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122 Cards in this Set

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  • Back
What are the Worm drugs that interfere w/ muscular activity?
Niclosamide MOA?
Uncouples oxidative metabolism

Tapeworm scolex releases from the intestinal wall
Praziquantal MOA?
opens calcium channels to cause muscular tetany
-- spastic paralysis
-- causes tegmental damage which activates the host immune system
Albendazole, Mebendazole MOA?
inhibits microtubules needed for glucose intake --> ↓ [glycogen] and [ATP] --> death
Thiabendazole MOA?
inhibits mitochondrial fumurate reductase
Diethylcarbamazine MOA?
Immobilizes microfilariae via decreased muscular activity
-- also alters surface membranes to make organism more susceptible to host immune defenses
Worm drugs which interfere w/ synaptic transmission?
pyrantel pamoate
Pyrantel pamoate, levamisole MOA?
ganglionic nicotinic cholinergic agonists = muscular tetany
Piperazine MOA?
a GABA agonist at chloride channel in NM jxn
-- flaccid muscle paralysis
Ivermectin MOA?
releases GABA and ↑ GABA binding --> facilitate opening of chloride channels in NM junction
-- flaccid muscle paralysis in helminths, insects and ectoparasites
-- may also cause tonic paralysis of musculature of nematodes via glutamate-gated Cl- channels found only in invertebrates

Used a lot in the cow industry
What are the WORM drugs?
Cestodes (tapeworms) – NICLOSAMIDE is DOC on exams

PRAZIQUANTAL is DOC in real world

Third drug – MEBENDAZOLE
Treatment of roundworms?
Ascaris lumbricoides

Pyrantel pamoate
Treatment of pinworms?
Enterobius vermicularis

Mebendazole (a safety pin has a bend in it)
Pyrantel pamoate
Treatment of hookworms?
Necator americanus

Treatment of whipworms?
Truchuris Trichuria

Treatment of threadworms?
Strongyloides stercoralis

Ivermectin is the DOC
Treatment of trichinosis?
Trichinella spiralis

Treatment of filariasis?
Wucheria bancrofti
-- diethylcarbamazine

Onchocerca volvulus
-- Ivermectin is the DOC
Other uses of ivermectin?
Tx of onchocerciasis and strongyloidasis (threadworm), ectoparasites
Treatment of trematodes?
(flukes) Schistosoma

Praziquantal is the DOC
CLINICAL: Patient passes tape worm segments (proglottids) - most likely Taenia saginata (beef tapeworm) or a patient who likes to eat sushi passes tapeworm segments - most likely to be Diphyllobothrium latum (fish tapeworm) - treat with?
Niclosamide or Praziquantal

Fish tapeworm causes megaloblastic anemia because the worm takes up all the vitamin B12 in the gut

Always worry that patient may have Taenia solium, pork tapeworm, which may produce cysticercosis (larval cysts) in the brain, orbit, muscles, liver and lungs.
Tx cysticercosis w albendazole

Praziqunatel is DOC if identity of the type of tapeworm is uncertain
CLINICAL: Baby w anal itching (pruritis) and a postive “cellophane tape” test?
Pinworm infestation

Tx w/ mebendazole or pyrantel pamoate
CLINICAL: Patient w mixed infestation = cestode (tapeworm) + trematode (fluke). Tx?
Mixed infestations treat w/ praziquantal
What are the antiprotozoal drugs?

Pentamidine isethionate
Metronidazole MOA?
Reduced to active nitroderivative that inhibits DNA replication

Active against anaerobic protozoa and bacteria
Metronidazole is the DOC for?
Giardia lamblia
-- beaver fever
-- camper’s fever

-- trichomoniasis

C Diff infections
Metronidazole can also treat…?
Entamoiba histolytica (amebiasis)

Obligate anaerobic bacteria
-- Bacteroides
-- Clostridium difficile
S/E’s of Metronidazole?
disulfiram-like rxn w/ EtOH headache, n/v, flushing

MOA of Pentamidine isethionate?
Therapeutic use of Pentamidine isethionate?
Second-line drug for PCP (Trim-sulfa is first)
-- use if pt can’t take sulfonamides
What are the antimalarial drugs?
Primaquine S/E’s?
Can cause acute hemolysis in pt w/ malaria in pts w/
-- glucose-6-phosphate dehydrogenase deficiency
Chloroquine S/E’s?
Principal drawback is the wide-spread occurrence of resistance strains

tinnitus, headache
Mefloquine is DOC for…?
prophylaxis for areas w/ chloroquine-resistant strains
Sulfadoxine-pyramethamine is DOC for…?
treatment of chloroquine-resistant malaria b/c it has a different MOA than chloroquine
Sulfadoxine MOA?
inhibits dihydropteroate synthase
Pyrimethamine MOA?
inhibits DHF reductase
-- can cause megaloblastic anemia
What are the antiviral drugs?







Acyclovir MOA?
Converted to acyclovir-monophosphate by thymidine kinase.

Other enzymes convert it to acyclovir-triphosphate (acyclo-GTP)

Inhibits viral DNA polymerase.
Why isn’t acyclovir toxic to the host cells?
Mammalian cells phosphorylate acyclovir at 1/30-1/00 the rate of the HSV

Acyclo-GTP is 1/10-1/30 less active in inhibiting mammalian DNA polymerase
Acyclovir is for treatment of…?
What causes HSV resistance to acyclovir?
a mutation which causes a deficiency of thymidine kinase
CASE: Immunocompromised patient w mucocutaneous HSV infection. Treatment?
CASE: Patient w HSV encephalitis. Treatment?
CASE: Patient w genital HSV infection. Treatment?
Keratoconjunctivitus caused by HSV is treated with…?
Trifluridine (trifluorothymidine)
Ganciclovir MOA?
Phosphorylated to a triphosphate which inhibits DNA polymerase
-- triphosphate is a competitive substrate w deoxyguanosine triphosphate for incorporation into DNA

Stops DNA chain elongation to inhibit DNA synthesis
Ganciclovir is used to treat…?
Cytomegalovirus (CMV)
CASE: Immunocompromised patient w/ CMV infection. Treatment?
Idoxuridine MOA?
triphosphate inhibits viral DNA polymerase(resembles thymidine)
When HSV becomes resistant to idoxuridine, it will also be resistant to…?

B/C both drugs are thymidine derivatives which inhibit DNA polymerase
Amantadine MOA?
Inhibits the membrane coat ion channel that allows the acid-mediated dissociation of ribonucleoprotein complex early in replication.
-- This inhibition of uncoating prevents the transfer of viral RNA into the cytoplasm of the mammalian cell
Amantadine use?
Inhibits coating of influenza A and rubella viruses

Used prophylactically to prevent infection w/ influenza A
Zanamivir MOA?
Inhibition of viral neuraminidase
Zanamivir therapeutic use?
Treatment of flu
Zidovudine MOA?
Converted to an active triphosphate which either
1. inhibits viral DNA polymerase (reverse transcriptase) OR
2. is incorporated into DNA in the place of thymidine to stop DNA chain elongation.
Zidovudine therapeutic use?
AZT – HIV treatment
Zidovudine S/E’s?
bone marrow depression

HIV protease inhibitor

Inhibit HIV aspartic protease which converts polyproteins into functional core proteins and viral enzymes
Interferon MOA?
causes protein synthesis

1. 2,5 adenine synthetase
-- makes adenylate oligomers which activate RNAase to degrade viral RNA

2. protein kinase phosphorylates elongation factor 2 to prevent peptide viral chain initiation

3. PDEase degrades terminal nucleotide of t-RNA to inhibit viral peptide chain elongation

interferes w viral penetration, uncoating, assembly and release
-- interferes w the synthesis of viral mRNA
-- inhibition of the translation of viral mRNA
What are the antifungal drugs?
Ampho B



Trim Sulfa

Ampho B MOA?
Binds to ergosterol in fungal membranes to form pores
-- increases the permeability of the fungal membrane
-- cells lose ions and macromolecules
-- enhances penetration of other antifungal drugs such as flucytosine
Ampho B resistance?
Decreased membrane ergosterol or altered structure of ergosterol
Ampho B therapeutic use?
DOC for
-- Coccidiodes immitis
-- Aspergillis infections

Also effective against Candida
Ampho B S/E’s?
Clinical usefulness is limited by its nephrotoxicity
-- histological damage to renal tubules w cell necrosis
-- renal tubular acidosis (a defect of renal function that produces systemic acidosis because bicarbonate ion cannot be reabsorbed in the PT or DT).
-- hyperchloremic metabolic acidosis

Renal toxicity can be avoided by giving mannitol to induce a high rate of urinary flow
Ketoconazole MOA?
Inhibits fungal CYP450 which prevents the demethylation of lanosterol to ergosterol
-- so blocks cell wall synthesis

All –konazoles have same MOA
Therapeutic use of Ketoconazole?
Candida infections

Also effective against Coccidiodes immitis
CLINICAL: Why is ketoconazole contraindicated in a patient receiving tx w amphoterecin B?
Because ketoconazole will BLOCK the antifungal actions of amphoterecin B
Ketoconazole and drug interactions?
Inhibits CYP450 to ↑ the plasma conc of other drugs
-- esp. cyclosporine in transplant patients (can damage kidneys)
-- fluconazole also ↑ [cyclosporine] by MOA is unknown

Inhibits adrenal 17 & scc CYP450’s
-- adrenal insufficiency
-- ↓ [testosterone]
-- ↓ [estradiol] = gynecomastia
-- ↓ libido & potency in males
-- menstrual irregularities in females
Flucytosine MOA?
converted to fluorouracil
-- inhibits thymidylate synthesis
-- thus inhibits DNA synthesis
Fungal resistance to Flucytosine?
Develops rapidly and limits its clinical effectiveness, so amphoterecin B is used to treat systemic fungal infections, or flucytosine and amphoterecin B are given together

Ampho B enhances penetration of flucytosine: synergistic antifungal activity
Flucytosine S/E’s?
bone marrow depression
-- limits clinical usefulness
CLINICAL: Which drug is selectively toxic to fungi because mammalian cells are unable to catalyze its deamination?
Trim-sulfa is the DOC for…?
PCP (+ silver stain)

Secondary drug is pentamidine (espec if sulfa allergy)
Griseofulvin MOA?
Disrupts mitotic spindle by interacting w polymerized microtubules
-- fungal mitosis is inhibited

Inhibits fungal CYP450 to block synth of ergosterol
Griseofulvin therapeutic use?
used to tx dermatophytes w hypae
-- Trichophyton
-- Microsporum
-- Epidermophyton.

Can also tx athlete’s foot w miconazole

DOC for ringworm on USMLE (in real world –conazole)
interact w penicillin-binding proteins to inhibit transpeptidation and peptidoglycan synthesis
-- cell wall synthesis is inhibited
PCN elimination?
Eliminated by renal tubular secretion.

-- Probenecid increases the half-life by inhibiting renal secretion (clearance).

-- The [PCN] in serum ↑ whereas the [PCN] in the urine ↓
What can inhibit penicillinases (beta-lactamases)?


Which PCNs are resistant to beta-lactamases?
Acid labile
-- methcillin
-- nafcillin

Acid stabile
-- oxacillin
-- cloxacillin
-- dicloxacillin
What is the primary beta-lactamase producing bacteria?
S. aureus
What else is resistant to beta-lactamases?
-- resistant to beta-lactamase
-- metabolized by renal tubular dihydropeptidases
-- Cilastatin inhibits the renal peptidases to decrease renal clearance of imipenem to increase the half-life

-- block transpeptidase-dependent cross-linkage of peptidoglycan
PCN S/E’s?
HSN rxns are common to all the PCNs
Cephalosporin MOA?

Have the same MOA as the PCNs

1st generation – very good MSSA and Strep coverage, OK community GNR

2nd generation – better Strep coverage, but worse Staph coverage
-- better community GNR
-- better anaerobic coverage

3rd generation
-- G(+) coverage varies by drug
-- all have improved GNR coverage
-- some cover nosocomial GNR
-- ALL penetrate CNS better than 1st or 2nd generation, and thus are preferred for meningitis
CLINICAL: Patient w gonorrhea
Tx w penicillin for 8 weeks
CLINICAL: Patient returns with similar symptoms but no diplococci in urine (no longer has gonorrhea)
patient has Chlamydia infection

Tx w tetracycline unless patient is a PG female--then tx w erythromycin
CLINICAL: Patient has Streptococcus infection and is allergic to PCNs. Tx?
Erythromycin (macrolide)

These others are better b/c they don’t cause diarrhea:
-- Clarithromycin has better extracellular concentration
-- Azithromycin
Vancomycin MOA?

Binds to 30S subunit
-- interfere w/ initiation complex of peptide formation
-- causes misreading of mRNA and break polysomes into non-functional monosomes.
Vancomycin therapeutic use?
given i.v. for bacterial infections b/c not absorbed when given p.o

-- Serious life-threatening MRSA in the hospital
-- If MSSA, can use any PCN
-- outpatient, treat w/ trim-sulfa or clindamycin or doxycycline
If C.diff occurs w/ i.v. vancomycin…?
P.O. vancomycin will still cure it (but want to limit p.o. use b/c this can cause resistance)

But DOC is metronidazole
Aminoglycoside MOA?

Binds to 30S subunit
-- interfere w initiation complex of peptide formation
-- causes misreading of mRNA and break polysomes into non-functional monosomes
Aminoglycoside kinetics?
Decreased GFR increases the half-life of gentamicin

PCN’s enhance the cellular penetration of aminoglycosides = synergistic effects
Aminoglycoside toxicity?
1. ototoxic

2. nephrotoxic, more so in elderly patients

3. drug accumulates in cells of PT and causes necrosis so urinary excretion of brush border enzymes increases
-- effect usually reversible since cells of PT can regenerate

4. get defect of renal concentrating mechanism because gent acts on DT and CD to decrease the sensitivity to ADH

5. decreased GFR, mild proteinuria, hyaline and granular casts in urine

NET EFFECT = mild increase in serum creatinine, hypokalemia, hypocalcemia and hypophosphatemia
Trim-Sulfa MOA?

See pg 6 for schematic
Trimethoprim – why doesn’t it affect humans?
100,000x more active against bacterial enzyme vs. mammalian enzyme
Trim-Sulfa therapeutic use?
Patient w/ AIDS develop infection w/ PCP – treat w/ trim sulfa
Trim-sulfa S/E’s?
Sulfonamides can displace bilirubin from plasma protein binding sites

Can cause kernicterus in neonates
Tetracycline MOA?

Bind to 30S subunit to block aminoacyl t-RNA binding to the acceptor (A) site
Tetracycline therapeutic use?
Acts against gram (+) and (-) organisms, Rickettsiae, Mycoplasma, Chlamydia and amebas

NOT used for pneumococcal pneumonia
-- tx w/ PCNs, Cephalosporins, or Erythromycin
Tetracycline S/E’s?
Chelates Ca
-- adverse effect on formation of teeth and bones - fetus and babies
-- bioavailability decreased by milk and food in GI tract

Severe rash w/ sunlight
Lincosamide MOA?
Lincosamide = Clindamycin


Binds to 50S subunit and blocks aminoacyl translocation of peptide chain
Clindamycin therapeutic use?
First line for anaerobic coverage above the diaphragm

Second line for skin infections

Good staph, strep coverage
CLINICAL: You have treated a pt w/ clindamycin and they develop pseudomembraneous colitis. How do we treat this?
Tx w/ oral metronidazole (or oral vancomycin)
How do we treat TB?
Rifampin (induces CYP450)
Isoniazid S/E?
causes hepatic damage
Drugs which inhibit DNA gyrase?
nalidixic acid

-- ciprofloxacin

forms negative DNA supercoils
What are the protein synthesis inhibitors?
buy AT 30, CELL at 50

A = aminoglycosides (cidal) + spectinomycin (static) – use for FCN resistant gonorrhea
T = tetracyclines (static)

C = chloramphenicol (static)
E = erythromycin (static)
L = lincomycin (static)
L = cLindomycin (static)

Since chloramphenicol, macrolides and clindamycin work at the same site, do NOT use them together because they will interfere w/ each other
What are the bactericidal drugs?
PCNs, cephalosporins, aztreonam, imipenem
aminoglycosides (gentimicin, etc)
polymixin, colistin
FQ’s (norfloxacin, etc)
nalidixic acid
What are the bacteristatic drugs?
macrolides (erythromycin, etc)
nitrofurans = nitrofurantoin
How is bacterial resistance usually acquired?
Plasmid-mediated resistance is easily transferred by transduction to other species of bacteria
What are the β-lactams?

The transpeptidase enzymes which are inhibited by the β-lactams are called penicillin-binding proteins (PBPs) because they are the target site for these drugs
How do G (+) bugs become resistance to β-lactams?
1.production of bacterial β-lactamases (penicillinases)

2.altered PBP's with decreased affinity for β-lactams. Synthetic PCN's which are resistant to the β-lactamases may not be effective if if the bug also has altered PBP's

3. MRSA = mutations change the binding sites of the PBP = no β-lactam can bind to the PBP = MRSA is resistanct to all β-lactams (PCN's, cephs, imipenem, aztreonam)
How do we treat MRSA?
Tx MRSA w clindmycin, trim-sulfa or possibly doxycycline
How do G(-) bugs become resistant to β-lactams?
1.production of bacterial β-lactamases (penicillinases) which may be inducible

2. reduced permeability --> β-lactams gain access to the periplasmic space (the site of the peptidoglycan wall in gram negative bugs) by passing through channels (called porins) in the outer bacterial membrane.
-- A mutation which decreases the number of porins reduces the entry of the β-lactams to their site of action.
-- Thus a β-lactam could resistant to β-lactamases, and yet not be able to inhibit bacteria growth because it could not reach the PBP's
How do bugs become resistant to vancomycin?

Vancomycin inhibits cell wall synthesis by binding to the terminal D-ala of the nascent peptidoglycan side chain
-- this action inhibits transglycosylation, so both the elongation and the cross-linking of the peptidoglycan chain are inhibited.

Resistance occurs when a mutation changes the terminal D-ala to a D-lactate
-- vancomycin can no longer bind
How do bugs become resistant to FQs?
a single point mutation alters the binding of FQ's to the active site of DNA gyrase
How do bugs become resistant to aminoglycosides?
Aminoglycosides = gentamicin, tobramycin, amikacin

Plasmid-mediated enzymes are transferases which destroy the antibacterial effect of AG's by altering their structure

The altered drug is inactive in inhibiting bacterial protein synthesis.

Enzymatic alterations include acetylation of amine groups and phosphorylation of hydroxyl groups
How do bugs become resistant to macrolides?
Macrolides = erythromycin, clarithromycin, azithromycin, clindamycin

bacterial enzymes methylate the 23S ribosomal component of the bacterial 50S ribosome

This methylation prevents the binding of erthyromycin and clindamycin to the bacterial ribosome.
How do bugs become resistant to tetracyclines?
tetracyclines = doxycycline

Pumped into susceptible bugs by an energy-dependent transport system in their cellular membranes.

Plasmids carry resistance genes which decrease the intracellular accumulation and code for efflux pumps which extrude the drug from the cell
How do bugs become resistant to folate synthesis inhibitors?
folate synthesis inhibitors = trim-sulfa

a plasmid-coded gene synthesizes a form of dihyropteroate synthetase which does not bind sulfonamides even though it still binds PABA

Bacterial folate synthesis continues unabated
How do drugs become resistant to rifampin?
A mutation causing a single amino acid substitution in the beta-subunit of the DNA-direcdted RNA polymerase reduces the binding of rifampin
How do drugs become resistant to chloramphenicol?
plasma mediated

Involves the production of acetyltransferases which inactivates the drug