Project!

Project deferred. More to come....

Woooooh.

Yeah, passed all my units. That's all that counts I guess. Didn't manage any HDs which irked me a bit but hey, 3x D's + 1x C isn't TOO bad I guess. Not too good, yet not too bad.

que?

Overdue

Its been quite some time since I've last posted. Having said that, I've decided a new post/entry should be in order.

Anyhow, most of you would've finished exams by now (you lucky bastards, you). As for me, 3 of 6 completed. Absurd how I get 6 exams :(

As far as studying is concerned, I've hardly done any. The majority of time I allocated to studying was wasted on random gaming. So much for aiming for a D/HD average.

I intend to write more but I honestly cannot be bothered, so I guess i'll start studying for my exam tomorrow.....or not.

So i'm blogging in a lecture...

Using this as a notepad :D

An elderly person was suffering from hypertension and heart failure that was manifested by oedema in the lungs, causing pulmonary congestion, and peripheral oedema, causing swelling in the lower limbs.

(i) List the class of drugs that could be prescribed to decrease the patient's extracellular fluid volume, including an example of each type and their mechanism of action (3 mins)

• Loop diuretics - i.e. frusemide
• Thiazides - acting on distal convoluted tubules to inhibit Na/Cl reabsorption
  

(ii) On another visit to the doctor, the cardiac glycoside digoxin was prescribed as the patient was suffered from severe heart failure. What drug interactions should the doctor be aware of that may increase the toxicity of dogixin? Explain the mechanisms causing this potential drug interaction (4 mins)

• Thiazides, frusemide - loss of K+
  
• Digoxin competes for K+ channels - the less K+ present, more chance digoxin will bind to channels -> toxicity
  

On the patient's next visit, the doctor indicates that other treatment options also need to be considered because of the patient's electrolyte imbalance.

(iii) What is the likely ion imbalance? Give an example of each of the treatment options that the doctor should consider, including mechanisms of action for correction of the electrolyte imbalance (3 mins)

• K+ imbalance
• Potassium-sparing diuretics - i.e. aldosterone, Na+ channel blockers
• Potassium supplements

------------------------------------------------------------------------------------------------
The following drugs were prescribed to an elderly patient with 'heart problems': aspirin, simvastatin, captopril, atenolol, warfarin.

(i) For each drug, suggest a clinical state/disease for its intended use, and indicate the mechanisms of action that are likely to contribute to the beneficial effects observed in this situation.

• Aspirin - irreversible COX inhibitor
• simvastatin - lipid lowering drug
• captopril - ACE inhibitor
• atenolol -selective beta-1 adrenoceptor antagonist
  
• warfarin - anticoagulant
  

-------------------------------------------------------------------------------------------------
An elderly man is diagnosed with hypertension and benign prostatic hyperplasia.

(i) List the symptoms of these 2 conditions.

(ii) Discuss the treatment options for benign prostatic hyperplasia.

• Surgery
• 5-alpha reductase inhibitors - i.e. finasteride
  
• alpha blockers
  

(iii) The doctor prescribes a class of drugs and explains that this will 'provide benefit for both the hypertension and benign prostatic hyperplasia'. Give an example of this particular class of drug and discuss its mechanism(s) of action for both conditions, as well as potential side-effects.

• alpha blocker - anti-hypertensive, blocks tonic activity in blood vessels and prostate.
• Side-effects = dizziness
  

Hectic.

Its been quite a while since I've last updated. Or rather, its been a while since I've been able to update. These past few weeks (namely this current week) have been my most busiest weeks this year, let alone during my uni life (albeit, its been quite short).

The amount of assessment deadlines this week would be considered nothing short of madness, insanity, absurd even. My educated guess would be that most uni students would be in the same position I'm in right now with all the assessments and whatnot.

In other news, I've decided to apply for a Pharmacology Research Project next semester! After several emails back and forth with the Unit Coordinator, I found out quite a bit of information regarding the unit. The prerequisite for said project is a Distinction (≥70%) average in both first semester Pharmacology units (PHA3011 and PHA3021). Judging by my progress so far, its going smoooooothly, as one would put it. Albeit, my PHA3011 average dropped a fair bit after the results of the group assignment was released yesterday qq (although an average of 80% is still good). PHA3021 progress has been really good thus far, but in perspective, its not all that much considering we've only completed practicals (15%) and a mid-semester test (15%).

Having said that, the list of potential projects (and their respective supervisors) was posted up just recently. Of the listed projects, only two of them really stand out (to me, at least);

• Monash Venom Group; Details

• Drug Discovery Biology (maximum of 3 students); Details
  

I'm leaning towards Drug Discovery Biology as the field of research that's associated with it (G-protein coupled receptors; GPCRs) really appeals to me. Alas, they just recently moved their lab to Parkville so I might end up having to go to Parkville for one day, Clayton for the remainder of the week. Else, I'll just go with Venoms and Toxins (awesome stuff) and stay in Clayton.

The only disadvantages I could find with undertaking with said project are that;

1. 12 contact hours per week; 6 hour lab + 6 hours of self-direct learning (analysing data, reading scientific literature, preparing presentations, working on reports).
2. For a major unit like this (12 contact hours!), its only worth 6 credit points; the same amount of credit points to that of a normal unit :(

So I guess for the next few days, I'll be contacting relevant individuals to the aforementioned projects, filling a myriad of forms then hope I do reasonably well in the upcoming exams in order for me to get into the unit. If it all doesn't go according to plan, well, I rather not think about that.

NB: this post was updated from the placeholder inserted here a while back, hence the old posting date. This post has been published as at 27/05/09.

I'm on the brink of insanity!

I'm this close |-----| to cracking it.





I just realized I am incapable of blogging more than a few lines.

I'm awesome!

Huh?!

Pharmacology Mid-semester test - HD.

D:

Not much to blog about~

jrwivhjnegswildshfiuwasdghfuwiocbdwlfhuewiulso stress.

Just spent countless hours on a report I severely underestimated. Sure the instructions were short and simple. But I just HAD to extend it and go into so much damn detail. Well there goes my weekend.

What was meant to be a simple 3-4 page report mutated into a 10 page; 2764 word wall of text.

Ah well.

Zzz...

Well that was short-lived. Lost motivation to update now :D

Drug Receptor Interactions

Pharmacodynamics - what the drug does to the body
Pharmacokinetics - what the body does to the drug

Pharmacokinetics follows the ADME scheme;

• Absorption
• Distribution
• Metabolism
• Excretion

Definitions

KD = dissociation constant. Measures ability for an object to dissociate into smaller objects.

Clark's Model

• Magnitude of response in proportional to drug-receptor (DR) complex

=> maximal response occurs when all receptors are occupied

EC50

• Concentration of agonist that produces a response which is 50% of its maximum
• Measure of agonist potency
  
• pD2 = -logEC50

Affinity

• Ability of a drug or ligand to bind to a receptor site

Efficacy

• Ability of a drug or ligand to generate a response once bound to a receptor

Potency

• Dose or concentration at which a drug produces an effect

Molecular targets for drug actions

Receptors

• Nicotinic / muscarinic receptors

Ion channels

• Ca2+ channels
• Na+ channels

Enzymes

• Acetylcholinesterase

Carrier proteins

• Noradrenaline transporters

Antagonism

Competitive

• Occupies receptor site but generates no response
• No depression of maximum
• Parallel shifts rightwards
• Reversible
  

Non-competitive

• Covalently binds to receptor site
• Depression of maximum at high concentrations
• Irreversible
• i.e. Phenoxybenzamine (PBZ)

Schild Plot

• Tests for competitive antagonism
• Linear plot = competitive

pA2

• Negative log10 of the antagonist concentration by which it is necessary to double the antagonist concentration to produce the same response as was obtained in the absence of the antagonist

• Only relevant when antagonist is competitive

• Compares relative potency of two competitive antagonists

• pA2 increases = decrease in the concentration of antagonist required to shift the concentration-response curve ( = more potent the antagonist)

Introduction

As you can see, this blog is relatively empty. Over the next few days (....or weeks), I'll post text-only summaries for topics covered in PHA3011 (Principles of Drug Action). Don't ask why :)