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Infectous Disease > Dr. Roane Antimycobacterials EXAM 3 > Flashcards

Dr. Roane Antimycobacterials EXAM 3 Flashcards

1
Q

What is tuberculosis known for?

A

White plague (paleness of patients), consumption (pt lose weight)

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2
Q

Synonym for Hansens disease

A

Leprosy

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3
Q

Which patient population is associated with Mycobacterium Avium/intracellulare?

A

Immunocompromised patients

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4
Q

What are the first-line drugs for Tuberculosis?

A

-Ethambutol
-Isoniazid
-Pyranizamide
-Rifampin/Rifapentine
-Streptomycin (aminoglycoside - only injectable)

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5
Q

What does Rifampin, Rifabutin, Rifapentine have in common?

A

Similar structure

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6
Q

Which diseases can be treated with Rifampin?

A

-Tuberculosis
-Leprosy

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7
Q

Is Tuberculosis transmissible in latent patients?

A

No, but w/o treatment they may develop the disease at some point in their life

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8
Q

What prevents the TB bacteria from spreading within the alveola tissue?

A

Granuloma contains of macrophages and other immune cells
-> When the Granuloma breaks open the TB bacteria multiplies and causes the disease

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9
Q

Where in the body are TB bacteria found?

A

-In the lungs: pulmonary

-other parts of the body (via the bloodstream): Extrapulmonary

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10
Q

Why is Mycobacterium tuberculosis hard to treat?

A

-mycolic acid (fatty acid, waxy) on the cell wall: less susceptible to antibiotics
-slow growing
-Resistance may occur -> more than one drug is required

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11
Q

What are the important drug targets for Mycobacteria tuberculosis?

A

-Synthesis of Mycolic acid (fatty acid, waxy) on the outer cell wall

-Synthesis of the arabinogalactan (sugar-chain)

-Inhibition of protein synthesis

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12
Q

How to test for tuberculosis?

A

-Mantoux test (skin test)
-A positive test means that the body has produced antibodies against tuberculosis (have been exposed to the bacteria; doesn’t mean you have the disease!

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13
Q

How does the tuberculosis bacteria get to the brain?

A

Through lymphatics

-can infect any tissue in the body

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14
Q

What does Granuloma look like on the tissues?

A

-Caesation: “cheese”-like tissue

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15
Q

What is the recommended treatment for latent TB infections?

A

changed recently from long-term Monotherapy of Isoniazid to a short-course regimen

-Isoniazid + Rifapentine (3mo, 1xweekly)
-Rifampin (4mo, daily)
-Isoniazid - Rifampin (3mo, daily)

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16
Q

What does TDR or XDR mean?

A

MDR: Multi-drug-resistant TB
TDR: Totally-drug-resistant tuberculosis
XDR: broadly drug-resistant TB

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17
Q

How many drugs are required to treat TB?

A

-At least 2 bacteriocidal drugs
-usually Isoniazid and Rifampin
-compliance is an issue

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18
Q

MOA of Isoniazid

A

-Inhibits bacterial enzymes
-The exact cidal MOA is unknown, more cidal when the bacteria is rapidly dividing
-pro-drug -> that is activated by bacterial enzymes -free radical is formed -> formation of an adduct -> inhibits mycolic acid

-disrupts the synthesis of mycolic acid (cell wall)

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19
Q

Form of Resistance of Tuberculosis

A

-Failure to activate the pro-drug
-Neutralize active compound (catches free radicals and prevents its effect?)

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20
Q

Which patient should be treated with caution when INH is used?

A

-Patients with liver disease

-INH itself also damages the liver

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21
Q

Adverse effects of Isoniazid

A

-Hepatitis
->increases with age and rifampin
-> No alcohol allowed
-> Threshold for acetaminophen toxicity is lower

-Peripheral neuritis (tingling - corrected by pyridoxine V6 supplement)
-other neurological effects, rash, fever

22
Q

What is a major route of Metabolism of INH?

A

Hepatic acetylation
-Slow acetylators are common, more common
in Mediterainean peoples

23
Q

What part of the population is vulnerable to INH use?

A

-Hispanic, African-American

24
Q

How can the adverse effect of peripheral neuritis (pins and needle tingling) be treated?

A

pyridoxine V6 supplement (similar structure)

25
Q

Which enzyme is inhibited by Isoniazide and what is the effect?

A

-Monooxidase
-anti-depressive effect

26
Q

Which INH-relative drug led to the discovery of Isocarboxazid?

A

-Iproniazid

-Isocarboxazid (MOA inhibitor treating depression)

27
Q

Which disease is known to be treated with Rifampin?

A

-Leprosy

-also: May treat mycobacterium avium-intracellulare, seen in AIDS patients

28
Q

MOA of Rifampin

A

Blocks prokaryotic DNA-dependent RNA
polymerase

29
Q

Where is Rifampin derived from?

A

-Soil Streptomyces

-belongs to the family of rifamycins (rifapentine, rifabutin and rifaximin)

30
Q

Mechanism of Resistance of the Bacteria against Rifampin

A

Mutations -> lowering of the affinity

-Not All or one, varies in affinity for the target

31
Q

Pharmacokinetics and side effects of Rifampin

A

-Penetrates tissues well
-Active orally
-Enterohepatic circulation
-Major p450 induction
-Urine, feces, tears, and sweat are colored orange-red

32
Q

What is a characteristic of rifampin’s metabolism?

A

It accelerates its own metabolism by inducing CYP450, as well as the metabolism of other drugs

-dose may have to be increased??
does CYP450 metabolism lead to more metabolites, hence more side effects??

-patients are often concerned about the efficacy of oral contraceptives when taking Rifampin

33
Q

What are the side effects of Rifampin?

A

-Fever, rash, N/V, liver damage
-Caution in patients with liver problems, alcoholics, elderly

34
Q

How does Pyrazinamide (PZA) work in the body?

A

-orally synthetic agent
-needs to be activated by the bacteria -> converted into pyrazonic acid with bacterial pyrazinamidase

-resistant bacteria lack pyrazinamidase

35
Q

What can be caused by the intake of PZA, INH, and Rifampin?

A

-liver dysfunction in 1-5% of patients
-gout (elevation of uric acid)

36
Q

How does Ethambutol work?

A

-orally active
-bacteriostatic
-inhibits arabinogalactans synthesis in the cell wall
-no resistance when used in Combination

37
Q

What are the side effects of Ethambutol?

A

-Optic neuritis (eye pain)
-Blurred vision
-Loss of red/green color discrimination

38
Q

Other drugs to treat Mycobacteria

A

-Streptomycin and other Aminoglycosides
-Capreomycin (a cyclic peptide)
-Macrolides (azithromycin)
-Fluoroquinolones (ciprofloxacin or others)

39
Q

Which anti-TB drug showed promising results when tested against MDR tuberculosis strains in a study?

A

-Tebepenem, oral carbapenem

-alone: MIC range of 0.125 to 8 μg/ml
-with clavulanate: 2 μg/ml or less

40
Q

Which drugs are recommended by a recent protocol for patients with a low bacterial count?

A

Rifapentine and Moxifloxacin

41
Q

Which drug is the first new anti TB drug in 40 years?

A

Betaquiline (Sirturo)
-MOA: inhibts mycobacterial ATP synthetase
-T1/2= about 55 days

42
Q

Which drug would lower the plasma level of Betaquiline due to drug interaction with CYP3A4?

A

Rifampin: CYP3A4-inducer

decrease Betaquiline leves by 50%

43
Q

Which drug would increase the plasma level of Betaquiline due to drug interaction with CYP3A4?

A

Ketoconazole: CYP-inhibitor

increase Betaquiline leves by 25%

44
Q

What is in the Black Box Warning of Betaquiline?

A

prolonged QT interval
-> Also for FQ and clofazamine

45
Q

What is the new drug Pretomanid used for?

A
  • txt of MDR-TB in combination with Linezolid and betaquiline

-Pretomanid inhibits mycolic acid synthesis
-Betaquiline inhibits bac. ATP synthetase
-Linezolid inhibits protein synthesis at the
ribosome

46
Q

What is BPaL referred to?

A

combination of Pretomanid, betaquiline, and Linezolid

47
Q

What is Leprosy?

A

-not highly contagious infection of M. leprae
-multi-drug therapy: 6-24 months
-Hansen’s Disease

48
Q

Which drugs are used to treat Leprosy?

A

-Dapsone (sulfonamide-like PABA-antagonist)
-Clofazimine
-Rifampin

-in combination for 6-24 months

49
Q

Side effect of Dapsone

A

-hemolytic anemia (red blood cell die), especially in patients with G6P-DH deficiency

-G6P-DH is involved in making ribose sugars and NADPH

50
Q

Side effect of Clofazimine

A

-phenazine dye, produces toxic free radical that inhibits DNA template function

-dyes patient to reddish-brown
(Rifampin colors fluids red)

51
Q

What is the consequence of Leprosy?

A

Sensory nerve damage -> patients can’t feel injuries -> infection -> Lost body parts

Infectous Disease (29 decks)

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