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Pharm SJSM > Extra B3 stuff > Flashcards

Extra B3 stuff Flashcards

1
Q

(GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin)

What drug class are they?

A

Aminoglycosides

MOA:
They Inhibit bacterial protein synthesis 30s subunit. Causes mRNA misreading.

● Resistance: Enzymatic modification.

● Side Effects: Nephrotoxicity, ototoxicity

● Clinical Use: Gram-negative bacilli, synergistic with beta-lactams.

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2
Q

MOA:
They Inhibit bacterial protein synthesis 30s subunit. Causes mRNA misreading.

● Resistance: Enzymatic modification.

● Side Effects: Nephrotoxicity, ototoxicity

● Clinical Use: Gram-negative bacilli, synergistic with beta-lactams.

A

Aminoglycosides

(GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin)

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3
Q

MOA:
They Inhibit bacterial protein synthesis 30s subunit. Causes mRNA misreading.

● Resistance: Enzymatic modification.

● Side Effects: Nephrotoxicity, ototoxicity

● Clinical Use: Gram-negative bacilli, synergistic with beta-lactams.

A

Aminoglycosides

(GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin)

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4
Q

Which drugs cause hemolytic anemia in patients with G6PD Deficiency?

A

Dapsone, Sulfonamides. Antimalarials (primaquine, chloroquine)

● Side Effects: Hemolytic anemia in G6PD deficiency.

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5
Q

Dapsone, Sulfonamides. Antimalarials (primaquine, chloroquine) All cause which side effect?

A

● Side Effects: Hemolytic anemia in G6PD deficiency.

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6
Q

Primaquine, Chloroquine, Mefloquine, Artensuate

A

Antimalarials

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7
Q

What is the MOA of Primaquine? (antimalarial)

A

○ It interferes with the electron transport in the mitochondria of the malaria parasite,
which is crucial for its energy metabolism.

● Side Effects:
1) G6PD deficiency hemolysis

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8
Q

○ It interferes with the electron transport in the mitochondria of the malaria parasite,
which is crucial for its energy metabolism.

● Side Effects:
1) G6PD deficiency hemolysis

A

Primaquine

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9
Q

What is the MOA of Chloroquine? (antimalarial)

A

○It inhibits heme polymerization.

Clinical use:
Antimalarial used to treat P. vivax, P. ovale & some strains of P. falciparum

● Side Effects:
1) Retinopathy

● Resistance due to efflux pump

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10
Q

What is the MOA of Mefloquine? (antimalarial)

A

○ It disrupts heme detoxification within the parasite’s food vacuole.

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11
Q

What is the MOA of Artesunate? (antimalarial)

A

○ It is rapidly hydrolyzed to dihydroartemisinin, which generates free radicals that damages the proteins and membranes in the malaria parasite.

○ Treats chloroquine-resistant P. falciparum and P. vivax in pregnant females.

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12
Q

○It inhibits heme polymerization.

Clinical use:
Antimalarial used to treat P. vivax, P. ovale & some strains of P. falciparum?

● Side Effects:
1) Retinopathy

● Resistance due to efflux pump

A

○ Chloroquine

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13
Q

Antimalarial used to treat severe & complicated P. falciparum malaria?

A

Artesunate

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14
Q

What are the clinical uses of Artesunate?

A

○ Treats severe and complicated P. falciparum malaria

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15
Q

Rifampin, Isoniazid (INH), Pyrazinamide, Ethambutol, & Streptomycin Are all examples of?

A

. Anti-TB: First Line Drugs (RIPES)

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16
Q

○ MOA:
Inhibits DNA-dependent RNA polymerase in Mycobacterium tuberculosis, preventing RNA synthesis.

○ Side Effects:
1) Hepatotoxicity
2) orange body fluids (urine, tears, sweat)
3) flu-like symptoms
4) Can also induce cytochrome P-450 enzymes, causing drug-drug interactions

A

Rifampin

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17
Q

Rifampin

A

○ MOA:
Inhibits DNA-dependent RNA polymerase in Mycobacterium tuberculosis, preventing RNA synthesis.

○ Side Effects:
1) Hepatotoxicity
2) orange body fluids (urine, tears, sweat)
3) flu-like symptoms
4) Can also induce cytochrome P-450 enzymes, causing drug-drug interactions

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18
Q

○ MOA:
Inhibits the synthesis of mycolic acids, essential components of the mycobacterial cell wall.

○ Side Effects:
1) Hepatotoxicity
2) peripheral neuropathy (preventable with pyridoxine/vit b6)
3) Can also cause drug-induced lupus.

A

Isoniazid (INH)

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19
Q

Isoniazid (INH)?

A

○ MOA:
Inhibits the synthesis of mycolic acids, essential components of the mycobacterial cell wall.

○ Side Effects:
1) Hepatotoxicity
2) peripheral neuropathy (preventable with pyridoxine/vit b6)
3) Can also cause drug-induced lupus.

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20
Q

○ MOA:
Disrupt mycobacterial cell membrane metabolism and transport functions.

○ Side Effects:
1) Hepatotoxicity
2) hyperuricemia (can precipitate gout attacks)
3) non-gout polyarthralgia.

A

● Pyrazinamide

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21
Q

● Pyrazinamide

A

○ MOA:
Disrupt mycobacterial cell membrane metabolism and transport functions.

○ Side Effects:
1) Hepatotoxicity
2) hyperuricemia (can precipitate gout attacks)
3) non-gout polyarthralgia.

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22
Q

○ MOA:
Inhibits arabinosyl transferase, an enzyme involved in the synthesis of the mycobacterial cell wall.

○ Side Effects:
1) Optic neuritis (leading to color blindness and visual field loss)

A

● Ethambutol

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23
Q

● Ethambutol

A

○ MOA:
Inhibits arabinosyl transferase, an enzyme involved in the synthesis of the mycobacterial cell wall.

○ Side Effects:
1) Optic neuritis (leading to color blindness and visual field loss)

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24
Q

○ MOA:
An aminoglycoside antibiotic that inhibits protein synthesis by binding to the 30S ribosomal subunit of the mycobacterium.

○ Side Effects:
1) Ototoxicity (both auditory and vestibular)
2) nephrotoxicity
3) allergic reactions

A

● Streptomycin

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25
Q

Streptomycin?

A

○ MOA:
An aminoglycoside antibiotic that inhibits protein synthesis by binding to the 30S ribosomal subunit of the mycobacterium.

○ Side Effects:
1) Ototoxicity (both auditory and vestibular)
2) nephrotoxicity
3) allergic reactions

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26
Q

● MOA:
Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.

● Resistance: Mutation in DNA gyrase, efflux pumps.

● Side Effects: Tendon rupture, QT prolongation.

● Clinical Use: Broad spectrum - respiratory, urinary, GI infections.

A

Fluoroquinolones

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27
Q

What is the MOA of Fluoroquinolones?

A

● MOA:
Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.

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28
Q

● MOA:
Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.

A

Fluoroquinolones

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29
Q

How do organisms develop resistance against fluoroquinolones?

A

● Resistance: Mutation in DNA gyrase, efflux pumps.

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30
Q

What are the adverse effects of Fluoroquinolones?

A

Side Effects:
1) Tendon rupture
2) QT prolongation.

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31
Q

Side Effects:
1) Tendon rupture
2) QT prolongation.

A

Fluoroquinolones

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32
Q

What are the clinical uses of Fluoroquinolones?

A

● Clinical Use: Broad spectrum - respiratory, urinary, GI infections.

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33
Q

● Clinical Use: Broad spectrum - respiratory, urinary, GI infections.

A

Fluoroquinolones

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34
Q

Aminoglycosides and Tetracyclines

A

Protein Synthesis Inhibitors: 30S inhibitors

“Buy AT 30, SELL at 50”

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35
Q

Streptogramin, Erythromycin, Lincosamides, and Linezolid

A

Protein Synthesis Inhibitors: 50S inhibitors

“Buy AT 30, SELL at 50”

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36
Q

■ MOA: Bind to 30S. Interferes with initiation complex of protein synthesis.

■ Note: These are bactericidal and are primarily effective against aerobic Gram-negative bacteria.

A

Aminoglycosides (e.g., Gentamicin, Streptomycin):

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37
Q

■ MOA:
They bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA to the mRNA-ribosome complex.

■ Mechanism of Resistance:
1) Efflux pumps (actively pumping the drug out of the
bacterial cell)
2) Ribosomal protection (altering the ribosomal binding site to reduce drug binding).

■ Note: These are generally bacteriostatic and have a broad spectrum of activity, including against some Gram-positive and Gram-negative bacteria, as well as atypical organisms.

A

○ Tetracyclines (e.g., Doxycycline, Tetracycline):

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38
Q

What is the MOA of Tetracyclines?

A

■ MOA:
They bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA to the mRNA-ribosome complex.

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39
Q

■ MOA:
They bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA to the mRNA-ribosome complex.

A

Tetracyclines

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40
Q

What is the MOA of Aminoglycosides?

A

■ MOA: Bind to 30S. Interferes with initiation complex of protein synthesis.

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41
Q

■ MOA: Bind to 30S. Interferes with initiation complex of protein synthesis.

A

Aminoglycosides

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42
Q

■ MOA:
They bind to the 50S subunit, but they do so in a sequential manner. One component inhibits the early phase of protein synthesis, while the other inhibits the late phase. Together, they produce a
synergistic bactericidal effect.

■ Note: Used mainly for resistant Gram-positive infections.

A

○ Streptogramins (e.g., Quinupristin/Dalfopristin)

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43
Q

■ MOA:
These drugs bind to the 50S ribosomal subunit and block the translocation step of protein synthesis.

A

○ Erythromycin (and other Macrolides):

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44
Q

What is the MOA of Erythromycin (and other Macrolides)?

A

■ MOA:
These drugs bind to the 50S ribosomal subunit and block the translocation step of protein synthesis.

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45
Q

■ MOA:
It binds to the 50S ribosomal subunit and prevents the formation of the 70S initiation complex.

■ Note: Mainly used for Gram-positive bacteria, including resistant strains such as MRSA and VRE.

A

○ Linezolid

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46
Q

What is the MOA of Streptogramins (e.g., Quinupristin/Dalfopristin)

A

■ MOA:
They bind to the 50S subunit, but they do so in a sequential manner. One component inhibits the early phase of protein synthesis (Quinupristin), while the other inhibits the late phase (Dalfopristin). Together, they produce a synergistic bactericidal effect.

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47
Q

What is the MOA of Linezolid?

A

■ MOA:
It binds to the 50S ribosomal subunit and prevents the formation of the 70S initiation complex.

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48
Q

■ MOA:
It binds to the 50S ribosomal subunit and inhibits peptide bond formation

A

○ Lincosamides (e.g., Clindamycin):

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49
Q

○ Lincosamides (e.g., Clindamycin):

A

■ MOA:
It binds to the 50S ribosomal subunit and inhibits peptide bond formation

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50
Q

● Drug: Doxycycline, Amoxicillin and Cefuroxime (in pregnancy). Are all examples of drugs to treat what?

A

Lyme Disease

Pregnancy: Amoxicillin and cefuroxime preferred due to teratogenic potential of doxycycline (bone abnormalities).

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51
Q

MOA: 2 DRUGS

1) Inhibits neuraminidase
2) Amantadine blocks viral uncoating.

● Resistance: Mutations in neuraminidase and targets M2 protein, respectively

● Clinical Use:
Influenza treatment and prophylaxis. (A for A) ________ for JUST Influenza A, & _____ for both

A
  1. Oseltamivir
  2. Amantadine
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52
Q

Which drugs are used to treat influenza viruses?

A

Amantidine for influenza A

Oseltamivir for Influenza A & B

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53
Q

Which Lyme disease treatment drugs are preferred & why?

A

Amoxicillin & Ceftriaxone (& other cephalosporins) because Doxycycline is a teratogen (bone abnormalities)

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54
Q

Antiherpes Drugs

● MOA:
Inhibit viral DNA polymerase.

● Resistance: Thymidine kinase mutations

● Clinical Use: Herpes simplex & Varicella-zoster

A

Acyclovir

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55
Q

● Classes: NRTIs, NNRTIs, Protease Inhibitors, Integrase Inhibitors. Are all examples of drugs that treat»>

A

HIV

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56
Q

What are the drugs of choice for treating CMV?

A

Ganciclovir & Valganciclovir (prodrug of ganciclovir)

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57
Q

What is the drug of choice for treating HSV & VZV?

A

Acyclovir

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58
Q

What are the drugs of choice when treating HBV?

A

IFN-a & Lamivudine

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59
Q

What is the drug of choice of treating influenza A & or B?

A

Oseltamivir

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60
Q

Atazanavir, Darunavir, Indinavir, Ritonavir are all examples of which class of drugs that treat which condition?

A

Protease inhibitors that inhibit HIV protein cleavage to treat HIV

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61
Q

Tenofovir, Emtricitabine, Lamivudine, Abacavir, & Zidovudine are all examples of which class of drugs that treat which condition?

A

NRTI’s that act as a nucleoside & nucleotide RT inhibitor to inhibit HIV DNA synthesis by terminating DNA chain elongation

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62
Q

Efavirenz & Nevirapine are all examples of which class of drugs that treat which condition?

A

NNRTI’s that act as allosteric RT inhibitors to inhibit HIV DNA synthesis by terminating DNA chain elongation

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63
Q

Dolutegravir & Raltegravir are all examples of which class of drugs that treat which condition?

A

Integrase inhibitors that inhibit HIV DNA integration into the hosts genome

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64
Q

Enfuvirtide is an example of which class of drugs that treat which condition?

A

Fusion inhibitor which prevents HIV fusion with a target cell membrane by binding to gp41

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65
Q

Maraviroc is an example of which class of drugs that treat which condition?

A

CCR5 antagonist tht inhibits HIV entry by blocking the HIV gp120allosteric interactions with CCR5

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66
Q

Zidovudine is associated with which side effect?

A

Myelosuppression/bone marrow suppression

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67
Q

Abacavir is associated with which side effect?

A

Fever & rash (allergic reaction)

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68
Q

Didanosine is associated with which side effect?

A

Pancreatitis

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69
Q

Stavudine is associated with which side effect?

A

Lipodystrophy

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70
Q

Lamivudine is associated with which side effect?

A

Least toxic form of Hep B

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71
Q

Tenofovir is associated with which side effect?

A

Gi upset

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72
Q

Azole, Amphotericin B, Caspofungin

A

Antifungal:

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73
Q

What is the MOA of Azoles?

A

● MOA:
inhibit ergosterol synthesis

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74
Q

What is the MOA of Amphotericin B

A

● MOA:
B binds ergosterol;

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75
Q

What is the MOA of Caspofungin?

A

● MOA:
Caspofungin inhibits cell wall synthesis.

76
Q

What are the side effects of Azoles?

A

Hepatotoxicity

77
Q

What are the side effects of Amphotericin B?

A

nephrotoxicity and thrombophlebitis at injection
site

78
Q

What are the drugs of choice for treating Chlamydia?

(Mucopurulent discharge, pleomorphic gram-negative, intracellular)

A

Azithromycin or Doxycycline

79
Q

What are the drugs of choice for treating Gonorrhea?

○ Yellow-green discharge, gram-negative intracellular diplococci

A

Ceftriaxone + Azithromycin or Doxycycline.

80
Q

What are the drugs of choice for treating Syphilis?

○ Painless chancre, gram-negative spiral-shaped bacteria

A

Penicillin G.

81
Q

What are the drugs of choice for treating Trichomoniasis?

○ Foul-smelling, yellow -green purulent discharge, trophozoites w/multiple flagella

A

Metronidazole or Tinidazole.

82
Q

What are the drugs of choice for treating Herpes?

○ Pain, pruiritis, rash

A

Antivirals like Acyclovir, Valacyclovir.

83
Q

What are the drugs of choice for treating Candida Vaginosis?

○ Milky, curdy white discharge, yeast infection

A

Fluconazole, clotrimazole

84
Q

What are the drugs of choice for treating Bacterial Vaginosis (Gardnerella)?

○ Grayish milky discharge, whiff test: fishy odour, clue cells, pleomorphic gram negative
rods.

A

Metronidazole

85
Q

Albendazole, Praziquantel, Pyrantel Pamoate are examples of which type of medication

A

Anthelminthics

86
Q

○ MOA:
It inhibits microtubule synthesis in helminths, impairing glucose uptake and depleting glycogen stores in the worm, which eventually leads to its death.

○ Clinical Uses:
* Broad spectrum of activity against intestinal and tissue parasites:
1) hookworms
2) pinworms
3) roundworms
4) tapeworms (e.g., Taenia solium),

  • cystic hydatid disease caused by Echinococcus granulosus.
A

● Albendazole:

87
Q

What is the MOA of Albendazole?

A

○ MOA:
It inhibits microtubule synthesis in helminths, impairing glucose uptake and depleting glycogen stores in the worm, which eventually leads to its death.

88
Q

○ MOA:
It increases the permeability of cell membranes in worms to calcium ions, causing severe muscular contractions, paralysis, and death of the parasite.

○ Clinical Uses:
1) schistosomes (blood flukes)
2) flukes (like liver and lung flukes)

A

● Praziquantel

89
Q

What is the drug of choice for schistosomiasis and many other trematode infections.

A

● Praziquantel

90
Q

What is the MOA of Praziquantel?

A

○ MOA:
It increases the permeability of cell membranes in worms to calcium ions, causing severe muscular contractions, paralysis, and death of the parasite.

91
Q

○ MOA:
A depolarizing neuromuscular blocking agent that paralyses a helminth (it’s expelled in poop)

○ Clinical Uses:
1) Intestinal nematodes Pinworms (Enterobius
vermicularis)

Roundworms (Ascaris lumbricoides)

Hookworms
(Necator americanus and
Ancylostoma duodenale).

A

● Pyrantel Pamoate

92
Q

Which Anthelminthic is preferred in preggos with a Scotch tape test +?

A

pyrantel pamoate

93
Q

What is the MOA of pyrantel pamoate?

A

○ MOA:
It acts as a depolarizing neuromuscular blocking agent, causing spastic paralysis of the helminth. The paralyzed worms are then expelled from the gastrointestinal tract by peristalsis.

94
Q

● MOA: 2 Drugs

Alkylating agents, cross-link DNA; marked effect on B cells than T cells

● Side Effects:
1) Hemorrhagic cystitis
2) myelosuppression
3) early menopause.

Clinical uses:
1) Bone marrow transplantation
2) Autoimmune disorders.

● Management: MESNA to prevent hemorrhagic cystitis, hydration.

A
  1. Ifosfamide & Cyclophosphamide
95
Q

Ifosfamide & Cyclophosphamide, Which one is the least leukemogenic (causing acute myelogenous leukemia)?

A

Cyclophosphamide

96
Q

What is the MOA of Ifosfamide & Cyclophosphamide?

A

Alkylating agents, cross-link DNA; marked effect on B cells than T cells

97
Q

● MOA: Inhibit microtubule formation. Blocking M phase.

● Side Effects:
1) Peripheral neuropathy
2) myelosuppression.

● Management: Dose adjustment, supportive care.

A
  1. Vincristine & Cell Cycle Specific Agents
98
Q

What is the MOA of Vincristine & Cell Cycle Specific Agents?

A

● MOA: Inhibit microtubule formation. Blocking M phase.

99
Q

● MOA:
Inhibits interleukin-1 and interleukin-2 receptor → inhibits T-cell activation.

● Side Effects:
1) Nephrotoxicity
2) hypertension.

● Clinical Use: Prevent transplant rejection, autoimmune disorders.

A
  1. Cyclosporine
100
Q

What is the MOA of Cyclosporine?

A

● MOA:
Inhibits interleukin-1 and interleukin-2 receptor → inhibits T-cell activation.

101
Q

MOA:
It Inhibits cytosine monophosphate dehydrogenase, and inhibits T-cell lymphocyte proliferation.

Clinical use:
1) Renal disease post SLE
2) Vasculitis

A

Mycophenolate Mofetil

102
Q

What is the MOA of Mycophenolate Mofetil?

A

MOA:
It Inhibits cytosine monophosphate dehydrogenase, and inhibits T-cell lymphocyte proliferation.

103
Q

● MOA:
Monoclonal antibody against CD20 on B cells.

● Side Effects:
1) Infusion reactions
2) immunosuppression

● Clinical Use:
1) Non-Hodgkin lymphoma
2) Rheumatoid arthritis.

A
  1. Rituximab
104
Q

What is the MOA of Rituximab?

A

● MOA:
Monoclonal antibody against CD20 on B cells.

105
Q

● MOA:
Inhibits ribonucleotide reductase halting the cell cycle in S phase.

● Side Effects: Myelosuppression

● Clinical Use:
1) Chronic myelogenous leukemia
2) Sickle cell anemia

A
  1. Hydroxyurea
106
Q

What is the MOA of Hydroxyurea?

A

● MOA:
Inhibits ribonucleotide reductase halting the cell cycle in S phase.

107
Q

● MOA:
They inhibit specific tyrosine kinase activity of protein product of bcr-abl oncogene (chronic
myelogenous leukemia) → philadelphia chromosome translocation.

● Side Effects/toxicity:
1) Diarrhea
2) rash
3) myelosuppression

● Clinical Use: Targeted cancer therapy.

A
  1. Tyrosine Kinase Inhibitors (Imatinib, Dasatinib, Nilotinib)
108
Q

● MOA:
Purine analogue, inhibits DNA synthesis, antimetabolite

● Side Effects:
1) Myelosuppression
2) hepatotoxicity

● Clinical Use:
1) Leukemias
2) autoimmune conditions

A

6-Mercaptopurine (6-MP)

109
Q

What can lead to severe 6-MP toxicity?

A

When 6-Mercaptopurine is given with Allopurinol, it inhibits xanthine oxidase resulting in increased levels of 6-MP and its active metabolites in the body.
This can lead to severe toxicity, including myelosuppression (bone marrow suppression), which can manifest as:

1) neutropenia
2) thrombocytopenia
3) anemia

110
Q
  1. Cancer Chemotherapy Toxicity and Management

Cisplastin, Methotrexate can both cause which form of toxicity?

A

● Renal Toxicity: Cisplastin, Methotrexate

○ Give Amifostine for Cisplatin (Platinum analogs)

111
Q
  1. Cancer Chemotherapy Toxicity and Management

Bleomycin, Busulfan, & Procarbazine can all cause which form of toxicity?

A

● Pulmonary Toxicity: Bleomycin, Busulfan, Procarbazine

112
Q
  1. Cancer Chemotherapy Toxicity and Management

Doxorubicin, Daunorubicin can both cause which form of toxicity?

A

● Cardiac Toxicity: Doxorubicin, Daunorubicin

113
Q
  1. Cancer Chemotherapy Toxicity and Management

Vincristine, Cisplatin can both cause which form of toxicity?

A

● Neurologic Toxicity: Vincristine, Cisplatin

114
Q
  1. Cancer Chemotherapy Toxicity and Management

Cyclophosphamide, Methotrexate can both cause which form of toxicity?

A

● Immunosuppressive Toxicity: Cyclophosphamide, Methotrexate

○ Give Leucovorin for methotrexate toxicity
○ Give Mesna for cyclophosphamide toxicity

115
Q

● Drugs: Tamoxifen, Trastuzumab are clinically used for

A
  1. Breast Cancer Treatment
116
Q

● MOA:
A selective Estrogen Receptor Modulator (SERM) → estrogen antagonist, preventing estrogen from binding to its receptor, thereby inhibiting the growth of estrogen-dependent breast cancer cells.

● Side Effects: Menopausal symptoms

● Clinical Use:
○ Tamoxifen is primarily used in the treatment of hormone receptor-positive breast cancer

A

Tamoxifen

117
Q

What is the MOA of Tamoxifen?

A

● MOA:
A selective Estrogen Receptor Modulator (SERM) → estrogen antagonist, preventing estrogen from binding to its receptor, thereby inhibiting the growth of estrogen-dependent breast cancer cells.

118
Q

● MOA:
A monoclonal antibody that targets the HER2/neu receptor, a protein overexpressed in some forms of breast cancer.

● Side Effects: cardiotoxicity

● Clinical Use:
treating HER2-positive breast cancer (more aggressive form)

A

Trastuzumab

119
Q

What is the MOA of Trastuzumab?

A

● MOA:
A monoclonal antibody that targets the HER2/neu receptor, a protein overexpressed in some forms of breast cancer.

120
Q

● If breast cancer patient are resistant to Tamoxifen, give them ____________:

A

aromatase inhibitors
( Anastrozole, Letrozole, and Exemestane)

121
Q

3 Drugs
● MOA:
These drugs inhibit aromatase, an enzyme that converts androgens to estrogens in
postmenopausal women, thereby reducing estrogen levels.

● Clinical use:
1) hormone receptor-positive breast cancer that is resistant to tamoxifen
(especially in postmenopausal women)

A

Aromatase inhibitors
● Drugs: Anastrozole, Letrozole, and Exemestane.

122
Q

What is the MOA of Aromatase inhibitors (Anastrozole, Letrozole, and Exemestane)?

A

● MOA:
These drugs inhibit aromatase, an enzyme that converts androgens to estrogens in
postmenopausal women, thereby reducing estrogen levels.

123
Q

MOA
It targets μ-opioid receptors in the myenteric plexus of the large intestine & acts as an agonist to reduce intestinal motility and increase the absorption of fluid and electrolytes. (antidiarrheal)

Clinical use:
1) Acute and Chronic diarrhea (It does not
readily cross the blood-brain barrier, so it has a lower risk of central opioid effects)

A

● Loperamide

124
Q

What is the MOA Loperamide?

A

It targets μ-opioid receptors in the myenteric plexus of the large intestine & acts as an agonist to reduce intestinal motility and increase the absorption of fluid and electrolytes. (antidiarrheal)

125
Q

What are Naloxone and Naltrexone?

A

They are opioid antagonists

Side effects: Withdrawal

126
Q

MOA:
It is a synthetic disaccharide that is not absorbed in the gut & metabolized by Gi flora into acid that draws water into the bowel (osmotic effect).(Laxative)

○ Key Point:
1) Constipation
2) Hepatic encephalopathy
(reduces ammonia absorption)

A

Lactulose

127
Q

What is the MOA of lactulose?

A

MOA:
It is a synthetic disaccharide that is not absorbed in the gut & metabolized by Gi flora into acid that draws water into the bowel (osmotic effect).(Laxative)

128
Q

MOA:
It blocks the D2 receptors in the chemoreceptor trigger zone and enhances the response to acetylcholine in the upper GI tract.

This promotes gastric emptying (prokinetic effect) and reducing nausea and vomiting (antiemetic effect).

○ Clinical use:
1) Diabetic gastroparesis
2) antiemetic

A

Metoclopramide

129
Q

What is a major side effect concerning Metoclopramide blocking D2 receptors?

A

extrapyramidal symptoms

130
Q

What is the MOA of Metoclopramide?

A

MOA:
It blocks the D2 receptors in the chemoreceptor trigger zone and enhances the response to acetylcholine in the upper GI tract.

131
Q

○ MOA: These irreversibly bind to and inactivate the H+/K+ ATPase (proton pump) in gastric parietal cells to reduce gastric acid secretion.

Clinical use:
1) GERD
2) Peptic ulcers
3) Zollinger-Ellison syndrome

A

● Proton Pump Inhibitors (PPIs): omeprazole

132
Q

○ Key Point: PPIs need an acidic environment to be activated, so they are usually taken before ______

A

meals

133
Q

What is the MOA of PPI’s?

A

○ MOA: These irreversibly bind to and inactivate the H+/K+ ATPase (proton pump) in gastric parietal cells to reduce gastric acid secretion.

134
Q

○ MOA: A PGE1 analogue that increases the production and secretion of gastric mucus and bicarbonate, to helps protect the gastric mucosa.
It also inhibits gastric acid secretion.

○ Clinical uses:
1) NSAID-induced peptic ulcers

A

● Misoprostol

135
Q

What is the MOA of Misoprostol

A

○ MOA: A PGE1 analogue that increases the production and secretion of gastric mucus and bicarbonate, to helps protect the gastric mucosa.
It also inhibits gastric acid secretion.

136
Q

○ MOA:
It blocks 5-HT3 receptors, particularly in the chemoreceptor trigger zone and the GIT to controls nausea and vomiting.

○ Clinical use:
1) chemotherapy-induced and postoperative nausea and vomiting.

A

● Ondansetron

137
Q

What is the MOA of Ondansetron?

A

○ MOA:
It blocks 5-HT3 receptors, particularly in the chemoreceptor trigger zone and the GIT to controls nausea and vomiting.

138
Q

Morphine (Opioid)

● Target: μ (mu), κ (kappa), and δ (delta) opioid receptors.

● MOA:
Primarily acts as an agonist at the μ-opioid receptors, leading to analgesia, sedation, euphoria, and respiratory depression & slowed Gi motility.

● Key Point: Widely used for pain relief but has a high potential for dependence and tolerance.

A

Morphine (Opioid)

139
Q

● Targets: Dopamine, norepinephrine, and serotonin reuptake transporters.

● MOA:
It inhibits the reuptake of these neurotransmitters, leading to their increased concentration at the synapse and causing euphoria, increased alertness, and vasoconstriction.

● Key Point: High abuse potential; acute overdose can lead to cardiac arrhythmias and
myocardial infarction.

A

Cocaine:

140
Q

acute overdose of this drug can lead to cardiac arrhythmias and myocardial infarction

A

Cocaine

141
Q

● MOA: Interferes with cellular respiration by inhibiting pyruvate dehydrogenase and
disrupting ATP production.

● Key Point: Symptoms include garlic breath, vomiting, diarrhea, QT prolongation, and hyperkeratosis.

A

Arsenic (As) poisoning treat with chelators & removal from the contaminant

142
Q

● MOA:
It inhibits various enzymes involved in heme synthesis and interferes with calcium metabolism.

A

Lead

143
Q

Abdominal pain, anemia, and neurologic symptoms
(e.g., encephalopathy, peripheral neuropathy).

A

Lead poisoning (plumbism)

Treat with a lead chelator:
Calcium disodium ethylenediaminetetraacetic acid (EDTA)

144
Q

● MOA:
It inhibits COX enzymes in the CNS, reducing pain and fever.

A

Acetaminophen (Paracetamol):

145
Q

● Overdose leads to hepatic necrosis

A

Acetaminophen toxicity

treat with N-acetylcysteine as an antidote to
replenish glutathione.

146
Q

● Target: Muscarinic acetylcholine receptors

● MOA:
It acts as a competitive antagonist at muscarinic receptors, to reduce parasympathetic activity (anticholinergic effects).

● Key Point: Used to treat bradycardia and as an antidote for organophosphate poisoning.

A

Atropine

147
Q

Hyperthermia, dry/flushed skin, tachycardia, constipation, dry eyes & dilated pupils

A

Atropine poisoning treat with physostigmine

148
Q

● MOA:
Inhibits acetylcholinesterase, leading to an accumulation of acetylcholine at
synapses and overstimulation of cholinergic receptors.

● Presents with DUMBBELSS symptoms
(Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation)

A

Organophosphate Poisoning treat with atropine & pralidoxime

149
Q

● MOA:
Binds to cytochrome c oxidase in mitochondria, inhibiting cellular respiration.

● Key Point: Presents with altered mental status, seizures, and lactic acidosis

A

Cyanide Toxicity it is treated with
hydroxocobalamin or sodium thiosulfate.

150
Q

● MOA:
Metabolized to toxic metabolites causing metabolic acidosis and renal failure.

● Key Point: Early symptoms include inebriation, vomiting, and respiratory depression; late
symptoms include renal failure and calcium oxalate crystal deposition.

A

Ethylene Glycol Poisoning:

Treat with
1) Sodium bicarbonate to correct the metabolic acidosis
2) Fomepizole or ethanol to inhibit the metabolism of ethylene glycol to its more toxic metabolites

151
Q

● Target: Nicotinic acetylcholine receptors

● MOA:
It acts as a (alpha 4 beta 2) partial agonist at these receptors, reducing craving and withdrawal symptoms.

● Key Point: Useful for smoking cessation but can cause mood changes and vivid dreams.

A

Smoking Cessation Medication – Varenicline

152
Q

● MOA:
Disulfiram inhibits aldehyde dehydrogenase, leading to the accumulation of acetaldehyde when ethanol is consumed.

● Key Point: Causes unpleasant symptoms like flushing, headache, nausea, and palpitations,
deterring alcohol consumption

A

Disulfiram Reaction (Enzyme: Aldehyde Dehydrogenase):

153
Q

Antibiotic resistance to penicillin occurs via

A

1) Beta-lactamase & ESBL
2) Mutated PBP
3) Mutated porin proteins

154
Q

Antibiotic resistance to vancomycin occurs via

A

1) Mutated peptidoglycan cell wall
2) Impaired influx/increased efflux

155
Q

Antibiotic resistance to Quinolones occurs via

A

1) Mutated DNA gyrase
2) Impaired influx/increased efflux

156
Q

Antibiotic resistance to Aminoglycosides occurs via

A

1) Aminoglycoside-modifying enzymes
2) Mutated ribosomal subunit protein
3) Mutated porin protein

157
Q

Antibiotic resistance to TCAs occurs via

A

1) Impaired influx/increased efflux
2) Inactivated enzyme

158
Q

Antibiotic resistance to Rifamycins occurs via

A

1) Mutated RNA polymerase

159
Q

What is the MOA of Amifostine?

What does it treat?

A

MOA:
It is a free radical scavenger (protects against them)

Treats:
Nephrotoxicity
(induced by platinum)

160
Q

What is the MOA of Dexrazoxane?

What does it treat?

A

MOA:
It’s an iron chelator

Treats:
Cardiotoxicity
(induced from anthracyclines)

161
Q

What is the MOA of Leucovorin acid (folinic acid)?

What does it treat?

A

MOA:
A tetrahydrofolate precursor

Treats:
Myelosuppression (from methotrexate & it enhances the effect of 5-FU

162
Q

What is the MOA of Mesna?

What does it treat?

A

MOA:
A sulfhydryl compound that binds acrolein (toxic metabolite of cyclophosphamide/ifosfamide)

Treats:
Hemorrhagic cystitis from cyclophosphamide/ifosfamide

163
Q

What is the MOA of Rasburicase?

What does it treat?

A

MOA:
A recombinant uricase that catalyzes metabolism of uric acid to allantoin

Treats:
Tumor lysis syndrome

164
Q

What is the MOA of Ondansetron & Granisetron?

What does it treat?

A

MOA:
A 5-HT3 receptor antagonist

Treats:
Acute nausea & vomiting (1-2hr post chemo or post op)

165
Q

What is the MOA of Prochlorperazine & Metoclopramide?

What does it treat?

A

MOA:
D1 receptor antagonist

Treats:
Acute nausea & vomiting (1-2hr post chemo or post op)

166
Q

What is the MOA of Aprepitant & Fosaprepitant?

What does it treat?

A

MOA:
An NK1 receptor antagonist

Treats:
Delayed nausea & vomiting (>24hrs after chemo)

167
Q

What is the MOA of Filgrastim & Sargramostim?

What does it treat?

A

MOA:
A recombinant G(M)-CSF

Treats:
Neutropenia

168
Q

What is the MOA of Epoetin alfa

What does it treat?

A

MOA:
Recombinant erythropoietin

Treats:
Anemia

169
Q

Drugs to treat alcohol abuse?

A

1) Disulfiram

2) Naltrexone (Reduce Craving Opioid Receptor Antagonist)

3) Acamprosate

4) BZDs

170
Q

1) Disulfiram

2) Naltrexone (Reduce Craving Opioid Receptor Antagonist)

3) Acamprosate

4) BZDs

Can all be used in therapy against ______abuse

A

Alcohol abuse

171
Q

Nicotine addition can be treated with which drugs?

A

1) Varenicline
2) Bupropion
3) Clonidine

172
Q

1) Varenicline
2) Bupropion
3) Clonidine

Can all be used in therapy against ______addiction

A

Nicotine

173
Q

Opioid addiction maintenance can be treated with which drugs?

Opioid intoxication on the other hand can be treated with?

A

Opioid Maintenance:
1) Methadaone
2) Buprenorphine
3) Clonidine
4) Naltrexone

Opiod Intoxication: Naloxone

174
Q

________Maintenance:
1) Methadaone
2) Buprenorphine
3) Clonidine
4) Naltrexone

________Intoxication: Naloxone

A

Opioid

175
Q

Which drugs can treat BZD abuse?

A

Flumazenil ( Overdose)

176
Q

Flumazenil ( Overdose) can treat _____

A

BZD OD

177
Q

Which metabolite causes a Disulfiram like reaction in alcohol abuse?

A

Aldehyde dehydrogenase

Causing elevated formic acid:
1) Respiratory failure
2) Severe anion gap metabolic acidosis
3) Ocular damage

178
Q

Cocaine vs Amphetamines

MOA

A

Cocaine MOA:
Blocks DA, NE, & 5-HT reuptake in the CNS to cause local anesthesia because of Na blockade

Amphetamine MOA:
Blocks NE & DA reuptake & it releases amines from a mobile pool to act as weak MAO inhibitors

179
Q

Cocaine vs Amphetamines

Effects

A

Cocaine

1) Increased NE causing sympathomimetic effects
(high HR, Contractility, BP, Mydriasis, CNS excitation)

2) Increased DA (psychotic episodes, paranoia, hallucinations, & dyskinesias)

3) Increased 5-HT (behavioral changes/decreased appetite)

Amphetamines

1) Increased NE causing sympathomimetic effects
(high HR, Contractility, BP, Mydriasis, CNS excitation)

2) Increased DA (psychotic episodes, paranoia, hallucinations, & dyskinesias)

180
Q

Cocaine vs Amphetamines

Toxicity

A

Cocaine

1) Excess NE (arrythmias, generalized ischemia + MI, strokes, & acute renal/hepatic failure)

2) Excess DA (major psychosis)

3) Excess 5HT (Serotonin syndrome)

Amphetamines

1) Excess NE (arrythmias, generalized ischemia + MI, strokes, & acute renal/hepatic failure)

2) Excess DA (major psychosis)

181
Q

Cocaine vs Amphetamines

Withdrawal

A

Cocaine & Amphetamines
Cravings
Severe depression
Anhedonia
Anxiety

182
Q

Benzodiazepines vs Barbiturates & Ethanol

MOA

A

BZD

Potentiates GABA interaction with GABA(A) receptors involving BZ1 & BZ2 binding sites

Barbiturates & Ethanol

Prolongs GABA, a GABA mimetic at high doses on GABA(A) receptors

183
Q

Benzodiazepines vs Barbiturates & Ethanol

Effects

A

BZD

Light-to-moderate CNS depression

Barbiturates & Ethanol

CNS depression

184
Q

Benzodiazepines vs Barbiturates & Ethanol

Toxicity

A

BZD

1) Sedation
2) Anterograde amnesia
(reverse with fluazenil)

Barbiturates & ethanol

1) Severe CNS depression
2) Respiratory depression
3) Death

185
Q

Benzodiazepines vs Barbiturates & Ethanol

Withdrawal

A

Benzodiazepines
1) Rebound insomnia
2) Rebound anxiety

Barbiturates & ethanol
1) Agitation
2) Anxiety
3) Hyperreflexia
4) Life threatening seizures
5) Hallucinations
6) Delirium tremens

186
Q
A

Pharm SJSM (23 decks)

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