21 Questions
What is the primary mechanism of action of beta blockers?
Competitive inhibition of beta receptors in the heart, thereby reducing heart rate and contractility.
How do alpha-2 agonists decrease blood pressure?
By stimulating alpha-2 receptors in the brain, which activates the parasympathetic nervous system, leading to decreased sympathetic tone and reduced blood pressure.
What is the mechanism of action of ACE inhibitors?
ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, thereby reducing blood pressure.
How do calcium channel blockers reduce blood pressure?
By blocking the influx of calcium ions into vascular smooth muscle cells, leading to relaxation of blood vessels and decreased blood pressure.
What is the primary effect of adrenergic neurotransmitters on the heart?
Increasing heart rate, contractility, and conduction velocity through stimulation of beta-1 receptors.
What is the mechanism of action of penicillins?
inhibiting cell wall synthesis
How do tetracyclines inhibit protein synthesis?
by inhibiting aa-tRNA binding to the A site
What is the common core structure of cell wall synthesis inhibitors?
B-Lactam
What are three possible mechanisms of penicillin resistance?
alterations at PBPs, prevention of B-lactams from accessing PBPs, and expression of B-lactamase
What class of antibiotics inhibits protein synthesis?
Aminoglycosides, tetracyclines, amphenicols, and macrolides
What is the difference between penicillins and cephalosporins?
Differences in antibacterial specificity explained by interactions with various penicillin binding proteins in bacteria
What are the pharmacokinetic characteristics of penicillins?
Acid stability varies, lipid insoluble, do not enter mammalian cells, cross blood/brain barrier only if meninges are inflamed, and most penicillins are eliminated renally
What is a common adverse reaction to penicillins?
Type 1&2 sensitivity reactions
What is the possibility of experiencing Candidiasis with prolonged use of antibiotics?
Candidiasis occurs with prolonged use
What is the unique characteristic of 5th generation cephalosporins?
Expanded G+, including MRSA, with high affinity binding
How are most cephalosporins administered and excreted?
Mostly administered parenterally, and excreted through renal tubular secretion
What is the main reason for cross-reactivity between penicillins and cephalosporins?
Similarity of sidechains between 1&2 gen ceph and penicillins
What is the primary mechanism of action of aminoglycosides in bacterial protein synthesis?
Inhibition of initiation, causing mRNA misreading
What is the effect of tetracyclines on bacterial protein synthesis?
Inhibition of tRNA binding
What is the adverse effect of aminoglycosides on the kidneys?
Nephrotoxicity, accumulation in proximal tubular cells
What is the consequence of prolonged use of tetracyclines on teeth?
Accumulation in teeth, leading to discoloration
Study Notes
Mechanisms of Action
- Penicillins inhibit cell wall synthesis
- Tetracyclines inhibit protein synthesis at tRNA by inhibiting aa-tRNA binding to A site
Cell Wall Synthesis Inhibitors
- Penicillins and cephalosporins are examples of cell wall synthesis inhibitors
- These inhibitors have a common core structure: B-Lactam
Penicillin Resistance
- Alterations at PBPs cause a decrease in drug binding ability at the protein, decreasing antibacterial activity
- Prevention of B-lactams from accessing and entering pore channels and reaching PBPs in the cell membrane of Gram-negative bacteria
- Expression of B-lactamase in certain bacteria
Protein Synthesis Inhibitors
- Aminoglycosides, tetracyclines, amphenicols, and macrolides are examples of protein synthesis inhibitors
- These inhibitors target different stages of bacterial protein synthesis
B-Lactams
- Penicillins and cephalosporins are examples of B-Lactams
- Amoxicillin is a synthetic, broad-spectrum penicillin with no B-lactamase resistance
- Clavulanic acid is a synthetic B-lactamase inhibitor
Penicillin Pharmacokinetics
- Acid stability varies among penicillins
- Lipid insoluble, do not enter mammalian cells
- Cross the blood-brain barrier only if meninges are inflamed
- Most penicillins are eliminated renally very quickly
Penicillin ADR
- Opening the B-lactam ring forms benzylpenicilloyl
- Type 1 & 2 sensitivity reactions
- Superinfection (e.g. Candidiasis) occurs with prolonged use
Cephalosporins
- 5th generation cephalosporins have expanded Gram-positive, including MRSA, and common Gram-negative coverage
- Binding with high affinity (ceftaroline)
Cephalosporin Pharmacokinetics
- Acid stable
- Most administered parenterally, with few orally
- Distribution: extracellular fluid, some cross blood-brain barrier to treat meningitis
- Excreted mostly through renal tubular secretion
Cephalosporin ADR
- Similar to penicillins
- Cross reactivity between penicillins and cephalosporins causes ADR
- Opening the B-lactam ring forms cephalosporoyl
Bacterial Protein Synthesis
- Initiation
- tRNA binding
- Peptide bond formation
- Translocation
- Elongation cycle
Bacterial Protein Synthesis Inhibitors
- Inhibit one of the four key steps in bacterial protein synthesis
- Most are bacteriostatic, except aminoglycosides which are bactericidal
Aminoglycosides
- Inhibit initiation
- MOA: [30s] inhibit codon-anticodon interaction, causing mRNA misreading
Tetracyclines
- Inhibit tRNA binding
- MOA: [30s] inhibit aa-tRNA binding to A site
Amphenicols
- Inhibit transpeptidation
- MOA: [50s] inhibit peptide bond formation
Antibacterial Macrolides
- Inhibit elongation and/or translocation
- MOA: [50s] prevent transfer of tRNA with the growing peptide from A site to P site
Bacterial PSIs: Aminoglycosides
- Bactericidal
- Active against Gram-positive and Gram-negative bacteria
- Time and concentration dependent, with AUC:MIC
- Pharmacokinetics: administered intramuscularly or intravenously, eliminated through glomerular filtration
- Ototoxicity: hearing loss and impaired vestibular function
- Nephrotoxicity: accumulation in proximal tubular cells
Bacterial PSIs - Tetracyclines
- Broad spectrum, active against Gram-positive and Gram-negative bacteria
- Bacteriostatic
- Generally administered orally, but also parenterally
- GI disturbance: direct irritation and modulation of gut flora with prolonged use
- Ca chelation: accumulation in teeth and bones
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