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4152 rehash > clw 6 > Flashcards

clw 6 Flashcards

tb, aki, nutrition, seizure, med chem (71 cards)

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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
how to know if pt is cured of tb
negative sputum culture or smear in last month of tx and on at least one previous occasion
26
when patient has AKI and tb, what to remember to do?
adjust the tb dose according to the improving/worsening crcl
27
do hcps need to report tb
yes, to moh under infectious disease act
28
counselling points for tb drugs
- 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
29
how to monitor effectiveness of tb treatment
CXR and clinical sample of smear after intensive phase (ie 2m)
30
how should airflow be for TB in hospital
- 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
do tb patients need to minimise contact with their household
nope, already exposed
32
non pharm for tb
- 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
labs for aki
accumulation of waste products (urea and Cr)
34
drugs causing aki
NSAIDs ACEi, ARB Contrast media Antimicrobials (aminoglycosides, amphotericin B, antivirals) Chemotherapy
35
prerenal aki what is it
- sudden and severe drop in bp (shock) - severe illness causing interruption of blood flow to kidneys
36
causes of prerenal aki
- volume depletion (haemorrhage, overdiuresis, vomiting, diarrhoea) decreased "effective" volume due to cirrhosis - heart failure - acei/nsaid
37
prerenal aki urine type
Urine is highly concentrated (high SG) and low in Na (FeNa < 1%)
38
what to avoid in pre renal aki
use of diuretics: can reduce circulating volume excessively and add further insult, worsening aki
39
what is intrinsic aki
direct damage to kidneys due to drugs, inflammation, reduced blood supply
40
intrinsic aki causes
Acute Tubular Necrosis (ATN) nephrotoxins (AG, contrast dyes, amphotericin B) ischemia penicillins, cipro, sulfonamides
41
what is postrenal aki
obstruction of urine flow due to enlarged prostate, kidney stones
42
GOT of AKI
- Minimize or remove insult to kidney - Reduce extrarenal complications - Restore patient’s renal function to pre-AKI baseline
43
how do NSAIDs and ACEi cause AKI
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
four phases of ATN
initiating, oliguric, diuretic, recovery
45
managing AKI
- diuretics for fluid management to prevent fluid accumulation - 2g of Na a day - managing electrolytes to prevent hyper K,Mg,P
46
diagnosing AKI
- 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
what kind of aki is most common in hospitalised patients
prerenal - decreased perfusion in kidneys
48
seizure non pharm
keto diet limit alcohol consumption adequate sleep manage stress
49
drug inhibitor effects vs inducer effect
drug inhibition (3-4d) vs peak effect of inducer (up to 2w later)
50
what is a carrier-linked prodrug
carries a pro-moiety which is subsequently hydrolysed to the active drug
51
what is a bioprecursor prodrug
converted to active forms via oxidation or reduction, do not have promoieties
52
properties of drugs with carrier linked prodrugs
physicochemical deficiencies that do not allow it to pass cross cellular barrier
53
advantages of bioprecursors
achieves site specific targeting by taking advantage of enzymes at that location
54
what kind of drugs are most likely to be converted to prodrugs
1. low solubility, high permeability 2. high solubility, low permeability
55
aim of prodrugs
- Improve solubility for parental and oral delivery - Improve passive permeability - Improve metabolic stability - Improve targeting and reduce side effects.
56
succinate chemical formula
c4h404(2-)
57
solubility of succinate due to
ionised terminal carboxylate
58
why are succinate esters easy to hydrolyse
intramolecular catalysis easy - terminal carboxylate is nucleophilic - side chain sufficient length to allow intramolecular reaction
59
what is the intestinal brush border rich with
membrane bound phosphatases to hydrolyse phosphate prodrug
60
what is Pe (permeability coefficient)
rate at which a cpd transverses a lipid barrier by passive diffusion (ie lipophilicity of solute)
61
adefovir/tenofivir (anti-hepatitis drugs) are activated by?
kinases - phosphorylated via introduction of two phosphate groups
62
what is phase 1 metabolism
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
what is phase 2 metabolism
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
glycine chemical structure
NH₂‐CH₂‐COOH
65
main enzymes for phase 1 rxn
oxidase, reductase, hydrolase
66
what is amidase
catalyze the hydrolysis of an amide, leading to the formation of carboxylic acid and ammonia,
67
main enzymes for phase 2 rxn
glutathione S-transferases, N-acyltransferases, N-acetyltransferases sulfotransferase (S04)
68
glutathione chem form
C10H17N3O6S
69
acyl vs acetyl
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
esterase
Esterases hydrolyze the compounds that contain ester, amide, and thioester bonds, which cause prodrug activation or detoxification.
71
crcl calculate
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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