Drugs

Question 1

Benzodiazepine (BZ)

Answer 1

BZ agonsists increase affinity of GABAa receptor for GABA; causes greater channel opening and greater influx of Cl- into the cell (inhibitory)

Question 2

BZ Agonists

Answer 2

Diazepam (sedative drugs, epilepsy drugs; increases amount of inhibition effect in brain as GABA is an inhibition drug) reduces stress/anxiety! Could cause general anaesthesia.

Question 3

BZ antagonists

Answer 3

Flumazenil (given antagonist to see if someone has an overdose of Diazepam)

Question 4

Inverse agonists for BZ

Answer 4

Betacarbolines (bind to BZ site and make it less likely that the receptor will open)

Question 5

Naloxone

Answer 5

Naloxone, sold under the brandname Narcan among others, is a medication used to block the effects of opioids, especially in overdose.

Question 6

Alprenolol

Answer 6

Alprenolol; treatment of angina; serotonin receptor antagonist

Question 7

Blockage of transfer of Ach into vesicle (NMJ)

Answer 7

VESAMILCOL

Question 8

Blockage of Choline transporter (NMJ)

Answer 8

HEMICHOLINIUM

Question 9

Blockage of exocytosis of vesicle (NMJ)

Answer 9

BOTULINIUM

Question 10

Non-depolarising neuromuscular blockers

Answer 10

D-tubocurarine

Question 11

Depolarising neuromuscular blockers

Answer 11

Suxamethonium

Question 12

Three cholinersterase inhibiters and their duration of action (NMJ)

Answer 12

Edrophonium- Ionic interaction (minutes)
Neostigmine- Covalent bonds (hours)
Organophosphates- phosphorylation (irreversible): Chemical weapon: pesticides

Question 13

Beta-blockers

Answer 13

beta-antagonists (e.g atenolol)

treat hypertension, heart failure, tremor

Question 14

Zidovudine

Answer 14

prevents/treats HIV/AIDS

Inhibits reverse transcriptase

Question 15

Nystatin (anti-fungal)

Answer 15

Like amphotericin B and natamycin, nystatin binds to ergosterol, a major component of the fungal cell membrane. When present in sufficient concentrations, it forms pores in the membrane that lead to K+ leakage, acidification, and death of the fungus.[12] Ergosterol is a sterol unique to fungi, so the drug does not have such catastrophic effects on animals or plants. However, many of the systemic/toxic effects of nystatin in humans are attributable to its binding to mammalian sterols, namely cholesterol. This is the effect that accounts for the nephrotoxicity observed when high serum levels of nystatin are achieved.

Question 16

Amphotericin

Answer 16

Amphotericin B binds with ergosterol, a component of fungal cell membranes, forming pores that cause rapid leakage of monovalent ions (K+, Na+, H+ and Cl−) and subsequent fungal cell death. This is amphotericin B’s primary effect as an antifungal agent.[42][43] It has been found that the amphotericin B/ergosterol bimolecular complex that maintains these pores is stabilized by Van der Waals interactions.[44] Researchers have found evidence that amphotericin B also causes oxidative stress within the fungal cell,[45] but it remains unclear to what extent this oxidative damage contributes to the drug’s effectiveness.[42] The addition of free radical scavengers or antioxidants can lead to amphotericin resistance in some species, such as Scedosporium prolificans, without affecting the cell wall.[citation needed]

Question 17

Ketoconazole

Answer 17

As an antifungal, ketoconazole is structurally similar to imidazole, and interferes with the fungal synthesis of ergosterol, a constituent of fungal cell membranes, as well as certain enzymes. As with all azole antifungal agents, ketoconazole works principally by inhibiting the enzyme cytochrome P450 14α-demethylase (CYP51A1).[18] This enzyme participates in the sterol biosynthesis pathway that leads from lanosterol to ergosterol. Lower doses of fluconazole and itraconazole are required to kill fungi compared to ketoconazole, as they have been found to have a greater affinity for fungal cell membranes.

Question 18

Mechanisms of resistance

Answer 18

The three fundamental mechanisms of antimicrobial resistance are (1) enzymatic degradation of antibacterial drugs, (2) alteration of bacterial proteins that are antimicrobial targets, and (3) changes in membrane permeability to antibiotics: bacteria produces a protein which stops antibiotic being incorporated into the membrane

e.g Penecillin- B-lactamase which breaks antibiotics structure, cancer cells break down drugs themselves

Transfer via intermediate viral infection: MRSA, plasmids, transposons (bacteria)
MRSA: aquires MecA gene which allows cell wall synthesis to continue in the presence of B-lactams and methicillin antibiotics –> passed gene on via horizontal gene transfer