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MBCHB1 exam > phase 1 week 4 > Flashcards

phase 1 week 4 Flashcards

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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
What are the b and m endings for connective tissue tumours?
oma | sarcoma
26
what are the b and m names for smooth muscle tumours?
leiomyoma | leiomyosarcoma
27
what are the b and m names for skeletal muscle tumours?
rhabdomyoma | rhabdomyosarcoma
28
what are the b and m names for bone forming tumours?
osteoma | osteosarcoma
29
what are the b and m names for cartilage tumours
chondroma | chondrosarcoma
30
what are the b and m names for fibrous tumours?
fibroma | fibrosarcoma
31
what are the b and m names for tumours of blood vessels
angioma | angiosarcoma
32
what are the b and m names for adipose tissue tumours?
lipoma | liposarcoma
33
what are the b and m names for lymphoid tumours?
n/a | lymphoma
34
what are the b and m names for haematopoetic tumours?
n/a | leukaemia
35
what are the b and m names fir primitive nerve cell tumours?
n/a | neuroblastoma e.g. retinoblastoma
36
what are the b and m names fir glial cell tumours?
n/a | glioma e.g. astrocytoma
37
what are the b and m names for tumours in melanocytes?
pigmented naevi | malignant melanoma
38
what are the b and m names for tumours in the mesothelium?
n/a | malignant mesothelioma
39
what are the b and m names for tumours in germ cells
teratoma | teratoma, seminoma
40
How do tumours get an adequate nutrient supply once they are larger than 1-2mm?
``` secrete VEGF (vascular endothelial growth factor) promotes production of new vascular tubules ```
41
what are MMPs?
matrix metalloproteinases (chew up basement membrane)
42
what is uPA?
urokinase plasminogen activator
43
What are some risk factors for cancer?
``` age alcohol cancer-causing substances chronic inflammation diet hormones immunosuppression infectious agents obesity radiation sunlight tobacco ```
44
what happens during G1?
growth in mass, centrosome duplication
45
what happens during s phase?
chromosome duplication - synthesis of DNA
46
what happens during G2?
cell grows in size, duplicating organelles and preparing for division
47
what happens during cytokinesis?
cleavage of daughter cells
48
what are the 5 stages of mitosis?
``` prophase pro-metaphase metaphase anaphase telophase ```
49
what happens during prophase?
chromatin condensation nucleolus disappears centrioles move to the poles of the cell
50
what happens during pro-metaphase?
nuclear membrane dissolves | chromosomes attach to microtubules and begin moving
51
What happens during metaphase?
spindle fibres align the chromosomes along the middle of the cell nucleus (metaphase plate)
52
What happens during anaphase?
paired chromosomes separate and move to opposite sides of the cell
53
What happens during telophase?
chromatids arrive at opposite poles of the cell new membranes form around the daughter nuclei chromosomes decondense spindle fibres disperse
54
What are cyclin-dependent kinases?
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
What are cyclins?
activator proteins that are up - or down - regulated depending on the phase of the cell cycle
56
What are cyclin-dependent kinase inhibitors?
small proteins that block cdk/cyclin activity either by forming an inactive complex or acting as a competitive CDK ligand
57
What is the cyclin / cdk complex needed at the end of G1?
CDK4/6 - cyclin D
58
What is the cyclin / cdk complex needed for progression through mitosis?
CDK1 - cyclin B
59
What is CDK1 - cyclin B also known as?
maturation promoting factor (MPF)
60
What are the four well established check points in the cell cycle?
``` restriction point (G1) DNA damage check points (end of G1 and G2) Metaphase check point ```
61
What is cell cycle progression dependent on?
growth factors
62
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?
cyclin D
63
What acts as the gate keeper at the restriction point?
retinoblastoma (RB)
64
What is the function of p53?
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
What are the benefits and limitations of X-rays?
good for bones chest X-ray abdomen limited
66
What are the benefits and limitations of CT scans?
excellent for bones chest and abdomen 25 seconds limited for soft tissues of spine, limbs and brain
67
What are the benefits and limitations of MRI?
great for brain, spine soft tissues, limbs less good for abdomen / pelvis no good for heart or lungs 25 minutes
68
What is CT?
A modern imaging tool that combines X-rays with computer technology to produce a more detailed, cross-sectional view of the body
69
How does an MRI work?
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
What are the 3 main stages of life before birth?
pre-implantation embryonic stage foetal stage
71
When is the pre-implantation stage?
week 1
72
When is the embryonic stage and what does it involve?
weeks 2-8 | organogenesis
73
When is the foetal stage and what does it involve?
weeks 9-38 | growth and development
74
Describe cleavage
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
Describe morula formation
around day 4, cells maximise contact with each other a cluster of cells forms held together by tight junctions enters the uterus
76
Describe blastocyst formation
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
What causes the blastocyst to "hatch"
ICM cells undergo proliferation and fluid builds up in cavity eventually blastocyst "hatches" from the zona pellucida to facilitate implantation
78
What happens in week 2?
implantation
79
what days does implantation occur?
7-12
80
Which cells implant first?
trophoblast
81
What does the trophoblast differentiate into?
cytotrophoblast | syncytotrophoblast
82
what makes up the bilaminal disk?
the epiblast and the hypoblast
83
Describe the amnion
continuous with the epiblast persists until birth cavity fills with amniotic fluid protection for developing embryo
84
Describe the yolk sac
continuous with the hypoblast important for nutrient transfer in weeks 2-3 disappears around week 20
85
Describe the chorion
trophoblast and extra embryonic mesoderm forms foetal component of placenta chorionic cavity seen early in pregnancy disappears when amnion expands
86
What is gastrulation?
a process of cell division and migration resulting in the formation of three germ layers
87
What are the three germ layers?
ectoderm mesoderm endoderm
88
Describe the formation of the three germ alters
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
Describe gap junction communication
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
What is endocrine signalling?
``` long range (blood) e.g. oestrogen ```
91
What is paracrine signalling?
local - neighbouring cells (via diffusion) | e.g. epidermal growth factor
92
What is autocrine signalling?
same cell | insulin-like growth factor 1
93
what is juxtracrine signalling?
signal adjacent to receptor | e.g. laminin
94
What is intracrine signalling?
signal produced in cell acts on nuclear or internalised receptor e.g. fibroblast growth factor 11
95
How do steroids work?
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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