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TAS > pharmacology > Flashcards

pharmacology Flashcards

1
Q

Describe Volume distribution

A

apparent volume into which the drug would have to distribute to achieve the measured concentration. The higher the VD the higher the loading dose of medication needed.

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2
Q

What is the formula for volume distribution

A

Amount of medication in mg/ plasma concentration of given medication

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3
Q

Define clearance

A

the ability of the body to remove a drug from the plasma or blood and is the sum of drug clearances of each organ (usually kidney + liver)

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4
Q

What formula is appropriate for calculating dosage of drugs given intravenously ?

A

(target concentration (mg/L)) x (clearance (L/hr/kg))

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5
Q

How does volume distribution relate to Neonates?

A

Neonates have higher body water, therefore they have a lower Vd for fat-soluble drugs and higher Vd for water-soluble drugs

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6
Q

Grapefruit juice contains potent inhibitors of what?

A

Cytochrome P450

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7
Q

Grapefruit juice increases the bioavailability of what medications?

A

Midazolam Carbamazepine Cyclosporin

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8
Q

What antibiotic groups require therapeutic drug monitoring and why?

A

Theophylline
Aminoglycosides -For gram negative
Glycopeptides- for gram positive
Both can cause oto/nephro toxicity

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9
Q

What is MOA of aminoglycosides?

A

bactericidal and works by irre­versibly binding the 30S subunit of the bacterial ribos­ome, and interfering with bacterial protein synthesis.

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10
Q

What is MOA of Glycopeptides?

A

Affect cell-wall synthesisi in gram positive bacteria. They bind to the end of the pentapeptide chains that are part of the growing cell wall structure. This inhibits the transglycosylation reaction and prevents incorporation.

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11
Q

Describe Red Man syndrome

A

Caused by Vanc. Flushing and erythematous skin usually of the upper body and face. Caused by a non-specific mast cell degranulation. Avoided with a slow infusion rate.

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12
Q

What are the phase 1 drug metabolism pathways?

A

OXIDATION hydrolysis reduction hydration

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13
Q

What are the phase 2 drug metabolism pathways?

A

Glucuronidation Methylation Sulfation Acetylation

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14
Q

What medications are metabolised by CYP3A4?

A

Carbamazepine Diazepam Erythromycin Fentanyl Midazolam Nifedipine Ondansetron Rifampicin

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15
Q

What medications are metabolised by CYP2D6

A

Amitriptyline Codeine Selective serotonin reuptake inhibitors

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16
Q

What medications are metabolised by glucuronidation?

A

Paracetamol Morphine

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17
Q

What medications are metabolised by CYP1A2?

A

Caffeine Theophylline

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18
Q

What medications are metabolised by CYP2C9?

A

Phenytoin Ibuprofen

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19
Q

What medications are metabolised by sulfation?

A

Paracetamol

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20
Q

What common group of enzymes control oxidation.

A

CYP450 phase 1 baby

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21
Q

How does Cystic fibrosis affect drug clearance?

A

Increases it. Will need higher doses of medication
Think Tobromycin

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22
Q

In what population of ceftriaxone prohibited?

A

premature infants
full-term infants with jaundice,
any child recieving calcium

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23
Q

Viral illness + what type of medication causes Reye’s syndrome?

A

Salicylates (Aspirin)

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24
Q

What is MOA of paracetamol?

A

Inhibition of COX enzymes prevents the metabolism of arachidonic acid to prostaglandins. In the central nervous system, inhibition of COX enzymes reduces concentrations of prostaglandin E2, which lowers the hypothalamic set-point to reduce fever, and activation of descending inhibitory serotonergic pathways to produce analgesia.

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25
Q

Where is paracetamol not effectively absorbed?

A

Gastric mucosa
Therefore give rectally/ IV to kids with poor gastric emptying.

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26
Q

How is paracetamol metabolised?

A

Glucuronide conjugation (accounting for 40–60% of a dose in adults), sulfate conjugation (20–40%), and N-hydroxylation via the cytochrome P450 isozyme CYP2E1 (<15%). This latter mecha­nism produces a highly toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI), which requires conjugation with glutathione to form a non-toxic metabolite that can be excreted.

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27
Q

What is mechanism of paracetamol overdose?

A

glucuronidation and sulfation pathways become saturated. More CYP2E1 metabolism, glutathione stores become depleted, resulting in excess quantities of NAPQI resulting in hepatotox­icity.

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28
Q

What is the treatment for paracetamol overdose?

A

N-acetylcysteine
increases the glutathione stores so that the buildup of NAPQI can be conjugated and excreted.

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29
Q

how do NSAIDs treat inflammation?

A

Inhibit cyclo-oxygenase, the enzyme that transforms arachidonic acid to prostaglandins and thromboxanes

30
Q

How do NSAIDs treat fever?

A

Inhibition of prostaglandin E2 (PGE2) synthesis, which normally triggers the hypothalamus to increase body temperature during inflammation.

31
Q

How is morphine metabolised?

A

Morphine is extensively metabolized by the gut wall and the liver. Glucuronidation by the liver enzyme UGT2B7 converts morphine to morphine-3-glucuronide (M3G) (70%) and morphine-6-glucuronide (M6G) (10%).

32
Q

What are the 3 types of antibiotics?

A

Cell wall inhibitors Protein synthesis inhibitors Nuclei synthesis inhibitors

33
Q

What are the classes and MOA of cell wall inhibitors?

A

β-Lactams are bactericidal and act by binding to enzymes known as penicillin binding proteins (PBPs) and inhibiting cell wall synthesis.

Glycopeptides -bind to the end of the pentapeptide chains that are part of the growing cell wall structure. This inhibits the transglycosylation reaction and prevents incorporation.

34
Q

What are the classes and MOA of protein synthesis inhibitors?

A

Aminoglycosides - bactericidal and works by irre­versibly binding the 30S subunit of the bacterial ribos­ome.

Chloramphenicol - blocks the action of peptidyl transferase thereby preventing peptide bond synthesis and subsequently inhibiting bacterial protein synthesis (binds to 50S subunit)

Macrolides - primarily bacteriostatic and act by binding to the 50S subunit of the ribosomes.

35
Q

What are the classes and MOA of Nucleic syntheis inhibitors?

A

Sulphonamides - bacteriostatic and act as competitive inhibitors of the enzyme dihydropteroate synthetase (DHPS) which is involved in bacterial folate synthesis.
Quinolone - inhibiting the activity of DNA gyrase and therefore preventing supercoiling of the bacterial chromosome. This prevents the bacterial cell from putting DNA into its cell

36
Q

Give an example of Quinolone and what is it used for?

A

Ciprofloxacin
Pseudomonal infections in children with CF or complicated UTIs

37
Q

Give an example of Macrolides and what is it used for?

A

clari/azithro/erythro -mycinatypical respiratory tract infections

38
Q

Give an example of sulphonamides and what is it used for?

A

Trimethoprim Gram negative e.coli in UTIs

39
Q

Give an example of Glycopeptides and what is it used for?

A

Vancomycin and teicoplanin
Gram positive staphylococci. MRSA/ c.diff

40
Q

Give an example of Aminoglycosides and what is it used for?

A

Gentamycin + tobramycin
Severe gram negative infections.
Gent synergises with β-lactams to treat group B strep hence benpen + gent.

41
Q

What are the types of β-lactam antibiotics?

A

Penicillins
Co-amoxiclav
2nd + 3rd generation cepholasporins

42
Q

Give an example of 2nd generation cephalosporins and what is it used for?

A

CefUROxime
Haemophilus influenzae or where there is resitance/ severity.

43
Q

Give an example of 3rd generation cephalosporins and what is it used for?

A

CefoTAXime, CefTRIaxoneGram-negative infections, such as Neisseria meningitides.

44
Q

What class of antibiotic is ceftazidime and what does it have good action against?

A

third-generation cephalosporin
Good against pseudomonas

45
Q

What is acetazolomide used for?

A

reducing ICP

46
Q

What is acetazolomide MOA?

A

carbonic anhydrase inhibitor. reduces hydrogen excretion in RENAL TUBULES and therefore more sodium, bicarbonate, potassium and water is excreted

47
Q

What are common complications of acetazolmaide?

A

Acute interstitial nephritis
Metabolic acidosis 2ndry to bicarb excretion

48
Q

What antiepiletics work on voltage gated sodium channels ?

A

Carbamazepine, phenytoin, lamotrigine

49
Q

What antiepileptics work on calcium channels?

A

lamotrigine

50
Q

What antiepileptics work on GABA systems?

A

phenobarbitone, vigabatrin, diazepam, lorazepam

51
Q

What is MOA of sodium valproate?

A

It is known to act at voltage-dependent sodium channels, as well as increasing gamma-aminobutyric acid (GABA). It is also thought to act against certain calcium channels

52
Q

What is MOA of topiramate?

A

Blocks voltage-dependent sodium channels, promotes activity of GABA receptors, and antagonizes an NMDA–glutamate receptor.

53
Q

What is common side effect of topiramate?

A

weightloss

54
Q

What anti epileptic do you NOT give to women of child bearing age?

A

Sodium valproate

55
Q

What do you tell women re contraception if they’re on lamotrigine

A

oestrogen contraceptives will reduce effectiveness of lamotrigine
progesterone is fine

56
Q

What do you tell women re contraception if they’re on enzyme inducing antiepileptic? + what are common enzyme inducing epileptics?

A

Contraceptives less effective.
carbamazepine, phenytoin, topiramate.
medroxyprogesterone acetate injections or an intrauterine method unaffected

57
Q

acute tubule–interstitial nephritis can be caused by what groups of medicines?

A

S Sulfonamides
M Methicillin (a beta-lactam)
A Amipicillin (a beta-lactam)
R Rifampicin
T Thiazides
C Cimetidine
A Allopurinol
N NSAIDs (non-steroidal anti-inflammatory drugs)

58
Q

What is MOA of hyoscine butylbromide?

A

blocks muscarinic receptors

59
Q

What is mannitol used for and what’s it’s MOA?

A

Management of cerebral oedema
works in proximal renal tubules to promote osmosis

60
Q

What are the classes of antifungals?

A

polyenes, azoles and ednichocandins

61
Q

Describe polyenes + give examples

A

bind to fungal cell wall. broad spectrum
nystatin and amphoteracin

62
Q

Describe Azoles and give examples

A

Prevent ergosterol production synthesis and therefore cell wall dysfunction
fluconazole- candidia
Voriconazole -aspergillus

63
Q

Describe ednichocandins and give examples

A

inhibit enzyme responsible for beta glucan synthesis therefore disrupt cell wall
Micofungin, caspofungin

64
Q

WHY is ceftriaxone avoided in neonates?

A

It can cause +++ hyperbilirubinaemia by displacing it from albumin

65
Q

What is MOA of fenofexidine?

A

H1 antagonist, (second generation therefore less likely to be sedating )

66
Q

What is MOA of sildefanil?

A

Phosphodiesterase V inhibitor

67
Q

What is MOA of caffeine in neonates?

A

Blocks A1 and A2 adenosine receptors

68
Q

What is MOA of tocolizumab?

A

IL-6 blocker

69
Q

What is MOA of Azothioprine?

A

inhibits the synthesis of purine nucleosides and thus the proliferation of T and B lym-
phocytes and antibody formation

70
Q

What is MOA of Tacrolimus?

A

Calcineurin inhibitor
Calcineurin catalyses some of the intracellular processes associated with the activation of T-
lymphocytes.

TAS (18 decks)

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