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YSM Semester 2 > Antivirals, Antihepatitis, Antiparsitics, Antiretrovirals > Flashcards

Antivirals, Antihepatitis, Antiparsitics, Antiretrovirals Flashcards

Some GI + OBGYN

1
Q

What medications are Tenofovir and Adefovir? What are their indications? What’s its MOA? What are their contraindications?

A

Hepatitis B
tenofovir is also a HIV medication

MOA - nucleotide analogs - inhibits DNA polymerase + terminated transcription

contraindications: Cirrhosis

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2
Q

What are the medications tenofovir and adefovir? What is the MOA and their AEs?

A

Hep B meds
MOA - nucleotide analogs - inhibits DNA polymerase + terminated transcription

AEs
- nephrotoxicity
- headache + abdominal pain
- disease exacerbation

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3
Q

What are the medications Lamivudine, telbivudine, and entecavir? What are their indications? What is their MOA?

A

Nucleoside analogs

indications: Hep B
lamivudine - also HIV NRTI

MOA - reverse transcriptase

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4
Q

What are entecavid, lamivudine, and telbivudine? What is their MOA? What are their AEs and contraindications?

A

nucleoside analogs
MOA - inhibits reverse transcriptase

AE
- GI symptoms
- Fever
- Headache

contraindications: cirrhosis

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5
Q

Describe interferon + ribavirin. What is it indicated for and what is the MOA?

A

MOAs
- interferon - causes antiviral state in cells inhibits viral protein synthesis
- ribavirin - nucleoside analog that stops RNA synthesis

indications: hep C

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6
Q

What are the MOAs and AEs of interferon + ribavirin?

A

MOA
- interferon - inhibits viral protein synthesis
- ribavirin - nucleoside analog that stops RNA synthesis

AEs
- interferon: fever, myalgia, neutropenia, thrombocytopenia, hypothyroidism, depression

  • rivabirin: teratogenic, hemolytic anemia, depression, depression, rash, nausea, diarrhea

problematic agents: not well tolerated, poor response rates, risk of relapse, 48 week long therapy

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7
Q

What are boceprevir, telaprevir, simepravir? What are their indications and MOA?

A

indication: hep C direct acting agent
- ONLY genotype 1
- response rate increased when added to interferon + ribavirin

MOA: NS3A + 4A protease inhibitors = causes decreased viral replication

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8
Q

What are boceprevir, telaprevir, simepravir? What are their MOA? What are their AEs?

A

HCV-1
MOA: NS3A + 4A inhibitor = decreased viral replication

AE
- headache, fatigue
- diarrhea, abdominal pain
- rash, photosensitivity

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9
Q

What is sofosbuvir + ledipasvir? What is the indication and MOA for this combination?

A

indication: hep C genotypes 1, 4, 5, 6

MOA
sofosbuvir - nucleoside analog against HCV NS6B polymerase = prevents HCV
Ledipasvir - NS5A inhibitor

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10
Q

What is sofosbuvir + ledipasvir? What is the indication and AEs for this combination?

A

MOA
sofosbuvir - nucleoside analog against HCV NS6B polymerase = prevents HCV replication
Ledipasvir - NS5A inhibitor = prevents HCV RNA replication

AE
sofosbuvir: insomnia, asthenia, pruritus, headache, fatigue, nausea
ledipasvir - headache, fatigue, nausea, diarrhea

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11
Q

Describe sofocbuvir + vepatsavir. What are its indications and MOAs?

A

indication: ALL hep C genotypes

MOA:
sofosbuvir - nucleoside analog against NS5B polymerase
velpatsavir - NS5A inhibitor = prevents HCV RNA replication

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12
Q

Describe glecabrevir + pibrentasvir. What is its indication and its MOA?

A

indication: ALL Hep C genotypes

MOA:
glecabrevir - NS3A + 4A inhibitor = decreased viral replication
pibrentasvir - NSA5A inhibitor = inhibits protein synthesis

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13
Q

Describe glecabrevir + pibrentasvir. What is its MOA and AEs?

A

Pan-genotypic Hep C antiviral
MOA:
glecabrevir - NS3A + 4A inhibitor = decreased viral replication
pibrentasvir - NSA5A inhibitor = inhibits protein synthesis

AE
glecabrevir - headache, fatigue, nausea
pibrentasvir - headache, fatigue, nausea + diarrhea

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14
Q

What are the hep C pan-genotypic agents?

A

Sofosbuvir + velpatsavir
Glecabrevie + pibrentasvir

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15
Q

How do you monitor drug efficacy in hep b drug regimens?

A

HEP B
serum markers repeated every
- 12-24 weeks during therapy
- 6 - 12 months after

serum ALT

HBV DNA level - PCR test for viral load

HBeAg - hep B e-antigen
- negative = drug stopped/slowed viral replication

HBsAg quantitative
Anti-HB
Liver histology

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16
Q

How do you monitor drug efficacy for HCV?

A

quantitative HCV RNA levels
12-24 weeks after sustained virology response

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17
Q

Compare early virologic response and sustained virologic response

A

EVR - 100-fold+ reduction in viral load after first 12 weeks of tx

SVR - virus not detected in the blood 12 weeks+ after tx

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18
Q

Describe the meds acyclovir and famiciclovir. What are their indications and their MOA?

A

MOA - guanosine analogue + P = incorporated into viral DNA
- inhibits transcription via inhibition of viral DNA polymerase

indications:
herpes simplex
varicella zoster

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19
Q

Describe the meds acyclovir and famiciclovir. What are their MOA and AEs?

A

MOA - guanosine analogue + P = incorporated into viral DNA
- inhibits transcription via inhibition of viral DNA polymerase

AEs
acyclovir
- obstructive crystal-induced nephropathy + AKI: can be prevented w hydration/dose adj
- neurotoxicity - lethargy, confusion, delirium

BOTH:
- thrombotic thrombocytopenia purpura
- GI symptoms
- Increased ALT/AST

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20
Q

Describe ganiciclovir. What are its indications, MOA and AEs?

A

indication: anti CMV
- can also be used in CMV retinitis + prophylaxis

MOA: inhibits transcription via inhibition of viral DNA polymerase

AE:
- myelotoxocity: pancytopenia
- nephrotoxicity
- GI symptoms
- CNS - headache, confusion, paresthesia

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21
Q

Describe foscarnet. What are its indications and MOA?

A

indications - antiviral for
- ganiciclovir-resistant CMV retinitis
- acyclovir-resistant HSV
- VZV

MOA - pyrophosphate analog that binds to DNA polymerase to inhibit transcription

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22
Q

Describe foscarnet. What is its MOA and AEs?

A

MOA: pyrophosphate analog that binds to DNA polymerase to inhibit transcription

AE
- nephrotoxicity
- hypocalcemia, hypo magnesia, hypokalemia
- genital ulcerations - high [foscarnet] in urine
- CNS: headache, confusion, paresthesia
- leukopenia, neutropenia

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23
Q

Describe maribavir. What is its indication and its MOA?

A

indication: ganiciclovir + foscarnet resistant CMV
MOA - direct inhibitor of enzyme UL97
- exhibits encapsidation + viral capsid nuclear egress

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24
Q

Describe maribavir. What is its MOA and its AEs?

A

MOA - direct inhibitor of ganiciclovir + foscarned resistant CMV

AEs
- dysgeusia: metallic taste in mouth
- GI: diarrhea, NV
- Hematologic: anemia, thrombocytopenia
- CNS: fatigue
- renal: increased Cr

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25
Describe letermovir. What are its indications and its MOA? What about AEs and contraindications?
indication: CMV prophylaxis for pts that received stem cell or kidney transplant MOA: inhibits terminal helices enzyme complex of CMV - required for viral DNA processing + packing AEs - tachycardia, afib, peripheral edema - abdominal pain, diarrhea, NV - thrombocytopenia - fatigue, headache - cough contraindications: - pimozide - pitavastatin/simvastatin + cyclosporine
26
Describe chloroquine. What are its indications, MOA, and AEs?
indications: - malaria: vivid, malaria, oval, falciparum - extra intestinal amebiasis MOA - concentrates in acidic vacuoles in parasites - increased pH = inhibits parasite growth - inhibits polymerase that protects parasite from ferriprotoporphyrin IX = membrane damage AEs - headaches, dizziness, confusion - NV - cardiomyopathy - can lead to failure - retinal toxicity
27
Describe chloroquine. What is its MOA, clearance, and contraindications?
MOA: concentrated in acicid vacuoles in parasites - increased pH = inhibition of parasite growth - inhibits polymerase protection from ferriprotoprorphyrin IX = membrane damage clearance: alkylation in the liver, 50% excreted in urine contraindications: retinal/visual field changes of any etiology
28
describe proguanil/ateovaquone. What are its indications, MOA and AEs?
indications - malaria prophylaxis/treatment for falciparum MOA proguanil - inhibits dihydrofolate reductase atovaquone - inhibits parasite mitochondrial ETC AEs - generally well-tolerated - N/V, diarrhea, rash
29
Describe proguanil/atovaquone. What their MOAs, metabolism, and contraindications?
MOA - proguanil - inhibits dihydrofolate reductase - atovaquone - inhibits parasite mitochondrial ETC Metabolism - 40-60% excreted in urine - 10% in feces contraindications: severe renal impairment patients should not receive prophylaxis
30
Describe artemether-lumefantrine. What are their MOAs, indications?
indications: malaria treatment for P falciparum in regions with chloroquine resistance MOA artemether: increases amount of free heme - kills majority of parasites quickly lumefantrine - kills remaining parasites - prevents R to artemether
31
Describe artemether-lumefantrine. What are their MOAS, contraindications, and AEs?
MOA: artemether: increases amount of free heme - kills majority of parasite quickly Lumefantrine - kills remaining parasites - prevents R to artemether contraindications: strong CYP3A4 inducers AEs: QT prolongation inhibits CYP2D6
32
Describe artesunate. What is its MOA, indications, metabolism, AEs?
indications: - SEVERE malaria treatment (hospitalized, parasitemia ≥5%) - blood-stage plasmodium MOA: endoperoxidase bridge + heme iron binding = oxidative stress - inhibits protein + nucleic acid synthesis excreted in urine AE - post treatment hemolysis: monitor Hb 4 weeks - rare anaphylaxis
33
Describe quinine. What is its indications, MOA, and metabolism?
indication: malaria treatment for chloroquine-resistance falciparum + doxy MOA: depresses O2 update + carb metabolism - poorest therapeutic index of all antimalarial metabolism: liver
34
Describe quinine. What is its MOA, AEs, and contraindications?
MOA: depresses O2 uptake + carb metabolism AEs - Cinchonism - tinnitus, headache, NV - black water fever: massive hemolysis in P falciparum - rash - bone marrow suppression Contraindications - prolonged QT interval - Myasthenia gravis - optic neuritis
35
Describe doxycycline. What strain of malaria is it used for? What drug is its used with?
Doxy + quinine Malaria strain: acute falciparum in areas with resistance
36
What are the AEs and contraindications of doxy?
AEs: - photosensitivity - hyperpigmentation + dental staining - oral candidiasis - bone growth suppression in children contraindications - hypersensitivity to tetracycline - pregnant/breastfeeding women
37
Describe mefloquine. what are its indications, MOA and metabolism?
indications: prophylaxis/treatment for malaria from falciparum + vivax MOA: destruction of asexual blood forms of malaria - blood schizonticidal drug metabolism: liver by CYP3A4, excreted in bile + feces
38
Describe mefloquine. What are its MOA, AEs, and contraindications?
MOA - description of asexual forms of malaria (falciparum + vivax) = blood schizonticidal drug AEs: - psychosis, seizures, anxiety, vivid dreams - NV - cardiac conduction disturbances Contraindications: hx of seizures/psychiatric disorders
39
Describe albendazole. What are its indications and MOA?
indications: - echinococcosis: liver hydatid cysts - neurocystercercosis: T. sodium (pork tapeworm) MOA: inhibits microtubule synthesis in nematodes - impaired glucose uptake - larvicidal for: hydatid disease, neurocysterocosis, ascariasis, hookworm - ovicidal: ascariasis, hookworm, whipworm
40
Describe albendazole. What is its MOA, metabolism, and AEs?
MOA: inhibits microtubule synthesis in nematodes - impairs glucose uptake by organism metabolism: hepatic, excreted in urine + feces AE: NV, rash
41
albendazole is a very broad antibiotic for intestinal nematodes. What does it cover?
indicated for: - echinococcosis - liver hydatid cysts - neurocystercercosis - T. solium (pork tapeworm) off-label: - Ascariasis (roundworm) - A lubumocoides - hookworm - A. duodenal, Americans - whipworm - T. trichuris - pinworm - E. vermicularis - cutanoous larval migrans
42
Describe ivermectin. What are its indications and MOA and metabolism?
indications: - First line for: onchocerciasis (river blindness), strongyloidiasis - scabies - lice MOA - potentials opening of glutamate-gated Cl channels in nematodes + arthropods - located in nerve/muscles cells - hyper polarization = death Metabolized: hepatic CYP3A4, excreted in feces
43
Describe ivermectin. What is its MOA, metabolism, AEs?
MOA: potentiates opening of glutamate-gated Cl channels in nematodes + arthropods - located in nerve/muscle cells - hyper polarization = death AEs - generally well-tolerated - neurotoxicity - ataxia, confusion, encephalopathy, impaired consciousness - Mazzoti reaction: pruritus, skin rash, fever, fatigue, arthralgia, tachycardia, hypotension, abdominal pain
44
Describe metronidazole. What are its indications and MOA?
indications: - amebiasis - amoebic liver abscess - Entranomeba histolytic - giardiasis - G. lambia - trichomoniasis - T. vaginalis MOA - concentrates within the parasite and becomes electron sink - causes direct DNA damage due to free radicals
45
Describe metronidazole. What are its MOA, AEs and contraindications?
MOA - becomes electron sink in parasite - free radicals = DNA damage AEs - peripheral neuropathy, aseptic meningitis, ataxia, concussion, encephalopathy, seizures, vertigo - disulfiram-like reaction when consumed + alcohol - Nausea - metallic taste - vaginitis contraindications: - 1st trimester of pregnancy - disulfiram within 2 weeks - alcohol within 2 days - Cockayne syndrome
46
Describe how chloroquine resistance developed?
parasites decreased the uptake of chloroquine into the digestive vacuole - specific membrane protein in vacuole inhibited by Ca channel blocker
47
Describe nucleoside reverse transcriptase inhibitors. What are meds and what is the MOA? What step of HIV replication do they target?
tenofovir alafenamide/disoproxil fumarate lamivudine emtricitabine abacavir MOA: analogues that terminate the elongation of HIV DNA chain = inhibits reverse transcription target step 3 - transcription
48
Describe tenofovir alafenamide and disoproxil fumarate. What kind of meds are they and what are their AEs?
nucleoside reverse transcriptase inhibitor AEs TAF: no major ADR TDF: - renal toxicity - Fanconi syndrome - inadequate reabsorption in proximal tubules - decreased bone/mineral density - NV/diarrhea - lactic acidosis, hepatomegaly, NASH
49
Describe lamivudine. What are its indications, AEs and med type?
NRTI indications: HIV + Hep B BLACK BOX WARNING: lactic acidosis + hepatomegaly + steatosis AE: NV, diarrhea
50
Describe the commonalities of NRTIs
NRTIS: TAF, TDF, lamivudine, emtriciabine, abacavir - really adjusted (except abacavir) - all can cause NV, diarrhea - all can cause lactic acidosis + hepatomegaly + steatosis (lamivudine + abacavir black box)
51
Describe emtricitabine. What are its indications, MOA, and AEs?
indications: HIV and Hep B MOA: NRTI: terminates elongation of HIV DNA chain = inhibits reverse transcription AE - hyperpigmentated palms - lactic acidosis + hepatomegaly + steatosis
52
Describe abacavir. What is its indications, MOA, AEs?
indications - HIV MOA: NRTI - stops elongation of HIV DNA chain = inhibits reverse transcription AEs - INCREASED RISK OF MI - NV, diarrhea BLACK BOX WARNING - hypersensitivity - HLA-B5701 - lactic acidosis + hepatomegaly + steatosis BUT only NRTI that doesn't require renal adjustments!
53
Describe the MOA of NNRTIs. What are the medications? What are the commonalities between all of them?
MOA - binds to reverse transcriptase directly to reverse transcription efavirenz, filpivirine, doravirine commonalities: - 3A4 substrates - do NOT use strong inducers - can cause rash, Steven's Johnson - hepatotoxic
54
Describe efavirenz. What kind of HIV med is it? Describe its MOA and AEs
NNRTI MOA: binds to reverse transcriptase enzyme directly to inhibit reverse transcription AEs - abnormal dreams, confusion, dizziness, psychiatric effects - Qt prolongation - false positive on drug test - rash, SJS - increased LFTs (hepatotoxic) take on empty stomach strong 3A4 inducers
55
Describe rilpirivine. What type of HIV med is it? What's its MOA, AEs, contraindications?
NNTI MOA: binds to reverse transcriptase enzyme directly to inhibit reverse transcription contraindications - NO PPI - can use antacids + H2RA meds = spaced out AEs - Qt prolongation - rash, SJS - increased LFT (hepatotoxic) requires acidic environment for absorption - take with food
56
Describe integrate strand transfer inhibitors (INSTI). What are the meds, their MOA, and commonalities?
TEGRAVIRs: dolutegravir, raltegavir, bictegravir, alitegravir, cabotegravir MOA: bind to integrase active site to prevent insertion of viral DNA into the CD4 DNA commonalities: - can cause headache + insomnia - taken w/o regard to meal EXCEPT cations (Mg, Ca, Fe, Al)
57
Describe dolutegavir. What kind of med is it, what is its MOA and AEs?
INSTI MOA: binds to integrase active site to prevent insertion of viral DNA into CD4 DNA AEs - headache + insomnia - increases metformin levels
58
Describe raltegavir. What kind of med is it, its MOA, contraindications, and AEs?
INSTI MOA: binds to integrase active site to prevent insertion of viral DNA into CD4 DNA AE - headache + insomnia - THINK MUSCLES: CPK elevation, myopathy, rhabdomyolosis contraindications: avoid with statins
59
Describe bictegravir. What kind of med is it, its MOA and AEs
INSTI MOA: binds to integrase active site to prevent insertion of viral DNA into CD4 DNA AEs - headache, insomnia - less ADRs than other INSTI
60
Describe protease inhibitors. What are the meds, their MOAs, and their commonalities?
NAVIRs: darunavir, atazanavir MOA: binds to protease + inhibits cleavage of the long protein chains = inhibits formation of mature virus commonalities - taken with PK boosters: Ritonavir, cobicistat - 3A4 substrates - avoid inducers AEs: - hyperlipidemia, lipohypertrophy, hyperglycemia - rash + SJS - boosters: GI upset
61
Describe darunavir. What kind of med is it, what is its MOA and AEs?
PI MOA: binds to protease + inhibits cleavage of long protein chains = inhibits formation of mature virus AEs: - hyperlipidemia, lipohypertrophy, hyperglycemia - rash, SJS cautious in pts with sulfa allergy - sulfa-moiety
62
Describe atazanavir. What kind of med is it, its MOA, and AEs
PI MOA: binds to protease + inhibits cleavage of long protein chains = inhibit formation of mature virus AE: - hyperlipidemia, lipohypertrophy, hyperglycemia - rash, SJS - hyperbilirubinemia: jaundice + scleral icterus - PR interval elongation antacids + acid suppressants reduce absorption = requires spacing
63
What is the initial regimen for HIV treatment without cabotegravir prophylaxis?
All combinations start with 2 NRTI backbone. For 3rd med, you can use: integrase inhibitor (INSTI): preferred - dolutegravir (INSTI) + emtricitabine + TAF/TDF - bictegravir (INSTI) _ emtricitabine + TAF Protease inhibitor (NAVIRs) + booster Non-nucleoside reverse transcriptase inhibitor (NNTI)
64
What is the initial regimen for HIV treatment WITH cabotegravir prophylaxis?
2 NRTI backbone + PI + Booster 1. NRTI - TAF/TDF 2. NRTI- Emtricitabine 3. PI - Darunavir 4. Boosters - cobiscistat/ritonacvir
65

YSM Semester 2 (10 decks)

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