Pharmacology is all about drugs that patients are given to either nurse them back to health or help them maintain a healthy life. Test your Pharmacology knowledge that has been gathered these past months by taking up the interesting quiz below It is basically divided into Pharmacokinetics, Pharmacodynamics and pharmacogenetics. All the best and come back for more Pharmacology tests.
Kidney
Liver
Heart
Bladder
Pyridostigmine
Nicotine
Curare
Dopamine
Physostigmine
Sitagliptin
Pioglitazone
Echothiophate
Therapy with tracheal intubation
Adjunct therapy to surgical anaesthesia
Treatment of convulsions
ADHD
Gatifloxacin
Gemifloxacin
Besifloxacin
Ofloxacin
Ciprofloxacin
Levofloxacin
Norflaxacin
Moxifloxacin
Paromomycin
Streptomycin
Neomycin
Gentamycin
Ofloxacin was the first quinolone
They have poor bioavailability
Inhibition of topoisomerase II prevents decatenation of DNA
Mutations to strand cutting subunits is a common mechanism of resistance
Theophylline interaction
Photosensitivity
NSAID interaction
Chelation by cations
Azithromycin
Telithromycin
Chloramphenicol
Streptogramins
All preganglionic sympathetic neurons synapse with cholinergic receptors
All postganglionic sympathetic neurons synapse with cholinergic receptors
Cholinergic receptors exist in the CNS
All postganglionic parasympathetic neurons synapse cholinergic receptors
Cholinergic receptors exist in neuromuscular junctions
Acetylcholine is incorporated into the vesicle in the cell body of the neuron
Hemicholinium inhibits the incorporation of acetycholine into the vesicle.
There is one molecule of acetylcholine per vesicle.
Botulinum toxin inhibits the exocytosis of acetylcholine
Acetycholine is transported across the synapse by active transport
M2 and M4 are autoreceptors that respond to acetylcholine at parasympathetic terminals
Acetylcholine can inhibit the release of norepinephrine by binding to autoreceptors
Acetycholine can affect both cholinergic and adrenergic receptors
Curare inhibits nicotinic receptors
Nicotinic receptors can be found in the neuromuscular junction
Stimulation of nicotinic receptors in the adrenal medulla causes the release of EPI and NE
Stimulation of nicotinic receptors in the neuromuscular junction causes a hyperpolarization that relaxes the muscle
Muscarinic receptors are ligand gated ion channels that require two ligands to bind
M2 and M4, when bound, have inhibitory action on the cell
Muscarinic receptors in the heart, when bound by acetycholine, would increase heart rate
The larger the N-substituent the more potent the agonist
The nitrogen must be capable of forming a negative charge
There must be 5 atoms between the oxygen and nitrogen
Molecules should have a hydrogen bond accepting oxygen
Iris constriction
Iris dilation
Pupillary Dilation
Pupillary constriction
Increased salivation
Urinary retention
Urinary relaxation
Bronchiole relaxation
Asthma: Choline esters (muscarinic agonists) can produce bronchoconstriction. In the predisposed patient, an asthmatic attack may be induced.
Hyperthyroidism: Choline esters (muscarinic agonists) can induce atrial fibrillation in hyperthyroid patients.
Peptic ulcer: Choline esters (muscarinic agonists), by increasing gastric acid secretion, may exacerbate ulcer symptoms.
Coronary vascular disease: Choline esters (muscarinic agonists), as a result of their hypotensive effects, can further compromise coronary blood flow.
Sjogren's Syndrome: Choline esters (muscarinic agonists), as a result of their decreased salivary secretions, can further exacerbate dry mouth
Quaternary N compounds are the most potent and absorbed most efficiently
Atropine constricts the pupils
More than 5 atoms between the terminal H and Nitrogen increases the potency
The L isomer of atropine is the most potent
Decreased heart rate
Mydriasis
Xerostomia
Cycloplegia
Temperature elevation
Sarin (Nerve gas)
Parathion (Insecticide)
Botulinum Toxin
Entry of calcium into presynaptic knob
They are most effective against gram negative organisms
Gram negative organisms display resistance by secreting beta lactamase on the surface of their cell
The pentaglycine bridge links two D-alanine together to form a cross bridge
Enzymatic inactivation of beta lactams could occur by cleaving the beta lactam ring or the r group of the drug
It is not required that a beta-lactam bind to a PBP to exert any effect
Beta-lactams are an effective treatment against the intracellular infections such as chlamydia.
Beta-lactamase would most effective in the log phase of bacterial growth
Tetracyclines causes GI distress and should be taken with food or milk
An increase in dose of tetracyclines will lead to a lower percentage absorbed in the GI tract
Doxycycline is available in intravenous formulation
Tetracyclines block tRNA from binding to the A site in translation
Resistance to Tigecycline comes in the form of efflux pumps and ribosomal protection proteins
Tigecycline has greater gram negative activity than the rest of the tetracyclines
Erythromycin would be more stable to stomach acid than clarithromycin
Tigecycline is available parenterally and orally only
Sulfonamides
Beta-lactams
Trimethoprim
Fluroquinolones
Macrolides
Beta-lactam
Dihydrofolic acid
P-aminobenzoic acid
Folic acid
Weakly acidic
Weakly basic
Neutral
None of the above
Increased production of PABA
Decreased intracellular accumulation of drug
Methylation of PABA
Production of a folic acid synthesizing enzyme
M1
M2
M3
M4
M5
Penicillins
Cephalosporins
Tetracyclines
Macrolides
Inhibits the release of acetycholine from the vesicle
Inhibits the choline uptake system
Inhibits the fusion of SNAPS and VAMPS
Inhibits the movement of acetylcholine into the vesicle
Stimulation of the muscarinic receptor in SA node would decrease heart rate
Stimulation of the muscarinic receptor in the bronchiolar smooth muscle would relax that muscle
Stimulation of the muscarinic receptor in GI tract would increase motility and tone
Stimulation of the muscarinic receptor in the lacrimal gland would increase secretion
M1
M2
M3
M4
M5
Inhibition of further ACh release
Inhibition of NE release from adjacent neuron
Stimulation of further ACh release
No effect
Butyrlcholinesterase limits the effectiveness of giving acetylcholine orally
Muscarinic agonists decrease cardiac output
Acetylcholine can easily cross the BBB
Muscarinic agonists decrease blood pressure
Bacteria
Fungi
Actinomycetes
Viruses
Polymyxin
Clindamycin
Rifamycin
Tetracycline
Polymyxin
Cephalosporin
Minocycline
Sulfamethoxazole
Tuberculosis is an example of a mycobacterial disease
They are fairly resistant to antibiotics
They grow very quickly
Multiple antibiotics are usually necessary to treat mycobacterial diseases
They require two molecules of acetycholine to bind to them to activate
They are ligand gated ion channels
They are located only on preganglionic neurons
Nn and Nm are both pentamers
The binding sites are associated with the alpha subunit
They can cause the release of histamine
75-80% of nicotinic acetylcholine receptors must be blocked to have an effect
Acetylcholine can decrease their effect
Acetylcholinesterase inhibitors increase the effect of these antagonists through synergism
Macrolides interfere with the transpeptidation step of translation
Macrolides bind to the 50S ribosomal subunit and inhibit the tRNA from binding to the A site
Macrolides bind to the 30S ribosomal subunit and inhibit the tRNA from binding to the A site
Macrolides bind to the 30S ribosomal subunit and inhibit the formation of the initiation complex
Macrolides are bacteriostatic at all concentrations
Macrolides are better gram negative agents
Gram negative bacilli are generally resistant to macrolides
Bacteria that are resistant to clindamycin generally do not show cross resistance with macrolides
Efflux pumps
Decreased permeability
Mutation of 30S ribosome
Ribosomal protection
Hydrolysis of macrolide
All of the above are mechanisms of resistance
Erythromycin
Azithromycin
Clarithromycin
Erythromycin stearate
Erythromycin estolate
Erythromycin ethylsuccinate
Erythromycin lactobionate
Clarithromycin
Erythromycin
Telithromycin
A and B
All of the above
B and C
It is able to penetrate bone and abscesses to exert its effect
It is not particularly effective against anaerobes
It is very effective against gram positive bacteria
It is associated with fatal antibiotic-associated colitis
Clindamycin is metabolized by the liver
It is commonly prescribed because of its low toxicity
It has good activity against anaerobes
It is bactericidal towards some organisms
It inhibits P450 enzyme
Penicillin
Tetracycline
Moxifloxacin
Chloramphenicol
50:50
70:30
90:10
95:10
Nearly all their activity is against gram positives
They are effective at killilng Enterococcus faecalis and Enterococcus faecium
They inhibit CYP450
They are reserved for serious infections
Streptogramin
Linezolid
Chloramphenicol
Minocycline
Tigecycline
Streptogramins
Linezolid
All of the above have activity againt faecalis
Linezolid
Chloramphenicol
Streptogramins
Tigecycline
They bind to the 50S ribosomal subunit
Tobramycin is the first drug considered for treatment
They are time dependent killers
Nephrotoxicity is a concern
300mg every 6 hours
600mg every 12 hours
400mg every 8 hours
1200mg daily
Amikacin
Neomycin
Gentamycin
Tobramycin
Gram positive aerobes
Gram negative aerobes
Gram positive anaerobes
Gram negative anaerobes
Streptomycin
Trimethoprim
Tetracycline
Linezolid
Patients should be counseled to take with lots of water
Sulfamethoxazole/Trimethoprim should be dosed in a 20:1 ratio
Resistance is plasma-mediated
Trimethoprim is 20-100 times more potent than sulfamethoxazole
Sulfonamides
Beta-lactams
Macrolides
Aminoglycosides
Clindamycin
Sulfonamides
Chloramphenicol
Aminoglycosides
Moxifloxacin
Gemifloxacin
Ciprofloxacin
Levofloxacin
Gemifloxacin
Norfloxacin
Ciprofloxacin
Moxifloxacin
Norfloxacin
Ofloxacin
Levofloxacin
Moxifloxacin
Moxifloxacin
Ciprofloxacin
Levofloxacin
Ofloxacin
Gram Positive
Gram Negative
Anaerobic
Aerobic
Tetracyclines
Macrolides
Clindamycin
Aminoglycosides
Sulfonamides
Linezolid
Streptomycin
Tetracycline
Doxycycline
Lipid rich cell membrane
Slow growth
Intracellular presence
All of the above are mechanisms of resistance
A well known ADR of this medication is peripheral neuropathy
It has no activity against non-mycobacteria
Dosage depends on the patients genetics
It has good activity against Mycobacterium tuberculosis and Mycobacterium Avium
Tigecycline
Minocycline
Streptogramins
Ampicillin
Linezolid
Sulfamethoxazole/Trimethoprim
Minocycline
Rifampin
Demeclocycline
Doxycycline
Clavulonic Acid
Rezbactam
Tazobactam
Sublactam
Aminoglycoside
Glycopeptide
Macrolide
None of the above
Streptomycin
Gentimycin
Neomycin
None of the above
Inhibition of formation of initiation complex
Premature release of an incomplete polypeptide
Addition of an incorrect amino acid resulting in a non-functional polypeptide
Binding to 50S ribosome and inhibiting transpeptidation
Sulfonamide
Trimethoprim
Fluoroquinolone
Beta-lactam
It is a very good gram negative agent
It is a very good agent against aerobes
It is effective against Enterococci
It is indicated for intraabdominal infections
Ethionamide
Rifampin
Cycloserine
Amikacin
P-aminosalicylic acid
Rifampin
Streptomycin
Cylcoserine
Isoniazid
Dapsone
Rifampin
Clofazimine
Staphylococcus aureus
Streptococcus pyogenes
Enterococcus faecalis
None of the above
Isoniazid
Rifampin
Ethambutol
Pyrazinamide
Clindamycin
Aminoglycosides
Streptogramin B
Tetracyclines
MRSA
E faecalis
H pylori
T pallidum
Erythromycin
Azithromycin
Clarithromycin
These are ADR's of tetracyclines
Tetracyclines/Clindamycin
Beta-lactams/Ketolides
Tetracyclines/Sulfonamides
Sulfonamides/Clindamycin
Ethambutol
Pyrazinamide
Rifampin
Tetracyclines
Tetracyclines
Macrolides
Rifampin
Chloramphenicol
Streptogramins
Telithromycin
Rifampin
Erythromycin
Doxycycline
Chloramphenicol
Tetracycline
Azithromycin
Streptogramins
Capreomycin
Linezolid
INH
Pyrizinamide
Capreomycin
Streptogramins
Tetracyclines
Aminoglycosides
Tetracylines
Fluoroquinolones
Macrolides
Sulfamethoxazole/Trimethoprim
Clindamycin
Sulfamethoxazole/Trimethoprim
Rifamycin
INH
M1
M2
M3
M4
M5
Inhibition of RNA polymerase
Inhibition of transpeptidase
Inhibition of transglycosylase
None of the above
Aminoglycosides
Quinolones
Beta-lactams
Tetracyclines
INH
Rifampin
Sulfonamides
Vancomycin
Fidaxomicin
Clindamycin
Clarithromycin
Metronidazole
Ciprofloxacin
Levofloxacin
Moxifloxacin
Gemifloxacin
Ofloxacin
A potential ADR is metallic taste
50 percent of patients report GI upset
Pyridoxine is recommended for coadministration of the drug
Phototoxicity is a concern
Take with food
Take on empty stomach
Take with lots of water
Take 2 hours before antacids or 4 hours after
Telithromycin
Sulfamethoxazole/Trimethoprim
Clindamycin
Rifampin
Azithromycin
Ethambutol
Sulfamethoxazole/Trimethoprim
Rifampin
Rifampin
Clofazimine
Isoniazid
Dapson
Linezolid
Macrolides
Streptogramins
Tetracyclines
Chloramphenicol
Clindamycin
Linezolid
Macrolides
Fluoroquinolones
Tetracyclines
Macrolides
Streptogramins
Streptomycin is the least used first line agent
Streptomycin is effective against intracellular tubercles
Extracellular tubercles represent active disease
Dapsone inhibits dihydropteroate synthase