BMD225 revision cards for week 1 -4

What are the main factors regulating insulin secretion?

Blood Glucose concentration - main, GIT - gastrrointestinal tract hormones (GIP, GLP-1), Sulfonylureas - release insulin

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What does insulin do?

Increases glucose uptake by Glut-4 in adipose tissue and muscle, inhibits glycogen breakdown so makes glycogen, synthesises glycogen, anabolic hormone, has alpha and beta subunits

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Describe the insulin receptor?

A large transmembrane glycoprotein complex belonging to the tyrosine kinase linked type 3 receptor superfamily

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What is diabetes mellitus and what can it cause?

Total/relative insulin insufficiency, characterised by hyperglycaemia. Causes: polyuria, ketoacidosis,increased thirst and polydipsia, appearance of glucose in urine

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What are the two forms of DM?

Type 1 (IDDM/ Juvenile Onset Diabetes) and Type 2 (NIDDM)

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What are some facts about Type 1 diabetes?

Type 1; often autoimmune, absolute insulin deficiency , usually see in young but can be seen in all ages, not usually about obesity, problem is with B cells

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What are some facts about Type 2 diabetes?

Mainly due to obesity, accompanied by insulin resistance and by impaired insulin secretion, B cell function declines, treatment is initially dietary then oral methods

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On a graph comparing normal people with type 1 and type 2 diabetics what would you expect to see?

For normal - biphasic point in the 1st phase (rapid start then slow onset). Type 2; 1st phase missing, 2nd phase slightly present. Type 1; Both phases missing. In 1st phase also produced by AA, sulfonylureas, glucagon and GI tract

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What are the different types of insulin?

Rapid acting, short acting (Regular), intermediate acting (NPH), intermediate and short acting mixtures, long acting

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What are some diabetic complications (long term) ?

Neuropathy; nerve damage, can predispose someone to atherosclerosis, associated with accumulation of osmotically active metabolites of glucose produced by the action of aldose reductase. Nephropathy, Peripheral vascular disease, retinopathy, CHD,

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In the pancreas where there is beta cell dysfunction what are the drgus that work to decrease glucose level?

Sulfonylureas, Glinides, DPP-4 inhibitors

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In muscle and Fat, where there is insulin resistance, what are the drugs that work to decrease glucose level?

TZDs (Glitazones), Biguanides

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In the gut where there is glucose absorption, what are the drugs that work to decrease glucose level?

Alpha glucosidase inhibitors, Biguanides

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In the liver, where there is hepatic glucose overproduction, what are the drugs that work to decrease glucose level?

Biguanides, TDZs (Glitazones), DPP-4 inhibitors

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What type of insulin has the greatest range of activity?

Rapid actin because of the surface area causing it to take a long time to reach the peak

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What are the complications of insulin therapy?

Hypoglycaemia, Immune mediated responses

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What are the causes, symptoms and treatment for hypoglycaemia?

Insulin dose too large, individual misses a meal, physical exertion. Mental confusion, palpitations,sweating,trembling,coma. Glucagon administrtion

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#what nis the use of HbA(1c-smallscript)

Lowering it reduces risk of complications. It is called glysated haemoglobin and is often used as a marker for severity of a disease. The levels of it show a positive correlation with severity of diabetes.

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Tell me about Biguanides - metformin?

They don't require a functioning Beta cell for their therapeutic effect, They: slow down GI absorption of glucose, increase the uptake of glucose into skeletal muscle, reduce glucagon, decrease hepatic gluconeogenesis, affects insulin.

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What are the disadvantages/advantages of biguanides?

Not well tolerated by all which can lead to sulphonylureas. Adv: Doesn't cause hypoglycaemia/stimualte appetite.

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First generation examples of sulphonylureas?

Tolbutamide, Chlorpropamide.

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second generation examples of sulphonylureas?

Glibenclamide, Glipizide.

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What are the disadvantages of sulphonylureas?

Pronounced hypoglycaemia, stimulate appetitie, often cause weight gain.

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What is the mechanism of action for sulphonylureas?

Block ATP dependent K+ channels (that can be found on the surface membranes of B cells), Bind to an ABC causing channel to close, closure results in beta cell depolarisation, calcium entry and insulin release.

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What makes sulphonylureas different and similar to biguanides?

Similar: Treat Type 2 diabetes in its early stage. Difference: Requires functional Beta cells.

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What is the role of Glinides?

Modulate beta cell insulin release - regulates K+ efflux, control post prandial glucose increases - resotres initial insulin concentration.

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Benefit of glinides?

Lower hypoglycaemia because they associate adn dissociate from binding site more rapidly so provide a better overall safety profile when looking at occupancy for binding sites.

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Role of thiazolidinediones (Glitazones)?

Insulin sensitizers that act on the peroxisome proliferator activated receptor gamma. Enhance the effectiveness of endogenous insulin thereby reducing hepatic glucose output and increasing glucose uptake into muscle. Act on nuclear receptors.

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Thiazolidinediones by reducing blood glucose concentration what is the implication?

Reduced insulin, free fatty acid concentration, decline of triglycerides, LDL and HDL are unchanged/slightly increased. The proportion of small dense LDL particles is reduced

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Problem with thiazolidinediones?

Weight gain of approx 1-4 kg

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Tell me about alpha-glucosidase inhibitors - acarbose?

helpful for obese type 2 diabetes, slow carb absorption.

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What trial is used in relation to acarbose?

STOP_NIDDM) trial; therapy in orediabetic individualss, reduces new cases of type 2 diabetes, helps restore b cell function

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What are the problems with alpha-glucosidase inhibitors?

Has no effect on insulin secretion/it's tissue action and is less effective for achieving glycaemic control, flatulance, loose stools/diarrhoea, abdominal pain, bloating, oral absorbtion is very low.

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Benefit of alpha glucosidase inhibitors?

The slow carb absorption means the postprandrial increase in blood glucose is reduced.

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What are the two different types of incretin mimetics and enhancers?

GLP-1 agonists, Dipeptidyl peptidase 4 inhibitors -mimics effect of GLPs, don't cause weight loss/gain

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Of those types what are the examples?

1. Exrenatide - peptide found in saliva of Gilatide monsters, Liraglutide. 2. Vildagliptin, Sitagliptin - Both lower blood glucose by potentiating GLP1 + GIP which stimulate insulin secretion.

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Problems that incretin mimetics and enhancers can cause?

GI effects, Pancreatitis, Occasional Liver Disease, Worsening of heart failure

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What is amylin?

a peptide hormone cosecreted with insulin from the pancreatic Beta cell and is therefore deficient in diabetic people. It inhibits glucagon secretion, delays gastric emptying and acts as a safety agent.

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What are the 3 types of chemical communication?

Endocrine, Paracrine, Neurotransmitters

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What systems make up the autonomic nervous systerm and briefly what are their roles?

Sympathetic - Fight/Flight, Parasympathetic - Rest/Digest. ANS conveys message from CNS to rest of body, regulates contraction/relaxation etc.

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What did Loewi figure out?

Stimulation of the vagus caused the appearance in the perfusote of the frog heart of a substance capable of producing in a second heart an inhibitory effect. He named it "vagusstoff"

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What drugs inhibit cholinergic transmission?

ACHE (neostigmine) , Non depolarising blocking agents (Tubocuraine), Presynaptic toxins (Botulinum), Vesamicol, Hemicholinium

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What drugs activate cholinergic transmission?

Depolarising blocking agents (Suxamethonium)

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NAme some clinical uses of botulinum toxin?

Neuromuscular; Facial wrinkles, pain conditions. Autonomic - Hyperhidrosis, GI disorders

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What are the 3 types of ACHE?

Short duration, medium duration, irreversible.

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What are the criteria for identifying a neurotransmitter

Chemical must be found within a neuron, must be produced within a neuron. When a neuron is stimulated it must release the chemical. When chimcal is released it must act on a post-synaptic receptor and cause an effect. After release: inactivation

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What are the differences in the ganglionic fibres and location between parasympathetic and sympathetic?

Parasympathetic - Long preganglionic fibres, ganglion in target tissue, short postganglionic fibres. Sympathethic - reverse.

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In the autonomic nervous system what can be said about the other 2 ganglionic gibres of the efferent nerves.

To the somatic (voluntary) there is only a single fibre. To the adrenal medulla there is a shorter single fibre with the ganglion in the paravertebral chain.

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In the autonomic nervous system what neurotransmitters are released and where?

All nerve fibers leaving CNS release Ach. Parasympathetic - ACH in both post and pre. Sympathetic - NA/ACh (sweat glands)

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In the autonomic nervous system on what receptors do the neurotransmitters act on.

All nerve fibers leaving CNS act on nicotinic receptors. Parasympathetic: Post - acts on MUSCARINIC. Sympathethic - acts on alpha/beta adrenoreceptors or MUSCARINIC.

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What are the steps in neurotransmission?

Uptake of precursors, NT synthesis, NT storage, Breakdown of surplus NT, DEP, influx of Ca, Exocytosis release, Diffusion, Interaction with Post Membrane, Inactivation, Reuptake, Uptake by non neuronal, Presynaptic receptor interaction

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What are the two types of presynaptic modulation?

Heterotropic - can casue conversion between PS and S, A NT is affecting the release of another NT from a distinct site. Homotropic - causes feedback from site in which it's released.

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What is noradrenaline, what is its role?

ANS - postganglionic sympathetic nerve endings. Acts of alpha and beta adrenoreceptors. alpha 1 - activate phospholipase C, alpha 2 - inhibits adenylate cyclase, Beta 1,2,3 - stimulate adenylate cyclase.

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What is the route for synthesis of NA?

Tyrosine, DOPA, Dopamine, Noradrenaline, Adrenaline.

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How is NA released?

It's stored in vesicles, presynaptic mechanism regulates it's release, monoamine oxidase/ catechol-O-methly transferase involved in it's metabolism.

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In the smooth muscle how do adrenoreceptor agonists regulate it?

a1 - contraction, b2 - relaxation

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In the cardiac muscle how do adrenoreceptor agonists regulate it?

B1 - inotropic and chronotropic effects

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In metabolism how do adrenoreceptor agonists(sympathomimetic drugs) regulate it?

B1 - carbohydrate, B3 - lipid

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In the nerve terminals how do adrenoreceptor agonist regulate it?

a2 - main affect that mediates, effect is inhibitory, basis of action of clonidine

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What are the uses of b-adrenoreceptor antagonists?

In cardiovascular disease. Non selective - propranolol. B1 selective - atenolol, labetolol

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In the synthesis and release of Ach what are the compounds involved and their roles?

Choline - start, CHat - adds Acetyl Coa, VACHT - puts drugs that affect Ach storage and release in vesicles. Vesamicol - blocks VACHT. HC-3 - hemicholine transporter. ACHE

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What are the 2 different types of activity of exogenous Ach?

Muscarinic - aprasympathetic stimulation. Nicotinic - stimulation of autonomic ganglia.

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What are muscarinic receptors and what are the different types?

GPCR, much slower time course of action than with transmission mediated by nicotin receptors. M1(neural), M2(Cardiac), M3(glandular/smooth muscle

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What are some muscarinic agonists and their effects and uses?

Pilocarpine, Carbachol, Muscarine. Effects: parasympathetic: bradycardia, vasodilation, sweating. PEripheral actions mainly mediated by M2 and M3. Clinical uses: glaucoma and bladder hypotonia.

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What are muscarinic antagonists?

Parasympatholytics - tachycardia, smooth muscle relaxation. All competitive. Clinical applications: atropine - adjunct for anaesthesia, HI hypermotility.

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What differences can be seen between non depolarising and depolarising blocking agents?

Effect of anticholinesterase drugs, fasciculations as a prelude to paralysis.

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What are some examples of nicotinc agonists and antagonists?

Suxamethonium. Trimetaphan, Pancuronium, Atracurium, Vercutonium, Mivacurium.

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What differences can be seen between non depolarising and depolarising blocking agents?

Depolarising: bind to Ach receptors and generate AP. Not metabolised by ACHE so binding is prolonged; extended DP. NonDP - competitive antagonists - bind but unable to induce ion channel openings, prevent Ach from binding

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How do you experimentally deterimine affinity?

Looking at toal bs non specific total bound against concentration. Subtracting the two gives a specificity bound graph. Then a scratchard plot can be made and K and Bmax identified.

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How do you experimentally determine efficacy and potency?

"Take organs for a bath" - bioassay, using saline and adding drugs and measuring magnitude of concentration by force transducer.

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In a concentration response curve what is Emax and EC50 a measure of?

Emax - A measure of efficacy. EC50 - a measure of potency - effective concentration that produces 50% of that maximum response. The smaller the Ec50 the more potent - gets to maximal resposne ar a smaller conc of drug.

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Define efficacy and potency?

Efficacy: ability of a drug to cause a functional response as a result of binding to its receptor. Potency: a measure of drug activity governed by both affinity and efficacy.

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What are the difference and similarities between partial agonsits and full agonists?Partial have a lower efficacy than full agonists bu the same occupancy.

Partial have a lower efficacy than full agonists bu the same occupancy.

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What are the differences between reversible competitive antagonism and irreversible competitibe antagonism?

Reversibel: equilibrium can be shifted to the right by increasing the concentration of agonist and maximal response is unchanged. Irreversible: non equilibrium conditionds due to slow/no dissociation of antagonist from the receptor.

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Can full agonist occupancy be achieved in irreversible competitive antagonism?

No, and the observed maximal response if reduced.

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How do we quantify competitive antagonism?

Using a Schild Plot. Organ bath experiment needs to be conducted enabling the determination of a set of dose ratios plotted against antagonist conc.

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How do we quantify competitive antagonism?

No efficacy so agonist needed, the action of which the antagonist of interest can inhibit. The antagonist potency can be expressed in the form of a PA2 value

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What is the pA2 value?

The negative logarithm of the molar concentration of antagonist which will reduce the response of a tissue to a double dose of agonist to that of a singl dose of agonist.

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What are some other types of antagonism?

Chemical, Pharmacokinetic, Physiological.

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What is occupation governed by?

Affinity.

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What is activation governed by?

Efficacy

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What are the targets for drug interaction?

Receptors, Ion channels, enzymes, Carrier molecules/transporters

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What does the law of mass action give rise to and what does it relate to?

It give rise to Kd (dissociation constant), It relates to the principle that the rate of a chemical reaction is directly proportional to the concentrations of the reacting substances.

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What are the equations involved in the law of mass action?

D+R-->

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If there is a high affinity what does that mean for Kd?

Low

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What are the factors affecting drug metabolism?

Age, Disease State, Gender Differences, Diet, Environment, Drug Interactions, Genetic Differences

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What are the implications of inducing Cp450 enzymes?

Reduction in pharmacodynamic effect of the inducing drug, reduction in effect of coadministered drugs which are metabolised by the same route

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What happens to the laf life of warfarin after repeated rifampicin dosing?

Reduced plasma 1/2 life.

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How does age affect drug metabolism?

Heptic function is lower at birth and old age. Chloramphenicol can cause grey baby syndrome. Diazepam can cause mental confusion in elderly. There is an increase variability and increased 1/2 life with agin.

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How can environmental factors affect drug emtabolism?

They affect cP450 function - inducers/inhibitors. Examples: tobacco, heavy metals, industrial pollutants.

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How can disease state affect drug metabolism?

Liver disease causes lower hepatic function - microsomal oxidases affected, decreased capacity to metabolise drugs. Viral hepatitis causes slower diazepam metabolism - overdose and coma maybe

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How can diet affect drug metabolism?

GFJ interactions - increases plasma felodipine concentrations and alters it's oral bioavailability - increasing cardiac toxicity risk. Increases simvastatin serum concentration - prolonging life

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How else can diet affect drug metabolism?

Glucosinolates in brussel sprouts can induce p450 enzymes that are metabolising enzymes so drug effects and duration of action are diminished.

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How can genetic differences affect drug metabolism?

Causes a large fold variation in response to a drug, often due to SNPs

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How else can genetic differences affect drug metabolism?

CYP2D6 polymorphisms are responsible for the metabolism of a lot of important drugs. Within a european pop 4 phenotypes: PM, IM, EM (highest frequency in caucasians), UM.

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What is warfarin and how do genetic differences affect it's drug metabolism?

Anti coagulant, wide variation in dose requirements depending on haplotype. Gene guided dosing takes into account the patient genotype for CYP2C9 and VKORC1.

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What is isoniazid and how do genetic differences affect it's metabolism?

Anti-TB drug. Metabolised by acetylation. Two types: fast acetylators (may lead to higher blood levels of drug and increase in toxicity), slow acetylators (60%, respond well) - types inherited, ratio varies

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How does isoniazid compare with salicylate?

S - normally distributed. I- bimodial distribution.

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Do receptor polymorphisms as part of genetic differences play a part in drug response?

yes, eg %-HT2C - can cause increased body fat.

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How does gender affect drug metabolism?

Sex hormones can change expression pattern. In phase 1 and 2 only CYP2C9 shows no sex differences in clearance values. In phase 2 only conjugation N-acetyltransferase mixed with caffeine/dapsone will show no sex differences in clearing.

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Which hepatic gene mixed with which model substrate show increase in clearance in women.

CYP3A4 - midazolam.

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What are the different ways drugs can be administered?

Oral/Rectal, PErcutaneous, Intravenous, Intramuscular, Intrathecal, Inhalation.

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How can drugs be eliminated?

Urine, faeces, milk/sweat, expired air

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What is drug disposition?

The processes a drug is subjected to by the body upon administration. Includes: Absorption,Distribution,MEtabolism, Excretion.

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What is the concept of bioavailability?

It is defined as the fraction (F) of the administered dose that reaches the systemic circulation.

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Which route will have F as 1?

Intravenous injection

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Which route will have F

Particularly oral

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What does the bioavailability of

Gastirc inability of drug, 1st pass metabolism (liver), Reduced absorption into the circulation.

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What are the factors that affect drug absorption?

Gastric motility, area of absorbing surface, blood flow at absorbing surface, ingestion of food, plasma protein binding, nature of the drug.

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What are the different ways a drug can be absorbed across membranes?

Diffusion through lipid, diffusion through aqueous channel, via a carrier, pinocytosis.

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What occurs when a drug is diffused down an ion channel/ aqueous pore?

Movement is down a concentration gradient, the membrane contains small pores which allow water soluble molecules of < 100Da through. Eg Lithium. NOT A MAJOR ROUTE OF DRUG PERMEATION.

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What occurs when a drug moves via carrier mediated transport?

Active transport/facilitated diffusion. Important sites: renal tubule, BBB, GI tract. These transporters can become saturated limiting rate of drug permeation + competition can occur between two ligands that bind to such carriers.

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What occurs when a drug moves via pinocytosis?

Uptakes macromolecules; 1000Da molecular weight or more) e.g insulin crossing the BBB. Attempts to utilise it as target drug uptake mechanism - incorporating the drug into lipid liposomes.

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What occurs when a drug diffuses through lipid membranes?

Common route for most drugs, only small lipid soluble, non polar drugs. Depends on surface area and blood flow. Degree of permeation by this route dictated by Fick's Law.

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What relationship does Fick's law follow?

The amount of drug diffusing with time is directly proportional to the permeability coefficient x membrane area x (concentration of drug either side of the membrane) but is INVERSELY PROPORTIONAL to the membrane thickness.

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What is the implication of a highly lipid soluble drug?

It has a large transmembrane concentration gradient and will diffuse more rapidly than a drug of lower lipid solubility even when the concentration gradient on either side of the membrane is the same.

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What is the effect of ph on drug ionisation?

It allow prediction of absorption.

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What are the henderson hasselbach equations?

for a weak acid: pka=ph+log10[HA]/[A-], for weak base HA becomes BH+ and A- becomes B.

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What is the pKa?

A dissociation constant, negative logarithm of Ka, equal to the ph at which 50% if the drug molecules are ionised.

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What are ionised species and what is their implication?

BH+/A- --> have very low lipid solubility and are virtually unable to permeate membranes without a specific transport mechanism

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What are the implications of the uncharged species?

Lipid solubility depends on their chemical nature, for many they are sufficiently lipid soluble.

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In terms of distribution what body compartment has the largest?

Intracellular water.

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Order the body compartments from largest percentage to lowest.

Intracellular water, Fat, Interstitial water, Plasma water, Transcellular water

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What is the volume of distribution?

The volume of fluid required to contain the total amount of drug in the body at the same concentration as that present in the plasma (Cp)

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How cna Vd be calculated?

Vd= Dose/Cp

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What does the degree of ionisation give rise to?

Ion trapping

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For aspirin which body compartment has it's highest concentration and why?

Urine because urine is alkaline and ionisation of the acidic drug is greatest at alkaline ph.

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For pethidine which body compartment has it's highest concentration and why?

Gastric Juice because as the drug is a weak base ionisation is greatest at an acidic pH.

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How is Vd derived experimentally?

By plotting plasma concentration vs time and then log plasma concentration versus time.

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What are the sites of drug metabolism and what happens to drugs?

Few are eliminated from the body unchanged, most undergo biotransformation. The sites include: liver (major), kidney, lungs, skin, intestine.

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What is the consequence of first pass metabolism, in which organ can it be found and what is the circulation of drugs in that organ?

It reduces bioavailability, in the liver, oral medication--> intestinal tract--> along portal vein to liver--> exits liver from hepatic vein --> systemic circulation--> hepatic artery back into liver.

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What is the process of metabolism?

To change a drug into more water soluble molecules which increase polarity and aid excretion.

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What occurs to drugs in certain instances?

1. Drugs can be activated by metabolism -prodrugs. 2. Metabolites can produce more active metaboliteswhich contribute to the action of the drug

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What does metabolism often consist of?

Phase 1 and Phase 2. Drug --> Derivative (Phase 1) Derivative --> Conjugate (Phase 2)

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What processes are used in phase 1?

Ocidation, Hydroxylation, Dealylation, Deamination, Hydrolysis.

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What process is used in phase 2?

Conjugation.

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What occurs in Phase 1 reactions?

Often enzyme catalysed. Most important: microsomal mixed function oxidase - resides on smooth ER in liver, requires a reducing agent (NADPH) and molecular oxygen. Of these, Cytochrome P450 (a haem protein) is most important.

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What are the non mfo phase 1 reactions?

Oxidaative reactions, cytoplasmic in nature, metabolise ethanol. Mitochondrial: catecholamine metabolism by monoamine oxidase.

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What occurs in Phase 2 reactions?

Occur mainly in the liver, conjugation reactions which occur at polar groups(introdcued during phase 1 reactions), conjugated products are very water soluble, excreted in urine /bile

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What is the most common conjugation reaction and what does it utilise?

Glucoronidation. Uses an endogenous reactant (UDP glucorinic acid), attaches to N,O,S atoms.

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Does paracetamol get metabolised via phase 1/ phase 2 reaction?

Both. Phase 2: Glucoronide/ Sulphate conjugation. Phase 1: via CP450.

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What occurs in paracetamol metabolism?

90% conjugation. remainder oxidation - using CYP2E1 isoform

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How do drugs get excreted?

Mainly in the kidney via clearance.

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What is clearance?

A measure of elimination (depends on both metabolism and excretion). It can also be considered a proprtionality constant between the rate of elimination and the concentration of the drug.

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Is there an equation for clearance?

Rate of elimination/Plasma Concentration

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How can renal clearance be defined as?

A measure of elimination, defined as 'The volume of plasma cleared of drug by the kidney per unit time' (ml/min)

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What are the factors influencing clearance?

Renal processes: Glomerular Filtration, Passive reabsorption, Active Tubular Secretion.

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How can ion trapping cause the urinary pH to influence clearance.

In the example of phenobarbital (weak acid) clearance is greater in alkaline urine than in acidic urine because there is a greater degree of ionisation so the drug is more likely to be absorbed in the urine.

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State the drugs in order of lowest to highest clearance value.

Warfarin, Digitoxin, Diazepam, Ampicillin, Nifedipine, Lidocaine, Propranolol, Imipramine.

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