Friday, July 23, 2010

I'm not dead, and I haven't forgotten about you all

Just updating to say I intend on continuing this blog with the coming semester. However I left my pencil case in Geelong and my three year old sister (according to my mother) is having a lovely time with it. I'll go buy some more textas soon and try to get this week's lectures summarised. (I may ignore Melvin's lectures, because he annoys me, but if I can manage to find the time I'll do his.)

Here is a Cthulhu joke that I can't take credit for coming up with.

For those of you who don't know the Cthulhu Mythos, just trust me, it's hilarious.

Saturday, July 3, 2010

I'm on a zole!

Today we start on antimicrobials, beginning with antifungals.
The basic function of of azoles is to stop the conversion of lanosterol into ergosterol, which interferes with the membrane and prevents reproduction making it fungistatic.
Four main azoles: ketoconazole, not used all that much any more since it can be quite toxic, fluconazole, used for CNS infections such as meningitis as it enters the cerebrospinal fluid, itraconazle, usually used for dermatophytes, and miconazole, usually for GIT infections.
Aphoterecin puts holes in the membrane and lets all the potassium leak out, but can cause renal impairment. Nystatin is much the same but is not absorbed from the GIT.
Griseofulvin cleaves microtubules and echinocandins render ergosterol ineffective and lyse the cell walls.
Flucytosine (I know runny nose is a symptom of rhinovirus not influenza but shhhh, it helps me remember) is taken up by both human and fungal cells, but only fungal cells convert it into a toxin, although resistance develops quite quickly so it is usually used in concert with other antifungals.
Turbinafine is a drug absorbed with great affinity for keratin and adipose tissue, it fills the cell wall with squaline and destroys it. In 10% of patients it has side effects.

I'm leaving for QC in a matter of hours, I'll probably have internet while I'm away but I doubt I'll be doing much for this, I rather hope I won't have time. When I get back we'll cover the rest of the antimicrobials.

Friday, July 2, 2010

Turning the Yellow Tide

The week we studied kidneys was the same week that my glandular fever decided to make its final stand to see just how much it could mess up my life. I therefore missed the introduction to the kidneys, and subsequently didn't understand a damn thing for the next few weeks. It is human nature to fear that which we do not understand, fear leads to anger, and anger leads to hate. God I hated the kidneys for the longest time. Then I jumped on this "studying" band wagon. They're like the coolest things ever, you just have to look a little deeper.
The majority of this section is about diuretics, you know, being the kidneys and all. I've divided them up according to which section of the nephron they act upon. There are few drugs that act upon the Proximal Convoluted Tubule, the main one is acetazolamide, causing excretion of bicarbonate and along with it more water.
Loop diuretics act upon the thick ascending limb and are the most powerful diuretics. They inhibit absorbtion of Na+ and Cl- and secretion of Mg2+ and Ca2+ resulting in what can be described as a "torrential flow" of urine which can cause a number of problems if not monitored. The most common loop diuretic is Fureosemide and is commmonly marketed under the name Lasix. They have a degree of vasodilation as well.
Thiazide diuretics act upon the Distal Convoluted tubule in a similar manner to loop diuretics (inhibiting Na+ and Cl- absortion), they are commonly used as anti-hypertensives.
Spironolactone and Eplerenone are potassium sparing diuretics and are often used alongside non-potassium sparing diuretics as they are quite weak in isolation. They act as aldosterone antagonists, inhibiting water and potassium absorbtion.
Amiloride and triamterene act on the collecting duct and are also potassium sparing diuretics.
There is only one common osmotic diuretic and that is mannitol. It is filtered by the glomerulus but is not absorbed, thus is raises the osmotic pressure within the nephron causing more water to be excreted.
Moving on from the diuretics we come to drugs used to alter urine pH. Why? Apparently carbonic anhydrase inhibitors and citrate will raise the pH and this reduces incidence of kidney stones. Ammonium chloride will lower the pH but no-one uses it any more.
Finally there are drugs to alter excretion of uric acid. The two main drugs that do this are probenecid, which stops reabsorbtion and allopurinol, which stops synthesis. These are important in relation to gout.

Leaving for QC tomorrow, and so far I've packed... A jacket. Yep, that's really it. Although I did have to go out and buy a case to pack it in. You'd think that's something I also would have considered earlier. Anyway....

Thursday, July 1, 2010

Pharmacology makes me fit with rage

*sigh* Antiepileptics represent the reason I have always hated pharmacology. Rang & Dale cover fourteen antiepileptics, each of them different enough from each other that you have to learn them separately. They don't lend themselves at all to summarisation and several of them don't even have understood mechanisms of action. So instead of making fourteen rather repetitive pictures I've drawn a reference table. If you want to learn these drugs get Rang and Dale, this is just a memory tool (which most of this blog is supposed to be, but these especially) for revision. There are three major methods of action of antiepileptics, Na+ channel blockers, Ca2+ channel blockers and GABA agonists. They treat three types of seizures, partial seizures, generalised seizures (tonic-clonic) and generalised (absent).
Phenytoin - Sodium channel blocker - All but absent
Carbamazepine - Sodium channel blocker - All but absent
Valproate - Weak calcium channel blocker and is possibly a GABA agonist - All types
Levetiracetam - Mechanism unknown - Partial seizures
Phenobarbital - GABA agonist and possibly a sodium channel blocker - All except absent seizures
Benzodiazepines - Strong GABA agonist - All seizures but is usually only used in status epilepticus
Vigabatam - GABA transaminase inhibitor - All seizures, even when there are drug resistances
Lamotrigine - Sodium channel and possibly and calcium channel blocker - All types
Gabapentin - Not actually a GABA agonist, but may be a Ca2+ channel blocker - Partial seizures
Felbamate - NMDA antagonist and possibly a Calcium channel blocker -
Tiagabine - GABA agonist and inhibits GABA reuptake - Partial seizures
Topiramate - Unknown mechanism - All except absent
Ethosuxamide - Strong Calcium channel blocker - Absent seizures, exaggerates tonic-clonic seizures
Zonisamide - Sodium channel blocker - Partial seizures

Tomorrow I'll put up the kidney drugs. They're much more fun. :D