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Pharm > Drugs > Flashcards

Drugs Flashcards

1
Q

Morphine equiv:

PO to IV

A

2:1 (halve PO dose)

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2
Q

Morphine equiv:

morphine to hydromorph

A

5:1
PO or SC
5mg morphine = 1mg hydromorph

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3
Q

Morphine equiv:

morphine to codeine

A

10:1

3mg morphine = 30mg codeine

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4
Q

Morphine equiv:

PO to SC

A

2:1 (halve SC dose)

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5
Q

Morphine equiv:

morphine to Bup (SL)

A

1:40
or divide microg by 2.5
8mg morphine = 200ucg buprenorphine

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6
Q

Morphine equiv:

Transderm fentanyl/buprenorphine

A

Calculate to 24hrs ~100:1

30mg morphine = 300ucg fentanyl, = 12ucg/hr patch

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7
Q

P-glycoprotein MoA

A

Transport protein - Efflux transporter (reduces absorption of substrate) in gut
ie outside of metabolism
p-gp inhibitors INCREASE substrate
p-gp inducers DECREASE substrate

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8
Q

P-glycoprotein - common inducers

A

NOT MANY!! Usual inducers like CYP
Phenytoin
Rifampicin
Co-trimox
Midazo

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9
Q

P-glycoprotein - common substrates

A

DIGOXIN
Cyclosporine
Ivermectin
Hormones - hydrocort, Est, Progest
HIV protease
ChemoRx

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10
Q

P-glycoprotein - common inhibitors

A

IF asked to guess - guess inhibitors (decrease substrate)
CCB
-azoles
Amiodarone
Macrolides
Ceftriaxone
CNI

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11
Q

Warfarin - drugs which INCREASE INR

A

Most drugs increase AC - so we should lower Warfarin

Amiodarine
Azoles
Verapamil
etc etc

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12
Q

Warfarin - drugs which DECREASE INR

A

These drugs LOWER INR (watch if valve, need to increase Warfarin dose)

CBZ
Pheny
Rifampicin
St JOHns Owrt
Cholestyramine

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13
Q

Warfarin - drugs with NO EFFECT on INR

A

“ABs” don’t change INR
ACE/ARBS
B Blockers
Statins

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14
Q

Anticholinergic verse cholinesterase-inhibitors (MoA & Examples)

A

CholinesterASE inhibitors block enzyme that degrades cholinesterase - ie increases ACh. Anti cholinergics decrease ACh.

Anti-cholinesterase/Cholinesterase INHIBITORS:
(prevent breakdown in synapse to increase chance of Ach connecting w/ post synapse neuron)
- Pyridostigmine in MG; Donepezil, Rivastigmine in AD

Anti-cholinergics - act presynaptic to prevent release
DIRECT effects:
-atropine; oxybutynin; ipratropium (BD effect) ; antiparkinsons: amantidine, benztropine;

INDIRECT
TCA, antipsychotics, CBZ, antihist, analgesics, eye drops

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15
Q

Azithromycin - MoA, PK properties

A

Bacteriostatic (binds to 50S ribosomal subunit)

Long half life (70hrs) and lrg Vd 
High concentrations (eg in macrophages) at site of inflammation 
Hepatic metabolism & faeces excretion but no CYP interactions
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16
Q

HAGMA - calculation & Causes

A

(Na + K) - (Cl- + HCO3) 16 +/- 4

LIRK : lactic, ingested toxins, renal, ketones
MUDPILES: metformin, ureamia, DKA, paracetamol, iron, isoniazid, Lactic, lithium, ethanols, salicylates

17
Q

Toxic ETOH - Rx (clinical presentation)

A

Whatever to prevent it being rapidly absorbed - eg gastric lavage, charcoal, induced emesis (<1hr)
May need HD
Can give ETOH to competitive inhibit alcohol dehydrogenase, or Fomepizole which high affinity binding of ETOH dehydrogenase to prevent metabolism
(Clinical fx - HAGMA, oxalate crystals)

18
Q

Dose adjustment with concurrent AED

A

Half dose LAMOTRIGINE when given with VALPROATE

(Ginny is half size of Valerie ) lower both, synergistic effect. (lower lamotrigine w/ CBZ also)

19
Q

MAO-Inhibitors -MoA, Drugs & risks

A

MAO-A inhibition DEC breakdown of serotonin, norad, & dopamine
MAO-B inhibition DEC breakdown dopamine, phenethylamine

Selective MAO-B (PD): Selegeline, Rasagiline, Safinamide
Non selective (A/B) Hydrazine
Selective MAO-A : moclobemide (RIMA)
Linezolid has weak MAO-inh!

Tyramine HTN crisis (cheese, etoh, biltang, fermented)
- Tyramine releases Nor-ad, ordinarily MAO would breakdown excess Nor-ad, excess MAO-Ing -> adrenergic crisis (alpha 1, vasoconstriction etc)

SS - don’t use w/ SSRI. (RIMAs safer as reversible & displace from receptor in presence of tyramine but can still cause SS)\Need to taper to finish due to discontinuation

20
Q

CYP Inducers v Inhibitors & classic examples

A

Inhibitors (many inc -azoles) increase substrate (decrease prodrug)

Inducers (CBZ, Rifampicin) decrease substrate (increase prodrug)

21
Q

Serotonin syndrome v NMS

A

SS
1. NM hyperactivity - hyperreflexia, sustained clonus including BILATERAL, rigidity
2 Autonomic dysfxn (sympathetic) - FEVER, tachy/HTN, diaphoresis, diarrhea, trem
3. GCS/Mental state change

NMS - antipsychotics

  1. EPS (like PD) - as dopamine inhibited: lead pipe rigidity but no clonus
  2. Autonomic dysfxn - low grade temp, HTN
  3. GCS
22
Q

NMS - pathophys, Fx, RF

A

(Typical) antipsychotics block D2 to stop dopamine transmission in brain.
Triad:
1) EPS - no clonus, just dyskinesia, dystonia - leadpipe rigidity
2) Autonomic dysfxn
3) GCS

Rx: BZD, Bromocriptane, stop agents
RF: <40yrs, LBD, Stopping L-dopa rapidly, antipsych 2-5days

23
Q

Malignant hyperthermia - fx, RF, Rx

A

RF: Suxamethonium, succinylcholine, halothane/fluranes (NOT rocuron/vec, local)
+ (AD) RYR1 gene (releases stored Ca causing mm contraction)
Fx
1) autonomic dysfxn (temp is late finding)
2) mm rigidity
3) acidosis, rhabdo, hyperK, hypercapnia
Rx: Dantrolene (+ supportive)

24
Q

DOAC interference w/ meds

A

AED - Phenytoin, CBZ; Rifampicin
Both p-glycoprotein & CYP3A4/2 inhducer so drug decreased effect

-conazoles (fungals)
Potent g-gp CYP3A4 inhibition - INCREASES effect much higher
Fluconazole best w/ Rivaroxaban

Dabigatran & CNI C/I
Dabigatran & Verapamil (decreased NOAC dose & take together)
MIld effects w/ amiodaron, macrolides

25
Q

Phosphodiesterase inhibitor - MoA, types & examples

A

Blocks >1 of the 5 subtypes of enzyme PDE
Prevents inactivation of second cell messengeres (cAMP, cGMP)
eg. on SM of pulm vasculature

Non selective - caffeine, theophylline
PD4 selective - Anti-inflam like pulm COPD
PD5 selective - Sildafenil, Dipyridamole (safe in preg)

26
Q

Aspirin - MoA

A

Stops synthesis of Thromboxane A2

by inhibiting Cox-1 (irresversibly)

which converts Arachidonic Acid to Prostaglandin H2

27
Q

P2Y12 inhibitors - types & MoA

A

MoA: stop ADP binding to P2Y12 on plts which stops activation of GP IIb/IIIA

Clopidogrel is pro drug (IRREVERSIBLE)
- requires CYP2C19 to activate (5% ppl poor metabolizers)
Ticagrelor is hepatically metabolised (CYP3A4 but not activated) - REVERSIBLE

28
Q

Dipyridamole - MoA, S/E

A

PDE5 inhibitors
Blocks breakdown of cAMP (& uptake of Adenosine)
Higher [cAMP] decreases intracellular Ca & inhibits plt activation

S/E flushing - GI (watch it combo w/ nitraties)

29
Q

GP IIb/IIIA antagonists

A

Eptifibatide

Abcixumab

30
Q

Heparin - MoA & types

A

Binds to antithrombin III to inhibit factor 2a (thrombin) + Xa

UFH (measure via Xa level or APTT)
LMWH (Enoxaparin & Danaparoid) - higher Xa inactivation
Fodaparinux (binds to antithrombin, only indirectly inhibits Xa)

31
Q

Thiopurine: metabolites (& enzymes/mutations) - consequences

A

Azathiopurine → (Glutathione) → 6MP

  1. (XO) → 6TUA (Allopurinol blocks XO)
  2. (HGPRT) → 6TGN (effect - ie myelosuppression)
  3. (TPMT) → 6MMP (hepatotoxicity)

TPMT mutations (hetero/homo) mean more shunted down 6TGN

32
Q

Thiopurine: Metabolite results - interpretation & action

  1. Very low 6TGN & very low 6MMP (<50 either)
  2. Low 6TGN (<260) & low 6MMP (<5700)
  3. Low 6TGN (<260) & High 6MMP (>5700)
  4. Therapeutic 6TGN (260-450) & Low/High 6MMP
  5. High 6TGN (>450) & Low/high 6MMP
A
  1. Very low 6TGN & very low 6MMP (<50 either) - non-adherence
  2. Low 6TGN (<260) & low 6MMP (<5700) - underdosed
  3. Low 6TGN (<260) & High 6MMP (>5700) - preferential 6MMP shunter, Add Allopurinol & decrease dose by 25%
  4. Therapeutic 6TGN (260-450) & Low/High 6MMP - refractory, change Rx
  5. High 6TGN (>450) & Low/high 6MMP - overdosed/refractory
33
Q

β blocker - non selective (β1 & β2)

A
  • Carvedilol (also has α-1 blocking)
  • Propranolol
  • Sotalol
  • Timolol
34
Q

β blocker - cardioselective

A
  • Atenolol (β1-selective)
  • Bisoprolol
  • Metoprolol (β1-selective)
  • Nebivolol
35
Q

β-blockers - differences lipophilic/hydrophilic (examples)

A
  • Lipophilic:
  • Propranolol
  • Metroprolol
  • Bisoprolol
  • Carvediolol
  • GIT absorption easy, liver metabolised (impairment prolongs), lrg Vd, CNS penetrance
  • Hydrophilic:
  • Atenolol
  • Sotalol
  • less readily absorbed - longer t½ so OD but renal impairment can prolong
36
Q

Sulfasalazine A/E

A

Cutaneous hypersensitivity

Azoospermia

Pharm (3 decks)

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