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GI > Antivirals/fungals > Flashcards

Antivirals/fungals Flashcards

1
Q

RNA viruses?

A
  • Influenza A, B, C (vaccine and drug)
  • Measles (vaccine), mumps, (vaccine), RSV (drug)
  • Rabies (vaccine)
  • Polio (vaccine), rhinovirus
  • HIV (drug)
  • Rubella (vaccine), hepatitis (drug)
  • Reovirus (drug) rotavirus
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2
Q

DNA viruses?

A
  • HSV (drug)
    Varicella (vaccine and drug)
    CMV (drug- antivirals are used a lot against CMV in people who have been transplanted - only once immunocompromised, do they become a real problem)
  • Adenovirus
  • Papilloma virus (vaccine)
  • Smallpox (vaccination)
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3
Q

What are the targets of antivirals?

A

Fusion - fuses with cell
Uncoating so that it can get into the nucleus
Replication of the free virus by RNA/DNA
Protease needed to make protein coat
Release - flu virus (oseltamivir = tamiflu) - prevents being passed on

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4
Q

What are drugs that act on the fusion of viruses? How does it work?

A

Enfurvitide (HIV)

HIV: infected cell binds onto surface of uninfected cell, creates second infected cell, HIV then replicates within that cell - takes about 15 mins

Enfurvitide: binds to gp41 on HIV surface, inhibits CD4/HIV interaction - gp41 binds to the CD4+ cell

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5
Q

Enfurvitide info?

A

Difficult dosing regime

Side effects: injection site pain, depression, infections (especially bacterial pneumonia)

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6
Q

What are drugs that act on the uncoating of viruses? How does it work?

A

Amantadine (flu)

Uncoating requires reduced pH of the endosome

inhibits viral ion channel (H+) - the viral one only

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7
Q

Amantadine info?

A

Channel prone to mutations (over 90% resistance reported in some outbreaks)

Side effects: CNS (dopaminergic effects) - nervousness, anxiety, insomnia

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8
Q

What are drugs that act on the replication of nucleic acids?

A

Zidovudine (HIV)
Nevirapine (HIV)
Acyclovir (Herpes)

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9
Q

How does Zidovudine work?

A
  • inhibits reverse transcriptase
  • incorporates into viral DNA (nucleoside reverse transcriptase inhibitor)
  • Thymidine analogue, slows replication
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10
Q

How does Nevirapine work?

A

non-nucleoside

inhibits RT by binding at a non-active site

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11
Q

Side effects of antivirals acting on nucleic acid replication?

A

Zidovudine and nevirapine (HIV)
Anaemia, bone marrow suppression, liver toxicity

Acyclovir (Herpes)
Nausea, vomiting, headache

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12
Q

How does acyclovir work?

A

inhibits DNA polymerase

Incorporates into viral DNA

Guanosine analogue 100x affinity for viral cf cellular polymerase - leads to chain termination

Requires activation by viral enzymes (thymidine kinase) - increases specificity

Side effects: nausea, vomiting, headache

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13
Q

What are antivirals that act on the protein coat formation ? How do they work?

A

Indinavir - protease inhibitor (HIV)

Binds to active site of HIV protease (Proteases cleave new proteins required for formation and assembly of virus coat)

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14
Q

Indinavir info?

A

Side effects: kidney stones, hyperlipidaemia

Restriction on what food can be taken and requires precise dosing (every 8 hours)

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15
Q

What are drugs that act on the release of the virus? How do they work?

A

OSELTAMIVIR (tamiflu) (influenza)

Blocks viral release by inhibiting neuraminidase activity
e.g. H1N1 strain - N = neuraminidase

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16
Q

Oseltamivir side effects?

A
  • nausea
    • vomiting
    • diarrhoea
    • headache
    • possible neurological (self harm)
17
Q

How can resistance occur in different HIV drugs?

A

HIV RT nucleoside inhibitors: mutation of the drug binding site on RT enzyme
- use multidrug approach

HIV RT non-nucleoside inhibitors: single point gene mutations
- require two other antiretroviral drugs

HIV protease inhibitors: mutations in HIV target protein

Multiple mutations required for high level resistance (1/3 of aa can be changed without altering function)

  • Sequential use of protease inhibitors increases resistance
  • use in combination with two RT inhibitors
18
Q

Types of fungi?

A

True yeast: single celled eukaryotic organisms
e.g. Cryptococcus

Yeast like fungi - non-branching filaments
e.g. Candida albicans

Filamentous fungi - branching filaments (mycelium)
e.g. Aspergillus, dermatophytes (ring worm)

19
Q

Characteristics of fungal infections?

A
  • Mycoses
  • Generally superficial
  • Affect skin and mucous membranes (internal organs rare)
  • Increasingly common in immunosuppression
  • Also after broad spectrum antibiotics as opportunistic infections
20
Q

Fungal treatment?

A

Avoidance and good hygiene component of effective treatment

Cell wall synthesis inhibitors

  • POLYENES
  • IMIDAZOLE
  • TRIAZOLES
  • TERBINAFINE

Nucleic acid synthesis inhibitors
- FLUCYTOSINE

Mitotic spindle
- GRISEOFULVIN

21
Q

How does cell wall synthesis occur in fungi?

A

Squalene —> Lansosterol (squalene epoxidase)

Lansosterol –> Ergosterol (lansosterol demethylase)
Lansosterol also –> Cholesterol

22
Q

What are polyenes? How do they work?

A

AMPHOTERICIN, NYSTATIN

Generates pores in cell wall (binds to the ergosterol?)- loss of ions

23
Q

Polyene details?

A

Side effects: few, used topically
-some GI upset internally, nephrotoxicity

Mutation - cell wall synthesis even without ergosterol
- Resistance is rare, seen in immunocompromised

  • Neither absorbed orally, given for oral and perioral infection, local application
24
Q

Polyene uses?

A

Amphotericin: IV used for systemic fungal infection, most fungi and yeasts - C. albicans

Nystatin: C. albicans infection of skin and mucous membranes, oesophageal and intestinal candidiasis

25
Q

How do imidazoles work? Uses/info?

A

Inhibit lansosterol demethylase

Lead to growth arrest - fluidity of cell wall increases, cell permeability increases

Ketoconazole can also block adrenal gland hormone steroid formation

Enzyme (lanosterol 14a-demethylase) is P450 like
Miconazole - possible interactions

Local treatment of vaginal candidiasis, dermatophyte infections

Resistance rare except in long term use in HIV due to changes in enzyme target or increases pumping out of cell

26
Q

What are imidazoles?

A

CLOTRIMAZOLE
MICONAZOLE
KETOCONAZOLE

27
Q

What are the uses of each imidazole?

A

Clotrimazole

  • vaginal candidiasis
  • ring worm

Miconazole

  • locally for oral infections
  • intestinal infections
  • (possible drug interactions)

Ketoconazole

  • best oral absorption
  • fatal hepatotoxicity
  • systemic mycoses
  • vulval candiasis
28
Q

What are triazoles?

A

FLUCONAZOLE

- well absorbed orally
- CSF penetration
- candida
- cryptococcus

ITRACONAZOLE

  • mucocutaneous candidiasis
  • dermatophytes
  • used with caution in those at risk of heart failure
  • contraindicated with calcium channel blockers - increased negative inotropic effect

VORICONAZOLE

  • wide spectrum
  • life threatening
  • aspergillosis

Similar spectrum to imidazoles

29
Q

How does terbinafine work? Uses/effects?

A

Inhibits squalene epoxidase

  • Membrane disruption and death
  • Toxic levels of squalene build up

Active against dermatophyte (ringworm) of the nail
- Can exacerbate sub-acute cutaneous lupus

30
Q

What is a fungal nucleic acid inhibitor? How does it work? Info?

A

Flucytosine

  • Base analogue, gets converted to flurouracil (by cytosine deaminase) and tries to get incorporated into viral DNA/blocks process

Resistance occurs readily through mutation or excessive production of uracil to compete

Only used in combination with amphotericin or fluconazole

31
Q

What is a microtubule antifungal?

A

Griseofulvin

  • Polymerised microtubules - against dermatophytes
  • Keratin precursor cells in skin and hair (keratinocytes)
  • Long duration of therapy as keratin/Gris complex has to enter skin/nail before coming into contact with fungus

GI (12 decks)

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