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Pharm Exam 5 > Antifungals and TB > Flashcards

Antifungals and TB Flashcards

1
Q

Steroid found in the cell membrane of fungi.

A

Ergosterol

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2
Q

Binds to ergosterol in the fungal cell membrane, creating pores to increase cell permeability and thus cause death.

A

Amphotericin MOA

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3
Q

Amphotericin mechanism of resistance.

A

The sterols (ergosterol) are altered in the membrane, so amphotericin cannot bind.

OR

There’s a decreased amount of sterols in the cell membrane.

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4
Q

Adverse reaction of Amphotericin

A

1) Kidney toxicity, causing the patient to waste K and Mg.
2) Idiosyncratic hypotension and arrhythmias.
3) Fever, chills, and rigors.

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5
Q

These antifungals bind to cyt P450 enzymes to inhibit 1,4-alpha demethylation of Lanosterol (fungal steroid found in cell membranes).

A

Azole antifungals

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6
Q

Adequate hydration may decrease the toxicity caused by this drug.

A

Amphotericin

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7
Q

Azole used for candida albicans.

A

Fluconazole

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8
Q

This antifungal has the least drug-drug interactions of all the azoles.

A

Fluconazole

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9
Q

Antifungal against Aspergillus (a fungus).

A

Voriconazole

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10
Q

Another azole antifungal.

A

Posaconazole

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11
Q

Need to be aware of this with all azole antifungals.

A

Drug-drug interactions!

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12
Q

Antifungal that’s part of the Echinocandin family.

A

Caspofungin

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13
Q

This antifungal inhibits beta 1,3-glucan.

A

Caspofungin

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14
Q

This antifungal works at a different site of action from the azoles and amphotericin.

A

Caspofungin

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15
Q

Also members of the Echinocandin family.

A

Micafungin

Anidulofungin

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16
Q

These bacteria have chains of mycolic acid (types of fatty acids).

A

Mycobacteria

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17
Q

Where does TB infection begin in the lungs?

A

Alveoli

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18
Q

Large or small TB droplets lodge in the alveoli?

A

Small

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19
Q

Why are the majority of TB bacilli destroyed or inhibited once inhaled?

A

Alveolar macrophages ingest them.

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20
Q

T/F: A small number of TB molecules multiply in the alveolar macrophages (intracellularly), and are released when the macrophages die.

A

TRUE

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21
Q

Immune responses soon develop to kill the bacilli.
Within how many weeks after infection does the immune system halt the multiplication of the tubercle bacilli, preventing further spread?

A

2-10 weeks

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22
Q

When is a person INFECTED with TB?

A

When their immune system tries to halt the multiplication of the tubercle bacilli.

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23
Q

What percent of people infected with TB will develop the disease?

A

10%

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24
Q

The TB infection is controlled by the immune system in what percent of people? They will not develop CLINICAL TB.

A

90%

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25
Q

What percent of the 10% infected that get the disease will develop it in the first two years?

A

5%

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26
Q

What percent of the 10% infected that get the disease will develop it over the remaining lifetime?

A

5%

27
Q

What is latent TB infection?

A

When you’re infected (have immune response against TB), but don’t have the disease.

28
Q

If you’re infected with TB, but don’t have the disease, can you spread TB?

A

No

29
Q

Total body burden of tuberculosis bacilli in LATENT TB infection.

A

Less than 10 ^4

30
Q

Drug used for latent TB infection.

A

Isoniazid

31
Q

How many organisms are in ACTIVE TB disease?

A

10^9-10^10

32
Q

Isoniazid MOA

A

Inhibits mycolic acid synthesis in the cell wall.

33
Q

Isoniazid/INH is what kind of drug?

A

Prodrug

34
Q

This enzyme metabolizes isoniazid to its active form.

A

Catalase/peroxidase enzyme (katG)

Cat activates the Ise;

Nat breaks down the Ise.

35
Q

Strains which cannot break down Isoniazid bc they have a defective catalase/peroxidase are __________ to Isoniazid.

A

resistant

36
Q

What metabolizes Isoniazid and where is it metabolized?

A

N-acetyl transferase; Liver

NAT breaks down ISE

37
Q

The rate of isoniazid acetylation is determined as what type of genetic trait?

A

Autosomal recessive.

38
Q

Does the rate of isoniazid acetylation alter therapy clinically?

A

No, just the weekly administration schedules

39
Q

Isoniazid adverse reactions.

A

1) Hepatitis

2) Neurotoxicity

40
Q

Peak hepatitis incidence when using Isoniazid.

A

First 4-8 weeks

Hepatic failure can occur, which then leads to death if you continue to take the drug.

41
Q

What percent of Isoniazid patients get elevated transaminases?

A

15%

42
Q

What causes neurotoxicity when using Isoniazid?

A

Increased pyridoxine excretion.

43
Q

Pyridoxine is what vitamin?

A

B6

44
Q

Concomitant administration of what vitamin is given when taking Isoniazid?

A

B6

45
Q

Clinical uses of Isoniazid

A

1) Treat latent TB (positive PPD, but no active disease).

2) Combo therapy for active TB at any stage.

46
Q

Rifampin MOA

A

Inhibits DNA dependent RNA polymerase of mycobacterial cells.

47
Q

Human enzyme is insensitive to the effects of this tuberculosis drug.

A

Rifampin

48
Q

Rifampin mechanism of resistance.

A

Alteration of DNA-dependent RNA polymerase (rpoB).

Occurs at about the same frequency as INH in the absence of drug 10^-6.

49
Q

Rifampin has excellent _____ absorption and wide distribution, including the __.

A

Oral; CNS

50
Q

How is Rifampin metabolized?

A

HEPATIC via cytochrome P450 (deacylation).

51
Q

This drug induces its own increased metabolism.

A

Rifampin

52
Q

Rifampin adverse reactions.

A

Hepatotoxicity is manifest as cholestatic changes (increase alkaline phosphatase, increased bilirubin), but can also be necroinflammatory with elevated transaminases.

INH and rifampin may potentiate hepatotoxicity of the other agent.

53
Q

Marked drug interaction secondary to the induction of CYT P450 occurs with this drug.

A

Rifampin

54
Q

Increased metabolism of coumarin, oral contraceptives, and phenytoin may occur with this drug.

A

Rifampin

55
Q

Interaction with verapamil causes marked reduction in verapamil levels when using this drug.

A

Rifampin

56
Q

What do elevated transaminases in the blood indicate?

A

The liver cells are inflammed or damaged, and they leak liver enzymes, like transaminases.

57
Q

Pyrazinimide MOA

A

Used to treat tuberculosis, and inhibits fatty acid synthesis.

58
Q

M. tuberculosis has this enzyme, which activates pyrazinamide to its active form (pyrazinoic acid) at acidic pH.

A

Pyrazinamidase.

59
Q

Pyrazinamide mechanism of resistance?

A

Unknown

60
Q

Pyrazinamide adverse reaction.

A

Hepatotoxicity

Gout

61
Q

Ethambutol MOA

A

An antimetabolite for tuberculosis, affecting RNA synthesis.

62
Q

Ethambutol Mechanism of Resistance

A

Unknown

63
Q

Most dangerous adverse reaction of ethambutol.

A

Retrobulbar neuritis.

64
Q

How does retrobulbar neuritis usually develop?

A

Decreased acuity and change in color vision (yellow and green).

Associated with high doses; peripheral neuropathy can also occur.

Pharm Exam 5 (8 decks)

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