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MBCHB1 exam > phase 1 week 4 > Flashcards

phase 1 week 4 Flashcards

1
Q

What is a tumour?

A

A tumour is formed by an excessive, uncontrolled proliferation of cells as a result of irreversible genetic change which is passed from one tumour cell to its progeny

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2
Q

What is cancer?

A

A neoplastic disease of which the natural course of which is (often) fatal

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3
Q

For epithelial tumours what is the normal way in which cells change to become cancerous?

A

normal > dysplasia > benign > pre-malignant > malignant

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4
Q

What is dysplasia?

A

“Bad growth” - loss of architectural orientation and development of cellular atypic. Cannot yet invade neighbouring tissue so is not cancer

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5
Q

What is metaplasia?

A

cells change from one differentiated tissue to another. Unstable environment so high chance of mutations in DNA - precursor to dysplasia and cancer

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6
Q

What are some modes of cancer spread?

A

local invasion
lymphatic spread
blood spread
transcolaemic spread

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7
Q

What do proto-oncogenes do?

A

Code for proteins that are needed for normal cell proliferation

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8
Q

What is a oncogene?

A

a mutated proto-ongogene

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9
Q

what are activating mutations?

A

only certain mutations in a proto-oncogene will convert it to the oncogenic form

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10
Q

What does the activation of proto-oncogenes do?

A

allows cells to bypass the need for extracellular growth signals

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11
Q

Why are porto-oncogenes described as dominant acting?

A

only one allele of a photo-oncogene needs to be acquire an activating mutation

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12
Q

What do oncogenes code for?

A 
a hyperactive version of a protein product
or
normal protein BUT
in abnormal quantities
at the wrong time
in the wrong cell type
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13
Q

What mutations can lead do hyperactive proteins being formed?

A

point mutation - e.g ras Ki-ras in colon cancer
deletion
chromosomal rearrangement e.g. ber-able in CML

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14
Q

What mutations can cause proteins to be formed in the wrong place, time or amount?

A 
gene amplification (HER2) breast cancer 
Chromosomal rearrangement - places gene downstream of a promoter e.g lg-myc
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15
Q

What external signals for growth be mutated to lead to cancer?

A

hormones

peptide growth factors

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16
Q

Give examples of cell surface receptors that can be mutated

A

HER2

EGFR

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17
Q

Give examples of intracellular molecules that can be mutated?

A 
signal transducers (ras)
cyclins (cyclin D)
transcription factors (myc)
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18
Q

What can constitutive telomerase expression do?

A

hay flick limit not reached so the cell is immortalised

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19
Q

What is a benign tumour?

A

stay localised at their site of origin

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20
Q

What is a malignant tumour?

A

able to invade and spread to different sites

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21
Q

What are the b and m endings for epithelial tumours?

A

oma and carcinoma

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22
Q

what are the b and m names for covering epithelium tissues?

A

papilloma and carconoma

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23
Q

what are the b and m names for glandular epithelial tumours?

A

adenoma, adenocarcinoma

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24
Q

What are the b and m names for tumours in the epithelium forming organs (e.g. liver)

A

adenoma

carcinoma e.g. hepatocarcinoma

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25
Q

What are the b and m endings for connective tissue tumours?

A

oma

sarcoma

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26
Q

what are the b and m names for smooth muscle tumours?

A

leiomyoma

leiomyosarcoma

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27
Q

what are the b and m names for skeletal muscle tumours?

A

rhabdomyoma

rhabdomyosarcoma

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28
Q

what are the b and m names for bone forming tumours?

A

osteoma

osteosarcoma

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29
Q

what are the b and m names for cartilage tumours

A

chondroma

chondrosarcoma

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30
Q

what are the b and m names for fibrous tumours?

A

fibroma

fibrosarcoma

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31
Q

what are the b and m names for tumours of blood vessels

A

angioma

angiosarcoma

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32
Q

what are the b and m names for adipose tissue tumours?

A

lipoma

liposarcoma

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33
Q

what are the b and m names for lymphoid tumours?

A

n/a

lymphoma

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34
Q

what are the b and m names for haematopoetic tumours?

A

n/a

leukaemia

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35
Q

what are the b and m names fir primitive nerve cell tumours?

A

n/a

neuroblastoma e.g. retinoblastoma

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36
Q

what are the b and m names fir glial cell tumours?

A

n/a

glioma e.g. astrocytoma

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37
Q

what are the b and m names for tumours in melanocytes?

A

pigmented naevi

malignant melanoma

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38
Q

what are the b and m names for tumours in the mesothelium?

A

n/a

malignant mesothelioma

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39
Q

what are the b and m names for tumours in germ cells

A

teratoma

teratoma, seminoma

40
Q

How do tumours get an adequate nutrient supply once they are larger than 1-2mm?

A 
secrete VEGF (vascular endothelial growth factor)
promotes production of new vascular tubules
41
Q

what are MMPs?

A

matrix metalloproteinases (chew up basement membrane)

42
Q

what is uPA?

A

urokinase plasminogen activator

43
Q

What are some risk factors for cancer?

A 
age
alcohol
cancer-causing substances
chronic inflammation
diet
hormones 
immunosuppression
infectious agents
obesity
radiation
sunlight
tobacco
44
Q

what happens during G1?

A

growth in mass, centrosome duplication

45
Q

what happens during s phase?

A

chromosome duplication - synthesis of DNA

46
Q

what happens during G2?

A

cell grows in size, duplicating organelles and preparing for division

47
Q

what happens during cytokinesis?

A

cleavage of daughter cells

48
Q

what are the 5 stages of mitosis?

A 
prophase
pro-metaphase
metaphase
anaphase
telophase
49
Q

what happens during prophase?

A

chromatin condensation
nucleolus disappears
centrioles move to the poles of the cell

50
Q

what happens during pro-metaphase?

A

nuclear membrane dissolves

chromosomes attach to microtubules and begin moving

51
Q

What happens during metaphase?

A

spindle fibres align the chromosomes along the middle of the cell nucleus (metaphase plate)

52
Q

What happens during anaphase?

A

paired chromosomes separate and move to opposite sides of the cell

53
Q

What happens during telophase?

A

chromatids arrive at opposite poles of the cell
new membranes form around the daughter nuclei
chromosomes decondense
spindle fibres disperse

54
Q

What are cyclin-dependent kinases?

A

serine / threonine kinases that require the binding of cyclin for full activity
regulate progression through the cell cycle
activity must be tightly regulated
waves of expression of specific cyclins
phosphorylation / dephosphorylation

55
Q

What are cyclins?

A

activator proteins that are up - or down - regulated depending on the phase of the cell cycle

56
Q

What are cyclin-dependent kinase inhibitors?

A

small proteins that block cdk/cyclin activity either by forming an inactive complex or acting as a competitive CDK ligand

57
Q

What is the cyclin / cdk complex needed at the end of G1?

A

CDK4/6 - cyclin D

58
Q

What is the cyclin / cdk complex needed for progression through mitosis?

A

CDK1 - cyclin B

59
Q

What is CDK1 - cyclin B also known as?

A

maturation promoting factor (MPF)

60
Q

What are the four well established check points in the cell cycle?

A 
restriction point (G1)
DNA damage check points (end of G1 and G2)
Metaphase check point
61
Q

What is cell cycle progression dependent on?

A

growth factors

62
Q

the accumulation of which cyclin means that no growth factors are required for the rest of the cell cycle and that cell is committed to cell division?

A

cyclin D

63
Q

What acts as the gate keeper at the restriction point?

A

retinoblastoma (RB)

64
Q

What is the function of p53?

A

cellular stress e.g. DNA damage leads to transcription of p53
at low levels this results in p21 expression which arrests the cell cycle and allows time for the DNA to be repaired
at high levels it promotes apoptosis of the cell

65
Q

What are the benefits and limitations of X-rays?

A

good for bones
chest X-ray
abdomen limited

66
Q

What are the benefits and limitations of CT scans?

A

excellent for bones
chest and abdomen
25 seconds
limited for soft tissues of spine, limbs and brain

67
Q

What are the benefits and limitations of MRI?

A

great for brain, spine soft tissues, limbs
less good for abdomen / pelvis
no good for heart or lungs
25 minutes

68
Q

What is CT?

A

A modern imaging tool that combines X-rays with computer technology to produce a more detailed, cross-sectional view of the body

69
Q

How does an MRI work?

A

Magnetic field around the patient
pulses radio waves
radio waves cause tissues to resonate
a computer measures the rate at which various tissues give of vibrations and converts it into a 2D picture

70
Q

What are the 3 main stages of life before birth?

A

pre-implantation
embryonic stage
foetal stage

71
Q

When is the pre-implantation stage?

A

week 1

72
Q

When is the embryonic stage and what does it involve?

A

weeks 2-8

organogenesis

73
Q

When is the foetal stage and what does it involve?

A

weeks 9-38

growth and development

74
Q

Describe cleavage

A

mitotic divisions of fertilised oocyte
overall size remains the same
allows passage down narrowest part of the uterine tube (isthmus)
surrounded by a glycoprotein coat - zona pellucida - to prevent premature implantation

75
Q

Describe morula formation

A

around day 4, cells maximise contact with each other
a cluster of cells forms held together by tight junctions
enters the uterus

76
Q

Describe blastocyst formation

A

first sign of cellular differentiation
inner cell mass - goes on to form embryo and extra-embryonic tissues
outer cells form trophoblast - contributes to placenta
fluid enters via the zona pellucida into the spaces of the inner cell mass
A fluid-filled blastocyst cavity forms

77
Q

What causes the blastocyst to “hatch”

A

ICM cells undergo proliferation and fluid builds up in cavity
eventually blastocyst “hatches” from the zona pellucida to facilitate implantation

78
Q

What happens in week 2?

A

implantation

79
Q

what days does implantation occur?

A

7-12

80
Q

Which cells implant first?

A

trophoblast

81
Q

What does the trophoblast differentiate into?

A

cytotrophoblast

syncytotrophoblast

82
Q

what makes up the bilaminal disk?

A

the epiblast and the hypoblast

83
Q

Describe the amnion

A

continuous with the epiblast
persists until birth
cavity fills with amniotic fluid
protection for developing embryo

84
Q

Describe the yolk sac

A

continuous with the hypoblast
important for nutrient transfer in weeks 2-3
disappears around week 20

85
Q

Describe the chorion

A

trophoblast and extra embryonic mesoderm
forms foetal component of placenta
chorionic cavity seen early in pregnancy disappears when amnion expands

86
Q

What is gastrulation?

A

a process of cell division and migration resulting in the formation of three germ layers

87
Q

What are the three germ layers?

A

ectoderm
mesoderm
endoderm

88
Q

Describe the formation of the three germ alters

A

once the cells have invaginated, some displace the hypoblast creating the endoderm and others between the epiblast and the newly created endoderm form the mesoderm
the remaining cells in the epiblast form the ectoderm
the cells in these layers give rise to all tissues and organs in the embryo

89
Q

Describe gap junction communication

A

sieve like structure at plasma membranes of opposing cells
hemi-channels composed of connexin molecules
Hemi-Channels of one cell align with those of another
physical sharing of ions and small cytoplasmic molecules
cells behave as a syncytium

90
Q

What is endocrine signalling?

A 
long range (blood)
e.g. oestrogen
91
Q

What is paracrine signalling?

A

local - neighbouring cells (via diffusion)

e.g. epidermal growth factor

92
Q

What is autocrine signalling?

A

same cell

insulin-like growth factor 1

93
Q

what is juxtracrine signalling?

A

signal adjacent to receptor

e.g. laminin

94
Q

What is intracrine signalling?

A

signal produced in cell acts on nuclear or internalised receptor
e.g. fibroblast growth factor 11

95
Q

How do steroids work?

A

diffuse across plasma membrane
bind directly to intracellular receptors
hormone-receptor complex acts as a transcription factor
Affects gene expression directly

MBCHB1 exam (28 decks)

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