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DDT > Trigger 5 > Flashcards

Trigger 5 Flashcards

1
Q

Describe the MAPK cascade (mitogen activated protein Kinase)

A

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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2
Q

What is DCC

A

deleted in colorectal carcinoma

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3
Q

Role of DCC

A

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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4
Q

Role of APC

A

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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5
Q

desrcibe the stages of Wnt siganlling when absent

A 
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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6
Q

desrcibe the stages of Wnt siganlling when present

A 
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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7
Q

What is Inflammatory bowel dsease

A

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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8
Q

tests for IBD

A 
primarily done without lab tests
lab tests
-stool culture 
- ova and parasite examination of stool
- coalic test 
- WBC test
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9
Q

treatments for IBD

A

anti-inflammatory drugs
steroids
immunosuppressants
antibiotics

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10
Q

Crohns disease

A

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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11
Q

symptoms of Crohns

A 
diarrohea
abdominal pain
fatigue
weight loss
blood or mucous in faeces
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12
Q

Ulcerative colitis

A

primarily affects the surface lining the colon

tissue inflammation normally continous

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13
Q

symptons of Ulcerative colitis

A

diarrohea
cramping pain
fatigue
loss of appetite

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14
Q

What are colon polyps

A

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

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15
Q

sypmtons of colon cancer

A 
change in bowel habits 
rectal bleeding 
persistent abdominal discomfort 
weight loss 
weakness/fatigue
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16
Q

diagnosing colon cancer

A

colonscopy

blood test

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17
Q

What are DNA repair genes

A

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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18
Q

Lynch syndrome/HNPCC

A

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

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19
Q

desribe the metastic cascade

A

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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20
Q

What is bioavailabilty

A

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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21
Q

Factors that influence bioavailabilty

A

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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22
Q

Volume of distribution

A

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

23
Q

factors affecting Volume of dustribution

A 
drug size 
drug lipophilicty 
plasma protein binding 
body compostion 
patient age/gender
24
Q

measuring volume of distribution

A

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

25
Q

Drug clearance

A

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

26
Q

Zero order kinetics

A

constant amount of drug cleared per unit of time

irrelevant of how much you intake

27
Q

first order kinetics

A

constant proportion of drug cleared per unit of time

double amount of drug - double time taken to clear

28
Q

plasmas half life

A

time taken for plasma conc of a drug to reduce by half

drug clearence and volume of distibtuion affect plasma half life

29
Q

Drug targeting

A

targeting of drug delivery to site of action

30
Q

benefits of drug targeting

A

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

31
Q

recombinant proteins

A

produced by gentically modified organisms

follows same process as recombinant dna

32
Q

advantages of recombinant proteins

A

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

33
Q

oral administraion

A

via mouth and swallowed

absorbed in small intestine

34
Q

sublingual adminstration

A

absorbed directly from oral cavity

pass directly into systemic circiualtion

35
Q

rectal administration

A

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

36
Q

stage of glycolysis

A 
glucose 
glucose 6P
fructose 6P
fructose 1-6P
G3P
pyruvate
37
Q

glycolysis

A

breakdown of glucose

38
Q

gluconeogenis

A

non CHO stores forming glucose

39
Q

stages of gluconeogenis

A 
TCA cycle - Oxalocate 
pyruvate and phophophoenolpyruvate 
G3P
fructose 1-6P
fructose 6P
glucose 6P
glucose
40
Q

Glycogenolysis

A

fromation of glucose from glycogen

41
Q

glycogenolysis stage

A 
glycogen
          (phosphorylase b --> phophoryalase a) 
glucose 1P 
          (phosphoglucomutase)
glusoce 6P
          (glucose 6 phosphatase)
glucose
42
Q

glycogensis

A

formation of glycogen

43
Q

stages of glyogensis

A 
glucose
         (hexokinase)
glucose 1P 
        (phosphoglucomutase)
glucose 6P
UDP glucose 
a glucose 
         (glycogen synthase)
glycogen `
44
Q

Glucagon

A

relaesed from islets of langerhans

stimulated by decreased blood glucose

45
Q

effects of glucagon

A

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

46
Q

glucose transporters

A

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

47
Q

GLUT 1

A 
found in most cells 
function - glucose uptake
48
Q

GLUT 2

A 
found in - liver, kidneys, small intestine, pancreas 
function - rapid uptake or relase of glucose
49
Q

GLUT3

A 
found in - brain, kidneys, placenta 
function - glucose uptake
50
Q

GLUT 4

A 
found in - liver, muscle and fat 
function - insulin stimulated glucose uptake
51
Q

GLUT 5

A 
found in - small intestine
function - glucose uptake
52
Q

inuslin

A

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

53
Q

Insulin recepetor

A 
transmembrane, tyrosin kinase receptor 
two alpha and two beta subunits 
insulin binds to alpha subunit 
beta subunits phosophrylate themsleves 
activates intracellular proteins 
generates response
54
Q

electromagentic sepectrum order

A 
radio wave 
microwaves 
infrared 
visible light 
ultraviolet
xrays 
gamma rays

DDT (10 decks)

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