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Knowledge Test > Integrity - Cancer > Flashcards

Integrity - Cancer Flashcards

1
Q

Excessive Immune response stages

A

Pro-inflammatory cytokines and chemokines are released.
This increases vascular permeability, bacterial killing, increased peripheral resistance, tachypnea, fever, tachycardia.
This leads to oedema, tissue damage, organ failure.

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2
Q

Scar formation

A
  1. hemostasis phase - clots the bleeding
  2. defensive/inflammatory phase - destroys bacteria
  3. proliferative phase - replace the tissue
  4. maturation phase - collagen fibers reorganise
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3
Q

Tissue targeted autoimmunity (Type 1 diabetes)

A

T cells target pancreatic beta cells, leading to insulin deficiency

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4
Q

Tissue targeted autoimmunity (MS)

A

T cells target neuron myelin sheath leading to demyelination and neurodegeneration

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5
Q

Tissue targeted autoimmunity (graves’ disease)

A

Ab stimulants target TSH receptor leading to hyperthyroidism

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6
Q

Tissue targeted autoimmunity (myasthenia gravis)

A

Ab blocks Ach receptor leading to neuromuscular transmission blockade

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7
Q

Tissue targeted autoimmunity (primary biliary cholangitis)

A

T cells target small bile duct epithelium leading to cholestasis and liver fibrosis

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8
Q

Atrophy

A

shrunken tissue from reduced cell size or number

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9
Q

hypertrophy

A

enlargement of cells in a tissue

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10
Q

hyperplasia

A

increased number of normal cells in a tissue

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11
Q

transdifferentiation

A

A switch of differentiation direct from one mature phenotype to another which is normally present in that tissue

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12
Q

metaplasia

A

a switch of differentiation from one mature phenotype to another which is not normally present in that tissue, in response to an environmental change

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13
Q

dysplasia

A

disordered microscopic appearance and maturation of cells implying neoplasia

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14
Q

tumour

A

abnormal lump of no specific cause

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15
Q

cyst

A

abnormal fluid filled lesion lined with epithelium

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16
Q

hamartoma

A

disorganised mature normal tissue elements lacking autonomous growth

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17
Q

neoplasm

A

growth of genetically abnormal cells derived from a mutated ancestor seed cell

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18
Q

cancer

A

malignant neoplasm which invades (crosses tissue boundaries) and metastasises ( discontinous spread to survive and grow at remote sites)

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19
Q

Craniospinal venous system

A

2-way venous flow (no valves), links cranial and vertebral circulation with intercostal abdominal and pelvic venous plexuses, results in a direct route for metastisis to spine and brain

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20
Q

TNM system

A

cancer staging
T: local tumour extent, diameter, invasion
N; lymph node metastasis, regional, distant, number affected
M: metastais elsewhere

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21
Q

Worrying ulcer

A

best biopsied at the edge

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22
Q

polyp

A

epithelium covers a raised core of connective tissue

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23
Q

papilloma/papillary neoplasm

A

epithelium covers long thin branches of connective tissue - much greater surface area than polyp of similar size

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24
Q

problems resulting from benign neoplasms

A

compression, obtruction, haemorrhage, infarction, secreted proucts, progression to malignancy

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25
Q

cancer forming

A

over time mutations occur, clonal expansion can lead to a large number of mutated cells. This increases with chronic inflammation and carcinogens

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26
Q

inside a cancer

A

cancer cells, non-cancer cells , nerves, blood vessels and lymphatics, high interstitial fluid pressure produces a core environment of ischaemia. Interstitial fluid flows from core into nearest lymphatics
Large uncontrolled angiogenesis with varied pO2. This surrounds a matrix structure.

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27
Q

Cancer hallmarks

A

replicative immortality, resist cell death, matrix degradation, angiogenisis, rtissue invasion, insensitivity to antigrowth

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28
Q

cancer stemness

A

cancer cells can move in and out of stemness if needed to replenish cell envrionment

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29
Q

cancer metabolism

A

anabolic (aerobic glycolysis) and chaotic vasculature that produces metabolic stress and depletes o2 and nutrients to healthy cells . This leads to immune dysfunction and CD8+ cell exhaustion and T cell senescence

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30
Q

Cancer cells and varying demands

A

cancers rebalance essential tasks via plasticity

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31
Q

cancer pre-cursor lesions

A

changes in the architecture of the epithelium, cytological morphology of the cells that precede invasion and metastasis. These have not invaded and stay on the epithelial side of basements membrane

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32
Q

cancer gene mutation targets

A

genes that control proliferation, cell death, genomic stability. regulate movement and adhesion. The transition from normal cell to malignant cancer requires several mutations

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33
Q

carcinogens

A

agents that induce cancer (mutagens): chemical, physical (UV or ionising radiation), biological (bacteria, viruses, parasites)

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34
Q

carcinogenisi

A

process of cancer induction.

  1. initiation: the alteration of a normal cell to a potentially cancerous cell.
  2. Promotion: a process which permits the clonal amplification of the initiated cell, promoters are not mutagens they induce proliferation ‘fix = make permanent’
  3. Progression: acquisition of further mutations within the neoplastic clone drive progression to a malignant neoplasm
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35
Q

dose response

A

a linear relationship between the amount of carcinogen delivered in a single dose and the number of tumours which develop

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36
Q

latent period

A

time lag between the administration of carcinogen and appearence of macroscopic tumours.

37
Q

threshold dose

A

there is a thershold dose of carcinogen below which no tumours form. (in the absence of secondary non carcinogenic stimulus e.g wounding)

38
Q

Replicative senescense

A

primary cells can only undergo a limited number of cell divisions (hayflick number) as the chromosome telomere ends shorten with each division until the cell is held in arrest (G0) and apoptosed

39
Q

telomerase

A

inhibits telomere shortening, present in germ and stem cells as well as cancer `

40
Q

Autosomal dominnant (heterozygous) cancer predispositions

A

retinoblastoma (Rb/Rb 1)
hereditary non polyposis colon cancer (MLH1,MSH2)
familial breast and ovarian cancer (BRAC-1/
brac-2)

41
Q

autosomal recessve (homozygous) cancer predispositions

A 
xeroderma pigmentosum (XP) 
fanconi's anemia (FA)
42
Q

What type of disease is cancer?

A

Genetic, and more than one mutation is necessary for progression

43
Q

Chemical carcinogens

A

synthetic - polycyclic hydrocarbons coal etc
aromatic amines & azo dyes hair dyes etc
naturally occurring - nitrosamines processed foods and beer. aflatoxin - peanut

44
Q

carcinogenic parasites

A

schistosoma haematobium

45
Q

carcinogenic bacteria

A

helicobacter pylori

46
Q

carcinogenic viruses

A

HPV, HBV,HCV, EBV, HTLV 1, HHV 8

47
Q

What gene classes are altered in cancer ?

A

Oncogenes (Onc) - normal version = proto-oncogenes, activated version = oncogenes . Cancer promoting genes that must be activated.
Tumour suppressor genes (TSG) - must be inactivated, suppress inappropriate proliferation

48
Q

p53

A

protector against aberrant oncogenes, mutation in p53 makes the cell genetically unstable and allows telomerase to overcome replicative senescense

49
Q

What is MMR

A

it corrects mismatched DNA bases

50
Q

what causes the disregard of apoptotic signals?

A

p53 inactivation, telomerase activation, BCL2 overexpression

51
Q

Cancer invasion

A

cancer cells move by destruction of nearby tissue using oedema. invasion requires change and or loss in cell-cell and cell-matrix adhesion, proteolysis of matrix, movement, break of cadherins that are central to adhesion

52
Q

How cancer metastises

A

detachment and invasion of surrounding tissues, neo-vascularisation, penetration in lymph and blood, release of tumor cells, evasion of host defences, adherence at the site of arrest

53
Q

lymphatic spread of 3 main cancers

A

breast - axillary lymph nodes
testicular - lower lumbar lymph nodes
colorectal - local mesenteric nodes and liver

54
Q

common metastatic sites

A

liver,lung,bone,brain

55
Q

cancer grading vs staging

A

grading - degree of differention

staging - invasion and metastasis

56
Q

Diagnosis of cancer

A

ultimately histoligical h and g stain

57
Q

causes of lung cancer

A

smoking, occupation (uranium, asbestos ), environmental exposures (radon gas), genetic (Li-Fraumeni Syndrome - mutated p53 genes)

58
Q

sarcoma

A

cancer that begins in the bone and in the soft tissue

59
Q

lymphoma

A

cancer beginning in the lymph

60
Q

melanoma

A

cancer of the skin

61
Q

hematoma

A

bruise

62
Q

Carcinoid lung tumour

A

relatively rare, slow progeression, present with haemoptysis or symptoms of airway obstruciton, younger adults and children

63
Q

lung cancer entity

A

it is not a single entity but a group of malignant epithelial tumours with different pathophysiologies

64
Q

Symptoms and signs of lung cancer

A

cough, dyspnoea, haemoptysis, weigh loss, chest/shoulder pain, hoarseness, fatigue, slow to clear pneumonia, finger clubbing, cervical lymphadenopathy, liver-bone-brain metastases, pleural effusion.

65
Q

Initial investigation of lung cancer

A

radiology - CXR, CT (lump)
Blood tests - high calcium, abnormal liver function tests
low serum sodium

66
Q

main cells of the epidermis

A

keratinocytes, melanocytes (neural crest derived), langerhan cells (bone derived)

67
Q

main cells of dermis

A

fibroblasts, ecm - collagen, mast cells

68
Q

keratinisation

A

differentiation in skin that leads to a dead anucleated cell called the stratum corneum

69
Q

cell compartments in epidermis

A

basal, spindle,granular,stratum corneum

70
Q

melanin

A

synthesised melanocytes

71
Q

appendageal structures

A

collective name for hair follicles, sebaceous glands, eccrine sweat glands. developed ONLY during first trimester of pregnancy

72
Q

erythema

A

red colour associated with increased blood flow to skin

73
Q

indomethacin

A

drug that inhibits some inflammatory pathways involved in sunburn

74
Q

phototherapy

A

treatment modality in dermatology, exposure to uv radiation

75
Q

fibroblasts

A

mesenchymal derived cells, that remodel extracellular collagen protein. found in the dermal papilla of the hair follicle

76
Q

mast cells

A

tissue basophil, contain and discharge (Degranulate) vasoactive chemicals including histamine

77
Q

inflammatory cells

A

lymphocytes, polymorphs, dermal macrophages

78
Q

vessels

A

there are no vascular elements in the EPIdermis

79
Q

epidermal differentiaton

A

as keratinocytes move from the basal layer to their terminally differentiated dead state in the stratum corneum they produce a proteins (keratins and filaggrin), and lipids

80
Q

keratins and filaggrin

A

keratins are alpha helical proteins bound in pairs one acidic one basic, they are aggregated by filaggrin

81
Q

classes of melanin

A

eumelanin - brown/black

pheomelanin - red or yellow

82
Q

skin colour differences

A

everyone has same number of melanocytes, differences arise due to amount and type of melanin produced by the same number of melanocytes

83
Q

Where is melanin produced

A

melanosomes that are passed down the dendrites into the surrounding keratinocytes

84
Q

albinism

A

same number of melanocytes, less melanin. mutation of tyrosinase key enzyme for melanin biosynthesis

85
Q

langerhan cells

A

antigen presenting cells, antigens are gathered and metabolised by langerhan cells before being presented to T-cells in the regional lymph node

86
Q

collagen

A

procollagen is synthesised, secreted and remodelled by fibroblasts, collagen is a triple alpha helix.

87
Q

marfan’s syndrome

A

mutation of fibrilin (skin elastic fibre)

88
Q

sebaceous cells

A

produce lipids that make up sebum, oestrogen decreases sebum excretion

89
Q

hair follicles

A

are formed in utero, once they are destroyed they cannot be regenerated

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