MICROBIOLOGY- Antimicrobials Flashcards

0
Q

This medication acts inhibiting the conversion from PABA to Dihydrofolate in DNA methylation

A

Sulfonamides

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1
Q

Which antimicrobials interfere with folic acid synthesis?

A

Sulfonamide

Trimethoprim

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2
Q

Who are examples of sulfonamides?

A

Sulfamethoxazole
Sulfisoxazole
Sulfadiazine

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3
Q

This antimicrobal inhibits the convertion of DHF to THF

A

Trimethoprim

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4
Q

How are classified the antimicrobials who inhibit cell wall synthesis?

A

Peptydoglycan synthesis

Peptydoglycan cross linking

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5
Q

Who are consider inhibitors of peptydoglycan synthesis?

A

Glycopeptides

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6
Q

Which medicines are glycopeptides?

A

Vancomycin

Bacitracin

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7
Q

Which families are from peptydoglycan cross linking?

A
Penicillinase sensitive penicillins
Penicillinase resistant penicillins
Antipseudomonals
Cephalosporins
Carbapenems
Monobactams
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8
Q

Which is the mechanism of action for Fluoroquinolones and quinolones?

A

Inhibiting DNA topoisomerase

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9
Q

This antimicrobial damages directly bacterias DNA

A

Metronidazole

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10
Q

Which is the mechanism of action of Rifampin?

A

Inhibits mRNA synthesis by inhibiting RNA Polymerase

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11
Q

How are classified antimicrobials who inhibit proteins?

A

Inhibitors of 50 S subunit

Inhibitors of 30 S subunit

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12
Q

They are classified as Inhibitors of 50 S subunit

A
Chloramophenicol
Clindamycin
Linezolid
Macrolides
Streptogramins
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13
Q

Which antimicrobials inhibit 30 S subunit?

A

Aminoglycosides

Tetracyclines

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14
Q

Who are consider penicillinase sensitive penicillins?

A

Penicillin G, V
Ampicillin
Amoxicillin

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15
Q

Who are consider prototype beta lactam antibiotics?

A

Penicillin G and V

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16
Q

Which is the way of administration for penicillin G?

A

IV and IM form

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17
Q

How do you administer penicillin V?

A

Oral

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18
Q

Which is the mechanism of action of Penicillin G, V?

A

Blind penicillin-binding proteins (transpeptidase)
Block transpeptidase cross-linking of peptidoglycan
Activate autolytic enzymes

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19
Q

Which is the clinical use for penicillin G and V?

A

Mostly used for gram-positive organisms

Also used for N. Meningitidis and T. Pallidum

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20
Q

Which gram-positive organisms are concealer penicillinase sensitive?

A

S. Pneumoniae
S. Pyogenes
Actinomyces

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21
Q

For which bacterias are penicillin G and V consider bactericidial?

A

Bactericidial for gram-positive cocci, gram-positive rods, gram negative cocci and sphirochetes

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22
Q

These are consider toxicity reactions to penicillin G and V

A

Hypersensitivity reactions

Hemolytic anemia

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23
Q

Who are consider resistant to penicillin V and G?

A

Penicillinase in bacteria (a type of beta lactamase) cleaves beta lactam ring

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24
Q

Who are consider aminopenicillins?

A

Ampicillin, amoxicillin

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25
Q

Which is the mechanism of action of ampicillin and amoxicillin?

A

Same as penicillin

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26
Q

Who has wider spectrum between aminopenicillin and penicillin? Why?

A

Aminopenicillin

Penicillinase sensitive

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27
Q

Which medicine is combined with aminopenicillins to protect against beta lactamase?

A

Clavulanic acid

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28
Q

Who has greater oral bioavailability between ampicillin and amoxicillin?

A

Amoxicillin

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29
Q

Which is the clinical use for Aminopenicillins?

A

Extended spectrum penicillin

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30
Q

Which bacterias are sensitive to aminopenicillins?

A
Haemophilus influenzae
E. Coli
Listeria monocytogenes
Proteus mirabilis
Salmonella
Shigella
Enterococci
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31
Q

Which are the clinical manifestations of toxicity caused by aminopenicillins?

A

Hypersensitivity reactions, rash and pseudomembranous colitis

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32
Q

Who can present resistance to aminopenicillins?

A

Penicillinase in bacteria (a type of beta lactamase) cleaves beta lactam ring

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33
Q

Which medicines are consider penicillinase resistant penicillins?

A

Oxacillin
Nafcillin
Dicloxacillin

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34
Q

Which is the mechanism of action of penicillinase resistant penicillins?

A

Same as penicillin. Narrow spectrum

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35
Q

Why do dicloxacillin has narrow spectrum than penicillin?

A

Because penicillin resistant penicillins only act for penicillinase resistant because bulky R group blocks access of Beta lactamase to beta lactam ring

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36
Q

Which is the principal use for Dicloxacillin (penicillinase resistant penicillin)?

A

S. Aureus

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37
Q

Is Every type of S. Aureus sensitive to penicillinase resistant penicillins?

A

No, MRSA is resistant because of altered penicillin binding protein target site

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38
Q

Which are adverse effects of penicillinase resistant penicillins?

A

Hypersensitivity reactions, interstitial nephritis

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39
Q

These medicines are consider antipseudomonals

A

Ticarcillin, pioeracillin

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40
Q

Which is the mechanism of action of antipseudomonals?

A

Same as penicillin but with extended spectrum

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41
Q

Which is the clinical use for ticarcillin?

A

Antipseudomonal

Pseudomonas spp and gram negative rods, susceptible to penicillinase

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42
Q

Which medicines are commonly used with pseudomonals?

A

Beta lactamase inhibitors

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43
Q

Who are considered beta lactamase inhibitors?

A

Clavulanic acid
Sulbactam
Tazobactam

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44
Q

Why do we add beta lactamase inhibitors to penicillin antibiotics?

A

To protect antibiotic from destruction by beta lactamase

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45
Q

Which is the effect penicillinase?

A

Destroy penicillin antibiotics by beta lactamase

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46
Q

How many generations do cephalosporins have?

A

5

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47
Q

This is how cephalosporin work

A

Beta lactam drugs that inhibit cell wall synthesis

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48
Q

Which is the problem of cephalosporins?

A

Less susceptible to penicillinases

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49
Q

How are cephalosporin consider bactericidal or bacteriostatics?

A

Bactericidal

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50
Q

Which organisms typically are not covered by cephalosporins?

A
Chephalosporins are LAME
Listeria
Atypicals (chlamydia, mycoplasma)
MRSA
Entericocci
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51
Q

Which cephalosporin covers MRSA?

A

Ceftaroline

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52
Q

What do first generation cephalosporins cover?

A

Gram positive cocci

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53
Q

Name some examples of first generation cephalosporins

A

Cefazolin

Cephalexin

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54
Q

Used prior to surgery to prevent S. Aureus wound infection

A

Cefazolin

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55
Q

Which bacteria are cover by second-generation cephalosporins?

A

Gram-positive cocci

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56
Q

Which are considered second-generation cephalosporins?

A

Cefoxitin
Cefaclor
Cefuroxime

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57
Q

These bacterias are cover by second generation cephalosporins

A
Haemophilus influenzae 
Enterobacter aerogenes
Neisseria spp
Proteus mirabilis
E. Coli
Klebsiella pneumoniae
Serratia marcescens
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58
Q

When is recommended the use of third-generation cephalosporins?

A

Serious gram-negative infections resistance to other Beta lactams

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59
Q

Name some third-generation cephalosporin

A

Ceftriaxone
Cefotaxime
Ceftazidine

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60
Q

When is recommended ceftriaxone?

A

Meningitis and gonorrhea

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61
Q

This third-generation cephalosporin is useful for pseudomonas

A

Ceftazidime

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62
Q

How is cefepime classified?

A

4th generation cephalosporin

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63
Q

Which is the mechanism of action of cefepime?

A

Increased activity against pseudomonas and gram-positive organisms

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64
Q

Consider the only fifth generation cephalosporin

A

Ceftaroline

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65
Q

What does Ceftaroline covers for?

A

Broad gram-positive and gram-negative organisms coverage, including MRSA

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66
Q

Which bacteria specially ceftaroline does not covers?

A

Pseudomona

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67
Q

When is consider that cephalosporins cause Toxicity?

A

Hypersensitivity reactions
Vitamin K deficiency
Low cross reactivity with penicillins
Increase nephrotoxicity of aminoglycosides

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68
Q

Which medicine is consider monobactam?

A

Aztreonam

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69
Q

How do you classify Aztreonam?

A

Monibactam resistant to beta lactamase

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70
Q

What does aztreonam prevents?

A

Prevents peptidoglycan cross linking by binding to penicillin binding protein 3

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71
Q

With which medication is aztreonam synergic?

A

Aminoglycosides

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72
Q

Do monobactams have cross allergenicity with penicillins?

A

False

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73
Q

Which are the only bacterias sensitive to aztreonam?

A

Gram negative rods

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74
Q

For which bacterias Aztreonam does not has activity

A

No activity against gram positives or anaerobes

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75
Q

When is recommended the clinical use of aztreonam (monobactams)?

A

For penicillin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides

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76
Q

How toxic is Aztreonam?

A

Usually nontoxic, occasionally GI upset

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77
Q

Who are categorized as carbapenems?

A

Imipenem
Meropenem
Ertapenem
Dorioenem

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78
Q

How is imipenem classified?

A

Broad spectrum, beta lactamase resistant carbapenem

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79
Q

Which medication it’s always administer with Imipenem?

A

Cilastatin

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80
Q

Why is cilastatin always administered with Carbapenems?

A

To decrease inactivation of drug in renal tubes

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81
Q

What does cilastatin inhibits?

A

Renal dehydropeptidase I

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82
Q

Ertapenem is limited to treat…

A

Pseudomona

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83
Q

Which is the clinical use for imipenem?

A

Gram positive cocci, gram negative rods and Anaerobes

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84
Q

When is recommended to use imipenem?

A

Wide spectrum but significant side effects limit use to life threatening infections or after other drugs have fail

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85
Q

Which is the advantage of meropenem compare to imipenem?

A

Meropenem has a decrease risk of seizures and is stable to dehydropetidase I

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86
Q

These are the adverse effects of imipenem

A

GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels

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87
Q

Which is the mechanism of action of vancomycin?

A

Inhibits cell wall peptidoglycan formation by binding D ala D ala portion of cell wall precursors

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88
Q

Is vancomycin a bactericidal or bacteriostatic?

A

Bactericidal

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89
Q

Which is a clinical use for vancomycin?

A

Gram-positive only serious multidrug resistant organisms including MRSA, enterococci and Clostridium difficile

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90
Q

When is recommended the use of vancomycin to treat Clostridium difficile?

A

Oral dose for pseudomembranous colitis

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91
Q

Although vancomycin is well tolerated, what are the risks for its use?

A

Nephrotoxicity, ototoxicity, Thrombophlebitis diffuse flushing

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92
Q

This adverse effect with vancomycin consists of diffuse flushing

A

Red man syndrome

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93
Q

How can you prevent red man syndrome caused by Vancomycin?

A

Pretreatment with antihistamines and slow infusion rate

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94
Q

When does resistance to vancomycin happens?

A

Occurs in bacteria via amino acid modification of D ala D lac

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95
Q

Which bacterial structure contains 30 s and 50 s subunits?

A

Ribosomes

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96
Q

Who are primarily target by protein synthesis inhibitors?

A

Smaller bacterial ribosome (70s made of 30s and 50s subunits)

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97
Q

Why is humman ribosome not affected by protein synthesis inhibitors?

A

They just affect 30s and 50 s subunits and the human ribosome is 80s

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98
Q

Consider 30s inhibitor bacteriostatic

A

Tetracyclines

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99
Q

Consider 30s bactericidal

A

Aminoglycosides

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100
Q

Who is considered 50 S inhibitor bacteriostatic?

A

Chloramphenicol, clindamycin

Macrolides (erythromycin)

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101
Q

50 S inhibitor but variable between bacteriostatic and bactericidal

A

Linezolid

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102
Q

These medicines are consider aminoglycosides

A

Gentamicin, neomycin, amikacin, tobramycin, streptomycin

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103
Q

How do aminoglycosides work?

A

Bactericidial, inhibit formation of initiation complex and cause misreading of mRNA
Blook translocation

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104
Q

Why aminoglycosides are ineffective against anaerobes?

A

Because aminoglycosides require O2 for uptake

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105
Q

When is recommended the clinical use for aminoglycosides?

A

Severe gram negative rod infections

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106
Q

Which medicines are synergistic with aminoglycosides?

A

Beta lactam antibiotics

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107
Q

What is recommended Neomycin?

A

For bowel surgery

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108
Q

Which are the toxicity risk for using Aminoglycosides?

A

Nephrotoxicity
Neuromuscular blockade
Ototoxicity
Teratogen

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109
Q

The use of aminoglycosides with these antibiotics increase the risk of nephrotoxicity

A

Cephalosporins

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110
Q

Which medicines when used in conjunction with aminoglycosides can increase the risk for ototoxicity?

A

Loop diuretics

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111
Q

Which is the mechanism from which bacterias inactivate aminoglycosides?

A

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

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112
Q

Who are considered tetracyclines?

A

Tetracycline, doxycycline, minocycline

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113
Q

This is the mechanism of action of tetracyclines

A

Bacteriostatic, bind to 30S and prevent attachment of aminoacyl-tRNA

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114
Q

How well tetracyclines penetrate to CNS?

A

Limited CNS penetration

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115
Q

How is doxycycline eliminated?

A

Fecally

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116
Q

In which patients can doxycyclin can be safely used?

A

Renal failure patients

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117
Q

In these occasions is not recommended the use of Tetracyclines

A

Do not take with milk (Ca2+), antacids (Ca2+ or Mg2+) or iron containing preparations

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118
Q

Why is not recommended the combination of tetracyclines with milk (Ca2+), antacids (Ca2+ or Mg2+) or iron containing preparations?

A

Because divalent cations inhibit its absorption in the gut

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119
Q

These bacterias are susceptible to tetracyclines

A

Borrelia burgdorferi

M. Pneumoniae

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120
Q

Which is the clinical use for tetracyclines?

A

Ricketssia and chlamydia

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121
Q

Why are tetracyclines effective against Chlamydia and Rickettsia?

A

Because tetracyclines have the ability to accumulate intracellularly

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122
Q

Which dermatologic disease can be treated with tetracyclines?

A

Acne

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123
Q

Name adverse effects of using tetracyclines

A

GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity

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124
Q

When are specially contraindicated tetracyclines?

A

Pregnancy

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125
Q

Which is the mechanism of resistance to tetracyclines?

A

Decrease uptake or increase efflux out of bacterial cells by plasmid encoded transport pumps

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126
Q

Who are classified as macrolides?

A

Azithromycin, clarithromycin, erythromycin

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127
Q

How do macrolides work?

A

Inhibit protein synthesis by blocking translocation

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128
Q

Where do macrolides bind?

A

To the 23 S RNA of the 50 S ribosomal subunits

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129
Q

Are macrolides bacteriostatic or bactericidal?

A

Bacteriostatic

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130
Q

When is clinically recomended the use of macrolides?

A

Atypical pneumonias
Sexually transmited diseases (chlamydia)
Gram positive cocci

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131
Q

Which bacteria can cause atypical pneumonias?

A

Mycoplasma
Chlamydia
Legionella

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132
Q

In streptococcal infections in patients allergic to penicillin which is the alternative treatment?

A

Macrolides

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133
Q

Which are adverse effects of macrolides?

A

Gastrointestinal motility issues, Arrhytmia caused by prologue QT, acute cholestatic hepatitis, rash, eosinophilia

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134
Q

Which medicines do macrolides increase serum concentrations?

A

Theophylines

Oral anticoagulants

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135
Q

This is the mechanism of resistance to macrolides

A

Methylation of 23 rRNA binding site prevents binding of drug

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136
Q

How does chloramphenicol works?

A

Blocks pepetydiltransferase at 50S ribosomal subunit

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137
Q

Is chloramphenicol bactericidal or bacteriostatic?

A

Bacteriostatics

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138
Q

Which cases is recommended the use of Chloramphenicol?

A

Meningitis (H. Influenzae, Neisseria meningitidis, S. Pneumoniae)
Rickettsia rickettssi

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139
Q

Why is limited the use of chloramphenicol?

A

Due to toxicities but often used in developing countries because of low cost

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140
Q

Which are the toxic effects caused by chloranphenicol?

A
Anemia (dose dependent)
Aplastic anemia (dose independent)
Gray baby syndrome
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141
Q

In whom and why chloramohenicol can cause gray baby syndrome?

A

In premature infants because they lack liver UDP glucuronyl transferase

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142
Q

What inactivates chloramphenicol?

A

Plasmid encoded acetyltransferase inactivates the drug

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143
Q

This is the mechanism of action of clindamycin

A

Blocks peptide transfer (translocation) at 50 S ribosomal subunit

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144
Q

Is clindamycin bactericidal or bacteriostatic?

A

Bacteriostatic

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145
Q

Which is the clinical use for clindamycin?

A

Anaerobic infections in aspiration pneumonia, lung abscesses and oral infections
Also effective against invasive group A streptococcal infection

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146
Q

Who are consider anaerobic bacterias treated with clindamycin?

A

Bacteriodes spp

Clostridium perfringens

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147
Q

Which is a mnemonic for treating anaerobes?

A

Clindamycin treats anaerobes above the diaphragm vs metronidazole treats anaerobic infections below diaphragm

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148
Q

These are some toxicity manifestations by clindamycin

A

Pseudomembranous colitis (C difficile overgrowth) fever, diarrhea

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149
Q

These three are consider sulfonamides

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

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150
Q

Which is the mechanism of sulfonamides?

A

Inhibit folate synthesis

Para aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase

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151
Q

Sulfonamides… Bactericidal or bacteriostatic?

A

Bacteriostatic

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152
Q

Which bacterias are susceptible to sulfonamides?

A

Gram positive
Gram negative
Nocardia
Chlamydia

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154
Q

Which clinical use of triple sulfas or SMX?

A

For simple UTI

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155
Q

What happens if G6PD is deficient and you administer Sulfonamides?

A

Hemolysis

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156
Q

Which could be the secondary effects of Sulfonamides?

A

Hypersensitivity reactions, hemolysis, nephrotoxicity, photosensitivity, kernicterus in infants

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157
Q

Which kind of nephrotoxicity can Sulfonamides cause?

A

Tubulointerstitial nephritis

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158
Q

How can sulfonamides affect other drugs?

A

Displace other drugs form albumin

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159
Q

Which is an example of drug that can be displace by sulfonamide?

160
Q

What can produce resistance to sulfonamides?

A

Altered enzymes (bacterial dihydrofolate synthase), ↓ uptake, or ↑ PABA synthesis

161
Q

Which enzymes do Sulfonamides inhibit?

A

Dyhydrofolate synthase

162
Q

Which enzyme is inhibited by Trimethoprim and pyrimethamine?

A

Dihydrofolate reductase

163
Q

Which convertions is catalyzed by dihydrofolate reductase?

A

Dihydrofolic acid to Tetrahydrofolic acid (THF)

164
Q

Which conversion is catalyzed by Dyhidrofolate synthase?

A

PABA+ Pteridine to Dihydropteroic acid

165
Q

Is Trimethoprim bactericidal or bacteriostatic?

A

Bacteriostatic

166
Q

What does the combination of Trimethoprim with Sulfametoxazole (TMP-SMX) allows?

A

Sequential block of folate

167
Q

What is the clinical use for TMP-SMX?

A

For UTIs, Shigellan Salmonella, pneumocystisi jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis

168
Q

Which are adverse effects of Trimethoprim?

A

Megaloblastic anemia
Leukopenia
Granulocytopenia

169
Q

The toxicity caused by Trimethoprim may be alleviate with…

A

Folinic Acid

170
Q

Who are consider Fluoroquinolones?

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacinm sparfloxacin, moxifloxacin, gemifloxacinm enoxacin

171
Q

This medicine is a quinolone

A

Nalidixic acid

172
Q

Which is the mechanism of action of Fluoroquinolones?

A

Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV

173
Q

Which topoisomerase is DNA gyrase?

A

Topoisomerase II

174
Q

Are fluoroquinolones bactericidal or bacteriostatics?

A

Bacteriostatics

175
Q

Which medicines must not be taken with fluoroquinolones?

176
Q

When is recommended the use of Fluoroquinolones?

A

Gram negative rods of urinary and GI tracts (including pseudomonas). Neisseria, some gram positive organisms

177
Q

Which could be the most common secondary effects to Fluoroquinolones?

A

GI upset, superinfections, skin rashes, headache, dizziness

178
Q

Which are less common toxicity effects of fluoroquinoles?

A

Tendonitis, tendon rupture, leg cramps, and myalgias

179
Q

When are fluoroquinoles contraindicated?

A

Pregnant women, nursing mothers and children under 18 years old due to possible damage to cartilage

180
Q

Consider a possible cardiac toxicity manifestation by fluoroquinoles

A

Prolonged QT interval

181
Q

Who are at higher risk of tendon rupture using fluoroquinolones?

A

People >60 years old and in patients taking prednisone

182
Q

This is the mechanism of resistance to Fluoroquinolones

A

Chromosome encoded mutation in DNA gyrase, plasmid mediated resistancem efflux pumps

183
Q

How does Metronidazole damages bacterias?

A

Forms free radical toxic metabolites in tje bacterial cell that damage DNA

184
Q

This antibiotic is also consider a antiprotozoal

A

Metronidazole

185
Q

Is metronidazole a bacteriostatic or bactericidal?

A

Bactericidal

186
Q

Which pathogens are suceptible to Metronidazole?

A
Giardia
Entamoeba
Trichomonas 
Gardnerella vaginalis
Anaerobes (Bacteroides, C. Difficile)
187
Q

In which medications does the triple therapy for H. Pylori consists?

A

Proton pump inhibitor
Clarithromycin
Metronidazole

188
Q

Which is the most common side effect of Metronidazole?

A

Disulfiram like reaction with alcohol

189
Q

What is the disulfiram like reaction?

A

Severe flushing
Tachycardia
Hypotension

190
Q

Which are the symptoms of Disulfiram like reaction with alcohol?

A

Headache

Metallic taste

191
Q

Who are consider mycobacterium?

A

M. Tuberculosis
M. avium- intracellulare
M leprae

192
Q

Which is the profilaxis treatment for M. tuberculosis?

193
Q

Which medicines are included in the treatment for M. Tuberculosis

A

Rifampin
Isoniazid
Pyrazinamide
Ethambutol

194
Q

For M. avium intracellulare, which is the prophylaxis treatment?

A

Azithromycin

Rifabutin

195
Q

Who is more resistant to treatment between M. Tuberculosis and M. avium intracellulare?

A

M. avium intracellulare

196
Q

Which is the recommended treatment for M. avium intracellulare?

A

Azithromycin or clarithromycin+ ethambutol.

Can add rifabutin or ciprofloxacin

197
Q

Is there any prophylaxis treatment for M. Leprae?

198
Q

How do you treat infection by M. Leprae, Tuberculoid form?

A

Long term treatment with dapsone and rifampin for tuberculoid form

199
Q

How is lepromatous form treated?

A

Long term treatment with dapsone and rifampin Add clofazimine for lepromatous form

200
Q

This is the mechanism of action of Isoniazid?

A

↓ synthesis of mycolic acids, Bacterial catalase- peroxidase(encoded by KatG) needed to convert Isoniazid to active metabolite

201
Q

Is there a difference of Isoniazid related to half lives?

A

Different Isoniazid half lives in fast vs low acetylators

202
Q

Which are the probable secondary effects of Isoniazid?

A

Neurotoxicity, hepatotoxicity

203
Q

This medicine can prevent neurotoxicity, lupus caused by Isoniazid

A

Pyridoxine (vitamin 6)

204
Q

Who are consider Ryfamycins?

A

Rifampin, Rifabutin

205
Q

How do Ryfamycins work?

A

Inhibits DNA dependent RNA polymerase

206
Q

Which is the advantage of combining Rifampin with Dapsone in Leprosy treatment?

A

Rifampin delays resistance to dapsone when used for leprosy

207
Q

When is Rifampin used as prophylaxis treatment?

A

Meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B

208
Q

Which are the possible side effects of Rifampicin?

A

Minor hepatotoxicity and drug interactions (↑P-450)

Orange body fluids

209
Q

When is preferred the use of Rifabutin more than Rifampicin?

A

HIV infections due to less cytochrome P-450 stimulation

210
Q

This is the mechanism of action of Pyrazinamide

A

Mechanism uncertain. Though to acidify intracellular enviroment via conversion to pirazinoic acid.

211
Q

On which enviroment is Pyrazinamide effective?

A

In acidic pH of phagolysosomes, where TB engulfed by macrophages is found

212
Q

These are consider toxic findings with Pyrazinamide use

A

Hyperuricemia

Hepatotoxicity

213
Q

Which is the mechanism of action of Ethambutol?

A

↓ carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

214
Q

This is the possible secondary effect of Ethambutol toxicity

A

Optic neuropathy (red green color blindness)

215
Q

This medication is used as prophylaxis for endocatitis with surgical or dental procedures

A

Penicillins

216
Q

You can use this medicine for Gonorrhea prophylaxis

A

Ceftriaxone

217
Q

In case of history of recurrent UTIs this is an alternative of treatment

218
Q

Drug of choice in meningococcal infection prophylaxis

A

Ciprofloxacin

219
Q

For Meningococcal infection prophylaxis this is the selected treatment for children

220
Q

Which is the prophylaxis treatmen for pregnant women carrying group B strep?

A

Ampicillin

221
Q

Prevention of gonococcal or chlamydial conjuntivitis in newborn

A

Erythromycin ointment

222
Q

Prevention of postsurgical infection due to S. aureus

223
Q

Phophylaxis of strep pharyngitis in child with prior rheumatic fever

A

Oral penicillin

224
Q

For syphilis this is the selected treatment

A

Benzathine penicillin G

225
Q

When CD4 counts are <200 cells/ mm3, which is the recommended prophylaxis?

226
Q

Which infection are you trying to prevent with TMP-SMX when CD4 counts are <200 cells/ mm3?

A

Pneumocystis pneumonia

227
Q

When CD4 counts are <100 cells/ mm3, which is the recommended prophylaxis? and which infections are prevented?

A

TMP-SMX

Pneumocystis pneumonia and toxoplasmosis

228
Q

When CD4 counts are <50 cells/ mm3, which is the recommended prophylaxis?

A

Azithromycin

229
Q

Which infection are you trying to prevent with TMP-SMX when CD4 counts are <50 cells/ mm3?

A

Mycobacterium avium complex

230
Q

In prophylaxis treatment in HIV if TMP-SMX is not tolerated by the patient, which is the alternative?

A

Aerolized pentamidine

231
Q

Can Aerolized pentamidine prevent Toxoplasmosis?

232
Q

Which bacterias are consider highly resistant bacterias?

A

MRSA (Methicillin Resistant S. Aureus)

VRE (Vancomycin Resistant Enterococcus)

233
Q

Which medicines work for MRSA?

A
Vancomycin
Daptomycin
Linezolid
Tigecycline
Ceftaroline
234
Q

Which adverse effect can Linezolid cause?

A

Serotonin syndrome

235
Q

For VRE which are the alternative treatment?

A

Linezolid and streptogramins

236
Q

Who are consider Streptogramins?

A

Quinuspristin/ Dalfopristin

237
Q

In Antifungal therapy these are the possible mechanisms of action inhibited?

A
Lanosterol Synthesis
Ergosterol Synthesis
Cell wal synthesis
Nucleic acid synthesis
Forms membrane pores
238
Q

Which group of medicines of Antifungal form membrane pores?

239
Q

Who are Polyenes?

A

Amphotericin B

Nystatin

240
Q

Which is the mechanism of action of Amphothericin B?

A

Binds ergosterol; forms memebrane pores that allow leakage of electrolytes

241
Q

When is recommended the clinical use of Amphotericin B?

A

Serious, systemic mycoses

242
Q

Who respond to Amphotericin B treatment?

A
Cryptococcus
Blastomyces
Coccidiodes
Histoplasma
Cnadida
Mucor
243
Q

For cryotococcal meningitis, what is the treatment?

A

Amphotericine B with/ without Flucytosine

244
Q

What is recommended for Fungal meningitis?

A

Intrathecally treatment

245
Q

What is recommended to supplement when you prescribe amphotericin B? Why?

A

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

246
Q

These are the possible secondary effects of amphotericin

A

Fever/ chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis

247
Q

What decreases the risk of nephrotoxicity when Amphotericin B is used?

248
Q

Which amphotericin has decrease risk of toxicity?

A

Liposomal amphotericin

249
Q

This is the mechanism of action of Nystatin

A

Binds ergosterol; forms memebrane pores that allow leakage of electrolytes

250
Q

Which is the administration way for Nystatin?

A

Topical form because too toxic for systemic use

251
Q

This is the clinical use for Nystatin

A

Swish and swallow for oral candidiasis (thrush)

Topical for diaper rash or vaginal candidiasis

252
Q

Who inhibit ergosterol synthesis?

253
Q

Name some Azoles

A

Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Miconazole, Voriconazole

254
Q

Which is the mechanism of action of Azoles?

A

Inhibit Fungal sterol (ergosterol) synthesis, by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol

255
Q

Which enzyme is inhibited by Azoles?

A

1,4 α demethylase

256
Q

This is the clinical use for Azoles

A

Local and less serious systemic mycoses

257
Q

When is recommended Fluconazole?

A

For chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types

258
Q

Itraconazole is recommended for…

A

Blastomyces, Coccidioides, Histoplasam

259
Q

Which Azoles are recomended for topical fungeal infections?

A

Miconazole and Clotrimazole

260
Q

These could be the Toxicity manifestations of Azoles

A

Testosterone synthesis inhibition, liver dysfunction

261
Q

What can Ketoconazole cause by Testosterone synthesis inhibition?

A

Gynecomastia

262
Q

Why can Azoles cause Liver dysfunction?

A

They inhibit cytochrome P 450

263
Q

This medicine inhibits nucleic acid synthesis

A

5- Flucytosine

264
Q

What mechanism of action does Flucytosine has?

A

Inhibits DNA and RNA biosynthesis by conversion to 5 fluorouracil by cutosine deaminase

265
Q

Which is the clinical use for Flucytosine?

A

Systemic Fungal infections (meningitis caused by Cryptococcus) in combination with amphotericin B

266
Q

You need to be careful to prescribe Flucytosine because can cause…

A

Bone marrow suppression

267
Q

This group of medicines inhibit cell wall synthesis in Fungal organisms

A

Echinocandins

268
Q

Who are consider Echinocandins?

A

Caspofungin, Micafunginm anidulafungin

269
Q

Which is the mechanism of action of Caspofungin?

A

Inhibits cell wall synthesis by inhibiting synthesis of β glucan

270
Q

When are Echinocandins recommended?

A

Invassive aspergillosis, Candida

271
Q

These are the clinical findings in case of Caspofungin toxicity

A

GI upset, flushing

272
Q

How do Echinocandins produce flushing?

A

Histamine release

273
Q

This medicine inhibits Lanosterol synthesis

A

Terbinafine

274
Q

Which enzyme is inhibited by Terbinafine?

A

Fungal enzyme squalene epoxidase

275
Q

Which is the clinical use for Terbinafine?

A

Dermatophytoses (especially onychomycosis- fungal infection of finger or toe nails)

276
Q

These are consider Toxicity manifestations of Terbinafine

A

GI upset, headaches, hepatotoxicity, taste disturbance

277
Q

This antifungal interferes with microtubule function; disrups mitosis

A

Griseofulvin

278
Q

Where does Griseofulvin deposits?

A

In keratin- containing tissues (eg. Nails)

279
Q

Which is the clinical use for Griseofulvin

A

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm)

280
Q

Which are the secondary effects of griseofulvin?

A
Teratogenic
Carcinogenic
Confusion
Headaches
↑ P450 and warfarin metabolism
281
Q

Name antiprotozoan therapy

A

Pyrimethamine
Suramin and Melarsoprol
Nifurtimox
Sodium stibogluconate

282
Q

For which microorganism is recomended Pyrimethamine

A

Toxoplasmosis

283
Q

Suramin and melarsoprol are used for…

A

Trypanosoma brucei

284
Q

An infection by… is recommended the use of Nifurtimox

285
Q

In this case we recommend sodium stibogluconate

A

Leishmaniasis

286
Q

How does Chloroquine works?

A

Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia

287
Q

For these cases Chloroquine is recommended

A

Treatment for Plasmodial species other than P. Falciparum

288
Q

Why the treatment with Chloroquine against P falciparum does not work?

A

Resistance is too high. Resistance due to membrane pump that ↓ intracellular concetration of drug

289
Q

So what is recommended to treat P. Falciparum infection?

A

Artemether/ lumefantrine or atovaquine/ proguanil

290
Q

What is recommended for life threatening malaria?

A

Quinidine in US (quinine elsewhere) or artesunate

291
Q

These are possible secondary effects due to Chloroquine use

A

Retinopathy; pruritus (specially in dark skinned individuals)

292
Q

These medicines are antihelminthic therapy

A

Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel

293
Q

Which is the effect of antihelminthic therapy?

A

Immobilize helminths

294
Q

When is recommended praziquantel?

A

Against flukes (trematodes) such as Schistosoma

295
Q

Which antiviral therapy inhibit the release of progency virus?

A

Oseltamivir

Zanamivir

296
Q

Which is the mechanism of action of Oseltamivir and Zanimivir?

A

Inhibit influenza neuroaminidase → ↓ the release of progency virus

297
Q

These antivirals are used for Treatment and prevention of both influenza A and B

A

Zanamivir

Oseltamivir

298
Q

How does Ribavirin works?

A

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase

299
Q

Which antiviral therapy may work for RSV and Hepatitis C?

300
Q

Which could be the secondary effects of Ribavirin?

A

Hemolytic anemia

Severe Teratogen

301
Q

These antivirals are Guanosine analogs

A

Acyclovir, Famcicloclovir, valacyclovir

Ganciclovir

302
Q

Who phosphorilates Acyclovir, Famcicloclovir, valacyclovir?

A

Monophosphorylated by HSV/ VZV thymidine kinase

303
Q

Which is the reason Acyclovir, Famcicloclovir, valacyclovir cause few adverse effects?

A

They just Monophosphorylated by HSV/ VZV thymidine kinase and not phosphorylated in uninfected cells

304
Q

Triphosphate formed by cellular enzymes

A

Acyclovir, Famcicloclovir, valacyclovir

305
Q

This is the mechanism of action of Acyclovir, Famcicloclovir, valacyclovir

A

Inhibits viral DNA polymerase by chain termination

306
Q

Which is the clinical use for Acyclovir, Famcicloclovir, valacyclovir?

A

HSV and VZV

Weak activity against EBV

307
Q

How much effectivity can Acyclovir, Famcicloclovir, valacyclovir have for EBV?

A

No activity against EBV

308
Q

Which case of HSV infection responds to Acyclovir, Famcicloclovir, valacyclovir?

A

HSV induced mucocutaneous and genital lesions as well as for encephalitis

309
Q

When is recommended the prophylaxis treatment with Acyclovir, Famcicloclovir, valacyclovir?

A

In immunocompromised patients

310
Q

Which cases of HSV and VZV infection have nos response to Acyclovir, Famcicloclovir, valacyclovir?

A

Latent forms of HSV and VZV

311
Q

Which is the prodrug of Acyclovir?

A

Valacyclovir

312
Q

Comparing Valacyclovir to Acyclovir which is the difference?

A

Valacyclovir has better oral bioavailabity

313
Q

For Herpes Zoster what is recommended?

A

Use a related agent, Famciclovir

314
Q

Which are the risk for using Acyclovir, Famcicloclovir, valacyclovir? How can we prevent them?

A

Obstructive crystalline neprhopathy and acute renal failure if not adequately hydrated

315
Q

This the mechanism of resistance to Acyclovir, Famcicloclovir, valacyclovir

A

Mutated viral thymidine kinase

316
Q

Triphosphate formed by cellular kinase

A

Ganciclovir

317
Q

How does Ganciclovir works?

A

Inhibits viral DNA polymerase

318
Q

When is recommended the clinical use for Ganciclovir?

A

CMV, especially in immunocompromised patients

319
Q

What is the product of CMV after the treatment with Ganciclovir?

A

5´monophosphate formed by a CMV viral kinase

320
Q

Which is the prodrug of Ganciclovir? and which is the advantage of the prodrug?

A

Valganciclovir, has better oral bioavailabity

321
Q

Which are the possible after effects of Ganciclovir?

A

Leukopenia, neutropenia, thrombocytopenia, renal toxicity

322
Q

Which medicine is more toxic to host enzymes between acyclovir and ganciclovir?

A

Ganciclovir

323
Q

This is the mechanism of resistance to ganciclovir

A

Mutated CMV DNA polymerase or lack of viral kinase

324
Q

Viral DNA polymerase inhibitor

325
Q

Where does Foscarnet binds?

A

Binds to pyrophosphate binding site of the enzyme

326
Q

Does foscarnet requires activation by viral enzymes?

327
Q

When ganciclovir fails to treat CMV, which medicine is the alternative?

328
Q

When is recommended the treatment with Foscarnet?

A

CMV retitnitis in immunocompromised patients when ganciclovir fails
Acyclovir resistant HSV

329
Q

This is the principal risk for using Foscarnet

A

Nephrotoxicity

330
Q

This is the mechanism of resistance to Foscarnet

A

Mutated DNA polymerase

331
Q

What does Cidofovir inhibits?

A

Viral DNA polymerase

332
Q

Does Didofovir requires phosphorylation by viral kinase?

333
Q

These are indications for Cidofovir

A

CMV retinitis in immunocompromised patients; acyclovir resistant HSV

334
Q

How is the half life of Cidofovir?

A

Long half life

335
Q

Posible toxic effect of Cidofovir

A

Nephrotoxicity

336
Q

What is recommended to decrease Cidofovir Nephrotoxicity?

A

Coadminister with probenecid and IV saline to ↓ toxicity

337
Q

Which is the main point in HIV therapy?

A

Highly active antiretroviral therapy (HAART)

338
Q

When is initiated HIV therapy?

A

When patients presetn with AIDS defining illness, low CD4 cell counts, or high viral load

339
Q

This CD4 cell count is when we consider starting HIV therapy

A

< 500 cell/ mm3

340
Q

How many drugs are used in HIV therapy?

341
Q

This is the regimen for HIV to prevent resistance

A

2 nucleotide reverse transcriptase inhibitors (NRTIs) +

1 non nucleoside reverse transcriptase inhibitor (NNRTI) OR 1 protease inhibitor OR 1 integrase inhibitor

342
Q

Which are consider protease inhibitors?

A
ALL NAVIR
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir
343
Q

What is needed for HIV assembly of virions?

A

Depends on HIV-1 protease

344
Q

Which is an alternative name for HIV-1 protease?

345
Q

What is the function of HIV-1 protease?

A

Cleaves the polypeptide products of HIV mRNA into their functional parts

346
Q

What is inhibited by protease inhibitors?

A

HIV-1 protease

347
Q

What does protease inhibitors prevent?

A

MAturation of new viruses

348
Q

Why do we need to have precautions in the use of Ritonavir?

A

Because can boost other drug concentrations by inhibiting cytochrome P-450

349
Q

These are consider toxicity situations caused by protease inhibitors

A

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy

350
Q

Which protease inhibitor can cause nephropathy and hematuria?

351
Q

Who are Nucleoside reverse transcriptase inhibitors?

A
Abacabir (ABC)
Didasone (ddl)
Emtricitabine (FTC)
Lamivudine (3TC)
Stavudine (d4T)
Tenofovir (TDF)
Zidovudine (ZDV)
352
Q

Formerly which names does Zidovudine received?

353
Q

Which is the mechaism if action of Nucleoside reverse transcriptase inhibitors?

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain(lack 3´OH group)

354
Q

Which is the only Nucleoside reverse transcriptase inhibitor that is Nucleotide?

355
Q

What is the requirement to activate Nucleoside reverse transcriptase inhibitors?

A

They need to be phosphorylated to be activated

356
Q

Which is the Nucleoside reverse transcriptase inhibitor that does not requires phosphorylation to be activated?

357
Q

Which Nucleoside reverse transcriptase inhibitor is used as general prophylaxis?

A

Zidovudine

358
Q

This Nucleoside reverse transcriptase inhibitor is used during pregnancy to decrease the risk if fetal transmission

A

Zidovudine

359
Q

Which toxic effects can Nucleoside reverse transcriptase inhibitors cause?

A

Bone marrow suppression

Peripheral neuropathy

360
Q

This secondary effects is just for Nucleoside reverse transcriptase inhibitors (nucleosides)

A

Lactic acidosis

361
Q

Which secondary effects is just for Nucleoside reverse transcriptase inhibitors (non-nucleosides)?

362
Q

This secondary effect is only for Zidovudine?

363
Q

This Nucleoside reverse transcriptase inhibitor can cause pancreatitis

A

Didanosine

364
Q

These medicines are Non nucleoside reverse transcriptase inhibitor

A

Efavirenz
Nevirapine
Delavirdine

365
Q

What is the difference between Non nucleoside reverse transcriptase inhibitor (NNRTIs) and Nucleoside reverse transcriptase inhibitors (NRTIs)?

A

NNRTIs bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be activate or compete with nucleotides

366
Q

What is the toxic effect common to all Non nucleoside reverse transcriptase inhibitor (NNRTIs)?

A

Rash and hepatotoxicity

367
Q

What can be expected with the use of Efavirenz?

A

Vivid dreams and CNS symptoms

368
Q

Which Non nucleoside reverse transcriptase inhibitor (NNRTIs) are contraindicated in pregnancy?

A

Delaviridine and efavirenz

369
Q

In case of bone marrow suppression caused by nucleoside reverse transcriptase inhibitors (NRTIs), what can reverse it?

A

Granulocyte colony stimulating factor (G-CSF) and erythropoietin

370
Q

Is an example of integrase inhibitor

A

Raltegravir

371
Q

This is the mechanism of action of Raltegravir

A

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase

372
Q

This is an adverse effect of Raltegravir

A

Hypercholesterolemia

373
Q

Name Fusion inhibitor medicines related to HIV

A

Enfuvirtide

Maraviroc

374
Q

This fusion inhibitor inhibits attachment of HIV

375
Q

This fusion inhibitor inhibits penetration of HIV

A

Enfuvirtide

376
Q

How does Enfuviride inhibits penetration of HIV?

A

Binds gp41, inhibiting viral entry

377
Q

This explain how Maraviroc inhibits the attachment

A

Binds CCR-5 on surface of T cell/ monocytes, inhibiting interaction with gp120

378
Q

For Maraviroc and Enfuvirtide this is the common side effect

A

Skin reaction at injection sites

379
Q

Which is the mechanism of action of Interferons?

A

Glycoproteins normally synthesized by virus- infected cells, exhibiting a wide range of antiviral and antitumoral properties

380
Q

Name the interferons

A

Interferon α
Interferon β
Interferon γ

381
Q

What is the clinical use for Interferon α?

A
Chronic hepatitis B and C
Kaposi Sarcoma
Hiry cell leukemia
Condyloma acuminatum
Renal cell carcinoma
Malignant melanoma
382
Q

This is the reason to use Interferon β

A

Multiple scleosis

383
Q

When is recommended the use of Interferon γ?

A

Chronic granulomatous disease

384
Q

Which are the toxic effects of Interferons?

A

Neutropenia, myopathy

385
Q

Antibiotics to avoid in pregnancy

A
Sulfonamides
Aminoglycosides
Fluoroquinolones
Clarithromicyn
Tetracyclines
Chloramphenicol
386
Q

Which antiviral is contraindicated in pregnancy?

387
Q

This antifungal needs to be avoided in pregnancy

A

Griseofulvin

388
Q

Which antibiotic increase the risk of kernicterus if used in pregnancy?

A

Sulfonamides

389
Q

What is the risk of using aminoglycosides in pregnancy?

A

Ototoxicity

390
Q

This is the reason why is not recommended the used of fluoroquinoles in pregnancy

A

Cartilage damage

391
Q

Why is important to avoid clarithromycin in pregancy?

A

Embryotoxic

392
Q

You need to be careful not to use tetracyclines in pregnant patients because risk for…

A

Discolored teeth, inhibition of bone growth

393
Q

You must not use Ribavirin in pregnant women because…

A

It is teratogenic

394
Q

This is the reason griseofulvin is contraindicated during pregnancy

A

Teratogenic

395
Q

This is the secondary effect of Chloramphenicol if used in pregant patients