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DDT > 5 - GI tract dysfunction > Flashcards

5 - GI tract dysfunction Flashcards

1
Q

what promotes cell cycle progression

A

cyclins

cdks

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2
Q

what stops cell cycle progressionq

A

cdk inhibitors

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3
Q

quiescence in the cell cycle

A

cells can exit and re-enter cell cycle through G0 phase

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4
Q

early phase of G0

A

mitogen-dependent

growth factors are required for progression beyond this point

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5
Q

once the cell progresses past the R point …

A

.. mitogens are no longer required for cell cycle progression

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6
Q

cancer stages

A

refers to the extent of the cancer
e.g. size of tumour, how far it has spread

TNM staging system

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7
Q

TNM staging system

A

T - size and extent of the main/primary tumour

N - number of nearby lymph nodes that have cancer.

M - whether the cancer has meta-stasized. This means that the cancer has spread from the primary tumor to other parts of the body.

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8
Q

name 4 types of eicosanoid

A

thromboxane
prostacyclin
prostaglandin
leukotriene

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9
Q

what two enzymes cut arachindonate

A

cycooxygenase (COX)

lipooxygenase

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10
Q

what do COX enzymes cut arachindonate into

A

prostacyclins H2

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11
Q

what are prostacyclin H2s cut into and what are they important for

A

prostaglandins - mucus in GI tract/pain/inflammation
thromboxane - clotting
prostacyclins - platelets

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12
Q

what cuts membrane phospholipids into arachindonic acid

A

phospholipase A2

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13
Q

inihbition of COX enzymes

A

NSAIDs
no prostaglandins produced
reduced pain/inflammation
potential stomach ulcers and gastric bleeding

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14
Q

what happens in G2

A

cell growth

proteins duplicated

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15
Q

what happens in G1

A

cell mass doubles

organelles copied

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16
Q

order of cell cycle

A

G1
S
G2
M

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17
Q

what happens in S phase

A

synthesis of complete copy of DNA

centrosome duplicates

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18
Q

order of stages in mitosis

A 
prophase
prometaphase
metaphase
anaphase
telophase
cytokinesis
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19
Q

where are the 3 cell cycle check points

A

late G1 (G1/S)
G2/M
metaphase-anaphase

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20
Q

function late G1 checkpoint

A

checks integrity of DNA

cell commits to cell cycle entry and chromosome duplication (occurs in S)

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21
Q

function of G2/M phase

A

checks proper chromosome duplication
checks environment is favourable
checks all DNA are replicated
triggers early mitotic events

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22
Q

cell cycle checkpoint metaphase-anaphase

A

checks proper attachment of kinetochore
stimulates sister chromatid separation
checks all chromosome are properly attached to the spindle

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23
Q

what is APC

A

adenomatous polyposis coli
tumour suppressor gene
negative regulator of B-catenin

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24
Q

somatic APC mutation

A

loss of binding to B-catenin
loss of inhibition of Wnt signalling
initiates tumour growth - loss of control of cell cycle

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25
Q

germline APC mutation

A

causes familial adenomatous polyposis

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26
Q

what is p53

A

tumour suppressor gene

involved in regulation of cell cycle and apoptosis

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27
Q

what triggers p53 production

A

DNA damagr

stress signal

28
Q

defective p53

A

abnormal cell proliferation

cancer

29
Q

function of mdm2

A

negative regulator of p53
maintains low conc of p53 at homeostasis
represses p53 by constant phosphorylation and ubiquitination

30
Q

what is mdm2

A

negative regulator of p53

31
Q

regulation of G1/S checkpoint

A

p53 activation stimulates p21

cell cycle arrest

32
Q

function of p21

A

stimluated by p53

cdk inhibitor p21-CDK2 complex causes cell cycle arrest

33
Q

what is ras

A

family of small gtp-ases

membrane-associated guanine nucleotide binding protein

34
Q

function of ras

A

regulates genes involved in cell growth, differentiation, survival
acts as an ‘on’ or ‘off’ switch

35
Q

GDP bound

A

resting state

36
Q

ras as a proto-oncogenes

A

mutant ras is always ‘on’

leading to continuous growth and proliferation

37
Q

examples of mitogens that bind to RTKs

A

vegf - insulin

growth factor

38
Q

outline steps in MAPK cascade

A 
ligand binds
receptor dimerisation + transautophosphorylation
Grb2 binds - SH2 domain
SOS (GEF)
activates Ras by GTP exchange
Ras.GTP complex phosphorylates Raf
raf phosphorylates MEK
MEK phosphorlates ERK
ERK translocates to nucleus
phosphorylation of transcription regulators 
transcripton
39
Q

mitogen

A

protein that binds and induces cell division and therefore mitosis

40
Q

when does the MAPK cascade stop

A

when a GTPase hydrolyses Ras.GTP to Ras.GDP

41
Q

importance of DNA repair genes

A

detect damaged DNA

repair DNA to facilitate accurate DNA replication

42
Q

mechanism of DNA repair genes

A

detect damaged dna e.g. hypoxia/cell injury
phosphorylate and activate p53
p53 transcribes apoptotic factors
p53 activates p21 - cell cycle arrest via CDK2

43
Q

example of DNA repair gene that is also a tumour suppressor

A

BRCA1

BRCA2

44
Q

longest wavelength on electromagentic spectrum

A

radio waves

45
Q

effect of longer wavelength on frequency and energy

A

longer wavelength = lower frequency and lower energy

46
Q

relationship between energy and wavelength

A

energy is directly proportional to wavelength

47
Q

radiotherapy as cancer treatment

A

x-rays targeted at tumours
ionising radiation causes cell death
cell cycle arrest
induced apoptosis

48
Q

whaat measurements are taken to TNM stage a patient

A

x-ray

lab test

49
Q

N in TNM staging

A

number of nearby lymph nodes that are cancerous

50
Q

uses of TNM staging

A

help plan treatment - indication of prognosis
assist in evaluation of results
indentify relevant clinical trials
enable global collation of information

51
Q

3 stages of gastric acid secretion

A

cephalic phase
gastric phase
intestinal phase

52
Q

what initiates cephalic phase

A

smell or taste of food

hunger

53
Q

what mediates cephalic phase

A

parasympathetic and enteric (submucosal plexus) NS

54
Q

when does cephalic phase of gastric secretion take place

A

before food has entered stomach

55
Q

when does gastric phase of secretions take place

A

when food arrives in stomach

56
Q

what effects does the presence of gastrin have

A

HCl secreted from parietal cells

histamine produced

57
Q

histamine production…

A

increases HCl produtcion

58
Q

why is HCl needed for digestion

A

to create acidic environment

proteins increase the pH

59
Q

why is intestinal phase of gastric secretions important

A

promotes continued digestion in small intestine

60
Q

what inhibits intestinal phase gastric secretions

A

CCK
somatostatin
secretin

61
Q

which nutrients are absorbed in intestine

A

proteins
carbohydrates
lipids

62
Q

protein absorption in intestine

A

brush border enzymes break peptides into amino acids in GI tract
amino acids transported by active transport from GI tract into enterocytes

peptides co-transported by PepT1 into enterocytes, then broken down into amino acids by peptidases

63
Q

how are absorbed proteins transported from enterocytes to liver

A

via hepatic portal vein

64
Q

carbohydrate absorption in intestine

A 
enzymes break carbohydrates into monosaccharides 
facilitated diffusion (Na+/H+ exchange pump)
GLUT channel-facilitated diffusion
65
Q

lipid absorption steps

A

bile salts- emulsifies fat globules to fat droplets
lipase forms micelles (fat droplets surrounded by bile salts) which can directly pass through intestinal endothelium - across enterocytes
micelles form chylomicrons (tiny fat droplets)

66
Q

how do absorbed fat droplets (chylomicrons) reach the liver

A

chylomicrons carried away by lacteals (lymphatic vessel) into lymphatic system into liver

67
Q

2 diseases making up IBD

A

chrons

ulcerative colitis

DDT (12 decks)

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