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Phrm3101 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What are the different ways to target bacteria?

A

Inhibition of cell wall synthesis
Inhibition of protein synthesis
Interference with metabolic pathways
Inhibition of nucleic acid synthesis
Disruption of the cell membrane

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2
Q

What drug classes are the beta-lactams?

A

Penicillins, cephalosproins, monobactams and carbapenams

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3
Q

How do beta-lactams work?

A

Inhibtion of penicillin-binding protein transpeptidase (PBP)

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4
Q

What is the function of PBP?

A

polymerize and modify peptidoglycan, the stress-bearing component of the bacterial cell wall.

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5
Q

What do beta-lactamases do?

A

They are the primary reason for resistance on beta-lactams. Beta-lactamases that target penicillin antibiotics and render them inactive are commonly referred to as penicillinases, while those that can hydrolyse cephalosporin antibiotics are known as cephalosporinases.

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6
Q

What are the beta-lactamase inhibitors called?

A

Clavulanic acid, tazobactam and avibactam.

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7
Q

What are the anti-staphylococcal penicillins? (except MRSA)

A

Dicloxacillin and flucloxacillin.

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8
Q

What are the aminopenicillins?

A

Amoxicillin and ampicillin.

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9
Q

What is the antipseudomonal penicillin?

A

Piperacillin (has action against pseudomonas aeruginosa.

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10
Q

What is the main difference between penicilins and cephalosporins?

A

Cephalosporins have a broader spectrum of activity.

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11
Q

What are features of 1st generation cephalosporins?

A

Cefalexin and cefazolin, moderate-spectrum, activity against s. aureus, used for streptococcal, do not cross BBB, increases risk of bleeding and effective against gram-positive.

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12
Q

What are the features of 2nd generation cephalosporins?

A

Cefaclor, cefoxitin and cefuroxime, moderate spectrum, improved gram-negative and weakened gram-positive coverage. Mainly used for bacterial upper respiratory tract infections. Do not cross BBB.

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13
Q

What are the features of 3rd generation cephalosporins?

A

cefotaxime, ceftazidine, ceftriaxone. Broad-specturm, more gram-negative coverage, can cross the BBB, strongly associated with clostridioides difficle-associated diarrhoea. Ceftazidime has anti-pseudomonal activity.

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14
Q

What are the features of 4th generation cephalosporins?

A

Cefepime. Broadest spectrum, similar Gram-positive coverage to the first-generation cephalosporins, covers many Gram-negative bacteria including, covers S. aureus. Reserved for treatment of multiresistant organisms, or for treating sepsis in neutropenic or immunosuppressed persons.

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15
Q

What are the features of 5th generation cephalosporins?

A

Only available for parenteral administration (ceftaroline fosamil, ceftolozane-tazobactam). Ceftaroline is the only cephalosporin for MRSA but does not cover pseudomonas aeruginosa. Ceftolozane-tazobactam has reduced Gram-positive coverage. In particular, it does not cover Staphylococci. It however does cover Pseudomonas aeruginosa.

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16
Q

What is the monobactam?

A

Aztreonam.

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17
Q

What are the features of aztreonam?

A

Safe for patients with allergies to other beta-lactams, except ceftazidime, Aztreonam has anti-pseudomonal activity. It is sensitive to inactivation by extended-spectrum beta-lactamases (ESBLs).

18
Q

What are the features of carbepanems?

A

only available for parenteral administration (imipenem-cilastatin, ertapenem, meropenem). Most broad-spectrum antibiotics available, active towards S. aureus but are not effective for MRSA or VRE. Ertapenem is given once daily and has poor activity against important hospital acquired infections (e.g. Pseudomonas aeruginosa, Enterobacter faecalis, Acinetobacter species). Imipenem is administered with cilastatin, which prevents its inactivation in the kidney.

19
Q

What are the glycopeptides?

A

Vancomycin and teicoplanin

20
Q

What are the features of glycopeptides?

A

preventing cross-linking of peptidoglycan. Non-covalently bind with high affinity to the D-Alanine-D-Alanine terminus, mainly active against Gram-positive bacteria, useful for treating Staphylococci, including MRSA, Streptococci and Clostridioides difficile. When infused too fast, can cause histamine release, which causes the patient to become warm, flushed and hypotensive (red man sydrome).

21
Q

Which drugs are aminoglycosides?

A

Amikacin, gentamicin, streptomycin and tobramycin.

22
Q

What is the MOA for aminoglycosides?

A

bind to the bacterial 30S ribosomal subunit. Results in the production of incorrect proteins, which can damage the cell membrane, enhancing aminoglycoside entry, and affecting other processes, resulting in bactericidal activity.

23
Q

Can aminoglycosides be administered with beta-lactams?

A

No as they are incompatible when mixed.

24
Q

What are the macrolides?

A

Erythromycin, clarithromycin, azithromycin and roxithromycin.

25
Q

What are the lincosamides?

A

Clindamycin and lincomycin.

26
Q

How do macrolides/lincosamides work?

A

binding to the bacterial 50S ribosomal subunit, which prevents translocation of the nascent peptide chain from the A-site to the P-site, and hence prevents addition of the next amino acid to the protein chain

27
Q

Are macrolides bacertiostatic or bacteriocidal?

A

Bacterostatic but may be bacertiocidal at higher concentrations.

28
Q

Which drugs are tetracyclines?

A

Doxycycline, minocycline and tetracycline.

29
Q

Which drug is a glycylcyclines?

A

Tigecycline.

30
Q

What is tetracyclines MOA?

A

Bind to the bacterial 30S ribosome, which prevents aminoacyl tRNA from accessing the acceptor (A) site, preventing incorporation of the next amino acid.

31
Q

What are tetracyclines adverse effects?

A

Damage to teeth, oesophageal ulcers, photosensitivity, dizziness and vertigo (minocycline) and absorption is affected by minerals.

32
Q

What toxicities is linezolid associated with?

A

Bone marrow suppression, lactic acidosis and peripheral and optic neuropathy. More common is used >14 days.

33
Q

How does chloramphenicol work?

A

binding to the bacterial 50S ribosomal subunit, at a similar site to macrolides and lincosamides, which results in inhibition of ribosomal peptidyltransferase activity.

34
Q

How do sulfonamides work?

A

competitive inhibitors of the enzyme dihydropteroate synthase in bacteria, which incorporates PABA into dihydropteroic acid, which is a precursor for folic acid synthesis, and ultimately the synthesis of DNA and RNA.

35
Q

How does trimethoprim work?

A

bacterial dihydrofolate reductase (DHFR) inhibitors such as trimethoprim function further down the pathway than sulfonamides, competitively inhibiting bacterial DHFR, which converts dihydrofolate to tetrahydrofolic acid.

36
Q

What is the only sulfonamide available in Australia?

A

Sulfamethoxazole.

37
Q

Which drugs are fluroquinolones?

A

Ciprofloxacin, norfloxacin, moxifloxacin and ofloxacin.

38
Q

Fluroquinolones MOA?

A

Involves inhibition of two enzymes, which are essential for bacterial DNA replication: DNA gyrase (also known as topoisomerase II) and topoisomerase IV. These enzymes are not present in eukaryotes, providing a mechanism for their bacterial selectivity.

39
Q

Important counselling points for nitrofurantoin?

A

May cause drowsiness (label 1), may turn urine a brown colour.

40
Q

Why is rifaximin used for traveller’s diarrheoa?

A

It is poorly absorbed following oral administration, and concentrates in the faeces.

41
Q

What are colistin’s side effects?

A

Nephrotoxicity, neurotoxicity and bronchospasm.

42
Q

Which antifungals function by disrupting the cell membrane?

A

Squalene epoxidase inhibitors, allylamines, lanosterol 14-a-demthylase inhibitors, ergosterol biosynthesis pathway inhibitors, membrane disruptors

Phrm3101 (7 decks)

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