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Foundations in Medicine 1 > Pathology (+neoplasia) > Flashcards

Pathology (+neoplasia) Flashcards

1
Q

What is meant by tumour heterogeneity?

A

where a tumour contains multiple cells that have different mutations that each have a selective advantage to evade the immune system/ avoid clearance

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2
Q

What is polyploidy?

A

exact multiple of your diploid state

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3
Q

what is aneuploidy?

A

inexact multiples of the diploid state

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4
Q

What is a carcinogen?

A

mutagenic substances that act on the DNA of cells causing tumours

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5
Q

What are HPVs two oncoproteins?

A

E6 and E7

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6
Q

What do oncoproteins bind to to suppress cell cycle repair mechanisms?

A

p53

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7
Q

What does the E7 viral oncoprotein of HPV cause?

A

tumour suppressor gene that encodes the retinoblastoma protein

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8
Q

What does the E6 viral oncoprotein of HPV act on?

A

TP53 preventing it from regulating DNA replication and initiating apoptosis

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9
Q

What is the function of retinoblastoma protein and which phase of the cell cycle does it act on?

A

regulates cell cycle progression at the G1-S phase

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10
Q

List the six steps of acute inflammation

A
  1. release of chemical mediators
  2. vasodilation
  3. increased vascular permeability (exudation)
  4. fluid accumulation
  5. cell recruitment
  6. phagocytsosis
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11
Q

What are the cardinal signs of inflammation?

A

redness
heat
swelling
pain
loss of function

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12
Q

what cytokine attracts neutrophils?

A

IL-8

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13
Q

neutrophils can undergo movement by rearranging their microtubules, true or false?

A

true

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14
Q

Name three types of opsonins from the complement system

A

C4b, C3b and C2a

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15
Q

Name three complement derived molecules that can induce chemotaxis of neutrophils

A

C5a, C3a and C567

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16
Q

Name the three steps in order for neutrophil migration

A
  1. margination
  2. adhesion
  3. emigration
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17
Q

what happens during emigration of neutrophils

A

they pass through the endothelium and through the basal lamina into the adventicia

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18
Q

list four chemicals involved in acute inflammation

A

leukotrienes
prostaglandins
serotonin
chemokines

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19
Q

what cell produces leukotrienes

A

neutrophils

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20
Q

why are prostaglandins involved in acute inflammation

A

they stmulate platlet aggregation

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21
Q

what is the process in which soluble fibrinogen is converted into fibrin

A

coagulation

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22
Q

what is the fucntion of serotinin in acute inflammation

A

vasconstrictor

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23
Q

What are four outcomes of acute inflammation

A

resolution (return to homeostasis)
chronic inflammation
suppuration (formation of ous from dead/dying neutrophils)
scarring/fibrosis tissue

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24
Q

what is an example of an inappropriate inflammatory response

A

anaphylaxis - allergic reaction

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25
Q

What is healing by secondary intention

A

where there has been excess tissue damage and loss that that the wound heals from the basal lamina upwards

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26
Q

what is granulation tissue made up of

A

capillaries, collagen and extracellular matrix

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27
Q

Name the five stages of bone healing post fracture

A

haematoma
inflammation
fibrovascular
bone formation
remodelling

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28
Q

if there is a loss of hepatocytes in the liver without damage to the architecture, can complete healing occur?

A

yes

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29
Q

What causes acute inflammtion to move into chronic inflammation

four points

A

causative agent is not removed
cellular exudate changes
suppurative not resolving
presence of foreign material

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30
Q

what cell line does not contain a hayflick limit

Henrietta Lacks :)))

A

HeLa

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31
Q

What is cellular senescense

A

cell ages but stops dividing

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32
Q

what is the hayflick limit

A

the number of times a somatic cell population will divide

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33
Q

What reduces the hayflick limit as we age

A

shortening telomeres

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34
Q

Why do cells undergo sensensence

relating to age of the cell

A

because their telomeres are too short

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35
Q

what are telomeres

A

caps at the end of the chromosome that shorten at each cell division

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36
Q

What is werners syndorme

“Adult progeria”

A

a mutation in ther WRN gene on chromosome 8 causes accelerated ageing post puberty and the adolescent growth spurt does not occur

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37
Q

What is the mutation in down syndrome

A

trisomy 21

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38
Q

What are the symptoms of down syndrome

A

accelerated ageing and shortened life expectancy

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39
Q

Which two proteins can prevent expression of hTERT and reduce/supress telomaerase activity?

A

RB and p53

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40
Q

Why are free radicals not always bad?

A

neutrophils and macrophages make them to kill pathogens (NADPH complex)

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41
Q

What is a detrimental effect of free radicals

A

causes DNA damage

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42
Q

What happens in Xeroderma pigmentosum

A

sun exposure causes UV damage to DNA and mechanisms of repair deffective to unable to repair the skin damage - can often develop skin cancers

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43
Q

What happens to the skin as we age?

A

less elastin and collagen and atrophy of the dermis

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44
Q

what are cardiovascular signs of ageing

A

elastin:collagen decreases
conduit arteries cannot stretch as much so increased systolic BP

45
Q

What is immunosenensence

and what immunological fucntions affect this

A

ageing of the immune system that it does not perform its optimal function - the thymus atrophies so less naiive cells are being generated resulting in more memory cells present

46
Q

what is osteoarticular ageing

A

osteoporosis - trabeculae are thinned out

47
Q

what is necrosis

A

cell death that can causes the cell to swell, a disruption to the cell membrane and expulsion of the cell contents

48
Q

What are the four types of necrosis?

A

coagulative
colliquative
caseuous
fat

49
Q

Where can coagualtive necrosis be found?

A

heart/kidneys (areas with a rich blood supply) - cell death with some bit of intact-ness

50
Q

Where can you find colliquative necrosis

A

in the brain (contains pus and liquid)

51
Q

Where can you find caseuous necrosis?

A

TB

52
Q

Where can you find fat necrosis?

A

in adipose tissue tends to be a pancreatitis - rupture of fat cells and chalky deposits

53
Q

what is apoptosis

A

programmed cell death that causes cell shrinking and is contained

54
Q

what happens during the intrinsic pathway of apoptosis

A

this is a mitochondrial pathway which causes the release of cytochrome C from the mitochondria - cleaves pro caspase 9 into caspase 9 - which cleaves procaspase 3 into active capsase 3 making an apoptosome triggering cell death

55
Q

What are the two extrinsic pathways of apoptosis

A

TNF and Fas

56
Q

What are the steps of the TNF pathway of apoptosis

A

TNF receptor activated by TNF - triggers TRADD domain and FADD domain
forms complex with procaspase 8 which cleaves into caspase 8 which then converts procaspase 3 into activated caspase 3 creating the apoptosome and apoptosis

57
Q

What are the steps in the FAS pathway of apoptosis

A

fas ligand binds to the fas receptor starts a complex of FADD procaspase 8 (death inducing sgnalling complex (DISC)) - cleaving procapspase 3 into active caspase 3 leading to apoptosis

58
Q

Give physiological examples in which apoptosis is used

3

A

embryogenesis (apoptosis of webbed fingers)
elimiination of cells from endometrium during menstrual phase
cancer prevention

59
Q

What is meant by a malignant neoplasm?

A

neoplasma with potentailly lethal abnormal characteristics that allow it to invade the body and metastasise

60
Q

what is a benign neoplasm

A

one that does not have the ability to metastatsise and invade the body but in some cases can still be harmful

61
Q

what are the four distinguishing features of a neoplasm

A

differentiation, local invasion, metastasis and rate of growth

62
Q

anaplastic refers to tumours that are well differentiated, true or false?

A

false, they are undifferentiated making it difficult to distinguish the tissue of origin

63
Q

are benign tumours usually more or less differentiated?

A

well-differentiated resembles its tissue of origin

64
Q

what is metaplasia?

A

change in the phenotype of the cells often in response to chronic irritation

65
Q

what is hypertrophy?

A

increased cell size often in response to increased work-load

66
Q

what is hyperplasia?

A

increase in cell number due to a stimulus such as growth factors etc

67
Q

what is a grade 3 tumour

A

one that is poorly differentiated and hence highly anaplastic some anaplasia

68
Q

what grade is a well-differentiated tumour?

A

grade 1

69
Q

What are the features of poor differentiation?

6 points

A

abnormal nuclear size and shape
abnormal nuclear features
increased mitotic activty
decreased cell order
necrosis
tumour giant cells

70
Q

What is displasia?

A

neoplastic change that is confined to the basal membrane

it can regress so does not always lead to malignancy

71
Q

why is displasia not always malignant?

A

because it is confined to the basal membrane and only when it breaches this does the tumour become malignant, displasia can also reverse

72
Q

malignant neoplasms are slow growing, true or false?

A

false

fast growing (benign are slow growing)

73
Q

what does the border of a benign tumour look like?

A

encapsulated and contained

fibrous capsule

74
Q

is carcinoma in situ malignant?

A

No, it is the highest grade of displasia

75
Q

what is the highest grade of displasia known as

A

carcinoma in situ

76
Q

what two subsets are epithelial tumours classed into?

A

surface/ non glandular and glandular

77
Q

breakdown the meaning of an adenoma

A

aden (glandular) oma (benign)

78
Q

what does a papilloma refer to

A

benign tumour of a non gladular surface/ epithelium

79
Q

what would a benign tumour of the skin be called?

A

squamous cell papilloma

80
Q

what is a benign tumour of the glandular epithelium in the colon called?

A

colonic adenoma

81
Q

benign tumor of the smooth muscle?

A

leiomyoma

82
Q

what is a chondroma?

A

benign tumour in the cartilage

83
Q

what is a malignant epithelial tumour called?

A

carcinoma

84
Q

what is an adenocarcinoma?

A

malignant tumour of the glandular epithelium

85
Q

what is a sarcoma?

A

malignant mesenchymal tumour

86
Q

what is a hamartoma?

A

non-neoplastic disordered overgrowth of normal tissue

87
Q

what is melanocytic naevus?

A

benign proliferation of melanocytes

88
Q

what is malignancy of melanocytes known as

A

melanoma

89
Q

define the following
1. lymphoma
2. myeloma
3. leukaemia

A
  1. malignancy of B or T cell origin (hogkins or not)
  2. malignancy of the plasma cells
  3. malignancy of white blood cells - begins in the bone marrow
90
Q

Name five hallmarks of cancer

A

avoiding immune destruction
enabling replicative immortality
evading growth suppressors
tumour promoting inflammation
activating invasion and metastasis
genomic instability
inducing angiogenesis
resisiting cell death
deregulating cellular energetics
sustaining proliferative signalling

91
Q

how do neoplastic cells become “immortal”

A

abnormal expression of oncogenes or innactiavtion of tumour suppressor genes
reduced apoptosis
increased telomerase activity

92
Q

what gene is expressed by tumours that can inhibt apoptosis

A

BCL-2

93
Q

what is an oncogene?

A

encodes for an oncoprotein that promotes neoplastic growth of cells (cancer will use this to enhance growth)

94
Q

is p53 an oncogene?

A

no, it is a tumour-suppressor gene

95
Q

how do we predict for carcinogens?

A

epidemiological evidence

96
Q

Give an example of a chemical carcinogen

A

aromatic amines
polycyclic aromatic hydrocarbons (smoking)
nitrosamines (tobacco and cured meats)
azo dyes
vinyl chloride

97
Q

What are the oncogenic viruses?

A

HPV
Epstein-barr
hep B and C
herpes
human T cell lymphotropic virus

98
Q

What type of tumour can be acquired from coinfection of HPV?

A

squamous cell carcinoma in the anogenital region

99
Q

How does HPV increase the risk of cancer?

A

the virus produces two oncoproteins which bind to p53 and RB both of which enhance cell cycle progression

100
Q

What cancer is EBV associated with?

A

b cell lymphomas and in some cases squamous cell carcinoma

not much is known about the carcinogenesis

101
Q

which tissues are the most sensitive to ionising radiation?

A

thyroid (Chornobyl)
bone
breast
haematopoetic tissue

102
Q

What bacteria can be associated with cancer acquisition?

A

helicoacter pylori (h.pylori)

103
Q

how does h. pylori lead to adenocarcinomas?

A

secrete toxins that activate oncoproteins

104
Q

What genes can increase susceptibility to breast cancer?

A

BRCA1 and BRCA2

105
Q

What hormone can be linked to carcinogenesis and how?

A

oestrogen and via increased production along with growth factors from adipose cells increasing cell proliferation

106
Q

What are the steps in metastasis?

A
  1. detachment
  2. invasion of surrounding tissue
  3. intravasation into vessels
  4. evasion of host defences
  5. adherence to endothelium elsewhere
  6. extravasation of cells from vessel to surrounding tissue
107
Q

whats transcoelomic metastasis?

A

when the cancer cells cross a body cavity along the peritoneum

108
Q

Name some examples of oncogenes?

A

PDGF
ras
src

109
Q
A

Foundations in Medicine 1 (11 decks)

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