Common Drugs Flashcards

Question

Etomidate? Class? MOA? Pharmacokinetics? SE? CI? Dose?

Answer 1

**_CLASS_****=** carboxylated imidazole derivative **_MOA_**= binds to GABA-A receptors & (1) increases affinity of GABA & also (2) mimics GABA at the GABA-A receptor site = **increases** Cl- conduction= hyperpolarizes cell= **decreases** neuronal transmission - producing sedation & hypnosis **_Pharmacokinetics_**= **75% PB**; _**lipid soluble**;_ onset- rapid 30-60sec; DOA- short 5-15 min (terminated by rapid redistribution); Vd- 3L/kg; E1/2= 3-5 hrs; water soluble in solution & mixed w/ propylene glycol (**burning on injection)**; **liver hydrolysis & metabolism by plasmaesterases** & excreted in urine (2%) & bile; _clearance dependent on HBF (_need HBF to clear drug, will be decreased clearance in time of decreased blood flow) **_SE_**= **decrease** CBF, CMRO2, ICP, & CMRO2- **can increase** **EEG- causing seizures;**; NO change in BP, HR, SVR, CO- very cardiac stable**; Potentiates NMB**; **30-40% N/V**; **myoclonus**; hiccups; **adrenocorticoid suppression** - may need cortisol replacement; pain on injection (**reversible inhibition of 11- b-hydroxlyase and 11-a-hydroxylase)** **_CI_**= seizures, porphyria, Addison’s disease/adrenal insufficiency **_Dose_**= induction- 0.3mg/kg; sedation- 5-8 mcg/kg/min; maintenance- 10 mcg/kg/min

Answer 2

**_CLASS_****=**non-barbiturate induction agent**_; phencyclidine derivative_** **_MOA_**= (1) blocks NMDA receptors to **inhibit** influx of Na+, Ca2+- inhibits the excitatory response of glutamate & produces a “**dissociative state anesthesia”** via depression of association areas of the brain (*depresses cerebral cortex and thalamaus while increasing hippocampus)***;** (1) analgesia effects by interacting with mu, kappa, delta & sigma receptors- (3) works on monoaminergic descending pain pathways & substance P in SC; (4) muscarinic (*antagonist*?) & (5) Ca++ channel antagonist **_Pharmacokinetics_**= **12% (poor) PB; highly lipid soluble**; onset- rapid 30-60sec; DOA= short 5-15min (short d/t redistribution); Vd- 3L/kg; E1/2- 2-3 hrs; acidic soluble & racemic mixture; metabolized by CYP450 to **norketamine** (active metabolite) then excreted in urine; _clearance dependent on HBF_ **_SE_**= **increase** CBF, ICP & CMRO2 & IOP; myoclonus, **hallucinations & emergence delirium** (can prevent with benzos); **increase** **SNS stimulation =** **increase** HR, SVR, BP; **direct myocardial depressant (*especially in critically ill patients that cannot surmount a SNS response)***; BRONCHODILATION (SNS); **increase** **PVR**; **increase** **saliva production (laryngospasm risk)**, potentiates NMB’s **_CI_**= psych disorders, head injury (**increase** ICP), eye injury, CAD, IHD, Systemic or pulmonary HTN **_Dose_**= induction- 0.5-2 mg/kg IV; sedation 0.2-0.5 mg/kg IV; maintenance- 1-2 mg/kg/hr IV; 5-10 mg/kg IM/PR

Answer 3

**_CLASS_****=** highly selective central-acting alpha 2 adrenergic agonist; GA/TIVA adjunct (a2/a1 1620:1) **_MOA_**= activates alpha 2 receptors- **decrease** SNS outflow & NE release causing sedation, anxiolysis, **decrease** neuroendocrine response; closely mimics sleep & causes analgesia by inhibiting substance P in SC (also locus ceruleus (hypnosis)) **_Pharmacokinetics_**= 90% PB; **water soluble**; Vd- **3L/k**g; redistributes in **6 min; E1/2- 2-3 hrs**- can build tolerance & dependence & has context sensitive ½ time- longer gtt on- longer it takes to metabolize; metabolized in the liver (rapid metabolism in liver by conjugaiton, n-methylation, hydroxylation) & excreted in urine & bile; antagonist- atipamezole **_SE_**= **decrease** CBF but **no change** in **CMRO2** & **ICP**; **decrease BP, HR** (most significant), SVR; **minimal** change in **RR** & small **decrease** in TV; depresses thermoregulation; **decreases** **MAC**/doses of other anesthetic agents. _**Attenuates CV resposne to noxious stimul**i, **no change in CO2 response**_ **_CI_**= Afib, HB, severe bradycardia, pts that cannot tolerate lower BP or HR **_Dose_**= 1 mcg/kg over 15 min bolus then 0.2-1 mcg/kg/**hr**

Answer 4

**_CLASS_****=** Depolarizing NMB; benzylisoquinolone **_MOA_**= **PARTIAL AGONIST-** Binds to alpha subunits of nicotinic Ach receptors **mimicking the action of ACh at the NMJ** opening Ca++ channels & depolarizing the motor endplate; fasciculations then flaccid paralysis occurs; Channels stay open & membrane cannot respond to subsequent ACh; effect terminated when SCh diffuses away from the NMJ **_Pharmacokinetics_**= water soluble; **small Vd (0.2L/kg) & PB**; onset- 30-60 sec; DOA- 8-15 min; E1/2- 2-4 min; rapidly hydrolyzed by plasmaesterases when diffuses away from the NMJ & excreted in the urine **_SE_**= **increase** ICP, IOP, IGP; histamine release - **decrease** HR & BP, **HYPERK+ (increae 0.5-1 mEq/L) (dysrhythmias);** masseter spasm, myalgias, fasciculations, rhabdomyolysis, myoglobinuria, **MH** **_CI_**= **MH, renal patient with high K+,** high K, **peds unless emergency**, caution asthma & COPD; atypical plasma esterase deficiency; muscles weakness like muscular dystrophy; sepsis, burn patients **_Dose_**= laryngospasm-10-20 mg IV; RSI/intubation- 1-1.5 mg/kg; infusion- 2-4mg/min

Answer 5

**COMPETITIVE ANTAGNOIST-** Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction

Answer 6

**_CLASS_****=** intermediate acting benzyllisoquinoline NDMR (-curium) pre and post NMJ AcH inhibition **_MOA_**: Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction **_Pharmacokinetics_**= water soluble; 80% PB; Vd: 0.2L/kg; onset- 2-3 min; DOA- 30-60 min; E1/2- 20 min; metabolized by ester hydrolysis 2/3 & Hofmann elimination 1/3 (temp & pH dependent) & excreted in the urine; has metabolite **Laudanosine** (can accumulate in RF & cause CNS problems like seizures- is a tertiary amine and can cross BBB) **_SE_**= Histamine release; **decrease** BP (minimal) & **increase** **HR**; skin flushing (all related to histamine release); muscle weakness; NMB can be potentiated with IA’s, ketamine, some abx, lithium, LA’s, antiarrhythmics, Mg++ **_CI_**= conscious patient, hypersensitivity; **caution with asthma, COPD, CAD, seizure hx**, muscle weakness, myasthenia gravis (increase sensitivity); **metabolite can accumulate with renal problems; prolonged action in acidosis & hypothermia** **_Dose_**= initial- 0.5 mg/kg IV; maintenance- 0.08 - 0.1 mg/kg q 20-45 min

Answer 7

**_CLASS_**= intermediate acting benzyllisoquinoline NDMR; (-curium) stereoisomer of Atracurium (A/C) **_MOA:_** Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction **_Pharmacokinetics_**= water soluble; Vd: 0.2L/kg; onset- 3-5 min; DOA- 30-60 min; E1/2- 30 min; metabolized 80% by **Hofmann elimination (temp & pH dependent**) & excreted in the urine; has metabolite Laudanosine 1/5 that of Atracurium (can accumulate in RF & cause CNS problems like seizures) **_SE_**= NO histamine & CV stable; good choice if CV instability or severe renal dysfunction, asthma or COPD or peds (immature liver); muscle weakness; potentiated NMB with IA’s, ketamine, some abx (such as aminoglycosides), lithium, LA’s, antiarrhythmics, Mg++ **_CI_**= conscious patient, hypersensitivity; muscle weakness, myasthenia gravis (give 1/10th of dose), **seizure hx; metabolite can accumulate with renal problems; prolonged action in acidosis & hypothermia** **_Dose_**= initial- 0.1-0.2 mg/kg IV; maintenance- 0.02 mg/kg IV q 40-60 min

Answer 8

**_CLASS_****=** short-intermediate acting steroid derivative NDMR **_MOA_**: Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction **_Pharmacokinetics_**= water soluble; Vd: 0.2L.kg; onset-30-60sec ; DOA- 30-90 min; E1/2- 2 hrs; hepatic metabolism with renal (30% unchanged) & biliary (50%) elimination (Prolonged effects in hepatic, renal, & biliary disease) **_SE_**= NO histamine & CV stable; bronchospasm; muscle weakness; effects potentiated IA’s, ketamine, some abx, lithium, LA’s, antiarrhythmics, Mg++ **_CI_**= conscious patient, hypersensitivity, myasthenia gravis, caution muscle weakness; **caution hepatic, renal, & biliary disease; hypothermia prolongs action** **_Dose_**= initial- 0.6-1.2 mg/kg (low = intubation; high = RSI); defasiculating- 0.06-0.1mg/kg (5-10 mg per lecture); maintenance- 0.1-0.2 mg/kg

Answer 9

**_CLASS_****=** intermediate acting steroid derivative NDMR **_MOA_**: Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction **_Pharmacokinetics_**= 80% PB; Vd: 0.2L/kg; onset-3-5 min; DOA- 30-60 min; E1/2- 1hr; hepatic metabolism with renal (30% unchanged) & biliary (50%) excretion (prolonged effects in hepatic, renal, & biliary disease); **active metabolite= 3-desacetyl vecuronium (was called 3-OH in lecture)** (50% as potent as parent) **_SE_**= NO histamine & CV stable; bronchospasm; muscle weakness, can cause **SA node exit block**; NMB potentiated with IA’s, ketamine, some abx, lithium, LA’s, antiarrhythmics, Mg++ **_CI_**= conscious patient; hypersensitivity; myasthenia gravis, caution muscle weakness; **caution hepatic, renal, & biliary disease; hypothermia prolongs action** **_Dose_**= initial- 0.1 mg/kg; defasiculating 0.01mg/kg IV; maintenance- 0.01-0.02mg/kg q 25-45 min

Answer 10

**_CLASS_****=** long acting steroid derivative NDMR **_MOA_**: Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction **_Pharmacokinetics_**= small PB; Vd: 0.2L/kg; onset- 3-5 min; DOA- 2-3 hours; E1/2- 2 hrs; 10-20% hepatic metabolism with **renal excretion (80% unchanged);** 3 active metabolites- most is the **3-desacetyl pancurounium (50% as potent as parent)**- (aka 3-OH in lecture) prolonged excretion in renal, hepatic disease, elderly & obese **_SE_**= SNS stimulation = **increase** HR, BP; bronchospasm; no histamine; muscle weakness, NMB potentiated with IA’s, ketamine, some abx, lithium, LA’s, antiarrhythmics, Mg++ **_CI_**= conscious patient, hypersensitivity, **renal dysfunction**; **CAD, HF or HD**, myasthenia gravis, caution muscle weakness **_Dose_**= initial- 0.1 mg/kg; maintenance- 0.01-0.02 mg/kg q 40-60 min

Answer 11

**_CLASS_**= short acting benzyllisoquinoline NDMR **_MOA:_** : Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction **_Pharmacokinetics_**= Vd: 0.2L/kg; onset- 1-2 min; DOA- 10-20 min; E1/2- 1hr; metabolized by plasma esterases & excreted (7% unchanged in the urine)- good for liver or renal failure **_SE_**= **HISTAMINE** release, **increase** HR & **DECREASE** BP, bronchospasm, flushing; muscle weakness **_CI_**= conscious patients, hypersensitivity, **atypical plasma esterase deficiency, asthma, COPD**; caution myasthenia gravis & muscle weakness; NMB potentiated with IA’s, ketamine, some abx, lithium, LA’s, antiarrhythmics, Mg++ _Dose_= initial- 0.2 mg/kg; maintenance- 0.01-0.1 mg/kg

Answer 12

**_CLASS_****=** quaternary ammonia acetylcholinesterase inhibitor (does not cross the BBB) **_MOA_**= **Covalently.** binds to the carbamyl group at the esteric site on acetylcholinesterases inhibiting it, thus inhibiting the breakdown of ACh & **increasing** its availability at the motor end plate; used to antagonize the effects of the NMB; most reliable with a deep block **_Pharmacokinetics_**= water soluble; Vd: 1L/kg; onset- 5-15 min; **peak 7-10 min**; DOA- 1 hr; E1/2- 70 min; metabolized by plasma & liver esterases 50% & excreted unchanged in the urine (50%) **_SE_**= **increase** salivation, bronchoconstriction, **decrease** HR, BP, SVR; N/V; **increase** gastric secretions; seizures **_CI_**= renal failure prolongs clearance, GI/GU obstruction, asthma, caution in CAD, prolongs effect os SUCCINYLCHOLINE d/t inhibiton of plasma esterases **_Dose_**= 0.04-0.07 mg/kg with Glyco 0.01 mg/kg

Answer 13

**_CLASS_****=** quaternary ammonia acetylcholinesterase inhibitor (does not cross the BBB) **_MOA_**= reversibe H+ binding to the acetylcholinesterases through an electrostatic attachment thereby inhibiting the breakdown of ACh & **increasing** its availability at the motor end plate; **has less severe muscarinic effects.** Fast onset than neostigmine and less effectiv ethan neostigmine**. Not effective for deep block (need TOF 4/4 to work)** **_Pharmacokinetics_**= water soluble; Vd: 1L/kg; onset- fast; peak- 1-2 min; DOA- short @ 1 receptor, but leaves that receptor & occupies another until eliminated which prolongs the DOA (1hr); **25% hepatic metabolism & _renal excretion 75% unchanged_** **_SE_**= **increases** salivation, bronchoconstriction, **decreases** HR, BP, SVR; N/V; **increase** gastric secretions; seizures **_CI_**= renal failure prolongs clearance, GI/GU obstruction, asthma, caution in CAD **_Dose_**= 0.5-1 mg/kg; given with atropine (0.01 mg/kg)

Answer 14

**_CLASS_****=** tertiary amine (crosses BBB) acetylcholinesterase inhibitor; **_MOA_**= **Reversibly** binds to the carbamyl group at the esteric site on acetylcholinesterases inhibiting it, thus inhibiting the breakdown of ACh & **increases** its availability at the motor end plate; can be used reversal of central anticholinergic syndrome. Not used for NMB reversal but used with central anticholinergic syndrome _Pharmacokinetics_= **lipid soluble & crosses BBB**; onset- 5 min; DOA- 1-5 hrs; E1/2- 30 min; hydrolyzed by cholinesterases & minimal renal excretion **_SE_**= **increase** salivation, bronchoconstriction, **decrease** HR, BP, SVR; N/V; **increase** gastric secretions; seizures; **inhibits somnolent effects of benzos, ketamine, IA & opioids** **_CI_**= GI/GU obstruction, asthma, caution in CAD **_Dose_**= 15-60 mcg/kg IV

Answer 15

**_CLASS_****=** quaternary ammonia acetylcholinesterase inhibitor (does not cross the BBB) **_MOA_**= **REVERSIBLY** binds to the carbamyl group at the esteric site on acetylcholinesterases, inhibiting the breakdown of ACh & **increase** availability at the motor end plate; used to antagonize the effects of the NMB; can be given orally for myasthenia gravis. Not used for reversal of NMB because of long onset of action also a very weak anticholinesterase inhibior. **_Pharmacokinetics_**= water soluble; Vd: 1L/kg; **onset- 10 min; peak- 12 min;** DOA- 1 hr; **25% hepatic metabolism & excreted in the urine 75% unchanged**; not used often as reversal d/t its slow onset and low potency **_SE_**= **increase** salivation, bronchoconstriction, **decrease** HR, BP, SVR; N/V; **increase** gastric secretions; seizures **_CI_**= renal failure prolongs clearance, GI/GU obstruction, asthma, caution in CAD **_Dose_**= 0.14-0.25 mg/kg; given with glyco (0.01 mg/kg)

Answer 16

Activates Mu, Kappa & delta G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically **increase K**+ conductance to hyperpolarize the cell & directly **decrease** neurotransmission; this **increasing** the pain threshold, alters pain perception & inhibits ascending pain pathways

Answer 17

**_CLASS_****=** Natural opioid agonist **_MOA:_** Activates Mu, Kappa & delta G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically increase K+ conductance to hyperpolarize the cell & directly decrease neurotransmission; this increasing the pain threshold, alters pain perception & inhibits ascending pain pathways **_Pharmacokinetics_**= **30% PB; 23% non-ionized (pKa= 7.9); low lipid solubility; Vd: 3L/kg** - IV peak- 15-30 min; DOA- 3 hrs; E1/2- 3-4 hrs - _Hepatic & renal metabolism to_ **morphine-3 glucoronide** (less active) & **morphine-6-glucoronide** (active metabolite which is 650x more potent) & excreted in the urine (1-12% unchanged) & feces **_SE_**= _analgesia, euphoria, sedation, N/V/C, pruritus, dry mouth, urinary retention; SOO spasm; dose-dependent respiratory depression (**decrease**_ _RR & **increase**_ _TV), dose dependent decrease_ _HR, BP, SVR_ more profound w/ **HISTAMINE release**; **inhibits SA/AV node;** delayed respiratory depression in epidural & spinals b/c not as lipid soluble **_CI_**= allergy, respiratory depression, asthma, COPD; **renal disease** (metabolites can accumulate); synergistic hypnosis & respiratory depression w/ Benzo’s & other CNS depressants; **decrease** dose in peds & elderly **_Dose_**= 0.01-0.2mg/kg – usually **2.5-15mg IV** (*in divided 1-4 mg doses q 5 min*) **Q 3-4 hours;** infusion 0.8-10mg/hr

Answer 18

**_CLASS_****=** phenyl-piperidine synthetic opioid agonist **_MOA:_** **Activates Mu, Kappa & delta G protein** coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing **Ca2+ channel inactivation presynaptically** to **inhibit** the release of **excitatory NT’s such as Epi, NE & Substance P or post synapatically increase** K+ conductance to **hyperpolarize** the cell & **directly** **decrease** **neurotransmission**; this increasing the pain threshold, alters pain perception & **inhibits** **ascending** **pain** pathways **_MOA cont.:_** **anti-cholinergic effects (atropine-like structure**), Alpha-2 agonist, blocks Na channels **_Pharmacokinetics_**= 1/10th as potent as morphine. **60% PB; nonionized- 10% (pKa: 8.5); low lipid solubility; Vd: 4L/kg**; - Onset fast; peak 5-10min**;** DOA- 3 hrs; E1/2: 3-4hrs - Liver metabolism to **normeperdine** (½ as potent as parent & can cause seizures & myoclonus) & excreted in the urine - **65% pulmonary 1^st pass effect** **_SE_**= _analgesia, euphoria, sedation; N/V/C, pruritus, dry mouth, urinary retention; SOO spasm_; _dose dependent respiratory depression (**increase**_ _RR & **decrease**__TV); dose dependent **decrease**_ _BP & SVR_ more profound w/ **HISTAMINE release**, decrease **shivering**; **sympathomimetic -** increase **HR & direct cardiac depressant** **_CI_**= allergy, respiratory depression, asthma, COPD; caution seizure hx, CAD; fatal interaction with **MAOIs**; **decrease** **dose in** **renal disease** (metabolites can accumulate); **decrease** dose in peds & elderly **_Dose_**= 50-100 mg IV; 12.5mg for shivering (total dose should not exceed 1 gram/24 hrs)

Answer 19

**_CLASS_****=** semi-synthetic opioid agonist that is derivative of morphine & 5x more potent than morphine **_MOA:_** Activates Mu G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically increase K+ conductance to hyperpolarize the cell & directly decrease neurotransmission; this increasing the pain threshold, alters pain perception & inhibits ascending pain pathways **_Pharmacokinetics_**= **8-19% PB**; onset \<30 minutes ; peak- 5-10 min; **DOA-2-4 hrs (**longer); E1/2- 1-3 hrs; **significant 1^st pass metabolism** in liver with 95% metabolized to Hydromorphone-3- glucuronide (inactive) & excreted in the urine **_SE_**= _analgesia, **more sedation & less euphoria than Morphine**; N/V/C, pruritus, dry mouth, urinary retention, SOO spasm; dose dependent respiratory depression (**decrease**_ _RR & **increase**__TV); Dose dependent **decrease**_ _HR, BP, SVR_ **_CI_**= allergy, respiratory depression; synergistic hypnosis & respiratory depression w/ Benzo’s & other CNS depressants; **decrease** dose in peds & elderly; increased ICP without controlled ventilation **_Dose_**= 1-4 mg IV q 4-6 hrs

Answer 20

**_CLASS_****=** Phenyl piperidine synthetic opioid agonist **_MOA:_** Activates Mu G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically increase K+ conductance to hyperpolarize the cell & directly decrease neurotransmission; this increasing the pain threshold, alters pain perception & inhibits ascending pain pathways **_Pharmacokinetics_**= 100x more potent than MSO4 (morphine) **- 80% PB; non-ionized- \<10% (pKa= 8.4); high lipid solubility; Vd-4L/kg** - Fast onset; peak- **6.4 min**; short DOA- 1 hr; E1/2- 3-6 hrs; - Liver metabolism (n-dealkylation & hydroxylation) that is **dependent on HBF** & excreted in the urine - Weak active metabolite **norfentanil** - _75% pulmonary 1^st pass effect & Secondary peak_ - **Longer context sensitive ½ time with infusions** **_SE_**= _analgesia, euphoria, sedation, N/V/C, pruritus, dry mouth, urinary retention; SOO spasm; dose-dependent respiratory depression (**decrease**_ _RR & **increase**__TV), dose dependent **decrease**_ _HR, BP, SVR_; **seizure like activity,** **muscle rigidity &** **wooden chest syndrome**; blunts SNS response to DVL **_CI_**= allergy, respiratory depression, caution in **hepatic/renal disease**, head trauma (**increase** ICP), gallbladder disease, bradyarrhythmias; synergistic hypnosis & respiratory depression w/ Benzo’s & other CNS depressants; **decrease** dose in peds & elderly **_Dose_**= bolus- 1-2 mcg/kg (analgesia); 25-100mcg (pre-med); infusion- 0.01-0.05 mcg/kg/min

Answer 21

**Sufentanil**- Phenyl-piperidine synthetic opioid agonist; most potent opioid **_MOA_**: Activates Mu G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically increase K+ conductance to hyperpolarize the cell & directly decrease neurotransmission; this increasing the pain threshold, alters pain perception & inhibits ascending pain pathways **_Pharmacokinetics_**= 1000x more potent than morphine **- 90% PB; 20% non-ionized (pKa= 8.0)** ; **highest lipid solubility; Vd-3L/kg** - Fast onset; peak – **6.2 min**; short DOA- 30 min; E1/2- 2.5 hr - **Liver & SI metabolism** & excreted in urine - Active metabolite **desmethylsufentanil** - _75% pulmonary 1^st pass effect & Secondary peak_ **_SE_**= _analgesia, euphoria, sedation, N/V/C, pruritus, dry mouth, urinary retention; SOO spasm; dose-dependent respiratory depression (**decrease R**__R & **increase**__TV), dose dependent **decrease**_ _HR, BP, SVR_; **_bronchospasm_**; **seizure like activity,** **muscle rigidity & wooden chest syndrome**; blunts SNS response to DVL cyp 3a inhibitors may increase levels of sufentanil **_CI_**= allergy, asthma, airway obstruction; caution in hepatic & renal dysfunction; synergistic hypnosis & respiratory depression w/ Benzos & other CNS depressants; **decrease** dose in peds & elderly **_Dose_**= analgesia -0.1-1 mcg/kg; infusion- 0.0015-0.01mcg/kg/min

Answer 22

**_CLASS_****=** tetrazole fentanyl derivative; synthetic opioid agonist **_MOA:_** Activates Mu G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically increase K+ conductance to hyperpolarize the cell & directly decrease neurotransmission; this increasing the pain threshold, alters pain perception & inhibits ascending pain pathways **_Pharmacokinetics_**= 90% PB; 90% non-ionized **(pka 6.5**); high lipid solubility; Vd- 0.4L/kg **- Onset- fastest**; peak- **1.4 min**; short DOA- 30-60 min; E1/2- 1.5hr - Metabolized in the **liver & SI** & excreted in the urine - Active metabolite **norfentanil** **- Context sensitive half time is 60 min for infusion up 8 hours (*longer than sufentanil despite similar DOA)*** **_SE_**= _analgesia, euphoria, sedation, N/V/C, pruritus, dry mouth, urinary retention; SOO spasm; dose-dependent respiratory depression (**decrease**_ _RR & **increase**_ _TV),_ **MINIMAL CHANGE in HR, BP, SVR; skeletal muscle rigidity,** blunts SNS response to DVL **_CI_**= allergy, respiratory depression, **untreated Parkinson’s,** **increase** ICP; synergistic hypnosis & respiratory depression w/ Benzo’s & other CNS depressants; **decrease** dose in peds & elderly **_Dose_**= initial- 10-20 mcg/kg; infusion- 0.25-0.75 mcg/kg/min

Answer 23

**CLASS=** phenyl-piperidine synthetic opioid agonist with ester link **_MOA:_** Activates Mu G protein coupled opioid receptors in the brain, spinal cord, & peripheral afferent neurons causing Ca2+ channel inactivation presynaptically to inhibit the release of excitatory NT’s such as Epi, NE & Substance P or post synapatically increase K+ conductance to hyperpolarize the cell & directly decrease neurotransmission; this increasing the pain threshold, alters pain perception & inhibits ascending pain pathways **_Pharmacokinetics_**= **80% PB; 65% non-ionized (pKa= 7.3); high lipid solubility**; **Vd- 0.4L/kg** - Onset 1-3 min; peak- 2 min; **DOA- shortest 10 min; rapidly metabolized by tissue & plasma esterases** **_SE_**= _analgesia, euphoria, sedation, N/V/C, pruritus, dry mouth, urinary retention; SOO spasm; dose-dependent respiratory depression (**decrease**_ _RR & **increase**_ _TV), dose dependent **decrease**_ _HR, BP, SVR;_ **skeletal muscle rigidity,** blunts SNS to DVL **_CI_**= allergy, respiratory depression**; do not use in epidural/spinals (d/t glycine prep); need plan for post-op pain**; synergistic hypnosis & respiratory depression w/ Benzo’s & other CNS depressants; **decrease** dose in peds & elderly **_Dose_**= initial- 1-2 mcg/kg; infusion- 0.05-0.25 mcg/kg/min

Answer 24

* Unsure of MOA- myer-overton theory that states anesthetic molecules caused hydrophiobic region to expand beyond critical amount and distorting channels has been debunked. Current theories are: * Presynaptic voltage gated Na channels * 2-pore potassium chennels * TREK and TASK channels * Ionotropic and metabotropic receptors * GABA, Glycine * Glutamate (NMDA, AMPA, Kainate)

Answer 25

**_CLASS_****=** inorganic gas with double bond b/t 2 N atoms **_Pharmacokinetics_**= eliminated by exhalation, biotransformation with 0.004% hepatic metabolism; - fast on & off b/c low BG coefficient; - can be used for **2^nd gas effect** - increases concentration & uptake of other gases; - potentiates NMB’s; - DECREASES MAC of other gases; - 34x more soluble than N2--\> diffuses into hollow cavitiies **_SE_**= odorless, sweet smell - **increase** CBF, ICP, CMRO2 (couples!) - SNS stimulation; direct myocardial depression; NO CHANGE/minimal **increase** in HR, BP, CO, SVR; **increase** PVR - **increase** RR & **decrease** TV; no change in resting PaCO2; **diffusion hypoxia (need O2 when d/c N2O!)** - **decrease** HBF; **decrease R**BF, GFR & UOP; **post op N/V; bowel distention** - Inhibits B12 dependent enzymes responsible for myelin formation & DNA synthesis; BM suppression; can impair immune response to infection - **Analgesic properties** **_CI_**= PTX, air embolism, tympanic membrane surgery, eye surgery, intestinal obstruction/bowel surgery, intracranial air, pulmonary HTN, immunosuppressed pts, caution CAD, sepsis, epinephrine use (dysrhythmias) **_Dose_**= VP- 39,000, BG- 0.47, MAC- 104, cannot be used as sole anesthetic

Answer 26

**CLASS=** halogenated methyl ethyl ether; isomer of enf **_Pharmacokinetics_**= pungent odor; eliminated by exhalation & biotransformation; hepatic metabolism \<0.2-2%; potentiates NM blockade **_SE_**= - **increase** CBF, ICP, **decrease** CMRO2;(mainly mac\>1)- effects reversed by hyperventilation; electrically silent EEg at 2 MAC; **enhances** CSF reabsorption - **decrease** SVR, BP but CO maintained; **increase** HR (mild Beta stimulation); CA vasodilator- **coronary steal (Not for CAD)**; BEST for patients going on bypass. **Anesthetic preconditioning-** brief exposure to VA can activate K-ATP channels- hyperpolarizing effect which proects tissue to subsequent ischemic episodes. *(hyperpolarizing decreases O2 requirement and makes cell tolerate lack of perf/reperfusion better)* - **increase** RR & decrease TV, bronchodilator; tachypnea less pronounced at 1 MAC compared to other agents; blunted response to hypoxia and hypercarbia; \>1 MAC, decreases hypoxic vasoconstriction, which can be detrimental in single lung ventialtion - **decrease** RBF, GFR & UOP; **maintains HBF** **_CI_**= peds- pungent causing coughing, laryngospasm; MH; ½ MAC in CAD & Neuro anesthesia; caution transient **increase** HR & BP w/ rapid **increase** concentration **_Dose_**= VP- 240, BG- 1.4, MAC- 1.2

Answer 27

**_CLASS_****=** fluorinated methyl ethyl ether; structure similar to iso **_Pharmacokinetics_**= pungent odor; uses Tec 6 vaporizer b/c VP is so close to atmospheric pressure; fast on & off; eliminated by exhalation & biotransformation; hepatic metabolism \<0.1%; highest risk of **CO formation from degradation by dried out CO2 absorbent** **_SE_**= - **increase** CBF, ICP, **decrease** CMRO2; - **decrease** BP, SVR, increase **HR (SNS stimulation when [] increase rapidly)**; CO maintained - increase RR & decrease TV; **irritating to the AW can cause coughing, bucking & laryngospasm** - **decrease** RBF, GFR, UOP, **decrease** HBF - Potentiates NMB’s **_CI_**= MH, peds for inhalational induction, asthma, **increase** ICP, caution CAD; caution transient **increase** HR & BP w/ rapid **increase** concentration **_Dose_**= VP- 669, BG- 0.42, MAC- 6

Answer 28

**_CLASS_****=** fluorinated methyl isopropyl ether **_Pharmacokinetics_**= ideal for peds- sweet & non-pungent with minimal AW irritation; expensive; fast on & of; eliminated via exhalation & biotransformation; hepatic metabolism 3-5% **_SE_**= - **increase** CBF, ICP, **decrease** CMRO2; - SLIGHT **decrease** SVR, BP, CO, no change HR**; no change in CVP** - **increase** RR & **decrease** TV; Bronchodilation - **decrease** RBF, GFR, UOP; **HBF maintained** - **Compound A** can form causing renal toxicity with low flows (keep flows at \>2L) - Potentiates NMB’s **_CI_**= MH, severe renal disease **_Dose_**= VP- 160, BG- 0.69, MAC- 2

Answer 29

**_CLASS_****=**amide LA (& Class IB antiarrhythmic – its active metabolite monoethyglycinexylidide blocks Na+ channels in cardiomyocytes,**decrease** AP duration & refractory period) - LA MOA- bind to H-gate of Na channel and physically obstruct the channel * keeps Na channel in closed/inactivated state and prevents further transmission AP (unionized portion diffuses across membrane, ionized portion blocks channel) **_Pharmacokinetics_**= - **pKa- 7.9; non-ionized- 24%, PB- 70% (PB 50% for antiarrhythmic); l**ow potency & low lipid solubility - **Fast onse**t & _moderate_ DOA (**1-2hr**); E1/2- 1.5hr (antiarrhythmic- 1-8 hrs) - **Intrinsic vasodilator activity; uptake into the lungs** - CYP450 liver metabolism that **depends on HB**F & excreted in urine - 2 active metabolites- **xylidide & monoethylglycinexylidide** **_SE_**= **TNS**, high incidence of cauda equina syndrome (*specfiically high concentraiton lidocaine)*; **BLUNT SNS TO DVL** LA toxicity **5-10 mcg/ml**: circumoral numbness, lightheadedness, tinnitus, skeletal muscle twitching, visual disturbances, systemic hypotension, myocardial depression, & tachycardia, decreased SVR & cardiac output. **10-15 mcg/ml:** seizures, unconsciousness **15-25 mcg/ml:** apnea, coma **\>25 mcg/ml**: cardiovascular depression/collapse **_CI_**= methemoglobinemia LA hypersensitivity to amide LA**, coagulopathies, infection, hypovolemia,** refusal, inability to cooperate inexperience of provider Antiarrhythmic hypersensitivity; WPW syndrome, HB, **hepatic disease**; CYP450 inhibitors such as Cimetidine & Propranolol **decrease** metabolism **_Dose_**= MAX: 4mg/kg & with epi 7mg/kg; Spinal MAX- 30-100mg (1-2mL) (1.5-5%) Epidural: 15-30 ml of 1-2% PNB- volume depends on location- 1-2% Intubation to blunt DVL & antiarrhythmic- 1-2 mg/kg (max antiarrhythmic: 3mg/kg)

Answer 30

**_CLASS_****=** amide LA **_Pharmacokinetics_**= **- pKa- 8.1; non-ionized- 17%, PB- 95%**; very potent & highly lipid soluble - **Moderate** onset & **long** **DOA** **(4-8hr)**; E1/2- 3.5hr - CYP450 liver metabolism that depends on HBF **_SE_**= **differential blockade**; TNS, "very low risk for neuro complications with spinal" (CB) ; **highly CV toxic hypotension, myocardial depression**, AV block, arrhythmias; local anesthestic toxicity *(cirucmoral numbness, tinnitus, vision changes, dizziness, restlessness, muscle twitching in face/extremities--\> seizures)--\> CNS depression, apnea, hypotension).* **_CI_**= refusal, inability to cooperate, **coagulopathies, hypovolemia, infection @ site**; inexperience of clinician; extreme caution in poor CV function & HB _Dose_= - MAX- 2.5mg/kg - Spinal MAX - spinal-15-20mg (0.5, 0.75%, 3-4 mL) - Epidural- 15-30 ml of 0.125-0.5% - PNB- amount depends on location- 0.25-0.5%

Answer 31

**CLASS=** non-steroidal anti-inflammatory drug **_MOA_****=** blocks cyclooxygenase 1 & 2; inhibits prostaglandin synthesis causing anti-inflammatory effects & analgesia effects; also blocks synthesis of thromboxane A2 causing REVERSIBLE inhibition of platelet aggregation **_Pharmacokinetics_****=**99% PB; onset- 10 min; peak- 2-3 hrs; DOA 6-8 hours; E1/2- 5 hrs (prolonged to 6-8 hrs in elderly); liver conjugation &**60%** excreted unchanged in urine **_SE_****=**no respiratory or CV depression; impaired bone healing,**increase**bleeding time,**GIB/ulcerations**; bronchospasm (**increase**leukotrienes), renal toxicity/ARF; black box- do not use peri-op in CABG, can cause**increase** CV effects like MI & stroke; can inhibit platelet function **_DDI’s_**= reduces effect of _diuretics, beta blockers, & ACEI’s_; **increased risk of bleeding when combined with other anticoagulants**; increases **levels of other protein bound drug**s such as Warfarin; AVOID with Probenecid =increases levels/prolongs action of Ketorolac **_CI_****=****_asthma--\> bronchospasm, ASA allerg_**y, **_RF_**, liver failure, GIB, coagulation problems, **_3^rd trimester;_** NO post-CABG **_Dose_****=** 30 mg IV x 1 or q 6 hrs (max daily is 120mg)- do not give longer than 5 days; decrease dose in elderly to 15mg

Answer 32

**_CLASS_**= central dopamine receptor antagonist & serotonin-4 receptor agonist **_MOA_**= blocks the DA2 receptors centrally in the CRTZ of the medulla preventing N/V; stimulates serotonin-4 receptors causing **increase** gastric motility & peristalsis; this is also accomplished by **increase** ACh @ the muscarinic post-synaptic receptors; **increase** LES tone & relaxation of pylorus & duodenum **_Pharmacokinetics_**= 30-40% PB;; Vd 2-4L/kg; onset- 1-3 min; DOA- 1-2 hrs; E1/2- 2-4 hrs; metabolized in the liver & 40% excreted unchanged in the urine **_SE_**= **increase** gastric motility, LES tone; **decrease** N/V; extrapyramidal SE, abdominal cramping (w/ rapid administration), sedation, prolactin secretion, dry mouth **_DDI’s_**= potentiates sedation of CNS depressants; **inhibits plasma cholinesterases thus may prolong Succinylcholine & Mivacurium** , **_MAOIS, TCA_**, pt with EPS **_CI_**= **Parkinson’s**, **bowel obstruction,** GI hemorrhage, seizure disorders, **_arrhythmias with Zofran_**; do not give with **phenothiazines**, **MAOI**, TCA, pt c EPS; pheochromocytoma **_Dose_**= 10-20 mg IV _over 3-5 min_ 15 min before induction

Answer 33

**_CLASS_****=** serotonin-3 receptor antagonist **_MOA_**= blocks serotonin receptors peripherally on vagal nerve terminals in GI tract & centrally in the CRTZ **_Pharmacokinetics_**= 70% **PB**; **Vd** 2-2.5 L/kg; **onset**- 30 min; **DOA**- 4-8 hrs; E1/**2**- 3-4 hrs; metabolized in the liver with renal excretion (5% unchanged) **_SE_**= HA with rapid administration, fatigue, arrhythmias (w/ Reglan), constipation, diarrhea **_CI_**= hypersensitivity, liver disease (decrease dose), SSRIs, Generally not recommended for treatment of existing chemotherapy-induced emesis or for prophylaxis of nausea from agents with little potential to cause nausea **_Dose_**= 4-8mg IV over 2-5 min

Answer 34

**_CLASS_****=** selective competitive H2 receptor antagonist (MOST potent) **_MOA:_** Competitively bind to H2 receptors, inhibiting the binding of histamine to gastric parietal cells, **decrease** cAMP & secretion of H+ ions, **decrease** gastric acid secretion from the parietal cells; can prevent Mendelsson syndrome or to treat GERD or ulcers; crosses BBB **_Pharmacokinetics_**= 20% PB; onset- 30 min; DOA- 8 hrs; E1/2- 3 hrs; liver metabolism with **75%** excreted unchanged in the kidneys; must be given IV d/t extensive first pass effect **_SE_**= dMultisystem disease and advanced age increase severity of side effects. Diarrhea, HA, fatigue, skeletal muscle pain, confusion (crosses BBB), arrhythmias; **rapid IV administration may cause bradycardia & hypotension (Give over 2 minutes for famotidine)** **_CI_**= caution liver/renal disease, hypersensitivity; may alter absorption of some drugs by increasing gastric pH **_Dose_**= 20 mg IV over 2 min

Answer 35

**_CLASS_****=** selective competitive H2 receptor antagonist **_moa:_** Competitively bind to H2 receptors, inhibiting the binding of histamine to gastric parietal cells, **decrease** cAMP & secretion of H+ ions, **decrease** gastric acid secretion from the parietal cells; can prevent Mendelsson syndrome or to treat GERD or ulcers; crosses BBB **_Pharmacokinetics_**= 15% PB, onset- 1 hr; E1/2- 2 hrs; 50% metabolized in the liver & **50%** excreted unchanged in the kidneys; must be given IV d/t extensive first pass effect **_SE_**= The frequency of severe side effects is low, and the risk of experiencing adverse side effects is increased by presence multiple medical illnesses, hepatic or renal dysfunction and advanced age.. HA, fatigue, dizziness, confusion, skeletal muscle pain, arrhythmias; rapid IV administration may cause bradycardia & hypotension **_CI_**= caution in RF & liver disease; hypersensitivity; may alter absorption of some drugs by increasing gastric pH **_Dose_**= 50 mg IV over 15-30 min preop; **decrease**in RF

Answer 36

**_CLASS_****=** selective competitive H2 receptor antagonist (least potent) **_MOA:_** Competitively bind to H2 receptors, inhibiting the binding of histamine to gastric parietal cells, **DECREASE** cAMP & secretion of H+ ions, **decrease** gastric acid secretion from the parietal cells; can prevent Mendelsson syndrome or to treat GERD or ulcers; crosses BBB **_Pharmacokinetics_**= 20% PB; onset- 1 hr; DOA- 4 hrs; E1/2- 2 hrs; liver metabolism with CYP450 & **75%** excreted unchanged in urine; must be given IV d/t large oral first pass effect **_SE_**= delays awakening from GA in RF; **decrease** HBF- transient **increase** liver enzymes; HA, fatigue, dizziness, confusion, skeletal muscle pain, arrhythmias; rapid IV administration may cause bradycardia & hypotension **_CI_**= caution in RF & liver disease, caution in asthma (may exacerbate bronchospasm with unopposed H1 bronchoconstriction) **_DDI’s=_** Inhibits CYP450 = prolonged effect of warfarin, diazepam, Lidocaine, Propranolol, morphine, CCB, TCAs, Phenytoin; may alter absorption of some drugs by increasing gastric pH **_Dose_**= 300 mg IV over 15-30 min; 1-2 hrs preop; **decrease** in RF

Answer 37

**_CLASS_****=** loop diuretic **_MOA_**= inhibits Na/2Cl/K pump in the thick ascending limb of loop of Henle causing excretion of H2O, Na+, Cl-, K+, Mg2+ & Ca2+; evokes renal production of prostaglandin; used for treatment of edema, hypercalcemia & differential diagnosis of oliguira **_Pharmacokinetics_**= 90% PB; onset of diuresis- 5 min; DOA- 2 hours; E1/2- 1 hr; hepatic metabolism with 50% excreted by kidneys (glomerular filtration & renal tubular secretion) & 30% excreted unchanged in the bile **_SE_**= hypotension, hyperglycemia, electrolyte imbalances = especially hypokalemia & hypochloremia, nephrotoxicity, ototoxicity, potentiates NMB, **decrease** clearance of lithium; possible cross reaction if have sulfa allergy **_CI/Caution_**= fluid & electrolyte abnormalities (hyperK), can **increase** risk of nephrotoxicity or ototoxicity if administered with aminoglycosides & cephalosporins **_Dose_**= 0.1-1 mg/kg IV; titrate & start with 5-40 mg IV

Answer 38

**_CLASS_****=** osmotic diuretic (6 carbon hexose sugar) **_MOA_**= **increase** osmolarity of the plasma drawing fluid into the intravascular space = causing **increase** UOP & diuresis; used to **decrease** ICP & IOP & differential diagnosis of oliguria **_Pharmacokinetics_**= onset- 15 min; DOA- 3-6 hrs; E1/2- 1 hr; cleared by the kidney 100% unchanged- none is reabsorbed **_SE_**= HA, convulsions, rash, blurry vision, pulmonary edema, hypovolemia, electrolyte imbalances; hypokalemic hypochloremic alkalosis; **decrease** ICP & IOP **_CI_**= hypovolemia, severe kidney disease, CV dysfunction, intracranial bleeding **_Dose_**= 0.25-1 g/kg over 30-60 min

Answer 39

**_CLASS_**= thiazide diuretic **_MOA_**= inhibits the reabsorption of Na+ & Cl- in the ascending loop of Henle & DCT, thereby enhancing Na+ & H2O excretion; used for treatment of HTN usually in combo with ßB **_Pharmacokinetics_**= 70% PB; onset- 2 hrs; DOA- 6-14 hrs; E1/2- 6-14 hrs; 100% excreted unchanged in the urine **_SE_**= hypotension, rash, hyperglycemia, **decrease** K+ & Mg2+, electrolyte imbalances, potentiates NMB, nephropathy, **increase** digoxin toxicity, low ceiling effect **_CI_**= renal failure, pregnancy, Antiarrhythmic agents that prolonged QTI causing torsades, **decrease** dose in elderly **_Dose_**= 25-100 mg/day PO in 1-2 doses; max 200 mg

Answer 40

**_CLASS=_** corticosteroid with **ONLY** glucocorticoid properties **_MOA_**= enters the cell & binds to glucocorticoid & receptors in the cytoplasm forming a steroid-receptor complex that enters the nucleus & affects DNA transcription; _Metabolically_ causes an **increase** nutrient availability by **increase** BG, amino acids, & Triglycerides; _inhibits the inflammatory process_ by inhibiting phospholipase A2 = **decrease** arachnidonic acid = **decrease** inflammatory mediators such as leukotrienes, cytokines, & prostaglandins ALSO- inhibits COX & Lipoxygenase pathways- may lead to analgesia effects; antiemetic property MOA unknown (poss. **decrease** prostaglandin, **increase** endorphins & appetite) Good: Antiemetic, analgesia, periop airway edema, cerebral edema **_Pharmacokinetics_**=DOA= 72hrs; E1/2- 3 hrs; liver metabolism with 30% excreted unchanged in the urine; antiemetic effect may last 24 hrs **_SE_**= **perineal burning**, **increase** BG, HTN, HYPOK+; immunosuppression, HPA axis suppression, delayed wound healing, fat redistribution, muscle & bone wasting **_CI_**= caution in DM, untreated infection, hypersensitivity **_Dose_**= 4-10 mg IV

Answer 41

**_CLASS_****=**corticosteroid with**equal** glucocorticoid & mineralcorticoid properties **_MOA_**= enters the cell & binds to glucocorticoid & mineralcorticoid receptors in the cytoplasm forming a steroid-receptor complex that enters the nucleus & affects DNA transcription; _Metabolically_ causes an **increase** in nutrient availability by **increase** BG, amino acids, & Triglycerides; _inhibits the inflammatory process_ by inhibiting phospholipase A2 = **decrease** arachnidonic acid = **decrease** inflammatory mediators such as leukotrienes, cytokines, & prostaglandins; **decrease** capillary membrane permeability; causes reflex Na+ & H2O retention with excretion of K+ in DCT **_Pharmacokinetics_**= 90% PB; DOA- 8-36 hrs; E1/2- 1-2 hrs; liver metabolism (conjugated) & 30% excreted unchanged in the urine **_SE_****=increase**BG,**increase**Na+ & H2O retention,**increase** appetite, HTN, HYPOK+; immunosuppression, HPA axis suppression, delayed wound healing, fat redistribution, muscle & bone wasting **_CI_****=** caution in DM, untreated infection, hypersensitivity _Dose_= Supplementation based on individual need and degree of surgery (multiple different mehodologies)- 100 mg IV q 6-8 hours for stress dose; Dosing depending on severity of surgery 25-150mg; 10-20mg/day average needed

Answer 42

**_CLASS_****=**corticosteroid with**MORE** glucocorticoid properties than mineralcorticoid properties **_MOA_**= enters the cell & binds to glucocorticoid & mineralcorticoid receptors in the cytoplasm forming a steroid-receptor complex that enters the nucleus & affects DNA transcription; _Metabolically_ causes an **increase** nutrient availability by **increase** BG, amino acids, & Triglycerides; _inhibits the inflammatory process_ by inhibiting phospholipase A2 = decrease arachnidonic acid = **decrease**inflammatory mediators such as leukotrienes, cytokines, & prostaglandins; **decrease** capillary membrane permeability; causes reflex Na+ & H2O retention with excretion of K+ in DCT GOOD for SC injuries, joint inflammation **_Pharmacokinetics_**= PB- 90%; DOA- 12-36 hrs; E1/2- 2-4 hrs; liver metabolism & 30% excreted unchanged in urine **_SE_**= **increase** BG, **increase** Na+ & H2O retention, HTN, HYPOK+; immunosuppression, HPA axis suppression, delayed wound healing, fat redistribution, muscle & bone wasting **_CI_**= caution in DM, untreated infection, hypersensitivity **_Dose_**= 10-250 mg IV

Answer 43

**_CLASS_****=** organic nitrate **_MOA_**= produces NO, which activates guanylate cyclase, **increase** cGMP inhibiting Ca2+ entry into cell & **increase** uptake of Ca2+ into the smooth ER causing peripheral & SM vasodilation; Dilates **Venous\> arterial** to **decrease** preload with _NO change in SVR & HR_; **increase**CA blood flow to ischemic areas; relaxes SM in GI tract and SOO **_Pharmacokinetics_= 60% PB**; **large** Vd; onset- immediate; DOA- 5min; E1/2- 5 min; metabolized rapidly with nitrate metabolite that is capable of producing methemoglobin by oxidation of ferrous to ferric ion in Hgb with \<1% excreted unchanged in the urine **_SE_**= **increase** ICP; dizziness, HA, syncope, N/V, MI, **decrease** venous return, CA vasodilation, **decrease** hypoxic vasoconstriction; **increase** bleeding time,; **relaxes** SM & SOO spasm,; can **_cause tachyphylaxis (need nitrate free periods);_** **_CI_**= _**do not use with PDIs;** hypotension, hypertrophic cardiomyopathy, aortic stenosis, **increase** ICP_, anemia, cardiac tamponade, caution in liver failure **increase** risk of methemoglobinemia, **_Dose_**= initially 5-10 mcg/min & titrate to 5-200 mcg/min; 200 mg at a time for SOO spasm

Answer 44

**_CLASS_****=** direct nonselective peripheral vasodilator **_MOA_**= prodrug that interacts with oxyhemoglobin dissociates to methemoglobin, NO, & cyanide; NO activates guanylate cyclase, **increase** cGMP inhibiting Ca2+ entry into cell & **increase** uptake of Ca2+ into the smooth ER causing peripheral & SM vasodilation; **equally** dilates venous to ê preload & arteries to **decrease** afterload; **_reflex increase_ _HR & contractility_** **_Pharmacokinetics_**= onset- immediate; E1/2- 5 min; metabolism- transfer of an electron from iron to SNP yields methemoglobin & SNP radical- 5 cyanide ions released; 1 reacts with methemoglobin to form cyano-methemoglobin (nontoxic) & the rest are metabolized in the liver & kidney & converted to thiocyanate which is cleared by the kidney (slowly cleared- takes 2-7 days) *keep bag covered- light can conver SNP--\> aquapentacyanoferrate and release hydrogen cyanide in the presence of light* **_SE_**= methemoglobinemia (higher risk with gtt \>2mcg/kg/min), cyanide toxicity (*s/s development is tachyphylaxis of drug)*, thiocyanate toxicity (causing seizures, & mental status changes), hypotension, tachycardia, **increase** bleeding time (plt inhib), **increase** ICP, Tachyphylaxis, hypoxia, lactic acidosis, **decrease** hypoxic vasoconstriction, **CORONARY STEAL** **_CI_**= **renal failure**, _hypotension, hypertrophic cardiomyopathy, aortic stenosis,_ **_increase_** _ICP_, caution CAD, don’t use with PDIs **_Dose_**= 0.3-10 mcg/kg/min (maintain \<2mcg/kg/min to reduce r/f toxicity) or 1-2 mcg/kg for HTN crisis bolus

Answer 45

**_CLASS_****=** vasodilator (vasodilator, more effective arteriole \>venous) **_MOA_**=from class----vasodilation via activation of guanylate cyclae--\> increases cGMP, decreases Ca entyr into cell. hyperpolarization--\> SM relaxation. Direct vasodilating effect on vascular SM to decrease SVR (arteries\> veins) another way to say it... activates guanylate cyclase causing **increase** cGMP directly dilating arterial \> venous; membrane hyperpolarizes causing K+ channel activation & inhibition of IP3 & Ca2+ release from SR in vascular SM thereby **decrease** SVR & BP **_Pharmacokinetics_**= 90% PB; onset- 15 min; DOA- 6 hrs; E1/2- 3 hrs; metabolized by the liver & excreted by the kidneys **_SE_=** **increase** ICP, HA, **reflex tachycardia**, angina (decreae in DBP \> SBP) ,**SLE syndrome**, **Na&H20 retention**, **_Tachyphylaxis_** **_CI_**= use with caution in CAD (tachy might **increase** O2 demand, also DBP decreases \> SBP), wait appropriate amount of time before redose or will get hypotensive **_Dose_**= 5-20 mg IV q 4 hrs; 2.5-10 mg IV in OR

Answer 46

**_Class:_** Antifibrionlytic: lysine analog **_MOA:_** Competitively inhibits plasminogen activation (binds to kringle domain in palce of lysine on plasminogen) reduces plasmin concentrationa nd fibrinolytic activity; TXA directly inhibits plasmin at high doses - Still examining exact MOA- Alternative hypothesis is that TXA improves survival via reduciton of proinflammatory plasmin activity **_Pharmacokinetcis:_** 3% PB vd 9-12 L; 95% excreted unchanged (reduce dose in renal pts) Onset 5-15 min; DOA 3 HOURS. E1/2T: 2-11 Hours **_S/E:_** Seizures (gaba blockade), vision changes, ureteral obstructionand bleeding, renal toxicity **_C/I: (not given in lecture...)_** from pfizer website: * In patients with subarachnoid hemorrhage. Anecdotal experience indicates that cerebral edema and cerebral infarction may be caused by CYKLOKAPRON in such patients. * In patients with active intravascular clotting. * In patients with hypersensitivity to tranexamic acid or any of the ingredients **_DOSE:_** 1 gm in 100 cc NS over 10 min then 1 gm in 100 cc NS over 8 hours. Do not admin in same line as blood, VIIa, or PCN. Stored 15-30C

Common Drugs Flashcards

I pulled what I thought were most common drugs/most likely to appear on the oral and placed them in a deck. Trying to narrow down my studying!