5 - GI tract dysfunction Flashcards by Sylvie Wilson

what promotes cell cycle progression

cyclins

cdks

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what stops cell cycle progressionq

cdk inhibitors

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quiescence in the cell cycle

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

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early phase of G0

mitogen-dependent

growth factors are required for progression beyond this point

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once the cell progresses past the R point …

.. mitogens are no longer required for cell cycle progression

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cancer stages

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

TNM staging system

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TNM staging system

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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name 4 types of eicosanoid

thromboxane
prostacyclin
prostaglandin
leukotriene

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what two enzymes cut arachindonate

cycooxygenase (COX)

lipooxygenase

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what do COX enzymes cut arachindonate into

prostacyclins H2

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

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

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what cuts membrane phospholipids into arachindonic acid

phospholipase A2

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inihbition of COX enzymes

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

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what happens in G2

cell growth

proteins duplicated

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what happens in G1

cell mass doubles

organelles copied

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order of cell cycle

G1
S
G2
M

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what happens in S phase

synthesis of complete copy of DNA

centrosome duplicates

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order of stages in mitosis

prophase
prometaphase
metaphase
anaphase
telophase
cytokinesis

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where are the 3 cell cycle check points

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

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function late G1 checkpoint

checks integrity of DNA

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

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function of G2/M phase

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

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cell cycle checkpoint metaphase-anaphase

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

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what is APC

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

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somatic APC mutation

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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germline APC mutation

causes familial adenomatous polyposis

what is p53

tumour suppressor gene | involved in regulation of cell cycle and apoptosis

what triggers p53 production

DNA damagr | stress signal

defective p53

abnormal cell proliferation | cancer

function of mdm2

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

what is mdm2

negative regulator of p53

regulation of G1/S checkpoint

p53 activation stimulates p21 | cell cycle arrest

function of p21

stimluated by p53 | cdk inhibitor p21-CDK2 complex causes cell cycle arrest

what is ras

family of small gtp-ases | membrane-associated guanine nucleotide binding protein

function of ras

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

GDP bound

resting state

ras as a proto-oncogenes

mutant ras is always 'on' | leading to continuous growth and proliferation

examples of mitogens that bind to RTKs

vegf - insulin | growth factor

outline steps in MAPK cascade

``` 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 ```

mitogen

protein that binds and induces cell division and therefore mitosis

when does the MAPK cascade stop

when a GTPase hydrolyses Ras.GTP to Ras.GDP

importance of DNA repair genes

detect damaged DNA | repair DNA to facilitate accurate DNA replication

mechanism of DNA repair genes

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

example of DNA repair gene that is also a tumour suppressor

BRCA1 | BRCA2

longest wavelength on electromagentic spectrum

radio waves

effect of longer wavelength on frequency and energy

longer wavelength = lower frequency and lower energy

relationship between energy and wavelength

energy is directly proportional to wavelength

radiotherapy as cancer treatment

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

whaat measurements are taken to TNM stage a patient

x-ray | lab test

N in TNM staging

number of nearby lymph nodes that are cancerous

uses of TNM staging

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

3 stages of gastric acid secretion

cephalic phase gastric phase intestinal phase

what initiates cephalic phase

smell or taste of food | hunger

what mediates cephalic phase

parasympathetic and enteric (submucosal plexus) NS

when does cephalic phase of gastric secretion take place

before food has entered stomach

when does gastric phase of secretions take place

when food arrives in stomach

what effects does the presence of gastrin have

HCl secreted from parietal cells | histamine produced

histamine production...

increases HCl produtcion

why is HCl needed for digestion

to create acidic environment | proteins increase the pH

why is intestinal phase of gastric secretions important

promotes continued digestion in small intestine

what inhibits intestinal phase gastric secretions

CCK somatostatin secretin

which nutrients are absorbed in intestine

proteins carbohydrates lipids

protein absorption in intestine

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

how are absorbed proteins transported from enterocytes to liver

via hepatic portal vein

carbohydrate absorption in intestine

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

lipid absorption steps

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)

how do absorbed fat droplets (chylomicrons) reach the liver

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

2 diseases making up IBD

chrons | ulcerative colitis