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4152 rehash > clw 6 > Flashcards

clw 6 Flashcards

tb, aki, nutrition, seizure, med chem

1
Q

what to check for TB tx initiation

A
  1. baseline liver enzymes
  2. (ethambutol) visual acuity, colour vision
  3. weight each visit
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2
Q

how are TB drugs dosed

A

by weight

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3
Q

first line TB tx drugs

A

rifampicin, isoniazid, pyrazinamide, ethambutol, streptomycin

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4
Q

common side effects of tb drugs

A

cutaneous rxn
photosensitivity
(PRI) gi s/e -> take after food

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5
Q

rifampicin metabolism

A

hepatic (monitor liver fx), cyp potent inducer

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6
Q

main ae associated with rifampicin

A

thrombocytopenia (feed mothers and neonates with VitK), SJS/TEN, flu-like syndrome

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7
Q

side effect of rifampicin to alert patients

A

ORANGE discoloration of bodily fluids eg. tears, sweat, urine

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8
Q

what to monitor for rifampicin

A

Renal fx - Rifampicin can cause acute renal failure

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9
Q

isoniazid metabolism

A

hepatic, N-acetyltransferase. kidney inactive metabolites excretion

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10
Q

isoniazid polymorphism

A

acetylation rate is related to genetic polymorphisms. chinese present rapid acetylator phenotype unlike indians

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11
Q

why can isoniazid exhibit hepatic toxicity?

A

toxic metabolite, hydrazine (not acetyl hydrazine)

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12
Q

isoniazid in pregnant patients / at risk of peripheral neuropathy give what

A

pyridoxine (vb6) for CNS function

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13
Q

avoid isoniazid with

A

carbs, tyramine, histamine

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14
Q

isoniazid inhibitor of

A

p450

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15
Q

main ae of isoniazid

A

peripheral neuropathy

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16
Q

importance of pyrazinamide

A

eliminates persistent bacilli responsible for relapse

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17
Q

which tb drugs can penetrate csf well

A

isoniazid, pyrazinamide

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18
Q

is pyrazinamide hepatotoxic

A

yes, avoid in patients with ALD

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19
Q

gout pts should be careful of pyrazinamide / ethambutol because

A

can lead to Increased uric acid levels

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20
Q

need adjust pyrazinamide / ethambutol for kidney pt?

A

yes, metabolites can accumulate. decrease dose

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21
Q

ethambutol ae

A

visual toxicity (esp kidney failure, elderly tx>2m)
gout

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22
Q

avoid ethambutol with

A

antacids, at least 2h

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23
Q

what can streptomycin replace

A

ethambutol

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24
Q

ae of streptomycin

A

ototoxicity, neuro, kidney toxicity

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25
Q

how to know if pt is cured of tb

A

negative sputum culture or smear in last month of tx and on at least one previous occasion

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26
Q

when patient has AKI and tb, what to remember to do?

A

adjust the tb dose according to the improving/worsening crcl

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27
Q

do hcps need to report tb

A

yes, to moh under infectious disease act

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28
Q

counselling points for tb drugs

A
  • reinforce importance of compliance to medication to eradicate bacteria
  • take after a light meal to reduce GI discomfort for PRI meds
  • space antacids 2h apart
  • cannot take concomitantly with tyramine and histamine-rich foods
  • pyridoxine helps to prevent peripheral neuropathy
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29
Q

how to monitor effectiveness of tb treatment

A

CXR and clinical sample of smear after intensive phase (ie 2m)

30
Q

how should airflow be for TB in hospital

A
  • In airborne infection isolation room with special air handling & ventilation system
  • Negative room pressure as compared to env: Unidirectional inward airflow frm the env to room → prevent contaminated air from pt’s room from flowing into env
31
Q

do tb patients need to minimise contact with their household

A

nope, already exposed

32
Q

non pharm for tb

A
  • cough etiquette
  • home should be well-ventilated
  • after 2 weeks of tx, do not need to avoid others
  • avoid allowing non-household contacts to visit
33
Q

labs for aki

A

accumulation of waste products (urea and Cr)

34
Q

drugs causing aki

A

NSAIDs
ACEi, ARB
Contrast media
Antimicrobials
(aminoglycosides,
amphotericin B, antivirals)
Chemotherapy

35
Q

prerenal aki what is it

A
  • sudden and severe drop in bp (shock)
  • severe illness causing interruption of blood flow to kidneys
36
Q

causes of prerenal aki

A
  • volume depletion
    (haemorrhage, overdiuresis, vomiting, diarrhoea)
    decreased “effective” volume due to cirrhosis
  • heart failure
  • acei/nsaid
37
Q

prerenal aki urine type

A

Urine is highly concentrated (high SG) and low in Na (FeNa < 1%)

38
Q

what to avoid in pre renal aki

A

use of diuretics: can reduce circulating volume excessively and add further insult, worsening aki

39
Q

what is intrinsic aki

A

direct damage to kidneys due to drugs, inflammation, reduced blood supply

40
Q

intrinsic aki causes

A

Acute Tubular Necrosis (ATN)

nephrotoxins (AG, contrast dyes, amphotericin B)
ischemia
penicillins, cipro, sulfonamides

41
Q

what is postrenal aki

A

obstruction of urine flow due to enlarged prostate, kidney stones

42
Q

GOT of AKI

A
  • Minimize or remove insult to kidney
  • Reduce extrarenal complications
  • Restore patient’s renal function to pre-AKI baseline
43
Q

how do NSAIDs and ACEi cause AKI

A

NSAID inhibits prostaglandin, cause afferent to constrict, inhibiting blood flow into the glomerulus

ACEi inhibits ag2, results in loss of constriction of efferent, intraglomerulus pressure drops

reduced pressure causes reduced urine formation

44
Q

four phases of ATN

A

initiating, oliguric, diuretic, recovery

45
Q

managing AKI

A
  • diuretics for fluid management to prevent fluid accumulation
  • 2g of Na a day
  • managing electrolytes to prevent hyper K,Mg,P
46
Q

diagnosing AKI

A
  • Increase in SCr by ≥ 26.5 μmol/L within 48 h
  • Increase in SCr to ≥ 1.5x baseline, within 7 days
  • Urine vol < 0.5 ml/kg/h for ≥ 6h
47
Q

what kind of aki is most common in hospitalised patients

A

prerenal - decreased perfusion in kidneys

48
Q

seizure non pharm

A

keto diet
limit alcohol consumption
adequate sleep
manage stress

49
Q

drug inhibitor effects vs inducer effect

A

drug inhibition (3-4d) vs peak effect of inducer (up to 2w later)

50
Q

what is a carrier-linked prodrug

A

carries a pro-moiety which is subsequently hydrolysed to the active drug

51
Q

what is a bioprecursor prodrug

A

converted to active forms via oxidation or reduction, do not have promoieties

52
Q

properties of drugs with carrier linked prodrugs

A

physicochemical deficiencies that do not allow it to pass cross cellular barrier

53
Q

advantages of bioprecursors

A

achieves site specific targeting by taking advantage of enzymes at that location

54
Q

what kind of drugs are most likely to be converted to prodrugs

A
  1. low solubility, high permeability
  2. high solubility, low permeability
55
Q

aim of prodrugs

A
  • Improve solubility for parental and oral delivery
  • Improve passive permeability
  • Improve metabolic stability
  • Improve targeting and reduce side effects.
56
Q

succinate chemical formula

A

c4h404(2-)

57
Q

solubility of succinate due to

A

ionised terminal carboxylate

58
Q

why are succinate esters easy to hydrolyse

A

intramolecular catalysis easy

  • terminal carboxylate is nucleophilic
  • side chain sufficient length to allow intramolecular reaction
59
Q

what is the intestinal brush border rich with

A

membrane bound phosphatases to hydrolyse phosphate prodrug

60
Q

what is Pe (permeability coefficient)

A

rate at which a cpd transverses a lipid barrier by passive diffusion (ie lipophilicity of solute)

61
Q

adefovir/tenofivir (anti-hepatitis drugs) are activated by?

A

kinases - phosphorylated via introduction of two phosphate groups

62
Q

what is phase 1 metabolism

A

Phase I: Yields a polar, water-soluble, metabolite that is often still active. Many of the products in this phase can also become substrates for phase II.

Oxidation with cytochrome P450 (most common)
Reduction
Hydrolysis

63
Q

what is phase 2 metabolism

A

Phase II: Yields a large polar metabolite by adding endogenous hydrophilic groups to form water-soluble inactive compounds that can be excreted by the body.

Methylation
Glucuronidation (most common)
Acetylation
Sulfation
Conjugation with glutathione
Conjugation with amino acids (glycine, taurine, and glutamic acid)

64
Q

glycine chemical structure

A

NH₂‐CH₂‐COOH

65
Q

main enzymes for phase 1 rxn

A

oxidase, reductase, hydrolase

66
Q

what is amidase

A

catalyze the hydrolysis of an amide, leading to the formation of carboxylic acid and ammonia,

67
Q

main enzymes for phase 2 rxn

A

glutathione S-transferases,
N-acyltransferases,
N-acetyltransferases
sulfotransferase (S04)

68
Q

glutathione chem form

A

C10H17N3O6S

69
Q

acyl vs acetyl

A

An acetyl is a type of acyl group. An acyl group can have any R group attached to the carbonyl (C=O).
An acetyl has a methane group attached to the carbonyl.

70
Q

esterase

A

Esterases hydrolyze the compounds that contain ester, amide, and thioester bonds, which cause prodrug activation or detoxification.

71
Q

crcl calculate

A

CrCl mL/min (males) = (140 - age) x weight(kg) / 0.814 x serum creatinine (micromol/L), for females, multiply result by 0.85.

4152 rehash (9 decks)

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