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PATH2220 > W11 > Flashcards

W11 Flashcards

1
Q

what is a neoplasm

A

A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues, and persists in the same excessive manner after apparent cessation of the stimuli which evoked the change.

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2
Q

what is hyperplasia

A

A potentially reversible increase in the mass of an organ or tissue due to an increase in the number of its component cells

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3
Q

what is hypertrophy

A

a potentially reversible increase in the size of an organ or tissue due to an increase in the size of its component cells. a physiological or pathological response to increased functional demand

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4
Q

explain the biology of cancer growth

A
  • First localised: pre-cancerous & pre-invasive (dysplasia/carcinoma in situ ) - may be asymptomatic
  • Penetrate the basement membranes/ capsules
  • Movement through extracellular matrix
  • Penetration of vascular channels
  • Survival/arrest in the circulation
  • Exit to new tissue sites
  • Survival and growth as metastasis evoking angiogenesis: growth factors are secreted- FGF, VEGF, TGF, PDGF
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5
Q

how can you classify a tumour

A
  • Behavioural
  • Histogenetic
  • Descriptive
  • Site of origin
  • Embryological • Aetiological
  • Molecular - emerging
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6
Q

what is mean if a tumour is benign

A

remain localised

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7
Q

what is mean if a tumour is malignant

A

not localised, spread to distant sites/invasion (primary or secondary (metastatic))

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8
Q

what is the different behavioural classifications

A

benign, malignant or intermediate

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9
Q

what is a carcinoma cancer

A

malignant epithelial

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10
Q

what is a mesenchymal cancer

A

sarcoma

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11
Q

what are the two different sites of origin for a cancer

A

primary and secondary

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12
Q

tissue type + oma

A

benign

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13
Q

cell/tissue + carcinoma

A

malignant

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14
Q

cell/tissue type + sarcoma

A

malignant

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15
Q

what is an adenoma

A

a benign epithelial neoplasm that forms glands or which derives from glandular tissue

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16
Q

what is an adenocarcinoma

A

a malignant counterpart of an adenoma

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17
Q

what is a polyp

A

any growth or mass protruding from a mucous surface

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18
Q

what are the different aetiologies of neoplasms

A 
Genetic:
• Chemical: polycyclic aromatics hydrocarbons, afla toxins
• Hormonal:
• Irradiation: ultraviolet, asbestos
• Mycrobial organisms:
• Chronic diseases: chronic ulcers
• Immune system disorders:
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19
Q

what are examples of the following: autsomal dominant inherited cancer syndromes

A

childhood retinoblastoma, Familial adenomatous polyposis (FAP)

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20
Q

what are examples of the following:Defective DNA repair syndromes and resulting DNA instability–

A

HNPCC, xeroderma pigmentosa

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21
Q

what are examples of the following: Familial cancers

A

colon, breast, ovary..

Complex interaction between genetic and non-genetic factors

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22
Q

what cancer is common in japan

A

gastric cancer

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23
Q

what cancer is common in australia and NZ

A

skin cancer

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24
Q

what cancer is common in australia and US

A

mesothelioma

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25
Q

what cancer is common in US

A

lung cancer

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26
Q

what chemical toxins can cause cancer

A

polycyclic hydrocarbons, aromatic amines, azo dyes, afla toxins

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27
Q

what cancers are caused by UV radiation

A

Squamous and basal cell carcinoma melanoma

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28
Q

what are some oncogenic DNA viruses

A

HepB – liver cancer

EBV – Burkitt’s lymphoma, nasopharyngeal carcinoma HPV – SCC of cervix, anogenital, some oral-laryngeal

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29
Q

what are some oncogenic RNA viruses

A

Human T cell leukaemia virus type 1

30
Q

what does helicobacter pylori cause

A

Gastric carcinoma and lymphoma

31
Q

what does a multiparous cervix look like

A

slit like

32
Q

what does does a nulliparous cervix look like

A

small and circular os

33
Q

what is the ectocervix lined with

A

non-

keratinising squamous epithelium

34
Q

what is the endocervix lined with

A

mucinous columnar epithelium

35
Q

what is the squamo-columbar junction

A

the point at which the squamous and columnar epithelium meet

36
Q

does and if so the squamo-columnar

junction change

A

yes under hormonal influences

37
Q

what is the transformation zone

A 
 The portion of columnar epithelium that is

ultimately replaced by squamous

epithelium is termed
the “transformation
zone”
This is where precancerous lesions and

squamous carcinomas develop
38
Q

what is the leading cause of cervical caner

A

HPV, accounts for more than 99% of cervical cancers

39
Q

what is HPV

A

 sexually transmitted infection

 extremely common – 80% women infected at some time

 peak prevalence in 20’s - commencement of sexual

activity
 subsequent decrease due to acquisition of immunity and transition to monogamous relationship

40
Q

where does HPV infect

A 
Infects basal cells present at the TZ

Requires damage to surface squamous

cells to give access to immature basal

cells
Most infections transient, asymptomatic

and eliminated by host immune response Persistent infection increases the risk of

precancerous lesions and subsequent
carcinoma
41
Q

what is the risk factors for HPV

A

HPV exposure – Age at first intercourse, multiple sexual partners

 Impaired immune response –
Immunosuppressive drugs, HIV infection
 Other co-factors - smoking, coexisting infections (HSV, Chlamydia), long term use

OCP, high parity, poor nutrition. Lack of regular pap smears

DES exposure (synthetic form of

oestrogen given to pregnant women in
1940-50’s to prevent miscarriage, affects
daughters exposed in utero)

42
Q

what is the most important HR types of HPV

A

16 and 18

43
Q

what types of HPV cause genital warts

A

HPV 6 and 11

44
Q

what is the clinical presentation of cervical cancer

A 
Most asymptomatic
 Abnormal pap smear
 Abnormal bleeding or vaginal discharge
Post-coital, intermenstrual, post menopausal

 Pain
 Late symptoms – bladder symptoms (pressure, direct extension), weight loss, metastases

45
Q

what are the macroscopic findings of cervical cancer

A 
Early lesions visible only on colposcopy

 Focal ulceration, elevated granular area that
bleeds on touch
 Advanced lesions can be either
Endophytic – ulcerated
Exophytic – polypoid tumour mass
46
Q

what are the cervical cancer subtypes

A 
Squamous cell carcinoma (80%)

 Precursor – High grade squamous
intraepithelial lesion (HSIL) or cervical
intraepithelial neoplasia (CIN)

Adenocarcinoma (15%)

 Precursor – Adenocarcinoma in situ
47
Q

what are uncommon cervical tumours

A 
Adenosquamous carcinoma

Direct invasion – endometrium, rectum,

bladder
Metastasis – breast,
ovary
48
Q

what is the histology of squamous cell carcinoma

A 
Malignant squamous epithelium invading

through basement membrane into stroma

graded as well, moderate, or poorly

differentiated
49
Q

what is the histology of adenocarcinoma

A

Proliferation of malignant cells showing

glandular differentiation

Usually moderately or well differentiated

 Multiple variants – eg clear cell with DES

50
Q

explain the spread of invasive carcinoma

A 
Advanced tumours extends by direct

spread to involve contiguous tissues

including bladder, ureters, rectum, and

vagina
Local pelvic and distant lymph nodes

Distant metastases - liver, lungs, bone marrow etc
51
Q

how do most patients with cervical cancer die

A 
Most patients with advanced cervical

cancer die due to local extension of the

tumor (eg into bladder and ureters, leading

to ureteric obstruction, pyelonephritis, and

uremia) rather than distant metastases
52
Q

what is the treatment of cervical cancer

A 
Depends on clinical stage

Early invasive carcinomas can be treated

with cone biopsy only

Most invasive lesions treated with
hysterectomy and lymph node dissection
Advanced lesions treated with surgery ±
adjunct radiotherapy and chemotherapy
53
Q

explain Low grade squamous intraepithelial
lesion



A 
HPV effect
Genital warts
lesion
(LSIL)
 Usually associated with HPV 6 and 11
 Low oncogenic potential 
CIN 1
60% of lesions regress spontaneously

30% persist
10% progress to HSIL

 LSIL does not progress directly to invasive

carcinoma
Treated by increased screening frequency
(1 yearly repeat pap, colposcopy if

persistent)

54
Q

discuss High grade squamous intraepithelial lesions

A 
 Usually associated with HPV 16 and 18

Significant malignant potential

 30% regress
 60% persist
 10% progress to carcinoma (months or many
years)
55
Q

how can you identify and treat precursor lesions

A 
Pap smear
 Identifies abnormality and grade

 Colposcopy
 Identifies exact site and extent of lesion
Cervical punch biopsy
 Exact histological diagnosis

LLETZ/Cone biopsy
 Surgically removes abnormal area
56
Q

what is a pap smear test

A 
Cells from transformation zone obtained

via spatula or brush
Smeared onto slide and stained using
Papanicolaou method
Liquid based medium
Screened by scientist
57
Q

what is HPV DNA testing

A 
Used as an adjunct to cytology on liquid

based preparations
Equivocal cytology
 Testing for women with a high grade
abnormality to ensure virus cleared (test of
cure)
58
Q

explain HPV vaccine

A 
Became available in
2006
Available in Australia

 Gardasil – quadrivalent (HPV 6,11,16,18)

 Cervarix – bivalent (HPV 16,18)

HPV 6/11 – account in Australia
for 90% genital warts
HPV 16/18 – 80% cervical cancer
Given to 12-13 girls/boys (school based programme). Vaccine prepared from non-infectious

virus-like particles
Induces serum antibodies to HPV

 Protection from infection for up to 5 years
after vaccination; longer follow-up studies
pending
59
Q

what is the clinical presentation of Suspicious symptoms and signs for bowel cancer

A

Blood in stool
• Change in bowel habit • Abdominaldiscomfort • Tiredness
• Weightloss

60
Q

what is the clinical presentation of Suspicious symptoms and signs for bowel cancer in the rectum

A

Brightredbloodinstool
• Tenesmus
• Stool appearing narrower than usual
• Rectal pain

61
Q

what is the clinical presentation for emergency presentation of bowel cancer

A
  • Intestinalobstruction
  • Acutegastrointestinal bleed
  • Perforationand peritonitis
62
Q

what is the gross classifications of bowel cancer

A
  1. endoluminal, 2. endophytic/ulcertaive 3. annular/ circumferential and 4. diffusely infiltrative
63
Q

what is the microscopic appearance of colon cancer

A 
• Infiltrating malignant glands
• Desmoplastic stroma
• Tall columnar cells – Pleomorphism
– Abnormalnuclear morphology
– Mitoses
– Loss of polarity 
 Variants:
– Mucinous adenocarcinoma
– Signet ring cell carcinoma
– Undifferentiated carcinoma – Others
64
Q

what are the precursor lesions of bowel cancer

A
  • Most, if not all, colorectal carcinoma arise from adenomas
  • Adenoma are intraepithelial neoplasms (benign)
  • Adenomas typically present as polyps in the colorectum
  • Residual adenoma identified in 10-30% of adenocarcinomas
65
Q

what are the two types of precursor lesions for bowel cancer

A
  1. Conventional adenoma

2. Serrated polyps – sessile serrated adenomas and traditional serrated adenomas

66
Q

explain covnetional adenomas

A

• Prevalence of adenomas parallels colorectal carcinoma
• Most arise in the rectosigmoid
• Risk: age and male sex correlated with
adenoma development
• Incidence rises at age 40, peak 60-70
• Asymptomatic – Anaemia, FOBT (occult bleeding). Precedes CRC by 10-15 years
• 10-15% chance of progression during 10 years
• Malignant risk:
– Polyp size (>1cm) – Villous
– High grade
• Removal of adenoma can help prevent development of adenocarcinoma

67
Q

what are the three pathways for colorectal carcinogenesis

A

– Chromosome Instability (CIN)
– Microsatellite instability (MSI)
– CpG Island Methylator Phenotype (CIMP)

68
Q

explain chromosome instability

A

Persistently increased rate of gains and losses of chromosomal material
• 70-80% CRC
• Aneuploidy
• Left-sided/distal CRC
• Precursor lesions: Conventional Adenoma
• Mutations APC/Wnt pathway
• ? Abnormal mitotic spindle segregation

69
Q

explain micro satellite instability

A

Widespread alterations in the sizes of repetitive DNA sequences.
• 10-15% CRC
• Diploid
• Markedly increased rates of mutation of coding sequences (somatic hypermutation).
• Right-sided/proximalcancers
• Precursor lesions: Serrated polyps
• Loss of mismatch repair protein function

70
Q

explain CIMP

A

Acquisition of widespread hypermethylation of CpG dinucleotides in the promoter regions of genes.
• Major mechanism of inactivation of tumor suppressor genes
– Eg. TP16, CDHI, and MLH1.
• 20-30% CRC
• Genetic and environmental eg smoking

71
Q

explain the national bowel cancer screening program

A 
• Definition:
– Testing for bowel cancer in people without symptoms
• Australians turning 50
• Rationale:
– Find polyps or early cancer
– Early treatmentCure
– Prevent cancer deaths
– Doing an FOBT every 1-2 years, can reduce risk of dying from bowel cancer by up to one third
• Method:
– Faecal Occult Blood Test (FOBT)

PATH2220 (14 decks)

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