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Apex NCE Board Prep 2020 > Pharmacology I > Flashcards

Pharmacology I Flashcards

1
Q

Volume of distribution

A

relationship between s drug’s plasma concentration after a specific dose (how a drug distributes throughout the body)

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2
Q

What does volume of distribution assume?

A
  • the drug distributes instantly

- the drug is not subject to biotransformation or elimination before it fully distributes

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3
Q

Equation for volume of distribution

A

Vd = amount of drug/desired plasma conc.

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4
Q

What does it mean when a drug’s Vd is greater than TBW?

A
  • the drug is lipophilic
  • the drug distributes into TBW and fat
  • will require a higher dose to achieve a given plasma concentration

ex: propofol, fentanyl

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5
Q

What does it mean when a drug’s Vd is less than TBW?

A
  • the drug is hydrophilic
  • it distributes into some or all of the TBW
  • does NOT distribute into fat
  • requires a lower does to achieve a given plasma conc.

ex: NMBs (ECF), albumin (plasma)

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6
Q

Loading dose calculation (IV and PO)

A

Loading dose = Vd x desired plasma conc / bioavailability

  • for IV drug, bioavailability is always 1 (all of the drug goes into the bloodstream)
  • PO drugs don’t get absorbed completely and subject to first pass by liver so bioavailability is reduced
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7
Q

Clearance

A
  • volume of plasma that is cleared of a drug per unit time
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8
Q

Clearance is directly proportional to…

A
  • blood flow to clearing organ
  • extraction ratio
  • drug dose
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9
Q

Clearance is inversely proportional to…

A
  • half-life

- drug concentration in the central compartment

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10
Q

Steady state

A
  • when the amount of drug entering the body is equivalent to the amount being eliminated
  • rate of admin = rate of elim
  • occurs after five half-times
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11
Q

What does the plasma concentration curve depict?

A
  • shows the biphasic decrease of a drug’s plasma concentration after a rapid IV bolus
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12
Q

Alpha distribution phase of plasma concentration curve

A
  • describes drug distribution from the plasma to the tissues
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13
Q

Beta distribution phase of plasma concentration curve

A
  • starts when plasma concentration falls below tissue concentration
  • concentration gradient reverses
  • drug re-enters the plasma
  • beta phase describes drug elimination from the plasma by the clearing organ
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14
Q

Half-times, % eliminated and % remaining

A
  • 0 half-time: 0% eliminated, 100% remaining
  • 1 half-time: 50% eliminated. 50% remaining
  • 2 half-time: 75% eliminated, 25% remaining
  • 3 half-time: 87.5% eliminated, 12.5% remaining
  • 4 half-time: 93.75% eliminated, 6.25% remaining
  • 5 half-life: 96.875% eliminated, 3.125% remaining
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15
Q

Context sensitive half-time

A
  • time required for the plasma concentration to decline by 50% after discontinuing the drug
  • normal half-times do NOT consider time
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16
Q

Context sensitive half-times for narcotics

A
  • context sensitive half-time for a fentanyl got increases the longer it was infused
  • longer infusion = more time to fill peripheral compartments = more fentanyl to be eliminated = longer elimination half-time
  • same thing with alfentanil and sufentanil
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17
Q

Remifentanil context sensitive half-time

A
  • remi is highly lipophilic BUT it is quickly metabolized by plasma esterase’s
  • has a similar context-sensitive half-time regardless of how long it was infused
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18
Q

What is the difference between a strong and weak acid or base?

A
  • difference is the degree of ionization
  • strong acid or strong base in water = will completely ionize
  • weak acid or weak base in water = fraction will be ionized and fraction will be unionized
  • acid donates H+
  • base donates OH-
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19
Q

What is ionization? What factors determine how much a molecule will ionize?

A
  • the process where a molecule gains a positive or negative charge
  • amount of ionization depends on the pH of the solution and the pKa of the drug
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20
Q

When the pKa and the pH are the same, _________________.

A

50% of the drug will be ionized and 50% of the drug will be unionized.

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21
Q

Ionization affect on solubility

A

IONIZED
- water = hydrophilic and lipophobic

UNIONIZED
- lipid = hydrophobic and lipophilic

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22
Q

Ionization and pharmacologic effects

A
  • ionized = not active

- unionized = active

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23
Q

Ionization and hepatic biotransformation

A
  • ionized = less likely

- unionized = more likely

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24
Q

Ionization and renal elimination

A
  • ionized = more likely

- unionized = less likely

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25
Q

Ionization and diffusion across lipid bilayer

A
  • ionized does NOT diffuse across the BBB, GI tract or placenta
  • unionized diffuses across the BBB, GI tract and placenta
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26
Q

Adding an acid in a basic solution

A
  • the acidic drug will be highly ionized in a basic pH
  • the acidic drug wants to donate protons and the basic solution wants to accept
  • acidic drug donates the protons and becomes ionized
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27
Q

Adding an acid to an acidic solution

A
  • the acidic drug will be highly unionized in an acidic solution (like dissolves like)
  • both the acidic drug and solution want to donate protons
  • there are no proton acceptors so the acidic drug retains them and remains unionized
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28
Q

Are most drugs acids or bases? Weak or strong?

A
  • most drugs are weak acids OR weak bases

- usually are prepared and a salt that dissociates in solution

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29
Q

Examples of weak acids

A
  • is usually paired with a positive ion like sodium, calcium or magnesium
    ex: sodium thiopental
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30
Q

Examples of weak bases

A
  • is usually paired with a negative ion like chloride or sulfate
    ex: lidocaine hydrochloride, morphine sulfate
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31
Q

Three key plasma proteins. and what kind of drugs do they bind?

A
  • albumin: primarily binds acidic drugs
  • alpha1- acid glycoprotein: binds basic drugs
  • beta-globulin: binds to basic drugs
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32
Q

What conditions reduce albumin concentrations?

A
  • liver disease
  • renal disease
  • old age
  • malnutrition
  • pregnancy
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33
Q

What conditions cause increased alpha1-acid glycoprotein concentration?

A
  • surgical stress
  • MI
  • chronic pain
  • Rheumatoid arthritis
  • advanced age
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34
Q

What conditions cause decreased alpha1-acid glycoprotein concentration?

A
  • neonates

- pregnancy

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35
Q

How do changes in plasma protein binding affect plasma drug concentrations?

A
  • decreased PP binding = increased Cp

- increased PP binding = decreased Cp

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36
Q

How do you calculate changes in plasma protein binding?

A

[free drug] + [unbound drug] = [bound drug]

  • if a drug is 98% bound and the bound fraction is reduced to 96% = the unbound/free fraction has increased by 100%
  • if the free fraction is 2% and it increases to 4%, then the free fraction has increased by 100%
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37
Q

First-order kinetics

A
  • a constant FRACTION of a drug is eliminated per unit time
  • most drugs follow this model

ex: a drug is cleared from the body at a rate proportional to its plasma concentration

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38
Q

Zero-order kinetics

A
  • a constant AMOUNT of drug is eliminated per unit time
  • rate of elimination is independent of the plasma drug concentration

ex: aspirin, phenytoin, warfarin, heparin, theophylline, alcohol

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39
Q

Function of a phase 1 reaction and list the three examples.

A
  • small molecular changes that make a molecule more water soluble to prepare it for phase 2 reaction
  • hydrolysis: adds water to a compound to split it up (usually an ester)
  • reduction: adds electrons to a compound
  • oxidation adds an oxygen molecule to a compound
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40
Q

How are most phase 1 biotransformations carried out?

A

P450 system

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41
Q

What is the function of phase 2 reactions? List the 5 common substrates.

A
  • adds a highly polar/water soluble substrate to the molecule making it inactive and ready for excretion
  • acetic acid
  • glucuronic acid
  • glycine
  • sulfate
  • methyl group
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42
Q

Enterohepatic circulation and a drug example

A
  • some conjugated compounds are excreted in the bile, reactivated in the intestine, and then reabsorbed into the systemic circulation
    ex: diazepam
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43
Q

What is the extraction ratio?

A
  • a measure of how much drug is delivered to a clearing organ vs. how much drug is removed by that organ
  • ER of 1.0 = 100% of drug delivered to clearing organ is removed
  • ER of 0.5 = 50% of drug delivered to clearing organ is removed
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44
Q

Flow limited elimination

A
  • for a drug with HIGH hepatic extraction ratio (>0.7), clearance depends on liver blood flow
  • hepatic blood flow greatly exceeds enzyme activity, so changes in liver enzyme activity has little effect
  • increased liver blood flow = increased clearance
  • decreased liver blood flow = decreased clearance
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45
Q

Capacity limited elimination

A
  • for a drug with a LOW hepatic extraction ratio (<0.3), clearance is dependent upon the ability of the liver to extract the drug from the blood
  • changes in enzyme activity or protein binding have profound impact on clearance
  • changes in liver’s intrinsic ability to remove drug from the blood is influenced by the amount of enzyme present
  • enzyme induction = increased clearance
  • enzyme inhibition = decreased clearance

** if a drug has a low hepatic extraction ratio, CYP inhibition will have a greater effect on its metabolism

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46
Q

Drugs with Low Hepatic ER

A
  • rocuronium
  • diazepam
  • methadone
  • thiopental
  • theophylline
  • phenytoin
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47
Q

Drugs with intermediate hepatic ER

A
  • midazolam
  • vecuronium
  • alfentanil
  • methohexital
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48
Q

Drugs with high hepatic ER

A
  • fentanyl
  • sufentanil
  • morphine
  • meperidine
  • naloxone
  • ketamine
  • propofol
  • lidocaine
  • bupivacaine
  • metoprolol
  • propranolol
  • alprenolol
  • nifedipine
  • diltiazem
  • verapamil
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49
Q

Hepatic enzyme inducer

A
  • increase clearance
  • decrease drug plasma level
  • drug dose increase may be required

ex: tobacco, barbs, ethanol, phenytoin, rifampin, carbamazepine

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50
Q

Hepatic enzyme inhibitors

A
  • decrease clearance
  • increase drug plasma levels
  • drug dose decrease may be required

ex: grapefruit juice, cimetidine, omeprazole, isoniazid, SSRIs, erythromycin, ketoconazole

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51
Q

Drug classes(2) and drugs (7) that are metabolized by pseudocholinesterase

A

NEUROMUSCULAR BLOCKERS

  • succinylcholine
  • mivacurium

ESTER LOCAL ANESTHETICS

  • chloroprocaine
  • tetracaine
  • procaine
  • benzocaine
  • cocaine (also metab by liver)
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52
Q

Six drugs that are metabolized by non-specific plasma esterases

A
  • esmolol
  • remifentanil
  • aspirin
  • clevidipine
  • atracurium (and Hoffman)
  • etomidate (and hepatic)
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53
Q

One drug that is biotransformed by alkaline phosphatase hydrolysis

A
  • fospropofol (propofol prodrug under trade name Lusedra)
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54
Q

Pharmacokinetics

A
  • what the body does to the drug
  • explains the relationship between the dose that you administer and the drug’s plasma concentration over time
  • absorption, distribution, metabolizm, excretion
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55
Q

Pharmacobiophysics

A
  • considers the drug’s concentration in the plasma and the effect site (bio phase)
56
Q

Pharmacodynamics

A
  • what the drug does to the body

- explains the relationship between the effect site concentration and the clinical effect

57
Q

What is potency and how is it measured?

A
  • dose required to achieve a given clinical effect (x-axis on dose response curve)
  • ED50 and ED90 are measures of potency: dose required to achieve a given effect in 50% and 90% of the population
58
Q

How is potency measured on the dose-response curve?

A
  • left shift = increased affinity for receptor = higher potency = lower dose required
  • right shift = decreased affinity for receptor = lower potency = higher dose required
59
Q

What is efficacy and how is it measured on the dose-response curve?

A
  • a measure of the intrinsic ability of a drug to produce a clinical effect
  • height of plateau on y-axis measures efficacy
  • higher plateau = greater efficacy
  • once the plateau is reached, additional drug does NOT produce additional effect
60
Q

What does the slope of the dose-response curve mean<

A
  • the slope depicts how many receptors must be occupied to elicit a clinical effect
  • steeper slope = small increase in dose can have a profound clinical effect
  • flatter slope = higher doses are required to increase the clinical effect
61
Q

Full agonist

A
  • binds to a receptor and turns on a specific cellular response
62
Q

Partial agonist

A
  • binds to a receptor
  • only capable to partially turning on a cellular response
  • less efficacious than a full agonist
63
Q

Antagonist

A
  • occupies the receptor and prevents and agonist from binding to it
  • does not tell the cell to do anything
  • does not have efficacy
64
Q

Inverse agonist

A
  • binds to the receptor and causes an opposite effect to that of a full agonist
  • has a negative efficacy
65
Q

Competitive antagonism and an example

A
  • is REVERSIBLE
  • giving more of the agonist can overcome the competitive antagonism

ex: atropine, vec, roc

66
Q

Noncompetitive antagonism and an example

A
  • is IRREVERSIBLE
  • drug binds to receptor via covalent bonds and its effect cannot be overcome by increasing agonist
  • effect of noncompetitive agonist can only be overcome by producing new receptors

ex: aspirin and phenoxybenzamine

67
Q

ED50

A
  • dose that produces the expected clinical response in 50% of population
  • is a measure of potency
68
Q

LD50

A
  • dose that will produce death in 50% of the population
69
Q

Therapeutic Index

A
  • helps determine the safety margin for a desired clinical effect

TI = LD50/ED50

  • drug with a narrow TI has a narrow margin of safety
  • drug with a wide TI has a wide margin of safety
70
Q

Chirality

A
  • division of stereochemistry that deals with molecules that have a center of 3D asymmetry
  • stems from carbon bonding
  • carbon binds to 4 different atoms
  • a molecule with one chiral carbon will have 2 enantiomer
  • the more chiral carbons in a molecule = more enantiomers created
71
Q

Enantiomers and their clinical relevance

A
  • chiral molecules that are non-superimposable mirror images of one another
  • different enantiomers can produce different clinical effects
  • 1/3 of drugs we administer are enantiomers

ex: side effects of one enantiomer of a drug can be different from another enantiomer of the same drug

72
Q

What is a racemic mixture? Examples?

A
  • racemic mixture Fontaine’s two enantiomers in equal amounts
  • 1/3 of the drugs we administer are enantiomers and almost all are prepared as racemic mixtures

ex: bupivacaine, ketamine, iso, and des (NOT sevo)

73
Q

Propofol MOA

A
  • direct GABA-A agonist = increased Cl- conductance = neuronal hyperpolarization
74
Q

Propofol dose

A
  • induction: 1.5-2.5 mg/kg

- infusion: 25-200 mcg/kg/min

75
Q

Propofol onset

A

30-60 seconds

76
Q

Propofol duration

A

5-10 mins

77
Q

Propofol clearance

A
  • liver (P450) and extrahepatic (lungs)
78
Q

Cardiovascular effects of propofol

A
  • decrease BP (decrease SNS tone and vasodilation)
  • decreased SVR
  • decreased venous tone = decreased preload
  • decrease contractility
79
Q

Respiratory effects of propofol

A
  • shifts CO2 response curve down and to the right = less sensitive to CO2 = respiratory depression/apnea
  • inhibits hypoxic ventilatory drive
80
Q

CNS effects of propofol

A
  • decreased cerebral oxygen consumption (CMRO2)
  • decreased cerebral blood flow
  • decreased ICP
  • decreased intraocular pressure
  • no analgesia
  • anticonvulsant properties
81
Q

What is propofol made from?

A
  • a 1% solution in an emulsion of egg lecithin, soybean oil and glycerol
  • most people with egg allergies are allergic to the whites. and lecithin is made from the yolk
  • no cross sensitivity b/w propofol and soy or peanuts
82
Q

Propofol infusion syndrome

A
  • propofol contains long chain triglycerides (LCT)
  • increased LCT impairs oxidative phosphorylation and fatty acid metabolism
  • cells (cardiac and skeletal muscle) get starved of oxygen
83
Q

Risk factors for propofol infusion syndrome

A
  • propofol dose > 4 mg/kg/hr (67 mcg/kg/min)
  • propofol infusion duration > 48 hours
  • children > adults
  • inadequate oxygen delivery
  • sepsis
  • significant cerebral injury
84
Q

Clinical presentation of propofol infusion syndrome

A
  • metabolic acidosis (base deficit > 10 mmol/L)
  • rhabdo
  • enlarged or fatty liver
  • renal failure
  • hyperlipidemia
  • lipemia (cloudy plasma or blood) may be an early sign
85
Q

How long is propofol good for in a syringe and as an infusion?

A
  • syringe: 6 hrs

- infusion/tubing: 12 hrs

86
Q

What preservatives are used in branded propofol?

A
  • Diprivan contains EDTA (disodium ethylenediamine tetraacetic acid) as a preservative
  • doesn’t cause issues for any specific patient population
87
Q

What preservatives are used in generic propofol?

A
  • metabisulfite: can cause bronchospasm in asthmatic patients
  • benzyl alcohol: avoid in infants
88
Q

How can propofol injection pain be minimized?

A
  • inject into a larger and more proximal vein
  • lidocaine
  • give an opioid prior to the propofol
89
Q

Antipruritic effects of propofol

A
  • 10mg of propofol can reduce itching caused by spinal opioids and cholestasis
90
Q

Antiemetic effects of propofol

A
  • 10-20 mg can be used to treat PONV

- or infusion at 10 mcg/kg/min

91
Q

How does fospropofol become active?

A
  • alkaline phosphatase converts fospropofol to propofol
92
Q

Ketamine MOA

A
  • NMDA antagonist (antagonizes glutamate)

- ketamine dissociates the thalamus (sensory) from the limbic system (awareness)

93
Q

What are the secondary receptor targets for ketamine?

A
  • opioid
  • MAO
  • serotonin
  • NE
  • muscarinic
  • Na+ channels
94
Q

Ketamine IV dose

A
  • induction: 1-2 mg/kg

- analgesia: 0.1 - 0.5 mg/kg

95
Q

Ketamine IM dose

A

4-8 mg/kg

96
Q

Ketamine PO dose

A

10 mg/kg

97
Q

Ketamine onset time

A
  • IV = 30-60 sec
  • IM = 2-4 mins
  • PO = variable
98
Q

Ketamine duration

A

10-20 mins

99
Q

Ketamine clearance

A
  • liver P450 enzymes
  • produces an active metabolite = norketamine (1/3-1/5 the potency of ketamine)
  • chronic ketamine use induces liver enzymes (ex: burn patients)
100
Q

Cardiovascular effects of ketamine

A
  • increased SNS tone
  • increased CO
  • increased HR
  • increased SVR
  • increased PVR
  • doses < 0.5 mg/kg don’t activate SNS
  • ketamine is actually a myocardial depressant. depressant effects will go unmasked in pt with depleted catecholamines (sepsis) or sympathectomy
101
Q

Respiratory effects of ketamine

A
  • bronchodilation
  • preserves upper airway muscle tone and reflexes
  • maintains respiratory drive
  • doesn’t significantly shift the CO2 response curve
  • increases oral and pulmonary secretions (increases risk of laryngospasm)
102
Q

CNS effects of ketamine

A
  • increased cerebral oxygen consumption (CMRO2)
  • increased cerebral blood flow
  • increased ICP
  • increased intraocular pressure
  • increased EEG activity
  • nystagmus
  • emergence delirium
103
Q

Ketamine emergence delirium (symptoms, treatment, risk factors)

A
  • s/s: nightmares and hallucinations
  • treat: Benzos (midaz > diazepam)
  • r/f: age > 15, female, dose > 2mg/kg, personality disorder
104
Q

Analgesic properties of ketamine

A
  • only induction agent that provides analgesia and opioid-sparing effect
  • relieves somatic pain > visceral pain
  • blocks central sensitization and wind-up in the dorsal horn of the spinal cord
  • prevents hyperalgesia after remi infusion
  • good for burn pt and chronic pain
105
Q

Etomidate MOA

A
  • binds to GABA and enhances receptors affinity for GABA neurotransmitter
106
Q

Dose of etomidate

A

0.2-0.4 mg/kg IV

107
Q

Onset of etomidate

A

30-60 sec

108
Q

Duration of etomidate

A

5-15 mins

109
Q

Clearance of etomidate

A

Hepatic P450 enzymes and plasma esterases

110
Q

Cardiovascular effects of etomidate

A
  • HD stability: minimal change in HR, SV or CO
  • SVR is decreased causing a small decrease in BP
  • does NOT block SNS response to intubation (esmolol or opioid will help)
111
Q

Respiratory effects of etomidste

A
  • mild respiratory depression
112
Q

CNS effects of etomidate

A
  • decreased CMRO2
  • decreased cerebral blood flow
  • decreased ICP
  • stable cerebral perfusion pressure
  • no analgesic effects
113
Q

Etomidate and myoclonus

A
  • involuntary skeletal muscle contraction, dystonia or tremor
  • etomidate causes an imbalance between excitatory and inhibitory paths in the thalamus = myoclonus
114
Q

Etomidate and seizure activity

A
  • in the patient with no seizure history, etomidate doesn’t increase the risk
  • if seizure hx: etomidate can increase seizure like activity and possibly seizures
115
Q

Etomidate and adrenal suppression

A
  • etomidate inhibits 11-beta-hydroxylase and 17-alpha-hydroxylase
  • cortisol and aldosterone synthesis are dependent on those enzymes
  • single dose of etomidate can suppress adrenal function for 5-8 hrs
  • avoid in septic or acute adrenal failure patients who need lots of cortisol
116
Q

What induction agent is most likely to cause PONV

A
  • etomidate
117
Q

What are the two sub-classes of barbiturates?

A

THIOBARBITURATES

  • sulfur in the second position that increases lipid solubility and potency
  • ex: thiopental, thiamylal

OXYBARBITURATES

  • oxygen in the second molecule
  • ex: methohexital, phenobarbital
118
Q

Thiopental MOA

A
  • GABA-A agonist: depresses the reticular activating system in the brainstem
  • low/normal dose: increases the affinity of GABA for its binding site
  • high dose: directly stimulates GABA-A receptor
119
Q

Thiopental dose

A
  • adult = 2.5-5 mg/kg

- child = 5-6 mg/kg

120
Q

Onset of thiopental

A

30-60 sec

121
Q

Duration of thiopental

A

5-10 mins

122
Q

Clearance of thiopental

A
  • liver (P450)
  • awakening is determined by redistribution (NOT metabolism)
  • repeat doses = tissue accumulation = prolonged wake up + hangover effect
123
Q

CV effects of thiopental

A
  • hypotension d/t ventilation and decreased preload
  • non-immunologic histamine release = hypotension (short lived)
  • baroreceptor reflex is preserved: reflex tachy helps to restore CO
124
Q

Respiratory effects of thiopental

A
  • repertory depression (shifts CO2 response curve to the right)
  • histamine release can cause bronchoconstriction
125
Q

CNS effects of thiopental

A
  • decreased CMRO2
  • decreased cerebral blood flow
  • decreased ICP
  • decreased EEG activity ( can cause burst suppression and/or isoelectric EEG = neuroprotection)
  • no analgesia
126
Q

When can thiopental be used for neuroprotection?

A
  • for focal ischemia (carotid endarterectomy or temporary occlusion of cerebral arteries)
  • NOT for global ischemia (cardiac arrest)
127
Q

Pathophysiology of acute intermittent porphyria

A
  • defect in heme synthesis where heme precursors build up (precursors can’t convert to heme)
  • heme is important in hemoglobin, myoglobin and P450 enzymes

succinylcholine-CoA + glycine = ALA synthase = precursors = heme

128
Q

Drugs to avoid in acute intermittent porphyria

A

Barbs, etomidate, glucocorticoids and hydralazine

*conditions to avoid: emotional stress, prolonged NPO

129
Q

Acute intermittent porphyria treatment

A
  • liberal hydration
  • glucose supplementation (reduces ALA synthase activity)
  • heme arginate (reduces ALA synthase activity)
  • prevention of hypothermia
130
Q

Risk of intra-arterial injection of thiopental and the treatment

A
  • causes intense vasoconstriction and crystal formation
  • leads to inflammation and tissue necrosis

TREATMENT

  • vasodilator (phentolamine or phenoxybenzamine)
  • sympathectomy: stellate ganglion or brachial plexus block
131
Q

Gold standard durch for electroconvulsive therapy and dose.

A
  • methohexital: decreases the seizure threshold producing a better quality seizure
  • dose: 1-1.5 mg/kg
132
Q

Dexmedetomidine MOA

A

Alpha2 agonist = decreases cAMP = inhibits locus coeruleus in the pons

133
Q

Demedetomidine dose

A
  • loading: 1 mcg/kg over 10 mins

- infusion: 0.4-0.7 mcg/kg/hr

134
Q

Demedetomidine onset

A

10-20 mins

135
Q

Demedetomidine duration

A

10-30 mins (after infusion stopped)

136
Q

Demedetomidine clearance

A

liver (P450)

Apex NCE Board Prep 2020 (5 decks)

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