Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm SJSM > Block 3 ALL > Flashcards

Block 3 ALL Flashcards

1
Q

What are the penicillinase-sensitive penicillin’s?

What are they used to treat?

A

These include Amino-penicillin’s (Amoxicillin & Ampicillin

Treat: gram +ve & gram -ve infections:
- Acute otitis media
- Syphilis
- Rheumatic fever
- Strep pharyngitis
- Listeria
- H. pylori (Amoxicillin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are penicillin V & G

A

G penicillin (natural)
V penicillin (acid-resistant)

beta-lactam antibiotics
D-Ala-D-Ala structural analog bind & block PBP to inhibit cell wall synthesis

Treats:
1) Mainly gram-positive organisms (Streptococcus spp., Actinomyces)
2) Some gram-negative cocci (N. meningitidis) and spirochetes (T. pallidum)

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

beta-lactam antibiotics
D-Ala-D-Ala structural analog bind & block PBP to inhibit cell wall synthesis

Treats:
1) Mainly gram-positive organisms (Streptococcus spp., Actinomyces)
2) Some gram-negative cocci (N. meningitidis) and spirochetes (T. pallidum)

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

A

G penicillin (natural)
V penicillin (acid-resistant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the Amino penicillin’s & what do they treat?

Adverse reaction?

A

gram +ve & gram -ve infections:

H. pylori (Amoxicillin)
H. influenzae
E. coli
Listeria monocytogenes
Proteus mirabilis
Salmonella
Shigella
Enterococci

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

These include Amoxicillin (oral) & Ampicillin (IV)

HHEELPSSS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the penicillinase-Resistant penicillin’s?

What are they used to treat?

Adverse effects?

A

They have bulky R groups that block access to their beta-lactam rings making them resistant to cleavage by penicillinase enzymes.

They are a great narrow spectrum antibiotic for S. aureus infections (except MRSA) (gram +ve species)

Includes:
Methicillin
Cloxacillin
Dicloxacillin
Naficillin
Oxacillin

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

They have bulky R groups that block access to their beta-lactam rings making them resistant to cleavage by penicillinase enzymes.

They are a great narrow spectrum antibiotic for S. aureus infections (except MRSA) (gram +ve species)

Includes:
Methicillin
Cloxacillin
Dicloxacillin
Naficillin
Oxacillin

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

A

penicillinase-Resistant penicillin’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are two ways that bacteria can become resistant to penicillin?

A

1) by making penicillinases that cleave the beta-lactam rings of penicillin (use beta lactamase inhibitors to avoid this!)

2) by mutating the transpeptidases that penicillin’s target so the penicillin can no longer bind (PBP mutations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which drug should be added to a drug regime with a penicillinase-sensitive penicillin?

A

Give a beta-lactamase (penicillinase) inhibitor like clavulanic acid, sulbactam, & tazobactam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which beta lactamase inhibitor should you give with Amoxicillin?

Which beta lactamase inhibitor should you give with Ampicillin?

Which beta lactamase inhibitor should you give with Ticarcillin?

Which beta lactamase inhibitor should you give with Piperacillin?

A

Amoxicillin-Clavulanate (Augmentin)

Ampicillin-Sulbactam (Unasyn)

Ticarcillin-Clavulanate

Piperacillin-Tazobactam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

clavulanic acid, sulbactam, & tazobactam are all examples of which type of drug?

A

beta-lactamase (penicillinase) inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does S. aureus become resistant to penicillin?

A

Mutations in penicillin-binding proteins (PBPs) the beta-lactam cannot bind to PBPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is penicillin?

What is the MOA?

Adverse effects?

A

A beta-lactam antibiotic
(aka D-Ala D-Ala analogue) that inhibits cell wall synthesis by competing with bacterial D-Ala D-Ala for enzymes & binding PBP (transpeptidases) to block cell wall cross-linking via peptidoglycans & activating autolytic enzymes.

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

A beta-lactam antibiotic
(aka D-Ala D-Ala analogue) that inhibits cell wall synthesis by competing with bacterial D-Ala D-Ala for enzymes & binding PBP (transpeptidases) to block cell wall cross-linking via peptidoglycans & activating autolytic enzymes.

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

A

Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which penicillin subtypes are involved in preventing cell wall synthesis (via B-lactams & PBPs)?

A

1) Penicillin-Sensitive Penicillin’s

2) Penicillin-Resistant Penicillin’s

3) Antipseudomonal penicillin’s

4) G & V penicillin’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which penicillin subtypes are involved in inhibiting peptidoglycan synthesis?

A

Vancomycin & Bacitracin

both are Beta lactam analogs that bind PBP to inhibit peptidoglycan formation & cross linking to inhibit cell wall building

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which type of penicillin is most effective against Pseudomonas aeruginosa?

A

Antipseudomonal penicillin’s like

Piperacillin, Ticarcillin or Carbenicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is vancomycin?

What is the MOA?

What is it used to treat?

Adverse effects?

Conferred resistance?

A

Glycopeptide antibiotic

MOA:
1) It inhibits cell wall peptidoglycan formation by binding D-Ala-D-Ala portion of cell wall precursors

Clinical use:
gram-positive bacteria only
**C.difficile
*MRSA

Others:
S. epidermidis &
Enterococci

Adverse effects:
1) Nephrotoxicity
2) Ototoxicity
3) Thrombophlebitis
4) Red Man Syndrome (Vancomycin infusion reaction)
6) DRESS syndrome

Organisms can modify the amino acids of D-Ala D-Ala to D- Ala D-Lac to confer resistance

(not susceptible to β-lactamases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Glycopeptide antibiotic

MOA:
1) It inhibits cell wall peptidoglycan formation by binding D-Ala-D-Ala portion of cell wall precursors
2) It also indirectly prevents transpeptidation

Clinical use:
#1 Best for treating C. difficile given orally for pseudomembranous colitis

Other:
- MRSA
- S. epidermidis
- Enterococcus species

Adverse effects:
1) Nephrotoxicity
2) Ototoxicity
3) Thrombophlebitis
4) Red Man Syndrome (Vancomycin infusion reaction)
6) DRESS syndrome

Organisms can modify the amino acids of D-Ala D-Ala to D- Ala D-Lac to confer resistance

(not susceptible to β-lactamases)

A

Vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is DRESS syndrome?

A

aka Drug reaction with eosinophilia and systemic symptoms

Manifestations include fever, lymphadenopathy, a diffuse rash, facial edema, and eosinophilia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of penicillin’s would you give?

A

Likely organism:
Pseudomonas aeruginosa infections

Treatment:
Give an Antipseudomonal Antibiotics like:

Penicillin’s
Carbenicillin, Piperacillin, or ticarcillin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of Carbapenems would you give?

A

Likely organism:
Pseudomonas aeruginosa infections

Treatment:
Give an Antipseudomonal Antibiotics like:

Carbapenems
Meropenem, Imipenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of Aminoglycosides would you give?

A

Aminoglycosides: Gentamicin, Amikacin, Tobramycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of Quinolones would you give?

A

Likely organism:
Pseudomonas aeruginosa infections

Treatment:
Give an Antipseudomonal Antibiotics like:

Quinolones
Ciprofloxacin, Levofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of Polymyxins would you give?

A

Likely organism:
Pseudomonas aeruginosa infections

Treatment:
Give an Antipseudomonal Antibiotics like:

Polymyxins
Polymyxin B and Colistin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of Monobactam would you give?

A

Likely organism:
Pseudomonas aeruginosa infections

Treatment:
Give an Antipseudomonal Antibiotics like:

Monobactam
Aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Patient presents with hot tub folliculitis, nosocomial pneumonia, nosocomial UTI

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the likely organism?
&
Which type of Cephalosporins would you give?

A

Likely organism:
Pseudomonas aeruginosa infections

Treatment:
Give an Antipseudomonal Antibiotics like:

Cephalosporins
3rd gen Ceftazidime &
Cefoperazone
4th gen Cefepime & Cefpirome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Microscopy shows motile gram-negative bacteria, catalase positive, oxidase positive.

What is the organism?

A

Pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are Carbapenems?
- 4 drugs

What is their MOA?

What are they used to treat?

Adverse effects?

Resistance?

A

Antipseudomonal Carbapenems

Imipenem
Meropenem
Ertapenem
Doripenem

MOA:
Beta-lactam antibiotics (DAlaDAla analogs) that bind & block PBP to prevent cross-linking of peptidoglycans thereby inhibiting cell wall synthesis

Clinical indications (broad spectrum β-lactamase resistant)
**Last-resort drugs
1. Pseudomonas aeruginosa infection

  1. Gram-positive cocci; except for MRSA

Adverse Effects:
1) GI distress
2) Rash
3) CNS toxicity (seizures) at high plasma levels
4) confusion

Mechanism of Resistance: They are inactivated by carbapenems (K. pneumonia, E. coli, E. aerogenes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Imipenem
Meropenem
Ertapenem
Doripenem

MOA: These are broad spectrum β-lactamase resistant carbapenems

Clinical Indications:
Pseudomonas aeruginosa infection

Adverse Effects:
1) GI distress
2) Rash
3) CNS toxicity (seizures) at high plasma levels
4) confusion

Mechanism of Resistance: They are inactivated by carbapenems (K. pneumonia, E. coli, E. aerogenes)

A

Antipseudomonal Carbapenems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why are carbapenems always given with cilastatin?

A

Cilastatin is a renal dehydroepeptidase inhibitor to reduce inactivation of the drug in renal tubules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which carbapenem has the lowest risk of seizures?

A

Meropenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the antipseudomonal penicillin’s?
- 3 drugs

What is their MOA?

What are their adverse effects?

A

Antipseudomonal Penicillin’s are Carbenicillin, Piperacillin, & ticarcillin.

MOA:
They are D-Ala-D-Ala analogs (B-lactams) that block transpeptidase peptidoglycan cross-linking & they bind PBP (transpeptidases) to activate autolytic enzymes to trigger lysis

Adverse Effects:
1) hypersensitivity reactions
2) Direct Coombs +ve hemolytic anemia
3) Interstitial nephritis
4) Pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are cephalosporins?

What is their MOA?

A

Cephalosporins (beta-lactam antibiotics)

MOA:
β-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases & they bind PBP (transpeptidases) to activate autolytic enzymes to trigger lysis

Adverse Effects:
1) hypersensitivity reactions
2) autoimmune hemolytic anemia
3) disulfiram-like reaction
4) vitamin K deficiency

Mechanism of Resistance: inactivated by cephalosporinases (type of β-lactamase) –– structural change in PBPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a concern when giving Cephalosporins with aminoglycosides?

A

There is a low rate of cross-reactivity even in penicillin-allergic patients resulting in an increase in nephrotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the MOA of Beta lactam antibiotics?

I.e All of these!

*Cephalosporins:
3rd gen:
Ceftriaxone
Cefotaxime
Cefpodoxime
Ceftazidime
4th gen:
Cefepime

*Antipseudomonal Penicillin’s are Carbenicillin, Piperacillin, & ticarcillin

*Penicillin
- Penicillin-sensitive penicillinase are Penicillin G & V, Ampicillin & Amoxicillin
- Penicillin-resistant penicillinase are Methicillin, Cloxacillin, & Dicloxacillin

*Antipseudomonal Carbapenems
Imipenem
Meropenem
Ertapenem
Doripenem

A

PBP/transpeptidase Inhibitor prevents cross linking of peptidoglycan to weaken the cell wall & trigger lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which antipseudomonal penicillin’s are considered Ureidopenicillins?

A

Piperacillin & Mezlocillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which antipseudomonal penicillin’s are considered Carboxypenicillin?

A

Carbenicillin & Ticarcillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are cephalosporins?

What is their MOA?

What are they used to treat?

A

Cephalosporins:

1st: Cefazolin
2nd: Cefotetan
3rd gen: ceftriaxone, cefotaxime, cefpodoxime, & ceftazidime
4th gen: cefepime & Cefpirome
5th: Ceftaroline & Ceftobiprole

MOA:
β-lactam antibiotic (transpeptidase/PBP inhibitor) that inhibits cell wall synthesis but that is less susceptible to penicillinases

AE:
1) Hypersensitivity (allergy) most common with cefazolin
2) Autoimmune hemolytic anemia (+ve Coombs test)
3) Disulfiram-like reaction to alcohol
4) Vitamin K deficiency
5) Increases nephrotoxicity of aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

1st: Cefazolin
2nd: Cefotetan
3rd gen: ceftriaxone, cefotaxime, cefpodoxime, & ceftazidime
4th gen: cefepime & Cefpirome
5th: Ceftaroline & Ceftobiprole

MOA:
β-lactam antibiotic (transpeptidase/PBP inhibitor) that inhibits cell wall synthesis but that is less susceptible to penicillinases

AE:
1) Hypersensitivity (allergy) most common with cefazolin
2) Autoimmune hemolytic anemia (+ve Coombs test)
3) Disulfiram-like reaction to alcohol
4) Vitamin K deficiency
5) Increases nephrotoxicity of aminoglycosides

A

Cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How do bacteria develop resistance against Cephalosporin drugs? (2 ways)

A

Cephalosporins get inactivated by cephalosporinases (type of β-lactamase) or structural change in PBPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the most important 5th generation cephalosporins used to treat MRSA & VRSA infections?

A

5th: Ceftaroline & Ceftobiprole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

4th generation cephalosporin drugs useful for treating life-threatning pseudomonas infection

A

Cefepime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

A 1st gen cephalosporin good for pre op prep in surgery because it’s targeted at gram +ve bacteria.

A

Cefazolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the most important 2nd & third generation cephalosporins that are effective in treating gram -ve bacteria?

A

2nd: Cefotetan

3rd gen: ceftriaxone, cefotaxime, cefpodoxime, & ceftazidime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is Aztreonam?

What are the adverse effects?

A

Monobactam (Beta-lactam antibiotic)

MOA:
It is less susceptible to β-lactamases & it prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3 (PBP3) it treats gram -ve infections (E.coli & pseudomonas)

Its Synergistic with aminoglycosides

Adverse Effects:
1) Gi upset
2) Phlebitis
3) Skin rash
4) Occasional liver dysfunction

only good for gram -ve bacteria (E.coli & pseudomonas) & it has no cross reactivity! (good for penicillin allergies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Monobactam (Beta-lactam antibiotic)

MOA:
It is less susceptible to β-lactamases & it prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3 (PBP3) it treats gram -ve infections (E.coli & pseudomonas)

Its Synergistic with aminoglycosides

Adverse Effects:
1) Gi upset
2) Phlebitis
3) Skin rash
4) Occasional liver dysfunction

only good for gram -ve bacteria (E.coli & pseudomonas) & it has no cross reactivity! (good for penicillin allergies)

A

Aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are Polymyxins (Colistin [polymyxin E], polymyxin B)? What are their adverse effects?

A

MOA:
Cation polypeptides that bind to phospholipids on cell membrane of gram-negative bacteria to disrupt the cell membranes integrity leading to leakage of cellular components and subsequent cell death

Adverse Effects:
1) nephrotoxicity
2) neurotoxicity (slurred speech, weakness, paresthesia)
3) respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MOA:
Cation polypeptides that bind to phospholipids on cell membrane of gram-negative bacteria to disrupt the cell membranes integrity leading to leakage of cellular components and subsequent cell death

Adverse Effects:
1) nephrotoxicity
2) neurotoxicity (slurred speech, weakness, paresthesia)
3) respiratory failure

A

Polymyxins (Colistin [polymyxin E], polymyxin B)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Imipenem, Meropenem, Doripenem, & Ertapenem are all considered which class of drug?

A

Carbapenems, they are synthetic beta-lactam antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Carbapenems, they are synthetic beta-lactam antibiotics include with 4 drugs?

A

Imipenem, Meropenem, Doripenem, & Ertapenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which carbapenem can cause nephrotoxicity & why?

A

Imipenem because it is metabolized in the kidney into an inactive form which can be toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which drug do you co-administer with imipenem to avoid nephrotoxicity?

A

Cilastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Cefazolin

A

1st gen cephalosporin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Cefotetan & cefotaxime

A

2nd gen cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

ceftriaxone, cefotaxime, cefpodoxime, & ceftazidime

A

3rd gen cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

cefepime & Cefpirome

A

4th gen cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Ceftaroline & Ceftobiprole

A

5th gen cephalosporin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are Beta-lactam inhibitors?

A

They bind Beta-lactam enzymes & prevent them from inactivating antibiotics these include Clavulanic acid, Sulbactam & Tazobactam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Clavulanic acid, Sulbactam & Tazobactam are examples of which type of drug?

A

Beta-lactam inhibitors that bind Beta-lactam enzymes & prevent them from inactivating antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are TCA’s?

What do they treat & was are the adverse side effects?

A

MOA:
They bind to 30S subunit of bacterial ribosomes to prevent the attachment of aminoacyl-tRNA & block bacterial protein synthesis.

Treat infections like cholera, Rocky Mountain Spotted Fever, Chlamydia, & Lyme disease

Adverse effects:
1) Gastric discomfort
2) Esophagitis
3) Hepatotoxicity at high doses (minocycline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MOA:
They bind to 30S subunit of bacterial ribosomes to prevent the attachment of aminoacyl-tRNA & block bacterial protein synthesis.

Treat infections like cholera, Rocky Mountain Spotted Fever, Chlamydia, & Lyme disease

Adverse effects:
1) Gastric discomfort
2) Esophagitis
3) Hepatotoxicity at high doses (minocycline)

A

TCAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Tetracycline, Doxycycline, & Minocycline are all examples of which type of drug?

A

TCAs (30s inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Aminoglycosides

Gentamycin
Neomycin
Amkimycin
Tobramycin
Streptomycin

A

Bactericidal drugs that inhibit the 30S subunit to inhibit the formation of the initiation complex, translocation, & causing misreading mRNA &
preventing bacterial protein synthesis.

It is used for treating serious gram -ve bacilli infections (pseudomonas)

Adverse effects:
1) Ototoxicity (avoid with loop diuretics)
2) Nephrotoxicity (ATN)
3) Neuromuscular paralysis (avoid in myasthenia gravis!)
4) Dermatitis (topical neomycin)
5) Teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Bactericidal drugs that inhibit the 30S subunit to inhibit the formation of the initiation complex, translocation, & causing misreading mRNA &
preventing bacterial protein synthesis.

It is used for treating serious gram -ve bacilli infections (pseudomonas)

Adverse effects:
1) Ototoxicity (avoid with loop diuretics)
2) Nephrotoxicity (ATN)
3) Neuromuscular paralysis (avoid in myasthenia gravis!)
4) Dermatitis (topical neomycin)
5) Teratogenic

A

Aminoglycosides

Gentamycin
Neomycin
Amkimycin
Tobramycin
Streptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Which TCA is safe to use in patients with renal failure & why?

A

Doxycycline because it is excreted in the poop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What do you want to avoid when taking TCAs?

A

Avoid milk, antacids, or iron-containing preparations because things like Calcium, magnesium, and iron ions (divalent ions) bind to drug, inhibiting drug’s absorption in gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Which organisms are TCAs effective against?

A

Rickettsia (Rocky Mountain Spotted Fever)
Borrelia burgdorferi
Chlamydia spp.
M. pneumoniae
Acne
Community-acquired MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How can organisms develop resistance against TCAs?

A

1) Plasmid-encoded active transport pumps will reduce the uptake or increased the efflux out of bacterial cells
&
2) By making a protein that enables translation despite TCA presence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Because aminoglycans requires O2 for uptake it can only treat which type of organisms?

A

Treats aerobic organisms only & especially Severe gram-negative rod infections (pseudomonas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Which Aminoglycoside is used for Bowel surgery infection prophylaxis?

A

Neomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Which aminoglycoside is used as a second line Mycobacterium tuberculosis treatment?

A

Streptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is a potential complication of nephrotoxicity as a side effect of aminoglycosides?

A

Acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is a potential complication of ototoxicity as a side effect of aminoglycosides?

A

Presents with hearing loss and tinnitus
Risk compounded with loop diuretics (also cause ototoxicity)
Damage to CN VIII can also lead to vestibular ataxia and vertigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How do organisms confer resistance to aminoglycosides?

A

Through enzyme modification of the drug, bacterial transferases inactivate the drug via acetylation, phosphorylation, & adenylation.

Seen with Enterococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Which drug do you give penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides

A

Aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How do organisms develop resistance to aztreonam?

A

They develop resistant against beta-lactamases (penicillinase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Red Man syndrome is a side effect of vancomycin, what is it?

A

Its a condition that is mediated by histamine (pseudo-allergic reaction) from mast cells, & it is not dependent on IgE signaling

Preventable with pre-treatment with antihistamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

They are beta lactam antibiotics

They are effective against gram-positive cocci like staph and strep bacteria so their used for preoperative antibiotic prophylaxis, to prevent wound infections caused by skin bacteria

A

What are first generation cephalosporins?

cefaZOLIN
cephaLEXIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are second generation cephalosporins?

cefoxitin, cefaclor, cefuroxime, and cefotetan

A

They are beta lactam antibiotics

highly effective against gram-positive cocci like staph and strep bacteria so they are used for preoperative antibiotic prophylaxis, to prevent wound infections caused by skin bacteria

Also good against some gram -ve:
H. influenzae
Enterobacter aerogenes
Neisseria
Serratia marcescens
Proteus mirabilis
E. Coli
Klebsiella pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

They are beta lactam antibiotics

highly effective against gram-positive cocci like staph and strep bacteria so they are used for preoperative antibiotic prophylaxis, to prevent wound infections caused by skin bacteria

Also good against some gram -ve:
H. influenzae
Enterobacter aerogenes
Neisseria
Serratia marcescens
Proteus mirabilis
E. Coli
Klebsiella pneumoniae

A

What are second generation cephalosporins?

cefoxitin, cefaclor, cefuroxime, and cefotetan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are 3rd generation cephalosporins?

cefTRIAXONE
cefTAZIDIME
CefoTAXIME
CefPODOXIME
ceFIXime

A

They are beta-lactam antibiotics that are widely used in the hospital setting.

They have broad coverage, as they are effective against both gram +ve and gram -ve bacteria.

Ceftriaxone is used to treat bacterial meningitis, Lyme disease, and gonorrhea. Ceftazidime can treat pseudomonas infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

They are beta-lactam antibiotics that are widely used in the hospital setting.

They have broad coverage, as they are effective against both gram +ve and gram -ve bacteria.

Ceftriaxone is used to treat bacterial meningitis, Lyme disease, and gonorrhea. Ceftazidime can treat pseudomonas infections.

A

What are 3rd generation cephalosporins?

cefTRIAXONE
cefTAZIDIME
CefoTAXIME
CefPODOXIME
ceFIXime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Ceftriaxone

A

a 3rd gen cephalosporin used to treat:

1) Meningitis: Crosses blood-brain-barrier (BBB)
2) Neisseria gonorrhoeae
3) Lyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Ceftazidime

A

a 3rd gen cephalosporin used to treat:

Pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

a 3rd gen cephalosporin used to treat:

1) Meningitis: Crosses blood-brain-barrier (BBB)
2) Neisseria gonorrhoeae
3) Lyme

A

Ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

a 3rd gen cephalosporin used to treat:

Pseudomonas aeruginosa

A

Ceftazidime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are 4th generation cephalosporins?

Cefepime

A

beta-lactam antibiotics that are relatively newer cephalosporin drugs.

Broad gram positive and negative coverage
& especially used to treat Pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Broad gram positive and negative coverage
Pseudomonas aeruginosa

A

What are 4th generation cephalosporins?

Cefepime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are 5th generation cephalosporins?

ceftaroline

A

A broad spectrum coverage against gram +ve and gram -ve bacteria,

Reserved as one of the only effective treatments against MRSA, or methicillin-resistant staph aureus.\

Does NOT cover Pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

A broad spectrum coverage against gram +ve and gram -ve bacteria,

Reserved as one of the only effective treatments against MRSA, or methicillin-resistant staph aureus.

Does NOT cover Pseudomonas aeruginosa

A

What are 5th generation cephalosporins?

ceftaroline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is Tigecycline?

A

Glycycline

a broad-spectrum antibiotic (TCA derivative) that binds & inhibits 30S to block bacterial protein synthesis.

It is used as a last resort treatment for multi-drug resistant organisms (MRSA & VRE)

Adverse effects:
Severe bleeding
Nausea/vomiting
Higher mortality rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Glycycline

a broad-spectrum antibiotic (TCA derivative) that binds & inhibits 30S to block bacterial protein synthesis.

It is used as a last resort treatment for multi-drug resistant organisms (MRSA & VRE)

Adverse effects:
Severe bleeding
Nausea/vomiting
Higher mortality rate

A

Tigecycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the macrolides? & What are they used for treating?

Suffix “-thromycin”

Azithromycin
Clarithromycin
Erythromycin.

A

MOA: Bacteriostatic
(Bind to the 23S rRNA of the 50S ribosomal subunit to block translocation to inhibit bacterial protein synthesis

Used for treating:
1) Atypical pneumonias (Legionella or Mycoplasma)
2) STI (chlamydia and gonorrhea)
3) Bordetella pertussis
4) Gram-positive cocci (streptococcal) in patients allergic to penicillin

Adverse:

Motility issues
Arrythmias (prolonged QT)
acute Cholestatic hepatitis (in patients with liver dysfunction)
Rash
eOsinophilia

“MACRO”

Complication:
Torsades de Pointes

Resistance:
Methylation of 23S rRNA-binding site prevents binding of drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

MOA: Bacteriostatic
(Bind to the 23S rRNA of the 50S ribosomal subunit to block translocation to inhibit bacterial protein synthesis

Used for treating:
1) Atypical pneumonias (Legionella or Mycoplasma)
2) STI (chlamydia and gonorrhea)
3) Bordetella pertussis
4) Gram-positive cocci (streptococcal) in patients allergic to penicillin

Adverse:

Motility issues
Arrythmias (prolonged QT)
acute Cholestatic hepatitis (in patients with liver dysfunction)
Rash
eOsinophilia

“MACRO”

Complication:
Torsades de Pointes

Resistance:
Methylation of 23S rRNA-binding site prevents binding of drug

A

adverse effects of macrolides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

(Bind to the 23S rRNA of the 50S ribosomal subunit to block translocation to inhibit bacterial protein synthesis)

A

Macrolides
Azithromycin
Clarithromycin
Erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Which macrolide accumulates into the macrophages, neutrophils, & fibroblasts

A

Azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is chloramphenicol?

A

MOA: Bacteriostatic
It binds the 50S subunit of bacterial ribosomes to prevent bacterial protein synthesis

It is used as a second- or third-line therapy for
1) Bacterial Meningitis (H.influenzae, N. meningitis, S.pneumoniae)
2) Rickettsial diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

MOA: Bacteriostatic
It binds the 50S subunit of bacterial ribosomes to prevent bacterial protein synthesis

It is used as a second- or third-line therapy for
1) Bacterial Meningitis (H.influenzae, N. meningitis, S.pneumoniae)
2) Rickettsial diseases

Adverse Effects:
1) Anemia (dose dependent)
2) Leukopenia
3) Thrombocytopenia
(Reversible by stopping medication)
4) Aplastic anemia (dose independent)
5) Gray-baby syndrome

Premature infants lack liver UDP-glucuronosyltransferase and cannot metabolize the drug, leading to toxic accumulation

Resistance:
acetyltransferase to inactivate the drug

A

chloramphenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Presents in babies as gray skin, vomiting, lethargy, and cardiorespiratory suppression

A

Gray baby syndrome, an adverse effect of Chloramphenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Chloramphenicol

A

MOA: Bacteriostatic
It binds the 50S subunit of bacterial ribosomes to prevent bacterial protein synthesis

It is used as a second- or third-line therapy for
1) Bacterial Meningitis (H.influenzae, N. meningitis, S.pneumoniae)
2) Rickettsial diseases

Adverse Effects:
1) Anemia (dose dependent)
2) Leukopenia
3) Thrombocytopenia
(Reversible by stopping medication)
4) Aplastic anemia (dose independent)
5) Gray-baby syndrome

Premature infants lack liver UDP-glucuronosyltransferase and cannot metabolize the drug, leading to toxic accumulation

Resistance:
acetyltransferase to inactivate the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is clindamycin?

A

MOA:
It targets the 50S subunit of bacterial ribosomes by blocking bacterial protein synthesis and stopping bacterial growth.

Treats:
1) anaerobic bacterial infections that arise above the diaphragm
e.g. Bacteroides spp., Clostridium perfringens
2) Aspiration pneumonia
3) lung abscesses
4) bacterial vaginosis
5) oral infections
6) Invasive group A streptococcal (S. pyogenes) infection

Adverse effects:
Pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

MOA:
It targets the 50S subunit of bacterial ribosomes by blocking bacterial protein synthesis and stopping bacterial growth.

Treats:
1) anaerobic bacterial infections that arise above the diaphragm
e.g. Bacteroides spp., Clostridium perfringens
2) Aspiration pneumonia
3) lung abscesses
4) bacterial vaginosis
5) oral infections
6) Invasive group A streptococcal (S. pyogenes) infection

Adverse effects:
Pseudomembranous colitis

A

clindamycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is a Linezolid? What does it treat?

A

MOA:
It binds the 50S subunit of bacterial ribosomes & blocks the formation of initiation complex to inhibit bacterial protein synthesis

Treats:
1) Gram-positive species including MRSA and VRE
(Usually as a last-resort for multi-drug resistant infections)

Adverse effects:
1) Bone marrow suppression
(Anemia, leukopenia, and thrombocytopenia)

2) Neuropathy
optic neuritis and peripheral neuropathy)

3) Serotonin syndrome
(Due to partial monoamine oxidase (MAO) inhibition
A higher risk with the use of other serotonergic drugs (e.g. MAOIs, SSRIs)

Resistance:
A Point mutation of ribosomal RNA that changes the 50S binding site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

MOA:
It binds the 50S subunit of bacterial ribosomes & blocks the formation of initiation complex to inhibit bacterial protein synthesis

Treats:
1) Gram-positive species including MRSA and VRE
(Usually as a last-resort for multi-drug resistant infections)

Adverse effects:
1) Bone marrow suppression
(Anemia, leukopenia, and thrombocytopenia)

2) Neuropathy
optic neuritis and peripheral neuropathy)

3) Serotonin syndrome
(Due to partial monoamine oxidase (MAO) inhibition
A higher risk with the use of other serotonergic drugs (e.g. MAOIs, SSRIs)

Resistance:
A Point mutation of ribosomal RNA that changes the 50S binding site

A

Linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are Polymyxins?

Colistin (polymyxin E)
Polymyxin B

A

MOA:
Cation polypeptides that disrupts cell membrane causing leakage of cellular components and cell death

Treat:
colistin and other polymyxins last-resort therapy for multidrug-resistant gram-negative bacteria
e.g. P. aeruginosa, E. coli, K. pneumoniae

Adverse effects:
1) Nephrotoxicity
2) Neurotoxicity (slurred speech, weakness, paresthesia’s)
3) Respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

MOA:
Cation polypeptides that disrupts cell membrane causing leakage of cellular components and cell death

Treat:
colistin and other polymyxins last-resort therapy for multidrug-resistant gram-negative bacteria
e.g. P. aeruginosa, E. coli, K. pneumoniae

Adverse effects:
1) Nephrotoxicity
2) Neurotoxicity (slurred speech, weakness, paresthesia’s)
3) Respiratory failure

A

Polymyxins

Colistin (polymyxin E)
Polymyxin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are streptogramins?

Quinupristin & Dalfopristin

A

MOA:
50S inhibitors to prevent bacterial protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are fluoroquinolones? What are they used to treat?

suffix “-floxacin”
Ciprofloxacin, Moxifloxacin, or Levofloxacin

A

MOA:
Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV
to impair bacterial DNA synthesis by preventing inhibiting DNA winding and unwinding, which causes the strand breaks

avoid antacids
(they reduce oral absorption of drug, reducing its efficacy)

Treat:
1) Gram -ve rods in urinary and GI tracts (e.g. Pseudomonas)
2) Some gram-positive organisms
3) Otitis externa

Adverse effects:
1) Tendonitis/Tendon rupture (Achilles tendon rupture)

2) Possible cartilage damage (Avoid in children)

3) Prolonged QT interval (Torsades de Pointes risk)

4) Superinfections

Resistance:
1) Mutated DNA gyrase/topoisomerase genes
2) Efflux pumps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

MOA:
Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV
to impair bacterial DNA synthesis by preventing inhibiting DNA winding and unwinding, which causes the strand breaks

avoid antacids
(they reduce oral absorption of drug, reducing its efficacy)

Treat:
1) Gram -ve rods in urinary and GI tracts (e.g. Pseudomonas)
2) Some gram-positive organisms
3) Otitis externa

Adverse effects:
1) Tendonitis/Tendon rupture (Achilles tendon rupture)

2) Possible cartilage damage (Avoid in children)

3) Prolonged QT interval (Torsades de Pointes risk)

4) Superinfections

Resistance:
1) Mutated DNA gyrase/topoisomerase genes
2) Efflux pumps

A

fluoroquinolones
suffix “-floxacin”

Ciprofloxacin, Moxifloxacin, or Levofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Which fluoroquinolone inhibits CYP450 enzyme?
& What is a potential complication of this?

A

Ciprofloxacin

Can lead to drug interactions (e.g. warfarin, theophylline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Bacteriostatic describes drugs that

A

Inhibit bacterial protein synthesis

30S inhibitors

50S inhibitors

Folate antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Bactericidal antibiotics are drugs that

A

that inhibit cell wall synthesis

Peptidoglycan synthesis inhibitors:
1) Glycopeptides

Peptidoglycan cross-linking:
1) Penicillinase-Sensitive penicillin’s
2) Penicillinase-resistant penicillin’s
3) Antipseudomonal
4) Cephalosporins
5) Carbapenems
6) Monobactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are the quinolones?

Nalidixic acids

A

Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV
to impair bacterial DNA synthesis by preventing inhibiting DNA winding and unwinding, which causes the strand breaks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV
to impair bacterial DNA synthesis by preventing inhibiting DNA winding and unwinding, which causes the strand breaks

A

Nalidixic acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are Sulfonamides?

Sulfamethoxazole (SMX)
Sulfisoxazole
Sulfadiazine

A

MOA: Folate antagonists (Impairs folate synthesis in bacteria)

The drugs have chemical analogs of para-aminobenzoic acid (PABA), a folic acid precursor for bacteria which binds to and inhibits dihydropteroate synthase, preventing bacterial conversion of PABA to folic acid

Clinical use (with trimethoprim):
1) Synergistic block of bacterial folate synthesis
2) Gram-positive organisms (e.g. Nocardia)
3) Gram-negative organisms

Adverse effects:
1) Hypersensitivity reactions (sulfa allergy)
2)Hemolysis with G6PD deficiency
3) Nephrotoxicity (tubulointerstitial nephritis)
4) Photosensitive rash (Can develop into Stevens-Johnson syndrome)
5) Infantile kernicterus
6) Causes drug interactions (e.g. raises warfarin levels)

Resistance:
1) Mutations in enzyme (bacterial dihydropteroate synthase)
2) Decreased uptake
3) Increased PABA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

If sulfonamides are given with ________ it causes it to be a bactericidal drug (i.e inhibits cell wall synthesis)

A

trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

MOA: Folate antagonists (Impairs folate synthesis in bacteria)

The drugs have chemical analogs of para-aminobenzoic acid (PABA), a folic acid precursor for bacteria which binds to and inhibits dihydropteroate synthase, preventing bacterial conversion of PABA to folic acid

Clinical use (with trimethoprim):
1) Synergistic block of bacterial folate synthesis
2) Gram-positive organisms (e.g. Nocardia)
3) Gram-negative organisms

Adverse effects:
1) Hypersensitivity reactions (sulfa allergy)
2)Hemolysis with G6PD deficiency
3) Nephrotoxicity (tubulointerstitial nephritis)
4) Photosensitive rash (Can develop into Stevens-Johnson syndrome)
5) Infantile kernicterus
6) Causes drug interactions (e.g. raises warfarin levels)

Resistance:
1) Mutations in enzyme (bacterial dihydropteroate synthase)
2) Decreased uptake
3) Increased PABA synthesis

A

sulfonamides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is trimethoprim? What does it treat?

A

MOA:
Folate antagonist (it inhibits bacterial folate synthesis) by blocking bacterial dihydrofolate reductase (DHFR)

Broad-spectrum when used in with sulfonamides:
1) Urinary tract infections (UTIs)
2) Shigella
3) Salmonella
4) Pneumocystis jirovecii pneumonia
5) Toxoplasmosis prophylaxis
6) Community-acquired MRSA

Adverse effects:
1) Hyperkalemia (high doses)

2) drug interactions (e.g. raises warfarin levels) by inhibiting CYP Enzymes

3) Displace warfarin from albumin, increasing effective dosing

4) Folate deficiency

5) Teratogenic (neural tube defects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

MOA:
Folate antagonist (it inhibits bacterial folate synthesis) by blocking bacterial dihydrofolate reductase (DHFR)

Broad-spectrum when used in with sulfonamides:
1) Urinary tract infections (UTIs)
2) Shigella
3) Salmonella
4) Pneumocystis jirovecii pneumonia
5) Toxoplasmosis prophylaxis
6) Community-acquired MRSA

Adverse effects:
1) Hyperkalemia (high doses)

2) drug interactions (e.g. raises warfarin levels) by inhibiting CYP Enzymes

3) Displace warfarin from albumin, increasing effective dosing

4) Folate deficiency

5) Teratogenic (neural tube defects)

A

trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

megaloblastic anemia, leukopenia, granulocytopenia; Bone marrow contains rapidly-dividing hematopoietic cells that are more affected by relative folate deprivation NO NEURO SYMPTOMS

A

Folate deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are the Rifampins?

Rifampin
Rifabutin

A

MOA:
Inhibits DNA-dependent RNA polymerase to reduce mRNA synthesis

Used to treat:
1) Mycobacteria (M. tuberculosis (TB)) (RIPE regimen)
2) M. leprae (Delays resistance to dapsone when used for leprosy)
3) M. avium complex
4) N. meningitidis (Used for prophylaxis of close contacts)
5) H. influenzae type b (Used for prophylaxis of close contacts)

Adverse effects:
1) orange body fluids
2) Induces CYP450 enzymes
3) Hepatotoxicity (Elevations of AST and ALT levels)
4) Nephrotoxicity (May cause acute interstitial nephritis)

Resistance:
1) Mutations in RNA polymerase reduce drug binding
2) Monotherapy in TB rapidly leads to resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

MOA:
Inhibits DNA-dependent RNA polymerase to reduce mRNA synthesis

Used to treat:
1) Mycobacteria (M. tuberculosis (TB)) (RIPE regimen)
2) M. leprae (Delays resistance to dapsone when used for leprosy)
3) M. avium complex
4) N. meningitidis (Used for prophylaxis of close contacts)
5) H. influenzae type b (Used for prophylaxis of close contacts)

Adverse effects:
1) orange body fluids
2) Induces CYP450 enzymes
3) Hepatotoxicity (Elevations of AST and ALT levels)
4) Nephrotoxicity (May cause acute interstitial nephritis)

Resistance:
1) Mutations in RNA polymerase reduce drug binding
2) Monotherapy in TB rapidly leads to resistance

A

Rifampins

Rifampin
Rifabutin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Rifampin, rifabutin, & rifapentine are all examples of which type of drug?

A

Rifampin’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Which Rifampin is favored & why?

A

Rifabutin is favored in patients with an HIV infection because of less CYP450 induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What is Metronidazole? What does it treat?

A

MOA:
It forms toxic free radicals in the bacterial cell wall that damage DNA
Bactericidal, antiprotozoal

Used to treat:
1) Giardia
2) Entamoeba histolytica
3) Trichomonas vaginalis
4) Gardnerella vaginalis
5) Anaerobes (Bacteroides, C. difficile)
6) Used to treat anaerobic infections below the diaphragm (clindamycin used above)
7) H. pylori (in patients with penicillin allergies)

Adverse effects:
1) Disulfiram-like reaction with alcohol (Inhibition of acetaldehyde dehydrogenase, a toxic buildup of acetaldehyde occurs)
2) GI upset (nausea, vomiting, abdominal pain)
3) Neuropathy (paresthesia’s, dizziness)
4) Headache

126
Q

MOA:
It forms toxic free radicals in the bacterial cell wall that damage DNA
Bactericidal, antiprotozoal

Used to treat:
1) Giardia
2) Entamoeba histolytica
3) Trichomonas vaginalis
4) Gardnerella vaginalis
5) Anaerobes (Bacteroides, C. difficile)
6) Used to treat anaerobic infections below the diaphragm (clindamycin used above)
7) H. pylori (in patients with penicillin allergies)

Adverse effects:
1) Disulfiram-like reaction with alcohol (Inhibition of acetaldehyde dehydrogenase, a toxic buildup of acetaldehyde occurs)
2) GI upset (nausea, vomiting, abdominal pain)
3) Neuropathy (paresthesia’s, dizziness)
4) Headache

A

Metronidazole

127
Q

Presents with severe flushing, tachycardia, hypotension
Metallic taste in mouth

A

Disulfiram-like reaction with alcohol (Inhibition of acetaldehyde dehydrogenase, a toxic buildup of acetaldehyde occurs)

128
Q

What is Daptomycin?

A

MOA:
Disrupts cell membranes by creating transmembrane channels
Causes intracellular leakage and membrane depolarization
Ultimately inhibits DNA, RNA, and protein synthesis, leading to bacterial death

Used to treat (Gram +ve bacterial infections):
1) Gram-positive cocci
2) S. aureus skin infections (esp. MRSA)
3) bacteremia
4) endocarditis
5) VRE

Adverse effects:
1) Myopathy
2) Rhabdomyolysis
3) Creatinine kinase (CK) levels may rise due to release from skeletal muscle

129
Q

MOA:
Disrupts cell membranes by creating transmembrane channels
Causes intracellular leakage and membrane depolarization
Ultimately inhibits DNA, RNA, and protein synthesis, leading to bacterial death

Used to treat (Gram +ve bacterial infections):
1) Gram-positive cocci
2) S. aureus skin infections (esp. MRSA)
3) bacteremia
4) endocarditis
5) VRE

Adverse effects:
1) Myopathy
2) Rhabdomyolysis
3) Creatinine kinase (CK) levels may rise due to release from skeletal muscle

A

Daptomycin

130
Q

What can Daptomycin NOT be used to treat & why?

A

Not used for pneumonia
Avidly binds to and is inactivated by alveolar surfactant

131
Q

Colistin (polymyxin E) & Polymyxin B

A

MOA:
Makes cation glycoproteins against cell membranes

A last-resort therapy for multidrug-resistant gram-negative bacteria
(P. aeruginosa, E. coli, K. pneumoniae)

Adverse effects:
1) Nephrotoxicity
2) Neurotoxicity (slurred speech, weakness, paresthesia’s)
3) Respiratory failure

132
Q

MOA:
Makes cation glycoproteins against cell membranes

A last-resort therapy for multidrug-resistant gram-negative bacteria
(P. aeruginosa, E. coli, K. pneumoniae)

Adverse effects:
1) Nephrotoxicity
2) Neurotoxicity (slurred speech, weakness, paresthesia’s)
3) Respiratory failure

A

Colistin (polymyxin E) & Polymyxin B

133
Q

What are Caspofungin, Micafungin, & Anidulafungin?

Clinical use
Adverse effect

A

Echinocandins:

MOA:
They inhibit cell wall synthesis by inhibiting the synthesis of B-glucan

Used to treat:
1) Invasive aspergillus
2) Candida infection

Adverse Effects:
1) Hepatotoxicity (Elevated AST and ALT)
2) GI upset (mild)
3) Infusion-associated hypersensitivity
(Rash, hypotension, bronchospasm, and angioedema rarely occur due to local histamine release)

134
Q

Echinocandins:

MOA:
They inhibit the synthesis of beta-glucan to block fungal cell wall synthesis (very good for Aspergillus and Candida)

Note: targets fungal wall, not fungal membrane

Adverse Effects:
1) Hepatotoxicity (Elevated AST and ALT)
2) GI upset (mild)
3) Infusion-associated hypersensitivity
(Rash, hypotension, bronchospasm, and angioedema rarely occur due to local histamine release)

A

adverse effects of Caspofungin, Micafungin, & Anidulafungin (Echinocandins)

135
Q

What are NRTI’s (Nucleoside Reverse Transcriptase Inhibitors)?

Abacavir (ABC)
Zidovudine (ZDV)
Emtricitabine (FTC)
Lamivudine (3TC)
Didanosine (ddI)
Stavudine (d4T)
Tenofovir (TDF)

Clinical use?

Adverse effect

A

MOA:
Nucleoside analogs inhibit reverse transcriptase by competing with nucleosides, leading to DNA chain termination. They lack a 3’OH group, preventing synthesis of DNA from viral RNA. Activation through phosphorylation is necessary, except for tenofovir.

Clinical use:
1) HIV (HIV 1 & 2)
2) ZDV (general prophylaxis and during pregnancy to reduce risk of fetal transmission)

Adverse effect:
1) Hypersensitivity (Abacavir)
2) Bone marrow suppression
3) Anemia (zidovudine)
4) Pancreatitis (didanosine)
5) Lipoatrophy
6) hepatic steatosis
7) Wasting of subcutaneous fat
8) Peripheral neuropathy
9) Lactic acidosis

136
Q

What is the association with the hypersensitivity reaction side effect of Abacavir?

A

Hypersensitivity (Abacavir) it is seen in patients with HLA B*57:01 allele. It is caused by Type 4 HSR with fever, nausea, vomiting, rash

137
Q

How can bone marrow suppression (Myelosuppression) as side effect of NRTI’s be reversed?

A

They can be reversed with granulocyte colony-stimulating factor (G-CSF) and erythropoietin

138
Q

MOA:
Nucleoside analogs inhibit reverse transcriptase by competing with nucleosides, leading to DNA chain termination. They lack a 3’OH group, preventing synthesis of DNA from viral RNA. Activation through phosphorylation is necessary, except for tenofovir.

Clinical use:
1) HIV (HIV 1 & 2)
2) ZDV (general prophylaxis and during pregnancy to reduce risk of fetal transmission)

Adverse effect:
1) Hypersensitivity (Abacavir)
2) Bone marrow suppression
3) Anemia (zidovudine)
4) Pancreatitis (didanosine)
5) Lipoatrophy
6) hepatic steatosis
7) Wasting of subcutaneous fat
8) Peripheral neuropathy
9) Lactic acidosis

A

NRTI’s

139
Q

What is an adverse effect of Abacavir

A

Hypersensitivity

140
Q

Which NRTI is a nucleotide?

A

Tenofovir (the rest are nucleosides)

141
Q

What is Zidovudine?

Adverse Effects: bone marrow suppression (reversed with G-CSF and erythropoietin), peripheral neuropathy, lactic acidosis, anemia

Clinical uses

Adverse effect

A

Classification: NRTI

MOA:
Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’OH group). It needs to be phosphorylated to be activated.

Clinical uses:
1) HIV therapy
2) General prophylaxis and during pregnancy to decrease risk of fetal transmission (ZDV)

Adverse effect:
1) bone marrow suppression (reversed with G-CSF and erythropoietin)
2) peripheral neuropathy
3) lactic acidosis
4) anemia

142
Q

Classification: NRTI

MOA:
Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’OH group). It needs to be phosphorylated to be activated.

Clinical uses:
1) HIV therapy
2) General prophylaxis and during pregnancy to decrease risk of fetal transmission (ZDV)

Adverse effect:
1) bone marrow suppression (reversed with G-CSF and erythropoietin)
2) peripheral neuropathy
3) lactic acidosis
4) anemia

A

Zidovudine

143
Q

What are the antivirals Acyclovir (famciclovir, valacyclovir)?

Clinical uses?

A

MOA:
They are Guanosine analog inhibits viral DNA polymerase. They causes DNA chain termination, to prevent viral DNA replication

NEED phosphorylation by HSV/VZV thymidine kinase to be activated

Clinical use:
1) HSV (used for mucocutaneous and genital lesions, meningoencephalitis but they can’t eliminate latent forms)

2) VZV (they can’t eliminate latent forms)

144
Q

MOA:
They are Guanosine analog inhibits viral DNA polymerase. They causes DNA chain termination, to prevent viral DNA replication

NEED phosphorylation by HSV/VZV thymidine kinase to be activated

Clinical use:
1) HSV (used for mucocutaneous and genital lesions, meningoencephalitis but they can’t eliminate latent forms)

2) VZV (they can’t eliminate latent forms)

A

Acyclovir, Valaciclovir, & Famciclovir

145
Q

What are the antivirals (acyclovir, valaciclovir, & famciclovir) are not very good at treating

A

They are negligible activity against EBV and CMV
(EBV and CMV produce different thymidine kinases with lower affinity for acyclovir, reducing phosphorylation and activation

146
Q

What are Fluroquinolones

Adverse effects

Resistance

A

MOA:
A bactericidal that inhibits prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV

Avoid with antacids

Adverse effects:
superinfections
Tendonitis/rupture

Resistance: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

147
Q

MOA:
A bactericidal that inhibits prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV

Avoid with antacids

Adverse effects:
GI upset
superinfections
Tendonitis/rupture
skin rashes
headaches
dizziness
leg cramps and myalgias

Resistance: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

A

fluroquinolones

148
Q

What are Rifampins?

Clinical uses?

Adverse effects?

A

Classification: rifamycin

MOA:
It inhibits DNA-dependant RNA polymerase

Used for treating:
1) Mycobacterium tuberculosis (delay resistance to Dapsone when used for leprosy)
2) meningococcal prophylaxis
3) chemoprophylaxis in contacts of children with H. influenza type b

Adverse Effects:
1) minor hepatotoxicity
2) drug interactions (increases cytochrome P450)
3) orange body fluids

Resistance:
mutations reduce drug binding to RNA polymerase –– monotherapy rapidly leads to resistance

149
Q

MOA:
It inhibits DNA-dependant RNA polymerase

Used for treating:
1) Mycobacterium tuberculosis (delay resistance to Dapsone when used for leprosy)
2) meningococcal prophylaxis
3) chemoprophylaxis in contacts of children with H. influenza type b

Adverse Effects:
1) minor hepatotoxicity
2) drug interactions (increases cytochrome P450)
3) orange body fluids

Resistance:
mutations reduce drug binding to RNA polymerase –– monotherapy rapidly leads to resistance

A

Rifampins

150
Q

What are Macrolides? What do they treat?

Adverse effects?

A

MOA: bacteriostatic
Inhibit protein synthesis by blocking translocation by binding to the 23S rRNA of the 50S ribosomal subunit

Clinical Indications:
1) atypical pneumonias (Mycoplasma, Chlamydia, Legionella)
2) STIs (Chlamydia)
3) gram positive cocci (streptococcal infections in patients allergic to penicillin)
4) B. pertussis

Adverse effects:
MACRO:
gastrointestinal Motility issues (stimulate motilin)
Arrhythmia (prolonged QT interval)
acute Cholestatic hepatitis
Rash
eOsinophilia

151
Q

MOA: bacteriostatic
Inhibit protein synthesis by blocking translocation by binding to the 23S rRNA of the 50S ribosomal subunit

Clinical Indications:
1) atypical pneumonias (Mycoplasma, Chlamydia, Legionella)
2) STIs (Chlamydia)
3) gram positive cocci (streptococcal infections in patients allergic to penicillin)
4) B. pertussis

Adverse effects:
MACRO:
gastrointestinal Motility issues (stimulate motilin)
Arrhythmia (prolonged QT interval)
acute Cholestatic hepatitis
Rash
eOsinophilia

A

Macrolides

152
Q

aminoglycosides?

Gentamycin
amikin
Neomycin
Streptomycin
Tobramycin

Clinical uses?

Adverse effects?

A

Classification: aminoglycosides

MOA: bactericidal
It irreversibly inhibits the initiation of the complex through binding of the 30S subunit which can cause misreading of mRNA & also block translocation.

They require O2 for uptake; therefore, ineffective against anaerobes.

Clinical Indications:
1) severe gram-negative rod infections (synergistic with β-lactam antibiotics)

Adverse Effects:
1) nephrotoxicity (proteinuria, hypokalemia, acidosis, acute tubular necrosis)
2) neuromuscular blockage (decrease release of Ach [absolute contraindication with MG])
3) ototoxicity (especially with loop diuretics)
4) teratogenicity

Resistance:
bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation MOA

153
Q

MOA: bactericidal
It irreversibly inhibits the initiation of the complex through binding of the 30S subunit which can cause misreading of mRNA & also block translocation.

They require O2 for uptake; therefore, ineffective against anaerobes.

Clinical Indications:
1) severe gram-negative rod infections (synergistic with β-lactam antibiotics)

Adverse Effects:
1) nephrotoxicity (proteinuria, hypokalemia, acidosis, acute tubular necrosis)
2) neuromuscular blockage (decrease release of Ach [absolute contraindication with MG])
3) ototoxicity (especially with loop diuretics)
4) teratogenicity

Resistance:
bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation MOA

A

Aminoglycosides

154
Q

Adverse Effects:
1) nephrotoxicity (proteinuria, hypokalemia, acidosis, acute tubular necrosis)
2) neuromuscular blockage (decrease release of Ach [absolute contraindication with MG])
3) ototoxicity (especially with loop diuretics)
4) teratogenicity

A

aminoglycosides

155
Q

How do organisms develop resistance against aminoglycosides?

A

bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation

156
Q

What is Chloramphenicol? What does it treat?

Clinical uses

Adverse effects?

A

Classification: bacteriostatic antibiotic

MOA:
It blocks peptidyl transferase at 50S ribosomal subunit ––

Clinical Indications:
1) meningitis (H. influenzae, N. meningitidis, S. pneumoniae)
2) rickettsial diseases (Rocky Mountain Spotted Fever)

Adverse Effects:
1) bone marrow suppression (dose dependant)
2) anemia (dose independent)
3) aplastic anemia (dose dependant)
4) gray baby syndrome (premature infants because they lack UDP-glucuronosyltransferase)

Resistance:
plasmid-encoded acetyltransferase inactivates the druga

157
Q

Classification: bacteriostatic antibiotic

MOA:
It blocks peptidyl transferase at 50S ribosomal subunit ––

Clinical Indications:
1) meningitis (H. influenzae, N. meningitidis, S. pneumoniae)
2) rickettsial diseases (Rocky Mountain Spotted Fever)

Adverse Effects:
1) bone marrow suppression (dose dependant)
2) anemia (dose independent)
3) aplastic anemia (dose dependant)
4) gray baby syndrome (premature infants because they lack UDP-glucuronosyltransferase)

Resistance:
plasmid-encoded acetyltransferase inactivates the druga

A

Chloramphenicol

158
Q

What is Ganciclovir?

Clinical uses

Adverse effects?

A

Classification: viral DNA/RNA polymerase inhibitor

MOA:
A Guanosine analog that inhibits viral DNA polymerase causing DNA chain termination & preventing viral DNA replication. It needs CMV kinase to phosphorylate it to its active triphosphate form

Clinical Indications:
1) CMV (especially in immunocompromised patients)

Adverse Effects:
1) hepatic and neurologic dysfunction
2) bone marrow suppression (leukopenia, neutropenia, thrombocytopenia)
3) renal toxicity
4) seizures (overdose)

Resistance:
through mutated viral kinase

159
Q

Classification: viral DNA/RNA polymerase inhibitor

MOA:
A Guanosine analog that inhibits viral DNA polymerase causing DNA chain termination & preventing viral DNA replication. It needs CMV kinase to phosphorylate it to its active triphosphate form

Clinical Indications:
1) CMV (especially in immunocompromised patients)

Adverse Effects:
1) hepatic and neurologic dysfunction
2) bone marrow suppression (leukopenia, neutropenia, thrombocytopenia)
3) renal toxicity
4) seizures (overdose)

Resistance:
through mutated viral kinase

A

Ganciclovir

160
Q

What is Valganciclovir?

A

a prodrug of ganciclovir that has better oral bioavailability

161
Q

acyclovir?

Clinical use

Adverse effects

Resistance

A

Classification: guanine analog

MOA:
monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells therefore few adverse effects. The triphosphate is formed by cellular enzymes & preferentially inhibits viral DNA polymerase by chain termination

Clinical Indications:
1) HSV and VZV

weak activity against EBV used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis

2) prophylaxis in immunocompromised patients

Adverse Effects:
1) nausea, diarrhea and headache (oral dosing)
2) obstructive crystalline nephropathy and acute kidney injury if not adequately hydrated

Resistance:
mutated viral thymidine kinase

162
Q

Classification: guanine analog

MOA:
monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells therefore few adverse effects. The triphosphate is formed by cellular enzymes & preferentially inhibits viral DNA polymerase by chain termination

Clinical Indications:
1) HSV and VZV

weak activity against EBV used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis

2) prophylaxis in immunocompromised patients

Adverse Effects:
1) nausea, diarrhea and headache (oral dosing)
2) obstructive crystalline nephropathy and acute kidney injury if not adequately hydrated

Resistance:
mutated viral thymidine kinase

A

acyclovir

163
Q

What is Zidovudine?

Clinical uses?

Adverse effects?

A

Classification: NRTI

MOA:
It competitively inhibits nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’OH group). It needs to be phosphorylated to be activated.

Clinical Indications:
1) HIV therapy
2) general prophylaxis and during pregnancy to decrease risk of fetal transmission

Adverse Effects:
bone marrow suppression (reversed with G-CSF and erythropoietin), peripheral neuropathy
lactic acidosis
anemia

164
Q

Classification: NRTI

MOA:
It competitively inhibits nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’OH group). It needs to be phosphorylated to be activated.

Clinical Indications:
1) HIV therapy
2) general prophylaxis and during pregnancy to decrease risk of fetal transmission

Adverse Effects:
bone marrow suppression (reversed with G-CSF and erythropoietin), peripheral neuropathy
lactic acidosis
anemia

A

Zidovudine

165
Q

What is Raltegravir? What is it used to treat?

Adverse effects?

A

Classification: integrase inhibitor

MOA:
It inhibits the HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase (HIV-1 and HIV-2). There are no CYP interactions making it relatively safe.

It is used to treat:
1) HIV

 Adverse Effects:
1) toxicity leads to increased creatine kinase

166
Q

Classification: integrase inhibitor

MOA:
It inhibits the HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase (HIV-1 and HIV-2). There are no CYP interactions making it relatively safe.

It is used to treat:
1) HIV

 Adverse Effects:
1) toxicity leads to increased creatine kinase

A

Raltegravir

167
Q

What is Foscarnet?

Clinical uses?

Adverse effects?

Resistance?

A

Classification: viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor

MOA: It binds to the pyrophosphate-binding site of enzyme & it does not require any kinase activation.

 Clinical Indications:
1) CMV retinitis in immunocompromised patients when ganciclovir fails 2) acyclovir-resistant HSV

 Adverse Effects:
1) nephrotoxicity
2) electrolyte abnormalities (hyper/hypocalcemia, hyper/hypophosphatemia, hypokalemia, hypomagnesemia) can lead to seizures

Resistance:
mutated DNA polymerase

168
Q

Classification: viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor

MOA: It binds to the pyrophosphate-binding site of enzyme & it does not require any kinase activation.

 Clinical Indications:
1) CMV retinitis in immunocompromised patients when ganciclovir fails 2) acyclovir-resistant HSV

 Adverse Effects:
1) nephrotoxicity
2) electrolyte abnormalities (hyper/hypocalcemia, hyper/hypophosphatemia, hypokalemia, hypomagnesemia) can lead to seizures

Resistance:
mutated DNA polymerase

A

Foscarnet

169
Q

What are Integrase Inhibitors? What do they treat?

Drug Names (-tegravir ending)
Raltegravir
Dolutegravir
Bictegravir
Elvitegravir

Adverse effects?

A

They Inhibit retroviral integrase & blocks integration of HIV viral DNA (made by reverse transcriptase) into host cell chromosome to prevent viral replication

Used to treat:
1) HIV
They are effective againstHIV-1 and HIV-2
(they are apart of the highly-active antiretroviral therapy (HAART)
Usually 3 drugs: 2 NRTIs and integrase or protease inhibitor)

Myositis (myopathy)
Increase creatine kinase levels

170
Q

They Inhibit retroviral integrase & blocks integration of HIV viral DNA (made by reverse transcriptase) into host cell chromosome to prevent viral replication

Used to treat:
1) HIV
They are effective againstHIV-1 and HIV-2
(they are apart of the highly-active antiretroviral therapy (HAART)
Usually 3 drugs: 2 NRTIs and integrase or protease inhibitor)

Myositis (myopathy)
Increase creatine kinase levels

A

Integrase Inhibitors

Drug Names (-tegravir ending)
Raltegravir
Dolutegravir
Bictegravir
Elvitegravir

171
Q

What is Amantadine? What are the adverse effects?

Adverse effects?

A

Classification: NMDA receptor antagonist (antiviral)

MOA:
It blocks muscarinic receptors to increase DA release and decrease DA reuptake

Adverse Effects:
1) insomnia
2) dizziness
3) confusion
4) ankle edema
5) atropine-like
6) livedo reticularis

172
Q

Classification: NMDA receptor antagonist (antiviral)

MOA:
It blocks muscarinic receptors to increase DA release and decrease DA reuptake

Adverse Effects:
1) insomnia
2) dizziness
3) confusion
4) ankle edema
5) atropine-like
6) livedo reticularis

A

Amantadine

173
Q

What is the trade name of Oseltamivir?

A

Tamiflu

174
Q

What do Oseltamivir and zanamivir treat?

Adverse effects?

A

Classification: Sialic acid analogs

MOA:
That bind & inhibit neuraminidase which prevents cleavage of viral progeny off of the cell surface & blocking the new viral particles to exit the cell. They may also slow the viral penetration into the airway epithelium

They treat:
1) Influenza virus (flu) both influenza A and B infections

Beginning within 48 hours of symptom onset can shorten course of illness

Adverse effects:
1) Gastrointestinal upset
2) Zanamivir may exacerbate COPD and asthma
(because it is an inhaled dry powder)

175
Q

Classification: Sialic acid analogs

MOA:
That bind & inhibit neuraminidase which prevents cleavage of viral progeny off of the cell surface & blocking the new viral particles to exit the cell. They may also slow the viral penetration into the airway epithelium

They treat:
1) Influenza virus (flu) both influenza A and B infections

Beginning within 48 hours of symptom onset can shorten course of illness

Adverse effects:
1) Gastrointestinal upset
2) Zanamivir may exacerbate COPD and asthma
(because it is an inhaled dry powder)

A

Oseltamivir and zanamivir

176
Q

What is Raltegravir? what does it treat?

Adverse effects?

A

Classification: integrase inhibitor

MOA:
It inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase (HIV-1 and HIV-2). It doesn’t have any CYP interactions

Clinical Indications: HIV therapy

Adverse Effects: toxicity leads to increased creatine kinase

177
Q

Classification: integrase inhibitor

MOA:
It inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase (HIV-1 and HIV-2). It doesn’t have any CYP interactions

Clinical Indications: HIV therapy

Adverse Effects: toxicity leads to increased creatine kinase

A

Raltegravir

178
Q

What is Ribavirin? What does it treat?

Adverse effects?

A

MOA:
It inhibits synthesis of guanine nucleotide by competitively inhibiting IMP dehydrogenase

Clinical Indications:
1)Hepatitis C
2)RSV

Adverse Effects:
1) Hemolytic anemia
2) severe teratogen

179
Q

MOA:
It inhibits synthesis of guanine nucleotide by competitively inhibiting IMP dehydrogenase

Clinical Indications:
1)Hepatitis C
2)RSV

Adverse Effects:
1) Hemolytic anemia
2) severe teratogen

A

Ribavirin

180
Q

What is Amphotericin B?

Clinical uses?

Adverse effects?

A

Classification: cell membrane integrity inhibitor (polyene)

MOA:
It binds ergosterol to form membrane pores that allow leakage of electrolytes

Clinical Indications:
1) serious, systemic mycoses
2) Cryptococcus
3) Blastomyces
4) Coccidiosis
5) Histoplasmosis
6) Candida
7) Mucor

Adverse Effects:
1) fever/chills
2) hypotension
3) nephrotoxicity
4) arrythmias
5) anemia
6)IV phlebitis

hydration helps decrease nephrotoxicity

181
Q

Classification: cell membrane integrity inhibitor (polyene)

MOA:
It binds ergosterol to form membrane pores that allow leakage of electrolytes

Clinical Indications:
1) serious, systemic mycoses
2) Cryptococcus
3) Blastomyces
4) Coccidiosis
5) Histoplasmosis
6) Candida
7) Mucor

Adverse Effects:
1) fever/chills
2) hypotension
3) nephrotoxicity
4) arrythmias
5) anemia
6)IV phlebitis

hydration helps decrease nephrotoxicity

A

Amphotericin B

182
Q

Amphotericin B is given with or without __________ when treating cryptococcal meningitis?

A

+/– flucytosine

183
Q

What should you give a patient experiencing the adverse effects of nephrotoxicity (Hypokalemia & Hypomagnesemia) when given Amphotericin B?

A

Supplement K+
and Mg2+ because of altered
renal tubule permeability

184
Q

What can decrease nephrotoxicity in patients being treated with amphotericin B?

A

Hydration reduces nephrotoxicity

185
Q

What is Caspofungin? What does it treat?

Adverse effects?

A

Classification: echinocandins (cell wall synthesis inhibitor)

MOA:
It inhibits cell wall synthesis by inhibiting synthesis of β-glucan

Clinical Indications:
1) invasive aspergillosis
2) Candida

Adverse Effects:
1) GI upset
2) flushing (r/t histamine release)

186
Q

Classification: echinocandins (cell wall synthesis inhibitor)

MOA:
It inhibits cell wall synthesis by inhibiting synthesis of β-glucan

Clinical Indications:
1) invasive aspergillosis
2) Candida

Adverse Effects:
1) GI upset
2) flushing (r/t histamine release)

A

Caspofungin

187
Q

What is Ketoconazole (azole)?

Clinical use?

Adverse effects?

A

Classification: ergosterol synthesis inhibitor (azoles)

MOA:
It inhibits fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme (14-α-demethylase) that converts lanosterol to ergosterol

Clinical Indications:
1) alternative drugs in candidemia and infections caused by Aspergillus, Blastomyces, Cryptococcus, and Histoplasma

Note ketoconazole is rarely used in systemic fungal infections

Adverse Effects:
1) testosterone synthesis inhibition (gynecomastia, decreased libido)
2) liver dysfunction (increased LFTs, hepatoxicity [inhibits cytochrome P-450])

188
Q

Classification: ergosterol synthesis inhibitor (azoles)

MOA:
It inhibits fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme (14-α-demethylase) that converts lanosterol to ergosterol

Clinical Indications:
1) alternative drugs in candidemia and infections caused by Aspergillus, Blastomyces, Cryptococcus, and Histoplasma

Note ketoconazole is rarely used in systemic fungal infections

Adverse Effects:
1) testosterone synthesis inhibition (gynecomastia, decreased libido)
2) liver dysfunction (increased LFTs, hepatoxicity [inhibits cytochrome P-450])

A

Ketoconazole

189
Q

Which drug interactions cause Hemolysis in G6PD
deficiency as a side effect?

A

Isoniazid, sulfonamides, dapsone, primaquine,
aspirin, ibuprofen, nitrofurantoin

“hemolysis is D PAIN”

190
Q

Isoniazid, sulfonamides, dapsone, primaquine,
aspirin, ibuprofen, nitrofurantoin

Drug interactions all result in what complication?

A

Hemolysis in G6PD
deficiency

191
Q

Which drug interactions cause Gray baby syndrome as a side effect?

A

Chloramphenicol

192
Q

Chloramphenicol

Drug interaction results in what complication?

A

Gray baby syndrome

193
Q

Which drug interactions cause Agranulocytosis as a side effect?

A

Dapsone, clozapine, carbamazepine,
propylthiouracil, methimazole, colchicine,
ticlopidine, ganciclovir

“Drugs Can Cause Pretty Major Collapse To
Granulocytes”

194
Q

Dapsone, clozapine, carbamazepine,
propylthiouracil, methimazole, colchicine,
ticlopidine, ganciclovir

Drug interactions all result in what complication?

A

Agranulocytosis

195
Q

Which drug interactions cause Aplastic anemia as a side effect?

A

Carbamazepine, methimazole, NSAIDs,
benzene, chloramphenicol, propylthiouracil

“Can’t Make New Blood Cells Properly”

196
Q

Carbamazepine, methimazole, NSAIDs,
benzene, chloramphenicol, propylthiouracil

Drug interactions all result in what complication?

A

Aplastic anemia

197
Q

Which drug interactions cause Direct Coombs ⊕
hemolytic anemia as a side effect?

A

Penicillin, methylDopa, Cephalosporins

“P Diddy Coombs”

198
Q

Penicillin, methylDopa, Cephalosporins

Drug interactions all result in what complication?

A

Direct Coombs ⊕
hemolytic anemia

199
Q

Which drug interactions cause Drug reaction with
eosinophilia and systemic symptoms as a side effect?

A

Allopurinol, antiBiotics, antiConvulsants, sulfa
drugs

“ABCs”

200
Q

Allopurinol, antiBiotics, antiConvulsants, sulfa
drugs

Drug interactions all result in what complication?

A

Drug reaction with
eosinophilia and systemic symptoms

201
Q

Which drug interactions cause Thrombocytopenia as a side effect?

A

Indinavir, heparin, quinidine, ganciclovir,
vancomycin, linezolid, abciximab

“I Have Quickly Gotten Very Low Amounts”

202
Q

Indinavir, heparin, quinidine, ganciclovir,
vancomycin, linezolid, abciximab

Drug interactions all result in what complication?

A

Thrombocytopenia

203
Q

Which drug interactions cause Rash (Stevens-Johnson
syndrome) as a side effect?

A

Anti-epileptic drugs (especially lamotrigine),
allopurinol, sulfa drugs, penicillin

“Steven Johnson has Epileptic Allergy to Sulfa
drugs and Penicillin”

204
Q

Anti-epileptic drugs (especially lamotrigine),
allopurinol, sulfa drugs, penicillin

Drug interactions all result in what complication?

A

Rash (Stevens-Johnson
syndrom

205
Q

Which drug interactions cause Tendon/cartilage
damage as a side effect?

A

Fluoroquinolones

206
Q

Fluoroquinolones

Drug interaction results in what complication?

A

Tendon/cartilage
damage

207
Q

Which drug interactions cause Myopathy as a side effect?

A

Statins, fibrates, niacin, colchicine, daptomycin,
hydroxychloroquine, interferon-α,
penicillamine, glucocorticoids

208
Q

Statins, fibrates, niacin, colchicine, daptomycin,
hydroxychloroquine, interferon-α,
penicillamine, glucocorticoids

Drug interactions all result in what complication?

A

Myopathy

209
Q

Where does enfuvirtide act & what does it do?

A

A → fusion inhibitor

210
Q

Where do NRTIs and NNRTIS act?

A

B → NRTIs and NNRTIS

211
Q

Where does oseltamivir act & what does it do?

A

C → It inhibits virion release because it’s a neuraminidase inhibitor

212
Q

Where does a de-Integrase inhibitor act?

A

D → Integrase inhibitor

213
Q

Where does Amantadine act, What does it do, & what does it specifically treat?

A

E → It inhibits uncoating of the influenza A virus only

214
Q

Fill in the boxes

A
215
Q

What is Amantadine?

Clinical use?

Adverse effect?

A

Classification: NMDA receptor antagonist (antiviral)

MOA:
It blocks the muscarinic receptors to increase DA release and decrease DA reuptake

Clinical use: HIV

 Adverse Effects:
1) insomnia
2) dizziness/confusion
3) ankle edema
4) atropine-like, livedo reticularis

216
Q

What are the azole antifungals?

Fluconazole
Itraconazole
Ketoconazole
Voriconazole
Isavuconazole
Clotrimazole
Miconazole

Clinical uses?

Adverse effects?

A

MOA:
They Inhibit fungal ergosterol synthesis by inhibiting the 14-alpha-demethylase (a cytochrome P450 enzyme), thereby blocking ergosterol synthesis Inhibits formation of fungal cell membrane (note: no effect on fungal cell wall)

Clinical uses:
1) Local and less serious mycoses
2) Cryptococcal meningitis in AIDS (fluconazole)
3) Candida (fluconazole)
4) Blastomyces
5) Coccidiodes
6) Histoplasma
7) Sporothrix schenckii (itraconazole)
8) Topical fungal infections (clotrimazole, miconazole)
9) Aspergillus (voriconazole, isavuconazole)

Adverse effects:
1) GI upset

2) Antiandrogen (Inhibits testosterone synthesis ie. gynecomastia)

3) Inhibits CYP450 Enzymes which can lead to drug interactions (e.g. with warfarin, theophylline)

4) Hepatotoxicity
(Mild hepatitis and liver dysfunction)

217
Q

MOA:
They Inhibit fungal ergosterol synthesis by inhibiting the 14-alpha-demethylase (a cytochrome P450 enzyme), thereby blocking ergosterol synthesis Inhibits formation of fungal cell membrane (note: no effect on fungal cell wall)

Clinical uses:
1) Local and less serious mycoses
2) Cryptococcal meningitis in AIDS (fluconazole)
3) Candida (fluconazole)
4) Blastomyces
5) Coccidiodes
6) Histoplasma
7) Sporothrix schenckii (itraconazole)
8) Topical fungal infections (clotrimazole, miconazole)
9) Aspergillus (voriconazole, isavuconazole)

Adverse effects:
1) GI upset

2) Antiandrogen (Inhibits testosterone synthesis ie. gynecomastia)

3) Inhibits CYP450 Enzymes which can lead to drug interactions (e.g. with warfarin, theophylline)

4) Hepatotoxicity
(Mild hepatitis and liver dysfunction)

A

azole antifungals

Fluconazole
Itraconazole
Ketoconazole
Voriconazole
Isavuconazole
Clotrimazole
Miconazole

218
Q

What is Nyastatin?

Clinical use?

Adverse effect?

A

MOA:
It binds to ergosterol to form holes in fungal membranes (unique to fungal membranes) causing membrane holes/pores, allowing electrolytes that cause fungal cell lysis to leak out

Clinical use:
1) Candidiasis (Swish and swallow for oral thrush)
2) Topical for diaper rash/vaginal candidiasis

Adverse effect:
Skin irritation or hypersensitivity

219
Q

MOA:
It binds to ergosterol to form holes in fungal membranes (unique to fungal membranes) causing membrane holes/pores, allowing electrolytes that cause fungal cell lysis to leak out

Clinical use:
1) Candidiasis (Swish and swallow for oral thrush)
2) Topical for diaper rash/vaginal candidiasis

Adverse effect:
Skin irritation or hypersensitivity

A

Nystatin

220
Q

What is Flucytosine?

Clinical use?

Adverse effects?

A

Antimetabolite:
A fungal DNA polymerase and RNA polymerase inhibitor

MOA:
Flucytosine is converted into 5-fluorouracil (5-FU) by cytosine deaminase a Fluorinated analog of cytosine which inhibits fungal DNA and RNA polymerase thereby blocking DNA replication and fungal protein synthesis

Clinical use:
Used in combination with amphotericin B to treat
1) Cryptococcal meningitis

Adverse effects:
1) Bone marrow suppression (anemia, thrombocytopenia, or leukopenia)

2) Nephrotoxicity

3) Hepatotoxicity

4) Nausea/vomiting

221
Q

How is Flucytosine cleared?

A

It is cleared renally so avoid in patients with renal failure

222
Q

Antimetabolite:
A fungal DNA polymerase and RNA polymerase inhibitor

MOA:
Flucytosine is converted into 5-fluorouracil (5-FU) by cytosine deaminase a Fluorinated analog of cytosine which inhibits fungal DNA and RNA polymerase thereby blocking DNA replication and fungal protein synthesis

Clinical use:
Used in combination with amphotericin B to treat
1) Cryptococcal meningitis

Adverse effects:
1) Bone marrow suppression (anemia, thrombocytopenia, or leukopenia)

2) Nephrotoxicity

3) Hepatotoxicity

4) Nausea/vomiting

A

Flucytosine

223
Q

What is Terbinafine?

Clinical use?

Adverse effects?

A

A squalene oxidase inhibitor (fungal enzyme)

MOA:
It inhibits the synthesis of lanosterol, a precursor to ergosterol, which forms fungal cell membrane

(Cleared via liver metabolism)

Clinical use:
1) Dermatophytosis (tinea) Especially onychomycosis - fungal infections of nails

2) Paracoccidioidomycosis

3) Seborrheic dermatitis

Adverse effects:
1) Headache
2) Loss of taste (dysgeusia) can lead to weight loss,
3) depression/anxiety
4) Hepatotoxicity
5) GI upset

224
Q

A squalene oxidase inhibitor (fungal enzyme)

MOA:
It inhibits the synthesis of lanosterol, a precursor to ergosterol, which forms fungal cell membrane

(Cleared via liver metabolism)

Clinical use:
1) Dermatophytosis (tinea) Especially onychomycosis - fungal infections of nails

2) Paracoccidioidomycosis

3) Seborrheic dermatitis

Adverse effects:
1) Headache
2) Loss of taste (dysgeusia) can lead to weight loss,
3) depression/anxiety
4) Hepatotoxicity
5) GI upset

A

Terbinafine?

225
Q

What are the first line drugs used in the treatment of TB?

“RIPES”

A

First line drugs -RIPES
1) ISONIAZID (H)
2) RIFAMPICIN (R)
3) PYRAZINAMIDE (Z)
4) ETHAMBUTOL (E)
5) STREPTOMYCIN (S)

226
Q

First line drugs -RIPES
1) ISONIAZID (H)
2) RIFAMPICIN (R)
3) PYRAZINAMIDE (Z)
4) ETHAMBUTOL (E)
5) STREPTOMYCIN (S)

A

TB

227
Q

What is Isoniazid (INH)?

Clinical use?

Adverse effects?

A

MOA:
It impairs the synthesis of mycolic acid (a key component of mycobacterial cell wall) that must be activated by bacterial catalase-peroxidase (encoded by KatG). It is an inactive pro-drug that must be converted into its active drug by an mycobacterial enzyme

Clinical use:
1) Mycobacteria (especially M. tuberculosis, RIPE therapy for active TB & a Monotherapy for latent TB, TB prophylaxis

Adverse effects:
1) Vitamin B6 (pyridoxine) deficiency
(Isoniazid inhibits pyridoxine phosphokinase, which normally activates vitamin B6 into its active form (PLP))

2) Inhibits CYP450 Enzymes it can lead to drug interactions (e.g. warfarin, theophylline)

3) Drug-induced lupus-like reaction

4) Hepatotoxicity

5) Anion gap metabolic acidosis

228
Q

MOA:
It impairs the synthesis of mycolic acid (a key component of mycobacterial cell wall) that must be activated by bacterial catalase-peroxidase (encoded by KatG). It is an inactive pro-drug that must be converted into its active drug by an mycobacterial enzyme

Clinical use:
1) Mycobacteria (especially M. tuberculosis, RIPE therapy for active TB & a Monotherapy for latent TB, TB prophylaxis

Adverse effects:
1) Vitamin B6 (pyridoxine) deficiency
(Isoniazid inhibits pyridoxine phosphokinase, which normally activates vitamin B6 into its active form (PLP))

2) Inhibits CYP450 Enzymes it can lead to drug interactions (e.g. warfarin, theophylline)

3) Drug-induced lupus-like reaction

4) Hepatotoxicity

5) Anion gap metabolic acidosis

A

Isoniazid (INH)

229
Q

What is Pyrazinamide (PZA)?

Clinical use?

Adverse effects?

A

an antibiotic used to treat active tuberculosis

MOA:
Exact mechanism is unknown but it is activated by the conversion to pyrazinoic acid by the mycobacterial enzyme pyrazinamidase
(more active at acidic pH (e.g. in macrophage phagolysosomes))

Clinical use:
Active Mycobacterium tuberculosis

(Part of RIPE regimen of rifamycin, isoniazid, pyrazinamide, and ethambutol)

Adverse effects:

1) Hepatotoxicity (Dose-dependent that is synergistic with rifampin’s hepatotoxic effect (also in RIPE treatment for TB))

2) Hyperuricemia/Gout
(Pyrazinamide competes with uric acid for secretion by the kidneys, resulting in increased uric acid levels)

3) Arthralgias8

230
Q

an antibiotic used to treat active tuberculosis

MOA:
Exact mechanism is unknown but it is activated by the conversion to pyrazinoic acid by the mycobacterial enzyme pyrazinamidase
(more active at acidic pH (e.g. in macrophage phagolysosomes))

Clinical use:
Active Mycobacterium tuberculosis

(Part of RIPE regimen of rifamycin, isoniazid, pyrazinamide, and ethambutol)

Adverse effects:

1) Hepatotoxicity (Dose-dependent that is synergistic with rifampin’s hepatotoxic effect (also in RIPE treatment for TB))

2) Hyperuricemia/Gout
(Pyrazinamide competes with uric acid for secretion by the kidneys, resulting in increased uric acid levels)

3) Arthralgias8

A

Pyrazinamide (PZA)

231
Q

What is Chloroquine?

clinical uses?

adverse effects?

develop resistance?

A

MOA:
It blocks the breakdown of heme to hemozoin by inhibiting heme polymerase it can also cause Heme accumulation is toxic to plasmodia

Treats:
1) Plasmodium spp. (Malaria)

Adverse effects:

1) Retinopathy (Rare chronic use)
2) Myopathy
3) Pruritus (Occurs more commonly in dark-skinned individuals)
4) GI upset
5) Headaches/dizziness

Resistance:
Membrane efflux pump

232
Q

MOA:
It blocks the breakdown of heme to hemozoin by inhibiting heme polymerase it can also cause Heme accumulation is toxic to plasmodia

Treats:
1) Plasmodium spp. (Malaria)

Adverse effects:

1) Retinopathy (Rare chronic use)
2) Myopathy
3) Pruritus (Occurs more commonly in dark-skinned individuals)
4) GI upset
5) Headaches/dizziness

Resistance:
Membrane efflux pump

A

Chloroquine

233
Q

Chloroquine-resistant P. falciparum is treated with which drugs?

A

artemisinins
atovaquone-proguanil
mefloquine (quinidine analog)

234
Q

What is Ethambutol?

What is the clinical use?

adverse effects?

A

MOA:
It inhibits arabinosyltransferase which prevents the production of arabinogalactan, a key component of mycobacterial cell wall

Clinical uses:
1) Mycobacterium tuberculosis
(Part of RIPE regimen of rifamycin, isoniazid, pyrazinamide, and ethambutol)

2) mycobacterium avium complex (MAC)

Adverse effects:
1) Optic neuropathy

Clinically manifests as red-green color blindness, decreased visual acuity, and central scotoma
Reversible with discontinuation of the drug

235
Q

MOA:
It inhibits arabinosyltransferase which prevents the production of arabinogalactan, a key component of mycobacterial cell wall

Clinical uses:
1) Mycobacterium tuberculosis
2) mycobacterium avium complex (MAC)

Adverse effects:
1) Optic neuropathy

Clinically manifests as red-green color blindness, decreased visual acuity, and central scotoma
Reversible with discontinuation of the drug

A

Ethambutol

236
Q

Antimycobacterial cyclic peptide that binds to the 30s ribosomal subunit

Treats:
M. TB, M. kansasi, & MYCOBACTERIUM AVIUM CELLULAR

Adverse effects:
Ototoxicity
Nephrotoxicity

A

Capreomycin?

237
Q

MOA:
Inhibits inhA gene & blocks mycolic acid synthesis

Treats: TB & Multidrug resistant TB

Adverse effects:
1) Postural hypotension
2) Depression
3) Drowsiness/anesthenia
4) Neurological toxicity

Recommended to be given with pyridoxine

A

Ethionamide

238
Q

MOA:
They bind to 30S ribosomal subunit

Treat:
TB
Mycobacterium Avium Cellular
DIC

the 2ns choice after streptomycin & Capreomycin to treat TB

Adverse effects:
1) Ototoxicity
2) Nephrotoxicity

A

Kanamycin
Amikacin

239
Q

MOA:
It inhibits DNA gyrase & topoisomerase

Treats:
TB

used in combination with other drugs to treat multi-drug resistant Mycobacterium Avium cellular in patients with AIDS

A

Fluoroquinolone
Ciprofloxacin

240
Q

MOA:
Binds to 30S ribosomal unit prevent formation of ‘initiation complex’ of peptide synthesis

Treats:
bactericidal mainly for extracellular bacilli

Adverse effects:
Ototoxicity
Nephrotoxicity
Hypersensitivity reactions
Anaphylaxis
Rash
Fever

A

Streptomycin

IM, IV

241
Q

MOA:
Cycloserine inhibits reactions in which D-alanine is involved in cell wall synthesis

Treats:
TB

Adverse effects:
Peripheral neuropathy
Dizziness tremors
Psychotic changes

A

Cycloserine

242
Q

MOA:
A less potent inducer of cyt p450.
Less interactions with PI/NNRTI

Treats:
Better activity
against MAC.
M.leprae/M.fortitum

Adverse effects:
Skin rash
GI intolerance
Hepatitis
Red orange discoloration of urine

A

Rifabutin

243
Q

Aminosalicylic acid (PAS)

A

MOA:
Inhibits folic acid synthesis of bacteria

Treats:
Bacteriostatic
Highly specific to M. TB

Adverse effects:
GI intolerance
HS reactions
Hematological
Abnormalities

244
Q

What is Bedaquiline?

A

diarylquinoline

MOA:
It targets C subunit of mycobacterial ATP synthase to Inhibit of proton pump activity.

It is good for shortening the duration of treatment without any increased risk of relapse

Used to treat:
MDR-TB

Adverse effects:
1) AST and/or ALT elevations
2) Amylase and/or lipase elevation
3) Musculoskeletal system abnormalities- myalgia
4) Cardiac rhythm disturbances (prolonged QT interval)
5) Gi issues

245
Q

diarylquinoline

MOA:
It targets C subunit of mycobacterial ATP synthase to Inhibit of proton pump activity.

It is good for shortening the duration of treatment without any increased risk of relapse

Used to treat:
MDR-TB

Adverse effects:
1) AST and/or ALT elevations
2) Amylase and/or lipase elevation
3) Musculoskeletal system abnormalities- myalgia
4) Cardiac rhythm disturbances (prolonged QT interval)
5) Gi issues

A

Bedaquiline

246
Q

What does Pretomanid treat?

A

Treatment:
XDR-TB or MDR-TB who are treatment-intolerant or non-responsive (collectively “highly drug-resistant TB”)

247
Q

What are Ifosfamide, Cyclophosphamide

Clinical uses

A

Classification: alkylating agents

MOA:
They cross-link DNA at guanine (N7) & they need require bioactivation by liver to be activated

Clinical Indications: 1
1) solid tumors
2) leukemia
3) lymphomas
4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s])

Adverse Effects:
1) alopecia
2) myelosuppression
3) SIADH
4) Fanconi syndrome (ifosfamide)
5) hemorrhagic cystitis and bladder cancer

248
Q

Classification: alkylating agents

MOA:
They cross-link DNA at guanine (N7) & they need require bioactivation by liver to be activated

Clinical Indications: 1
1) solid tumors
2) leukemia
3) lymphomas
4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s])

Adverse Effects:
1) alopecia
2) myelosuppression
3) SIADH
4) Fanconi syndrome (ifosfamide)
5) hemorrhagic cystitis and bladder cancer

A

Ifosfamide & Cyclophosphamide

249
Q

What is Vincristine?

Clinical use

Adverse effect

A

An [M-phase specific] microtubule inhibitor

MOA:
It is a vinca alkaloid that binds 𝛃-tubulin and inhibits its polymerization into microtubules which prevents the mitotic spindle formation (M-phase arrest) Overall it decreases microtubule polymerization

Clinical Indications:
1) solid tumors
2) leukemias
3) Hodgkin and non-Hodgkin lymphomas
4) Wilms

Adverse Effects:
1) alopecia
2) SIADH
3) neurotoxicity (areflexia, peripheral neuritis)
4) constipation (paralytic ileus)

no myelosuppression

250
Q

An [M-phase specific] microtubule inhibitor

MOA:
It is a vinca alkaloid that binds 𝛃-tubulin and inhibits its polymerization into microtubules which prevents the mitotic spindle formation (M-phase arrest) Overall it decreases microtubule polymerization

Clinical Indications:
1) solid tumors
2) leukemias
3) Hodgkin and non-Hodgkin lymphomas
4) Wilms

Adverse Effects:
1) alopecia
2) SIADH
3) neurotoxicity (areflexia, peripheral neuritis)
4) constipation (paralytic ileus)

no myelosuppression

A

Vincristine

251
Q

What is Doxorubicin?

Clinical use

Adverse effect

A

Classification: anthracyclines

MOA:
They generate free radicals which intercalates in the DNA leading to breaks in DNA resulting in decreased replication. It interferes with topoisomerase II enzyme

Clinical Indications:
1) solid tumors
2) leukemias
3) lymphomas

Adverse Effects:
1) cardiotoxicity (dilated cardiomyopathy)
2) myelosuppression, alopecia

252
Q

Classification: anthracyclines

MOA:
They generate free radicals which intercalates in the DNA leading to breaks in DNA resulting in decreased replication. It interferes with topoisomerase II enzyme

Clinical Indications:
1) solid tumors
2) leukemias
3) lymphomas

Adverse Effects:
1) cardiotoxicity (dilated cardiomyopathy)
2) myelosuppression, alopecia

A

Doxorubicin

253
Q

What should you use to prevent cardiotoxicity when giving Doxorubicin?

A

Use dexrazoxane (iron chelating agent) used to prevent cardiotoxicity

254
Q

What is Cyclosporine?

Clinical use

Adverse effect

A

Classification: calcineurin inhibitor

MOA:
It binds cyclophilin that blocks T-cell activation by preventing IL-2 transcription

Clinical Indications:
1) psoriasis
2) rheumatoid arthritis

Adverse Effects:
1) nephrotoxic
2) hypertension
3) hyperlipidemia
4) neurotoxicity
5) gingival hyperplasia
6) hirsutism

255
Q

What is Ifosfamide & Cyclophosphamide?

clinical use

adverse effects

A

Classification: alkylating agent (nitrogen mustards)

MOA:
They cross-link DNA at guanine (N7) & they need bioactivation by liver

Clinical Indications:
1) solid tumors
2) leukemia
3) lymphomas
4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s])

Adverse Effects:
1) alopecia
2) myelosuppression
3) SIADH, Fanconi syndrome (ifosfamide)
4) hemorrhagic cystitis and bladder cancer
(prevented with mesna [sulfhydryl group of mesna binds toxic metabolites] and adequate hydration [cyclophosphamide])

256
Q

Classification: alkylating agent (nitrogen mustards)

MOA:
They cross-link DNA at guanine (N7) & they need bioactivation by liver

Clinical Indications:
1) solid tumors
2) leukemia
3) lymphomas
4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s])

Adverse Effects:
1) alopecia
2) myelosuppression
3) SIADH, Fanconi syndrome
4) hemorrhagic cystitis and bladder cancer
(prevented with mesna [sulfhydryl group of mesna binds toxic metabolites] and adequate hydration

A

cyclophosphamide & ifosfamide

257
Q

Classification: alkylating agent (nitrogen mustards)

MOA:
They cross-link DNA at guanine (N7) & they need bioactivation by liver

Clinical Indications:
1) solid tumors
2) leukemia
3) lymphomas
4) rheumatic disease (SLE, granulomatosis with polyangiitis [Wegner’s])

Adverse Effects:
1) alopecia
2) myelosuppression
3) SIADH, Fanconi syndrome (ifosfamide)
4) hemorrhagic cystitis and bladder cancer
(prevented with mesna [sulfhydryl group of mesna binds toxic metabolites] and adequate hydration [cyclophosphamide])

A

Ifosfamide & Cyclophosphamide

258
Q

What is Doxorubicin?

CLinical uses

Adverse effects

A

Classification: anthracyclines

MOA:
It generates free radicals through intercalate in DNA causing breaks in DNA resulting in decreased replication which interferes with topoisomerase II enzyme

Clinical Indications:
1) solid tumors
2) leukemias
3) lymphomas

Adverse Effects:

1) cardiotoxicity (dilated cardiomyopathy) (use dexrazoxane (iron chelating agent) used to prevent cardiotoxicity

2) myelosuppression
3) alopecia

259
Q

Classification: anthracyclines

MOA:
It generates free radicals through intercalate in DNA causing breaks in DNA resulting in decreased replication which interferes with topoisomerase II enzyme

Clinical Indications:
1) solid tumors
2) leukemias
3) lymphomas

Adverse Effects:

1) cardiotoxicity (dilated cardiomyopathy) (use dexrazoxane (iron chelating agent) used to prevent cardiotoxicity

2) myelosuppression
3) alopecia

A

Doxorubicin

260
Q

What is Methotrexate?

Clinical uses

Adverse effects

A

Classification: antimetabolite

MOA:
It is a folic acid analog that competitively inhibits DHF reductase leading to decrease in dTMP resulting in decreased DNA synthesis

Clinical Indications:
1) cancers (leukemia [ALL], lymphoma, & choriocarcinoma sarcoma)
2) non-neoplastic (ectopic pregnancy & medical abortion)
3) rheumatoid arthritis
4) psoriasis
5) IBD
6) vasculitis

Adverse Effects:
1) myelosuppression (reversible with leucovorin [folinic acid] rescue)
2) hepatotoxicity
3) mucositis (mouth ulcers)
4) pulmonary fibrosis
5) folate deficiency
6) nephrotoxicity

261
Q

Classification: antimetabolite

MOA:
It is a folic acid analog that competitively inhibits DHF reductase leading to decrease in dTMP resulting in decreased DNA synthesis

Clinical Indications:
1) cancers (leukemia [ALL], lymphoma, & choriocarcinoma sarcoma)
2) non-neoplastic (ectopic pregnancy & medical abortion)
3) rheumatoid arthritis
4) psoriasis
5) IBD
6) vasculitis

Adverse Effects:
1) myelosuppression (reversible with leucovorin [folinic acid] rescue)
2) hepatotoxicity
3) mucositis (mouth ulcers)
4) pulmonary fibrosis
5) folate deficiency
6) nephrotoxicity

A

methotrexate

262
Q

What are the Tyrosine Kinase inhibitors? (-tinib)?

Imatinib
Gefitinib
Erlotinib
Dasatinib
Sunitinib
Adavosertib

Clinical uses

Adverse effects

A

MOA:
They are tyrosine kinase inhibitors of BCR-ABL (encoded by Philadelphia chromosome [t(9;22)] fusion gene in CML) and c-kit (common in GIST)

Clinical uses:
1) CML
2) GIST

 Adverse E8ffects: fluid retention

263
Q

MOA:
They are tyrosine kinase inhibitors of BCR-ABL (encoded by Philadelphia chromosome [t(9;22)] fusion gene in CML) and c-kit (common in GIST)

Clinical uses:
1) CML
2) GIST

 Adverse E8ffects: fluid retention

A

What are the adverse effects of Tyrosine Kinase inhibitors? (-tinib)

Imatinib
Gefitinib
Erlotinib
Dasatinib
Sunitinib
Adavosertib

264
Q

What is Vincristine?

Clinical uses

Adverse effect

A

Classification: microtubule inhibitors

MOA:
They are vinca alkaloids that bind β-tubulin and inhibit its polymerization into microtubules which prevents mitotic spindle formation (M-phase arrest) to decrease microtubular polymerization

Clinical Indications:
1) solid tumors
2) leukemias
3) Hodgkin and non-Hodgkin lymphomas
4) Wilms

Adverse Effects:
1) alopecia
2) SIADH
3) neurotoxicity (areflexia, peripheral neuritis)
4) constipation (paralytic ileus)

no myelosuppression

265
Q

Classification: microtubule inhibitors

MOA:
They are vinca alkaloids that bind β-tubulin and inhibit its polymerization into microtubules which prevents mitotic spindle formation (M-phase arrest) to decrease microtubular polymerization

Clinical Indications:
1) solid tumors
2) leukemias
3) Hodgkin and non-Hodgkin lymphomas
4) Wilms

Adverse Effects:
1) alopecia
2) SIADH
3) neurotoxicity (areflexia, peripheral neuritis)
4) constipation (paralytic ileus)

no myelosuppression

A

Vincristine

266
Q

What is 6-Mercaptopurine?

Clinical use

Adverse effect

A

Classification: antimetabolite

MOA:
A purine (thiol) analog that results in decreasing de novo purine synthesis that is activated by HGPRT

Clinical Indications:
1) preventing organ rejection
2) rheumatoid arthritis
3) IBD
4) SLE

Adverse Effects:
1) immunosuppression
2) myelosuppression
3) GI and liver toxicity
(metabolized by xanthine oxidase, therefore, increase risk of toxicity with allopurinol or febuxostat)

267
Q

Which medication is used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease

A

6-Mercaptopurine

268
Q

Classification: antimetabolite

MOA:
A purine (thiol) analog that results in decreasing de novo purine synthesis that is activated by HGPRT

Clinical Indications:
1) preventing organ rejection
2) rheumatoid arthritis
3) IBD
4) SLE

Adverse Effects:
1) immunosuppression
2) myelosuppression
3) GI and liver toxicity
(metabolized by xanthine oxidase, therefore, increase risk of toxicity with allopurinol or febuxostat)

A

adverse effects of 6-Mercaptopurine

269
Q

List the following adverse effects for:

Cisplatin & Carboplatin

Vincristine

Bleomycin & Busulfan

Doxorubicin

Trastuzumab

Cyclophosphamide

A

Cisplatin & Carboplatin:
Ototoxicity & nephrotoxicity

Vincristine: Peripheral neuropathy

Bleomycin & Busulfan: Pulmonary fibrosis

Doxorubicin: Cardiotoxicity

Trastuzumab: Cardiotoxicity

Cyclophosphamide: Hemorrhagic cystitis

270
Q

Topoisomerase inhibitors inhibit which parts of the cell cycle?

Etoposide
Teniposide
Irinotecan
Topotecan

A

S phase (DNA synthesis)
G2 (Double check repair)

271
Q

An anticancer drug that inhibits

S phase (DNA synthesis)
G2 (Double check repair)

A

Topoisomerase inhibitors:

Etoposide
Teniposide
Irinotecan
Topotecan

“Topoisomerase Inhibitors Are Tough Enough”

272
Q

Antimetabolites inhibit which part of the cell cycle?

Azathioprine
Cladribine
Cytarabine
5-Fluorouracil
Hydroxyurea
Methotrexate
6-Mercaptopurine

A

An anticancer drug that inhibits

S phase (DNA synthesis)

273
Q

An anticancer drug that inhibits only

S phase (DNA synthesis)

A

Antimetabolites:

Azathioprine
Cladribine
Cytarabine
5-Fluorouracil
Hydroxyurea
Methotrexate
6-Mercaptopurine

274
Q

Bleomycin inhibits which part of the cell cycle?

A

G2 phase (Double check repair)

275
Q

An anticancer drug that inhibits only

G2 phase (DNA synthesis)

A

Bleomycin

276
Q

Microtubule inhibitors inhibit which part of the cell cycle?

Paclitaxel
Vinblastine
Vincristine

A

M phase (Inhibits Mitosis)

277
Q

Which anticancer drug inhibits the M phase (mitosis)?

A

Microtubule inhibitors

Paclitaxel
Vinblastine
Vincristine

278
Q

What is Albendazole?

CLinical use?

Adverse effects?

A

Classification: anthelmintic

MOA:
It decreases the glucose uptake and decrease microtubular structure

Clinical Indications: most intestinal nematodes

 Adverse Effects:
1) leukopenia
2) alopecia
3) elevation of LFTs

279
Q

Classification: anthelmintic

MOA:
It decreases the glucose uptake and decrease microtubular structure

Clinical Indications: most intestinal nematodes

 Adverse Effects:
1) leukopenia
2) alopecia
3) elevation of LFTs

A

Albendazole

280
Q

What is Bleomycin?

A

MOA:
An antitumor antibiotic that binds to DNA in the G2 phase of the cell cycle and induces free radical formation to induce DNA breaks

281
Q

What are Dactinomycin & Actinomycin D?

Clinical uses?

Adverse effects

A

Dactinomycin and actinomycin D are two interchangeable names for the same intercalating agent.

MOA:
They intercalate into the DNA their molecules insert between two strands of DNA blocking RNA polymerases from accessing DNA strands preventing RNA synthesis in rapidly dividing cells.

Used for childhood tumors:
1) Wilms tumor
2) Ewing sarcoma
3) rhabdomyosarcoma

Adverse effects:
1) Myelosuppression (obvious)

282
Q

Dactinomycin and actinomycin D are two interchangeable names for the same intercalating agent.

MOA:
They intercalate into the DNA their molecules insert between two strands of DNA blocking RNA polymerases from accessing DNA strands preventing RNA synthesis in rapidly dividing cells.

Used for childhood tumors:
1) Wilms tumor
2) Ewing sarcoma
3) rhabdomyosarcoma

Adverse effects:
1) Myelosuppression (obvious)

A

Dactinomycin & Actinomycin D

283
Q

What are Doxorubicin and daunorubicin? (3 ways)

Adverse effects?

A

Doxorubicin and daunorubicin are chemotherapeutics

MOA:
1) They cause DNA strand breaks by inducing free radical formation

2) They can insert themselves or intercalate into DNA

3) These drugs inhibit topoisomerase II (prevents the enzyme from unwinding or fixing knots in DNA)

Adverse effects:
1) myelosuppression
2) alopecia
3) cardiotoxicity

284
Q

Doxorubicin and daunorubicin are chemotherapeutics

MOA:
1) They cause DNA strand breaks by inducing free radical formation

2) They can insert themselves or intercalate into DNA

3) These drugs inhibit topoisomerase II (prevents the enzyme from unwinding or fixing knots in DNA)

Adverse effects:
1) myelosuppression
2) alopecia
3) cardiotoxicity

A

Doxorubicin and daunorubicin

285
Q

What is Ivermectin?

clinical uses

Adverse effects?

A

 Classification: anthelmintic

MOA:
It intensifies GABA-mediated neurotransmission in nematodes and causes immobilization of parasites, facilitating the removal by the reticuloendothelial system (does not cross BBB)

 Clinical Indications:
1) onchocerciasis
2) cutaneous larva migrans
3) strongyloidiasis
4) filariasis

Adverse Effects:
1) fever/headache/
2) dizziness
3) rash/pruritus
4) tachycardia
5) hypotension
6) pain in joints, muscles and lymph glands

contraindicated in pregnancy

286
Q

 Classification: anthelmintic

MOA:
It intensifies GABA-mediated neurotransmission in nematodes and causes immobilization of parasites, facilitating the removal by the reticuloendothelial system (does not cross BBB)

 Clinical Indications:
1) onchocerciasis
2) cutaneous larva migrans
3) strongyloidiasis
4) filariasis

Adverse Effects:
1) fever/headache/
2) dizziness
3) rash/pruritus
4) tachycardia
5) hypotension
6) pain in joints, muscles and lymph glands

contraindicated in pregnancy

A

Ivermectin

287
Q

Metronidazole

Clinical use

Adverse effects?

A

Classification: nitroimidazoles (bactericidal & antiprotozoal)

MOA:
It forms toxic free radical metabolites in bacterial cell that damage DNA

Clinical Indications:
1) Giardia
2) Entamoebae
3) Trichomonas
4) Gardnerella vaginalis
5) Anaerobes (Bacteroides, C. difficile) –– can be used in place of amoxicillin in H. pylori ‘triple therapy’ in case of penicillin allergy

Adverse Effects:
1) disulfiram-like reaction (sever flushing, tachycardia, hypotension) with alcohol
2) headache
3) metallic taste

288
Q

Classification: nitroimidazoles (bactericidal & antiprotozoal)

MOA:
It forms toxic free radical metabolites in bacterial cell that damage DNA

Clinical Indications:
1) Giardia
2) Entamoebae
3) Trichomonas
4) Gardnerella vaginalis
5) Anaerobes (Bacteroides, C. difficile) –– can be used in place of amoxicillin in H. pylori ‘triple therapy’ in case of penicillin allergy

Adverse Effects:
1) disulfiram-like reaction (sever flushing, tachycardia, hypotension) with alcohol
2) headache
3) metallic taste

A

Metronidazole

289
Q

What is Isoniazid?

Clinical use

adverse effects

A

Classification: antituberculosis

MOA:
It decreases the synthesis of mycolic acid. It needs bacterial catalase peroxidase (encoded by KatG) in order to convert INH to active metabolite

Clinical Indications:
1) mycobacterium tuberculosis (only agent used as solo prophylaxis against TB and monotherapy for latent TB)

Adverse Effects:
1) hepatoxicity
2) hemolysis in G6PD deficiency
3) cytochrome P-450 inhibition
4) drug-induced SLE
5) anion gap metabolic acidosis
6) vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia)
7) seizures (high doses –– refractory to benzodiazepines) –– administer with pyridoxine

290
Q

Classification: antituberculosis

MOA:
It decreases the synthesis of mycolic acid. It needs bacterial catalase peroxidase (encoded by KatG) in order to convert INH to active metabolite

Clinical Indications:
1) mycobacterium tuberculosis (only agent used as solo prophylaxis against TB and monotherapy for latent TB)

Adverse Effects:
1) hepatoxicity
2) hemolysis in G6PD deficiency
3) cytochrome P-450 inhibition
4) drug-induced SLE
5) anion gap metabolic acidosis
6) vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia)
7) seizures (high doses –– refractory to benzodiazepines) –– administer with pyridoxine

A

Isoniazid

291
Q

How do organisms develop resistance to Isoniazid?

A

Mechanism of Resistance:
mutations leading to under expression of KatG

292
Q

What is a Sulfonamide?

Sulfamethoxazole (SMX)
Sulfisoxazole
Sulfadiazine

Clinical use

Adverse effects?

A

Classification: folic acid synthesis inhibitor

MOA:
They inhibit dihydropteroate synthase, thus inhibiting folate synthesis it is a bacteriostatic (bactericidal when
combined with trimethoprim)

 Clinical Indications:
1) Gram-positive organisms (e.g. Nocardia)
2) gram negative

Adverse Effects:
1) hypersensitivity reactions
2) hemolysis if G6PD deficient
3) nephrotoxicity (tubulointerstitial nephritis)
4) photosensitivity
5) SJS
6) kernicterus in infants
7) displace other drugs from albumin

293
Q

Classification: folic acid synthesis inhibitor

MOA:
They inhibit dihydropteroate synthase, thus inhibiting folate synthesis it is a bacteriostatic (bactericidal when
combined with trimethoprim)

 Clinical Indications:
1) Gram-positive organisms (e.g. Nocardia)
2) gram negative

Adverse Effects:
1) hypersensitivity reactions
2) hemolysis if G6PD deficient
3) nephrotoxicity (tubulointerstitial nephritis)
4) photosensitivity
5) SJS
6) kernicterus in infants
7) displace other drugs from albumin

A

Sulfonamides

Sulfamethoxazole (SMX)
Sulfisoxazole
Sulfadiazine

294
Q

How do organisms develop resistance to Sulfonamides?

A

Through altered enzyme (bacterial dihydropteroate synthase), decrease uptake or increase PABA synthesis

295
Q

What is Dapsone?

A

Classification: sulfones

MOA:
inhibit dihydropteroate synthase, to inhibit folate synthesis it is a bacteriostatic (bactericidal when combined with trimethoprim)

Clinical Indications:
1) leprosy
2) PJP prophylaxis or treatment when combined with TMP

Adverse Effects:
1) hemolysis if G6PD deficient
2) methemoglobinemia
3) agranulocytosis

296
Q

Classification: sulfones

MOA:
similar to sulfonamides, but structurally distinct
They inhibit dihydropteroate synthase, thus inhibiting folate synthesis it is a bacteriostatic (bactericidal when combined with trimethoprim)

Clinical Indications:
1) leprosy
2) PJP prophylaxis or treatment when combined with TMP

Adverse Effects:
1) hemolysis if G6PD deficient
2) methemoglobinemia
3) agranulocytosis

A

Dapsone

297
Q

What is 6-Mercaptopurine?

Clinical use

Adverse effect

A

Classification: antimetabolite

MOA:
A purine (thiol) analog leading to decrease de novo purine synthesis that is activated by HGPRT

Clinical Indications:
1) preventing organ rejection
2) rheumatoid arthritis
3) IBD
4) SLE –– used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease

Adverse Effects:
1) immunosuppression
2) myelosuppression
3) GI and liver toxicity (metabolized by xanthine oxidase, therefore, increase risk of toxicity with allopurinol or febuxostat)

298
Q

Classification: antimetabolite

MOA:
A purine (thiol) analog leading to decrease de novo purine synthesis that is activated by HGPRT

Clinical Indications:
1) preventing organ rejection
2) rheumatoid arthritis
3) IBD
4) SLE –– used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease

Adverse Effects:
1) immunosuppression
2) myelosuppression
3) GI and liver toxicity (metabolized by xanthine oxidase, therefore, increase risk of toxicity with allopurinol or febuxostat)

A

6-Mercaptopurine

299
Q

What is Primaquine? & what does it treat?

Adverse effects?

A

Classification: antiprotozoal
Mechanism of Action: unknown?

 Clinical Indications:
1) P. vivax
2) P. ovale
3) PJP

Adverse Effects:
1) GI distress
2) pruritus
3) headache
4) methemoglobinemia
5) blood cytopenia’s
6) hemolysis in G6PD deficiency

Contraindicated in pregnancy

300
Q

Classification: antiprotozoal
Mechanism of Action: unknown?

 Clinical Indications:
1) P. vivax
2) P. ovale
3) PJP

Adverse Effects:
1) GI distress
2) pruritus
3) headache
4) methemoglobinemia
5) blood cytopenia’s
6) hemolysis in G6PD deficiency

Contraindicated in pregnancy

A

Primaquine

301
Q

What are Tyrosine Kinase Inhibitors (-tinib)?

What do they treat?

What are the adverse effects?

A

MOA:
They are tyrosine kinase inhibitors of BCR-ABL (encoded by Philadelphia chromosome [t(9;22)] fusion gene in CML) and c-kit (common in GIST)

Clinical Indications:
1) CML
2) GIST

Adverse Effects: fluid retention

302
Q

MOA:
They are tyrosine kinase inhibitors of BCR-ABL (encoded by Philadelphia chromosome [t(9;22)] fusion gene in CML) and c-kit (common in GIST)

Clinical Indications:
1) CML
2) GIST

Adverse Effects: fluid retention

A

Tyrosine Kinase Inhibitors (-tinib)

303
Q

What is aspirin?

clinical use

Adverse effect

A

Classification: NSAID

MOA:
An NSAID that irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation leading to decrease synthesis of TXA2 and prostaglandins. It increases bleeding time but doesn’t effect PT & PTT

 Clinical Indications:
1) decrease platelet aggregation (low dose)
2) antipyretic and analgesic (intermediate dose)
3) anti-inflammatory (high dose)

Adverse Effects:

1) gastric ulceration
2) tinnitus (CN VIII)
3) allergic reactions (patients with asthma or nasal polyps)
4) acute kidney injury (chronic)
5) interstitial nephritis
6) GI bleeding

7) Risk of Reye syndrome in children treated with aspirin for viral infection

304
Q

Classification: NSAID

MOA:
An NSAID that irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation leading to decrease synthesis of TXA2 and prostaglandins. It increases bleeding time but doesn’t effect PT & PTT

 Clinical Indications:
1) decrease platelet aggregation (low dose)
2) antipyretic and analgesic (intermediate dose)
3) anti-inflammatory (high dose)

Adverse Effects:

1) gastric ulceration
2) tinnitus (CN VIII)
3) allergic reactions (patients with asthma or nasal polyps)
4) acute kidney injury (chronic)
5) interstitial nephritis
6) GI bleeding

7) Risk of Reye syndrome in children treated with aspirin for viral infection

A

Aspirin

305
Q

Respiratory alkalosis early, but transitions to mixed metabolic acidosis-respiratory. Describes which toxicity?

A

treatment of overdose: NaHCO3-.

306
Q

What is Ibuprofen?

clinical use

adverse effect

A

Classification: NSAID

MOA:
It reversibly inhibit cyclooxygenase (1 & 2) to block prostaglandin synthesis

Clinical Indications:
1) antipyretic
2) analgesic
3) anti-inflammatory

Adverse Effects:
1) interstitial nephritis
2) gastric ulcer (prostaglandins protect gastric mucosa)
3) renal ischemia (prostaglandins vasodilate afferent arteriole)
4) aplastic anemia

307
Q

Classification: NSAID

MOA:
It reversibly inhibit cyclooxygenase (1 &2 ) to block prostaglandin synthesis

Clinical Indications:
1) antipyretic
2) analgesic
3) anti-inflammatory

Adverse Effects:
1) interstitial nephritis
2) gastric ulcer (prostaglandins protect gastric mucosa)
3) renal ischemia (prostaglandins vasodilate afferent arteriole)
4) aplastic anemia

A

Ibuprofen

308
Q

What is Nitrofurantoin?

What is it’s clinical use?

What are the adverse effects?

A

Classification: anthelmintic

MOA: Bactericidal and bacteriostatic

 Clinical Indications:
1) UTI (not Proteus or Pseudomonas)

 Adverse Effects:
1) GI distress
2) rash
3) pulmonary infiltrates
4) phototoxicity
5) neuropathies
6) hemolysis in G6PD deficiency

309
Q

Classification: anthelmintic

MOA:
bactericidal and bacteriostatic

 Clinical Indications:
1) UTI (not Proteus or Pseudomonas)

 Adverse Effects:
1) GI distress
2) rash
3) pulmonary infiltrates
4) phototoxicity
5) neuropathies
6) hemolysis in G6PD deficiency

A

Nitrofurantoin

310
Q

What can Augmentin (Amoxicillin-Clavulanate) & Unasyn (Amoxicillin-Sulbactam) treat?

A

Acute sinusitis
Animal bites
Aspiration pneumonia

Pharm SJSM (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions