Trigger 5 Flashcards by Anna Parker

Describe the MAPK cascade (mitogen activated protein Kinase)

Grwoth factor and insulin ligands bind to receptor
Dimersation
tryosine domains trans-auto phosphorylate themselves
attarct any protien with a SH2 receptor
Grb2 attached
SOS activated, SOS is a GEF
activates Ras, GTP in activate site of RAS, stimulates pathway
activates Raf
phosphorylates futher kinase
ERK binds to DNA

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What is DCC

deleted in colorectal carcinoma

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Role of DCC

acts as a tumour supressor and proto oncogene
activates MAP kinase cascade
has its own ligand - nitrin 1
dependance receptor
with ligand, stimulates MAp kinase cascade
without lignad it actiavtes caspase leading to apoptosis

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Role of APC

inviolved in Wnt signalling
when there is no lignad, APC part of destruction complex

if APC mutated it inhibits kinase of destruction complex, unregulatted growth

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desrcibe the stages of Wnt siganlling when absent

no ligand binding to frizzled 
complex of APC, axin and a kinase = destruction complex 
phophorylates B-catein 
Bcatein ubiquinated
protesomnal degradation
no transcription

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desrcibe the stages of Wnt siganlling when present

Wnt binds to Frizzled 
dishevelled activated 
inhibits kinase of destruction complex 
B-catein not phosphorylted so not ubiquinated 
transolation to nucelus 
gene transcription

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What is Inflammatory bowel dsease

relapsing and remitting conditon chaarctized by chronic inflammatory at sites in the GI tract

results from cell mediated immune response in the GI mucosa

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tests for IBD

primarily done without lab tests
lab tests
-stool culture 
- ova and parasite examination of stool
- coalic test 
- WBC test

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treatments for IBD

anti-inflammatory drugs
steroids
immunosuppressants
antibiotics

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Crohns disease

can affect any part of the GI tract
80% in the SI
Affected areas are patchy
can casue narrowing of the GI tract, ulcers or fistulas

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symptoms of Crohns

diarrohea
abdominal pain
fatigue
weight loss
blood or mucous in faeces

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Ulcerative colitis

primarily affects the surface lining the colon

tissue inflammation normally continous

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symptons of Ulcerative colitis

diarrohea
cramping pain
fatigue
loss of appetite

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What are colon polyps

small clumps of cells that form on the lining on the colon
neoplastic
Non-neoplastic polpys

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sypmtons of colon cancer

change in bowel habits 
rectal bleeding 
persistent abdominal discomfort 
weight loss 
weakness/fatigue

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diagnosing colon cancer

colonscopy

blood test

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What are DNA repair genes

code for proteins whose normal function is to correct errors that arise when cells duplicate the DNA prior to cell division

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Lynch syndrome/HNPCC

inherited disorder that increase rick of many types of cancer
faulty repair genes
MLH1, MSH2, MSH6 and PMS2

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desribe the metastic cascade

release of tumour cell from primary tumour and invasion of basement membrane, secrete MMPs to breakdoen tissue
intravasion into a capillary
in the blood supply, invades the immune system
- leukocyte bind to it
- platelts bind, can be protective
- met with other tumour cells
arrest and extraversion into target organ, produces CAM1 to help stick to endothelium
growth in new environment and formation of secondary tumour

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What is bioavailabilty

the proportion of an administered drug that reached the systemic circulation

area under the curve or oral does/area under the curve of IV dose
% of measured relative to IV dose

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Factors that influence bioavailabilty

nature of the drug

- Gi transit and digestion 
- first pass metabolism - breakdown of the drug by the liver before it has entered the systemic circulation     - route of administraion - IV direct into blood stream, oral breakdown via GI tract     - Lipophilicty - ability to cross plasma membrane

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Volume of distribution

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apparent voulme of distrubution, theoritcal value
after absorption, drug equilibrate bewteen plasma and tissues
drug conc measure in plasma, less in plasma = more distrubuted

factors affecting Volume of dustribution

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drug size 
drug lipophilicty 
plasma protein binding 
body compostion 
patient age/gender

measuring volume of distribution

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measuerd following IV administraion of known amount of drug
amount of drug in body/plasma conc
e.g high plasma=low Vd = drug not widely distributed

Drug clearance

volume of plasma cleared of the active compound per unit of time

Zero order kinetics

constant amount of drug cleared per unit of time | irrelevant of how much you intake

first order kinetics

constant proportion of drug cleared per unit of time | double amount of drug - double time taken to clear

plasmas half life

time taken for plasma conc of a drug to reduce by half drug clearence and volume of distibtuion affect plasma half life

Drug targeting

targeting of drug delivery to site of action

benefits of drug targeting

reduces side effects, espcailly when non-specific mechanisms of action allows lower dose to be given more predictable biological effects

recombinant proteins

produced by gentically modified organisms | follows same process as recombinant dna

advantages of recombinant proteins

high % of purity recombinant protiens show higher specific activity continous supply high leves of consistency is seen in batch to batch productions

oral administraion

via mouth and swallowed | absorbed in small intestine

sublingual adminstration

absorbed directly from oral cavity | pass directly into systemic circiualtion

rectal administration

required for drugs to either produce a local effect or to produce systemic effects often unrelaible useful in patients who are vomiting

stage of glycolysis

``` glucose glucose 6P fructose 6P fructose 1-6P G3P pyruvate ```

glycolysis

breakdown of glucose

gluconeogenis

non CHO stores forming glucose

stages of gluconeogenis

``` TCA cycle - Oxalocate pyruvate and phophophoenolpyruvate G3P fructose 1-6P fructose 6P glucose 6P glucose ```

Glycogenolysis

fromation of glucose from glycogen

glycogenolysis stage

``` glycogen (phosphorylase b --> phophoryalase a) glucose 1P (phosphoglucomutase) glusoce 6P (glucose 6 phosphatase) glucose ```

glycogensis

formation of glycogen

stages of glyogensis

``` glucose (hexokinase) glucose 1P (phosphoglucomutase) glucose 6P UDP glucose a glucose (glycogen synthase) glycogen ` ```

Glucagon

relaesed from islets of langerhans | stimulated by decreased blood glucose

effects of glucagon

on blood glucose - stimulates glycogeolysis, inhibits glycogen - stimulates gluconeogensis, decreases PFK activity - increase blood glucose conc on blood fatty acid and ketoacid - increases lypolysisand inhibits fatty acid synthesis

glucose transporters

transmembrane proteins faciliates the movement of glucose across plasma membranes driven by concentration gradient binding of glucose causes a transforamtional change

GLUT 1

``` found in most cells function - glucose uptake ```

GLUT 2

``` found in - liver, kidneys, small intestine, pancreas function - rapid uptake or relase of glucose ```

GLUT3

``` found in - brain, kidneys, placenta function - glucose uptake ```

GLUT 4

``` found in - liver, muscle and fat function - insulin stimulated glucose uptake ```

GLUT 5

``` found in - small intestine function - glucose uptake ```

inuslin

peptide hormone prodcued by beta cells in the iselts of langerhans regulates metaboism of CHO, Lipid and protein

Insulin recepetor

``` transmembrane, tyrosin kinase receptor two alpha and two beta subunits insulin binds to alpha subunit beta subunits phosophrylate themsleves activates intracellular proteins generates response ```

electromagentic sepectrum order

``` radio wave microwaves infrared visible light ultraviolet xrays gamma rays ```

Trigger 5 Flashcards

(54 cards)