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pr3151 > antiTB > Flashcards

antiTB Flashcards

1
Q

what are the characteristics of mycobacterium tuberculosis

A

slow growing, acid fast bacilli, aerobic

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2
Q

what is tuberculosis caused by

A

caused by mycobacterium tuberculosis

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3
Q

which group of patients are more susceptible to have active TB

A

immunocompromised, elderly, HIV positive

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4
Q

is it active TB during initial infection

A

no it stays dormant and has no symptoms (latent TB) and risk of progression to active TB highest in first two years after initial infection

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5
Q

what are the measures taken to combat TB in singapore

A

promotion of directly observed therapy (DOT), national treatment surveillance registry to monitor treatment progress and outcome for all TB patients, contact investigations

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6
Q

how do you clinically diagnose TB

A
  1. history of close contact
  2. risk factors
  3. clinical presentation
  4. physical exam findings using sputum
  5. chest x ray findings
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7
Q

what are the risk factors of TB

A

immune status (HIV, DM), living conditions, nutritional status, age

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8
Q

what is the clinical presentation of TB

A

fever, night sweats, hemoptysis, weight loss

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9
Q

what is the test done using sputum for diagnosis of TB

A

ziehl neelson stain for acid fast bacilli

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10
Q

what are the principles of TB treatment

A

different subpopulations have different metabolic activity for active TB, treatment should be prolonged to prevent transmission and ensure eradication else may cause relapse, avoid monotherapy to prevent drug resistance

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11
Q

what are the MOH guidelines for TB treatment

A
  1. assess baseline liver enzymes before initiating
  2. if to start of ethambutol, assess patient’s visual acuity and colour vision
  3. document patient’s weight at every visit and adjust dose accordingly
  4. patients with high risk of drug induced hepatitis must be closely monitored
  5. 6 month regimen
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12
Q

what does the 6 month regimen comprise of

A

2months intensive phase of daily rifampicin, isoniazid, pyrazinamide, ethambutol
4months continuous phase of daily or 3x/w rifampicin and isoniazid

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13
Q

what is the moa of rifampicin

A

inhibit gene transcription by blocking DNA dependent RNA polymerase and prevents mRNA and protein synthesis thus leading to cell death

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14
Q

what is the moa of isoniazid

A

prodrug that is activated by catalase peroxidase to form oxygen derived free radicals that inhibit formation of mycolic acids of bacterial cell wall thus leading to DNA damage and cell death

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15
Q

what is the moa of pyrazinamide

A

prodrug which is converted into its active form pyrazinoic acid by pyrazinamidase microbial enzyme which enters bacilli passively -> rich high conc in bacterial cytoplasm where there is accumulation of pyrazinoic acid that decreases intracellular pH to levels that inactivate critical pathways necessary for bacterial survival

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16
Q

what is the moa of ethambutol

A

inhibit arabinosyltransferase enzyme encoded by embB gene and interfere with polymerisation of arabinose to arabinogalactan which is principal polysaccharide of mycobacterium cell wall thus affect integrity and facilitate entry of lipophilic abx like rifampicin and levofloxacin

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17
Q

what class is streptomycin

A

aminoglycosides

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18
Q

what is the moa of aminoglycosides

A

bind to 30S ribosomal subunit -> distorts structure of ribosomes -> block formation of initiation complex -> cause misreading of codons as wrong amino acyl tRNAs bind to A site without matching the codon present in mRNA at that position -> translocation inhibited

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19
Q

which phases of bacilli does rifampicin kill

A

metabolically active and bacilli in stationary phase

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20
Q

what are the indications of rifampicin

A

active TB in combi with other antimycobacterials, latent TB, leprosy against mycobacterium leprae

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21
Q

what are the resistance of mechanisms to rifampicin

A

mutations in gene which encodes RNA polymerase beta chain

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22
Q

PK characteristics of rifampicin

A

oral, best taken on empty stomach

cns conc 10-20%, penetration increased in meningitis

hepatically metabolised 65% excreted in bile
no renal dose adjustments as not renally cleared, monitor liver function due to hepatotoxicity

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23
Q

what are the adverse effects of rifampicin

A
  1. cutaneous syndrome that is self limiting and can be managed by antihistamine therapy, can continue treatment (flushing and/or pruritis, redness and watering of eyes)
  2. flu like syndrome (fever, chills, malaise, headache and bone pain)
  3. respiratory syndrome (sob)
  4. thrombocytopenia, hemolytic anemia and acute renal failure (rare)
  5. orange discolouration of bodily fluids (tears, sweat, urine)
  6. hepatitis due to hepatotoxicity (but less than isoniazid and pyrazinamide)
  7. GI symptoms like N, abdominal discomfort, anorexia - administer after light meal or before bedtime
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24
Q

what is the pregnancy category of rifampicin

A

category C

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25
Q

what should be given to pregnant mothers taking rifampicin and why

A

vitamin K to prevent postpartum hemorrhage

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26
Q

what should be monitored if give rifampicin to breastfeeding mothers

A

infant for jaundice

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27
Q

what is the c/i for rifampicin

A

history of hypersensitivity to rifampicins

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28
Q

what are the drug interactions for rifampicin

A

rifampicin can induce certain cyp450 which increases metabolism of drugs that are partially or completely metabolised by cyp450 like warfarin, corticosteroids, hormonal contraceptives, HIV protease inhibitors

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29
Q

what type of bacilli does isoniazid have effect on

A

bactericidal effect on rapidly growing bacilli, limited effect on slow growing and intermediate growing bacilli

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30
Q

what are the indications of isoniazid

A
  1. active TB in combi with other antimycobacterials
  2. latent TB
  3. prophylaxis
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31
Q

what are the mechanisms of resistance for isoniazid

A
  1. mutations to catalase peroxidase enzyme
  2. mutations to regulatory genes involved in mycolic acid synthesis
32
Q

PK characteristics of isoniazid

A

oral, best taken on empty stomach

half life 1hr for fast phenotype, 2-5h for slow phenotype, good csf penetration

metabolised through acetylation in liver by N-acetyltransferase (acetylation rate related to genetic polymorphism)

inactive metabolites excreted by kidney
monitor liver function, no renal dose adjustments as not renal cleared

33
Q

what are the adverse effects of isoniazid

A
  1. peripheral neuropathy (pricking pain, paresthesia, burning sensation in hands and feet)
  2. hepatitis due to hepatotoxicity (risk increases with age, ROH use, concomitant use of other nephrotoxic agents)
  3. rarely - convulsions, toxic psychosis, hematologic reactions, lupus like syndrome, hypersensitivity
34
Q

what should be given if pregnant take isoniazid

A

pyridoxine

35
Q

what should be given if breastfeeding take isoniazid

A

child and mother take pyridoxine

36
Q

what pregnancy category is isoniazid

A

category c

37
Q

what should be monitored if breastfeeding take isoniazid

A

monitor baby for jaundice

38
Q

what are the metabolic pathways of isoniazid

A

N-acetyltransferase 2 pathway (NAT2): produces acetyl-hydrazine
amidase pathway: produces hydrazine

39
Q

is isoniazid and its metabolites hepatotoxic

A

isoniazid and acetyl-hydrazine is not hepatotoxic, hydrazine is hepatotoxic

40
Q

what are the food interactions of isoniazid

A

carbs can reduce absorption by 57%, avoid tyrosine and histamine rich foods as they block monoamine oxidase enzymes and histaminase which can result in flushing and headache

41
Q

what are the drug interactions of isoniazid

A

cyp450 inhbitor thus can increase plasma conc of anticonvulsants and anticoagulants, separate antacids and isoniazid by 2hrs as antacids increase gastric pH which can delay absorption of isoniazid

42
Q

what is pyridoxine

A

naturally occurring B6 that is converted into active form pyridoxal phosphate after being absorbed from GI tract and the cofactor is involved in many metabolic processes

43
Q

what is the role of pyridoxine

A

prevent pyridoxine deficiency which is essential for cns function and can prevent peripheral neuropathy

44
Q

what can taking pyridoxine with isoniazid help with

A

prevent peripheral neuropathy

45
Q

what are the similarities between pyrazinamide and isoniazid

A

structurally similar

46
Q

does the similarities of pyrazinamide and isoniazid cause cross resistance

A

no

47
Q

what type of mycobacterial is pyrazinamide most effective for

A

resistant mycobacterium that are responsible for relapse

48
Q

what benefit does pyrazinamide have

A

reduces therapy of RIP to 6 months

49
Q

what are the indications for pyrazinamide

A

active TB in combi with other antimycobacterials

50
Q

what are the mechanisms of resistance to pyrazinamide

A

mutations in the gene encoding for pyrazinamidase

51
Q

PK characteristics of pyrazinamide

A

oral, well absorbed

widely distributed, high cns penetration

metabolite eliminated by kidney, renal dose adjustments needed as metabolites can accumulate if kidney failure

52
Q

what are the adverse effects of pyrazinamide

A

GI (N,V), photosensitivity, hepatotoxicity, hyperuricemia and arthralgia, exanthema (widespread rash) and pruritus

53
Q

what is the pregnancy category of pyrazinamide and can it be used in preganacy

A

category C, safe to use

54
Q

can pyrazinamide be used in breastfeeding, what should be monitored

A

compatible, monitor for jaundice

55
Q

why does pyrazinamide cause hyperuricemia and arthralgia

A

active form pyrazinoic acid inhibits renal tubular secretion of uric acid which results in gout like symptoms

56
Q

what are the c/i for pyrazinamide

A

generally avoid in hepatic failure else, closely monitor and go for labs frequently

57
Q

what type of effect and what kind of bacteria is ethambutol effective for

A

bacteriostatic, rapidly growing bacilli

58
Q

what type of effect and what kind of bacteria is ethambutol effective for

A

bacteriostatic, rapidly growing bacilli

59
Q

what are the indications for ethambutol

A

active TB in combi with other antimycobacterials

60
Q

what are the mechanisms of resistance to ethambutol

A

mutations in embB gene

61
Q

PK characteristics of ethambutol

A

oral, 75-80% absorbed

does not pass through healthy meninges, can reach therapeutic levels in meningitis

25% metabolised in liver, 25% excreted unchanged in feces, 50% unchanged in urine
renal dose adjustments required in kidney failure as ethambutol and metabolites can accumulate but can use full dose if liver failure

62
Q

what are the adverse effects of ethambutol

A
  1. visual toxicity (decrease in visual acuity, red green colour blindness, blurring, central scotoma)
  2. hyperuricemia due to reduction in uric acid excretion by kidney (P>E)
63
Q

what are the factors that increases risk of central scotoma effects by ethambutol

A

elderly, kidney failure, treatment >2m

64
Q

what pregnancy category is ethambutol and can it be used

A

category C, safe to use

65
Q

can ethambutol be used when breastfeeding

A

yes

66
Q

what are the drug interactions of ethambutol

A

separate by 2h with antacids

67
Q

what are the indications for streptomycin

A

first line antiTB drug in SG, can be used to replace ethambutol in intensive phase

68
Q

PK characteristics of streptomycin

A

IM, poor csf penetration, excreted unchanged in urine

69
Q

what are the adverse effects of streptomycin

A

ototoxicity (vertigo and ataxia, tinnitus, hearing loss), nephrotoxicity, neurotoxicity

70
Q

what factors increases risk of ototoxicity if take streptomycin

A

age >40 years, risk incr with dose, can cause fetal ototoxicity

71
Q

what circumstances are drug resistant TB present in

A

patients who were previously treated, fail treatment, known contacts of patients with MDR TB, from countries with high prevalence like India, Philippines, South Africa, Russia

72
Q

what constitutes as a cure for TB

A

initially culture pos patient demonstrating neg sputum smear or culture in the last month of treatment and at least one prev ocassion

73
Q

what constitutes as a treatment failure for TB

A

pos sputum on or after 5m of treatment

74
Q

what is a good marker for relapse of TB

A

nonconversion of sputum culture at 2m

75
Q

what must medical professionals do in relation to TB cases

A

must report both new or relapsed TB incl suspected cases and their treatment outcomes to MOH

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