and distant
metastases.
• Of greater clinical value than grading. e.g. TNM

50
Q

Laboratory Diagnosis of Cancers

A

• Cytologic Methods

o Fine Needle Aspiration (FNA)
o Cytologic Smears

  • Histopathology
  • Immunohistochemistry
  • Flow Cytometry
  • Circulating Tumour Cells
  • Molecular and Cytogenetic Diagnostics
  • Tumour Markers
51
Q

Tumor Markers

A

Biochemical assays for tumour-associated enzymes, hormones, and other tumour markers in the
blood.
Cannot be used for definitive diagnosis of cancer; however, they contribute to the detection of
cancer.
In some instances, are useful in determining the effectiveness of therapy or a recurrence.

Classes of tumour markers include:
• Hormones
• Oncofetal antigens
• Isoenzymes 
• Specific proteins

HORMONES
Human chorionic gonadotropin -Trophoblastic tumors, nonseminomatous testicular tumors
Calcitonin- Medullary carcinoma of thyroid
Catecholamine and metabolites -Pheochromocytoma and related tumors

ONCOFETAL ANTIGENS
α-Fetoprotein- Liver cell cancer, nonseminomatous germ cell tumors of testis
Carcinoembryonic antigen- Carcinomas of the colon, pancreas, lung, stomach, and heart

ISOENZYMES
Prostatic acid phosphatase- Prostate cancer
Neuron-specific enolase -Small-cell cancer of lung, neuroblastoma

SPECIFIC PROTEINS
Immunoglobulins -Multiple myeloma
Prostate-specific antigen and prostate-specific membrane antigen - Prostate cancer

MUCINS AND OTHER GLYCOPRETEINS
CA-125 - Ovarian cancer
CA-19-9 -Colon cancer, pancreatic cancer
CA-15-3 -Breast cancer

Anatomical pathology (13 decks)

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