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185 Cards in this Set

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Define pharmacokinetics.
what the body does to the drug.
What are the 4 paths involved in pharmacokinetics?
Absorption, Distribution, Metabolism, Elimination
List the routes of administration.
Topical, enteral (oral, rectal), parenteral (IV, subcut, transdermal, sunlingual).
Topical administration is not just skin, it's also...?
Inhalers (ie asthma - topically applied to smooth muscle of lungs), eye & ear drops.
What's special about topical admin?
It's the only route that doesn't involve using the blood stream! You apply the med to the affected site.
With oral meds, bioavailability is...? Because why?
Less because of the 1st pass effect (it goes to the liver 1st).
When administering enteral meds, you need to make sure the pt has a....?
Healthy GI so that they can absorb the medication - this goes for both oral and rectal meds.
What's special about all parenteral route meds?
They completely bypass the 1st pass effect because they're bypassing the GI. Pt doesn't need to have a healthy GI to get parenteral route meds.
With IV administration, bioavailability is...? Because why?
Full bioavailability because IV is going directly into the blood.
Define 'bioavailability'.
The ability of a drug to reach the bloodstream & it's target tissues.
Define 'absorption'.
The movement of the drug from the site of administration, across body membranes into circulating fluid (bloodstream).
6 factors that affect drug absorption?
(acronym = ADD BEG)

Admin route
Drug formulation (excipient)
Dosage
Blood flow to admin site
Enz's of GI
GI motility (ie having food in stomach delays drug abs. need to speed drug abs? -give on an empty stomach!)
Reasons to add excipient to a drug?
So that you can physically hand the person the pill because the amount of med needed to exert effects is so small you can't actually hold it in your hand.

Excipient is used for rapid & delayed release drugs too - to speed or slow dissolution rate (ie anti-depressants you want slow release from excipient; pain killers you want quick release from excipient).
Before meds are absorbed they must 1st be...?
Dissolved - to separate from the excipient. This can happen in the stomach or the small intestine. Like dissolves like and water soluble drugs dissolve well in stomach & small intestines where fluids are largely composed of water.
If fluids in the stomach and the small intestine are mostly water, how do we get lipid soluble drugs to dissolve?
Recommend fat soluble drugs be taken with food so they can dissolve easier (food has a little bit of fat content to it).
If a med is highly water soluble you can admin it...? But lipid soluble drugs can never be admin'd via this route because...?
IV. Lipid soluble drugs can't be admin'd this way because they can clump up in the bloodstream and kill the patient. :(
What aspect of pharmacokinetics does IV skip?
Absorption.
What are the 2 processes by which absorption happens? What types of particles are they used for?
Diffusion - for small non-polar meds (just use the [ ] gradient)

Active transport - for large polar meds (needs energy)
What does the med do as soon as it is absorbed? What happens when it does this?
Binds albumin in the blood & becomes inactive. Only free drug remains active and can distribute across to target tissue to cause effect.
Why would you need to hold a drug like Warfarin before doing surgery?
You need to give it time for the Warfarin to be pulled off of albumin. The concentration of Warfarin-albumin in the blood is high. So, if you don't hold Warfarin and wait for the drug to be eliminated, surgery could cause blood loss.
What form does an acid or a base need to be in for it to be absorbed through a lipid membrane?
Uncharged and non-polar form.
Describe why a weakly acidic drug so absorbed so well in the stomach.
AH + H2O <-> A- + H+ + H2O

The stomach is an acidic enviro therefore high [H+]. So when AH (the acid in the uncharged nonpolar form) dissociates and becomes charged (A-), a H+ is quick to bind it and return the acid to it's uncharged nonpolar form (AH) in which it can be absorbed through the lipid bilayer.
Why are weakly acidic drugs poorly absorbed in the small intestines?
Because the small intestine is a basic enviro and so low [H+]. Therefore the charged polar form of the acid is favoured (A-) and, in this form, it can not permeate the lipid bilayer.
Acids are...? Bases are...?
H+ givers. H+ getters.
An example of an acidic drug.
Aspirin.
What form is a weakly acidic drug in the stomach? In the small intestines? Where is it absorbed mostly?
Stomach - nonpolar & non-ionized
Small intestines - polar & ionized
Absorbed in the stomach
What form is a weakly basic drug in in the stomach? In the small intestines? Where is it absorbed mostly?
Stomach - polar & ionized
Small intestines - nonpolar & non-ionized
Absorbed in the small intestines
A drug is absorbed in the stomach so avoid ingesting...?
Anything that affects pH (ie Tums) - impairs drug absorption & decreases efficacy
A drug is absorbed in the small intestine so avoid ingesting...?
Anything that decreases intestinal transit time (ie laxatives) - impairs drug absorption & decreases efficacy
What's pKa?
The strength of an acid. The pH @ which [acid] in ionized form = [acid] in non-ionized form.
The faster the drug absorption the faster the...?
Onset of drug action. Which is why IV exerts effect so quickly b/c it skips absorption all together.
Local enviro directly influences drug abs via...?
Ionization. Can make this work to your advantage - ie enteric-coated oral meds will absorb in basic enviro of small intestine.
The patient has had a high fat meal - what will this do in terms of stomach motility and absorption of some oral drugs?
Slow stomach motility and therefore decrease absorption of some oral meds.
The patient has had some citrus fruit juice with her weakly acidic meds. What will happen?
Gastric acidity will increase and hasten the absorption of the weakly acidic meds.
The patient has consumed something basic with her enteric-coated meds. What will happen?
Premature break down of the drug before it reaches the small intestine
Define distribution.
Process of transporting drugs throughout the body.
4 factors that can affect distribution.
acronym: BOMS

Blood flow
Organ size (diffusion is slower in smaller organs)
Mechanical barriers (ie blood brain barrier; fetal-placenta barrier).
Solubility of med
Describe the distribution of parenteral admin drugs.
Drugs distribute to target tissue & exert bio/therapeutic effect b/c they go directly into the blood and have nothing to do with the GI and trying to get absorbed.
Describe the distribution of oral admin drugs.
Drugs first distributed to the liver via hepatic portal circuit (1st pass effect!)
How does the 1st pass effect affect oral admin drugs?
It metabolizes a fraction of the drug & renders it biologically inactive - it reduces bioavailability of the drug. Therefore you need to admin more than is needed to exert the desired therapeutic effect.
Describe the distribution of rectal admin drugs.
There's partial avoidance of the 1st pass effect before it's distributed to target tissues.
Steps of 1st pass effect?
-drug is absorbed
-drug enters hepatic portal circ & goes to liver
-hepatic microsomal enz's metabolize drug to inactive forms
-drug conjugates leave liver
-distribution to gen circ
Which tissues have the ability to accumulate & store drugs after abs?
bone marrow, teeth, eyes, adipose, tissue
Define metabolism.
Process by which drugs are biotransformed into water soluble compounds that are easily excreted via the kidneys.
3 things that can happen as a result of drug metabolism.
-bio active drug metabolized into an inactive water soluble metabolite thereby terminating therapeutic response OR
-bio active drug metabolized to form metabolites that are still bio active thereby prolonging therapeutic response
-bio inactive drug (PRODRUG) is activated via metabolism thereby initiating therapeutic response (ie chemo)
The main organ for drug metabolism.
Liver! Therefore it has a key role in terminating drug action and making drugs water soluble so that they may be excreted in the urine via the kidneys.
Phase 1 & phase 2 of drug metabolism other wise broadly known as...?
Hepatic drug metabolism.
Phase 1 rxns include?
acronym: HOR

Hydrolysis
Oxidation
Reduction

**may or may not inactivate drug***
Phase 2 rxns include?
Conjugation

**mostly inactivates drug**
What does a phase 1 rxn do?
Makes non-polar drugs polar by adding polar functional group (ie -OH, -SH, -NH2)
What enz's do phase 1 oxidation rxns use?
CYP-450, CYP-448, Liver Alcohol Dehydrogenase (LADH), Monoamine Oxidase (MAO - think psych meds for DA, NE, and serotonin!), Aldehyde Oxidase (AO; ***is ONLY for booze! - not a multifunction oxidase)
What do phase 1 reduction rxns do?
Add H+ (think OILRIG!)
What do CYP-450 enz's do?
Replace -CH or -NH groups w/ -OH
What do CYP-448 enz's do?
Add oxygen atom b/w C=C
What factors cause variation in [CYP]?
Ethnicity, age, pt health, some drugs (antibio's), smoking , grapefruit juice
How does smoking affect CYP activity?
Increases therefore increases oxidation rxns.
How does grapefruit juice affet CYP activity?
Decreases metabolism of drug therefore it stays active long -> OD risk!
How does Rifampin (antibio) affect CYP-450 enz's?
Increases CYP synth -> increases metabolism & decreases plasma [ ] of co-administered drugs (ie antidep's, estrogens, antiarrhythmics, etc).
How does Erythromycin (antibio) affect CYP-450 enz's?
Inhibits CYP activity -> decreases metabolism & increases plasma [ ] of co-administered drugs (ie antidep's, estrogens, antiarrhythmics, etc)
What do phase 2 rxns do?
Conjugate drug (or it's biotransformation product) w/ a very water soluble compound to increase it's water solubility.

Not every drug goes through phase 2 b/c some drugs are already water soluble enough to be excreted via urine.
What is the only thing that phase 2 rxns can activate?
Prodrugs.
What are the phase 2 enz's and what do they do?
Glucuronyl transferase - does glucuronidation (most important & most common) replaces -OH or -SH w/ glucuronic acid to increase water solubility

N-acetyltransferase - replace -OH, -SH, -NH2 w/ acetate to inc water solubility

sulfotransferase - replace -OH or -SH w/ sulfate to inc water solubility

glutathione S-transferase - forms adduct b/w drug & glutathione to inc water solubility
Under normal circumstances how is acetaminophen's drug action terminated?
Mostly by phase 2 rxns and a small amount my CYP-450 phase 1.
What happens in an acetaminophen overdose?
-Phase 2 hepatic enz's are over-saturated thereby causing reliance on phase 1 CYP-450 enz's.
-CYP-450 oxi's the tylenol producing NAPQI which binds liver proteins & causes permanent damage
-usually glutathione comes in & metabolizes NAPQI making it inert and water soluble for excretion but in cases of OD, glutathione is saturated
-liver failure 16-36hrs post-OD
What common socially consumed substance is known to induce phase 1 rxns (CYP-450 metabolism)?
Ethanol.
What is Acetylcysteine?
A drug that acts as a replacement for glutathione and can be used to treat acetaminophen overdose in that it metabolizes NAPQI so as to stop liver damage.
How can you treat ASA overdose?
-manipulate pH of the urine to excrete ASA as much as possible
-ASA is a wk acid
-pH of urine is acidic therefore ASA will be in it's non-ionized nonpolar form and as a result it can cross lipid bilayers and be reabsorbed from the filtrate which we don't want
-inc the pH of the filtrate so admin sodium bicarb so that ASA is in it's charged polar form and can't cross lipid bilayers therefore can't be reabsorbed from the filtrate and is excreted
If drugs are to be excreted through the kidneys, they should be in what form?
Polar & ionized.
How are highly fat-soluble metabolites eliminated? How are they excreted?
Eliminated in the bile.
Excreted in the feces.
Why might the drug action of highly fat soluble drugs be prolonged?
B/c they're highly fat soluble, they pass through lipid bilayer w/ ease and so they could get reabsorbed.
How would you adjust the dose of a drug for a patient with liver damage?
Decrease it.
The rate of excretion determines...?
-[drugs] in blood & tissues
-[drugs] in blood determines duration of action (liver & kidney fail can inc blood lvls)
What is the primary site of excretion?
Kidneys
What can pass through the glomerulus?
-free drugs, polar agents, electrolytes, small molecules
What cannot pass through the glomerulus?
-proteins, blood cells, conjugates, drug-protein complexes
What can pass through the renal tubules?
-non-ionized & lipid soluble molecules
What cannot pass through the renal tubules?
-ionized & water soluble molecules
Which to patient pop'ns should you pay special attention to with ability to excrete meds & why?
Infants & older adults b/c metabolic enz activity & secretion methods are less active.
Foods that acidify the urine?
Cranberries, cheese, eggs, lentils, pasta, grains, plums, prunes
Foods that alkalinize the urine?
Milk, veggies (not corn), fruits (not cranberries, plums, prunes)
What is the solubility of the agents that may be removed excreted via the lungs?
Water soluble (ie ethanol)
Factors that affect excretion of drugs via lungs?
Lung perfusion
Solubility
Diffusion
Gas exchange
Why might patients receiving IV meds have a funny taste in mouth?
Because water-soluble drugs can be secreted into saliva.

Water-soluble drugs can also be secreted in sweat & breast milk.
Define enterohepatic recirculation.
Bile circulated back to liver (re-using bile salts).
What happens to highly fat soluble drugs when they are reabsorbed from the GI?
They will ultimately be metabolized by the liver, go through hepatic drug metabolism, become water soluble and be excreted in the urine.
List pharmacokinetic pathways in order.
Absorption
Distribution
Metabolism & Elimination
Excretion
Define elimination.
Process by which drug is removed from systemic circulation.
What do the 4 pathways of pharmacokinetics control?
-Therapeutic [drug] in plasma
-Onset, peak, intesnity of drug action, duration
-dosing interval
Onset of drug action depends on?
Rate of absorption & distribution
Intensity of drug action depends on?
Amount of drug absorbed & distributed
Duration of drug action
Rate of drug metabolism & elimination
Define bioavailability.
% admin'd dose that reaches plasma in chem unchanged & bio active form
4 factors that influence bioavailability?
-1st pass hepatic metabolism
-chem instability
-drug formulation
-plasma protein binding
Define distribution.
Process by which drug reversibly leaves blood stream & enters body tissues.
Define Apparent Volume of Distribution.
-volume into which a drug is known to distribute w/in the body
-ratio of amt of drug in body to [drug] in plasma

Vd = (amt drug in body) / (plasma [drug])

-may be expressed in L or L/kg (if does is variable due to weight as w/ children & the obese)
Define Therapeutic Concentration.
-[drug] in plasma w/in therapeutic concentration range specific to that drug
-expressed as [D]th
-mg/L or ug/L
Define Loading Dose.
-Dose od drug to prime blood w/ a plasma lvl sufficient to quickly induce therapeutic response.
-Always > maintenance dose
-use top of therapeutic range ([D]o)

Wd = [D]o X Vd
How would you calculate single dose of a drug?
Wd = [D]pl X Vd

**[D]pl means middle of therapeutic range***
Define the Plateau Principle.
"95% of the steady state will be reached after 4 half-lives (t1/2)"
-drug EQM is reached after 4 t1/2's (at this point, what goes into systemic circulation is balanced by what is eliminated)
-after u start, stop or change a dosage regimen it will take 4 t1/2's for [drug] in plasma to be stable
-therapeutic effect may not be robust until this is over
Define Maintenance Dose.
Dose required to maintain plasma [drug] w/in therapeutic range.
-always < loading dose

Wd = [D]pl X T X Clr

**[D]pl is the middle of the therapeutic range***
Define Clearance.
Volume of plasma completely cleared of drug per unit time (L/hr)

Clr = k X Vd

k = 0.693 / (t1/2)
Define Dosing Interval.
Amount of time b/w doses.

log ( [D] / [Do] ) = - ( k / 2.303 ) X T

*** [D] is bottom of therapeutic range***
What is [Do]?
Top of therapeutic range
What is Vd?
Apparent volume of distribution; ratio of amt of drug in body to plasma [drug]
What is k?
Elimination rate constant.
k = 0.693 / (t1/2)
What is [D]pl?
Middle of therapeutic range.
What is T?
Dose interval (time b/w doses).
What is [D]?
[drug] in plasma after given amt of time

OR

Bottom of therapeutic range
How would you calculate dose when bioavailability is not 100%?
Loading Dose / Maintenance Dose
Henderson Hasselbalch Eq'n?
pH = pKa + log ( [A-] / [AH] )
How would you calculate the fraction (Fr) of a drug absorbed in a location (ie stomach, small intestine)?
1/Fr = 1 + [A-] / [AH]

And then multiply Fr by 100% to get it as a %.
How would you calculate mass of med abs'd in a location (ie stomach, small intestine)?
% med abs'd / 100% = X / dose(mg)

Solve for X.
How would you calculate amount of drug absorbed?
Amount of drug absorbed = Fr X amount of drug available for absorption
How would you calculate the amount of tablets to admin?
A = (D / H) x S

D is dose ordered OR desired dose
H is dose on hand OR available dose (dose per tab on drug label)
S is stock
How would you calculate the amount of liquid suspension to admin?
A = (D / H) x S
What is the pH of the stomach?
2
What is the pH of the small intestine?
8
Define Pharmacokinetics.
Study of drug mov'nt (kinetics!) throughout the body.
Define Pharmacodynamics.
Study of how drug changes (dynamics!) the body.
Quantal Data refers to...?
Yes/No patient response. (ie did the drug reduce systolic BP by 20mmHg? Y/N)
Does not discuss magnitude of response or maximal effect of drug.
What is ED50?
Median Effective Dose
-the dose needed to produce specific therapeutic response in 50% of pts
What is the standard dose?
ED50 - the Median Effective Dose
What is the average dose?
ED50 - the Median Effective Dose
Define Therapeutic Index?
Ratio of a drug's LD50 (or TD50) to it's ED50.

TI = TD50 / ED50
What is LD50?
Dose of drug that will be lethal in 50% of test animals.
What is TD50?
Dose that will produce a given toxicity in 50% of pts.
How would you calculate therapeutic index?
TI = TD50 / ED50

OR

TI = LD50 / ED50
Define Therapeutic Window.
Range based on minimum effective therapeutic [ ] & minimum toxic [ ] for a specific toxic effect.
What does it mean if a drug has a low therapeutic index?
Means the therapeutic window is narrow or ED50 & LD50 may even overlap some therefore it's a high alert medication b/c there is a small difference in amount of drug that could produce therapeutic response and lethal or toxic effects.
What info do dose-response curves give you?
Magnitude of bio effects of drug.
Info to determine:
-therapeutic range
-efficacy
-potency
Define Potency.
-compares the doses of 2 or more drugs w/ respect to how much drug is needed to produce a specific response.
-Str of a drug @ a specific [ ] or dose.
Define Efficacy.
Ability of drug to produce the desired effect.
The % of the max bio effect.
How much of a highly potent drug do you need to produce a therapeutic response?
A small dose.
Define Association.
Rate of drug-receptor complex formation. k1
Define Dissociation.
Rate of drug dissociating from receptor. k-1
What will the association (k1) and dissociation (k-1) be like for a drug that has high affinity for a receptor?
Association (k1) will be fast.
Dissociation (k-1) will be slow.
What will the association (k1) and dissociation (k-1) be like for a drug that has a low affinity for a receptor?
Association (k1) will be slow.
Dissociation (k-1) will be fast.
What is the dissociation constant?
(Kd) = k-1 / k1
What kind of affinity do drugs with a low Kd have for a receptor?
High.
What kind of affinity do drugs with a high Kd have for a receptor?
Low.
List 3 types of agonists.
-full
-partial
-inverse
List 4 types of antagonists.
-reversible
-competitive
-non-competitive
-irreversible
Define full and partial agonists.
Both bind same rec as endogenous ligand & produce same signal as endogenous ligand.

Full agonists - produce the full effect of the endogenous ligand.
Partial agonists - only part of the endogenous ligand effect.
Partial agonist efficacy vs full agonist efficacy.
Partial < Full
Define Inverse Agonist.
Binds same rec as natural ligand but induces opposite response of the natural ligand. This only happens when recs have an intrinsic (basal) lvl of activity (constitutive activity).
Define Constitutive Activity.
Receptors exert a bio effect independent of natural ligand.
What kind of efficacy do inverse agonists have?
Negative.
Define Antagonist.
Bind same rec as natural ligand but DON'T produce the same effect as the natural ligand.
What kind of efficacy do antagonists have?
None!
All agonists are _______ agonists.
Complete.
What are the 2 types of reversible antagonists?
Competitive and Non-Competitive.
Define Competitive Antagonist.
-competes for same rec as natural ligand
-blocks natural ligand from binding its rec
-always dissociates from rec
Define Non-Competitive Antagonist.
-binds a site other than endogenous rec binding site & changes conformation of rec so natural ligand can't bind
-poor clinical utility
-usually illicit drugs (ie PCP; ketamine)
Define Irreversible Antagonist.
Binds rec site & does not dissociate from rec.
k-1 = 0
Kd is very low and affinity is very high
poor clinical utility
bio weapons (ie cholinesterase inhibitors - 'nerve gases')
What's the only way an irreversible antagonist can be 'reversed'.
When the receptor ages and gets phagocytosized.
Why are G-protein coupled receptors (GPCR) the most sophisticated cell receptor?
B/c they're not just turning on/of.
They are used for neurotransmitters, light, odorants, hormones, prostaglandins.
What do G proteins do?
Stimulate effectors to produce intracellular changes.
What do Gs proteins do?
Stimulate effectors.
What do Gi proteins do?
Inhibit/tone them down effectors.
What effectors can G proteins stimulate?
Ion channels
Adenylyl cyclase
Phospholipase C (PLC)
Which effectors are Gs and Gi associated with?
Adenylyl cyclase
What does Adenylyl cyclase do?
It starts the cAMP signal transduction pathway. Adenylyl cyclase makes cAMP from ATP. cAMP is the 2nd MSN.
Which effector is Gq associated with?
Phospholipase C (PLC)
What does PLC do?
It starts the phosphatidylinositol signal transduction pathway. PLC cleaves PIP. This produces IP3 & DAG which are 2nd MSNs!
What's the 2nd MSN in ion channels?
The ion moving through the channel.
What is Gs action on adenylyl cyclase?
Stimulates.
What happens when adenylyl cyclase is stimulated?
Converts ATP into cAMP (2nd MSN) which binds & activates protein kinases. Protein kinases activate enz's via phosphorylation.
What is Gi action on adenylyl cyclase?
Inhibition.
What happens when adenylyl cyclase is inhibited?
No cAMP is being made and so no protein kinases are activated therefore no activation of enz's.
What is Gq action on Phospholipase C (PLC)?
Gq activates PLC which cleaves PIP to make two 2nd MSNs IP3 & DAG. IP3 binds sarcoplasmic reticulum & stims Ca2+ release into cytoplasm (for muscle contraction).
How does bronchodilation happen?
Salbutamol (bronchodilator) will bind beta 2 adrenergic rec. Activates Gs which activates adenylyl cyclase which converts ATP to cAMP which activates enz's which sequester Ca2+. Decreasing Ca2+ causes relaxation of bronchial smooth muscle.
How can we decrease stomach acid production?
Misoprostol (peptic ulcer drug) will bind Gi-linked prostaglandin E1 rec. Which inhibits adenylyl cyclase which decreases cAMP production. Protein kinases are not activated by cAMP and therefore enz's & pumps that help produce stomach acid are no longer activated. So stomach acid production goes down...
What is Misoprostol's other function? Why? And what is it called when it performs its other function?
Uterine contraction. Can be used for chemical abortion. Because prostaglandin E1 receptors are also located in the uterus. It's called Cytotech when used for chem abortion.
What is the drug that may be used to terminate postpartum hemorrhage? How do they work?
Ergonovine. Ergonovine binds Gq-linked prostaglandin E1 rec in uterus & Gq-protein linked alpha 1 adrenoreceptors in bv's. Rec binding stimulates PLC to be cleaved to IP3 and DAG (2nd MSNs). IP3 binds sarcoplasmic reticulum causing Ca2+ release into cytoplasm. Ca2+ release causes smooth muscle contraction in the uterus & blood vessels.
What is the bone major thing you should monitor the patient for when administering ergonovine for terminating postpartum hemorrhage?
Dangerous increases in BP b/c contraction of bv smooth muscles also happens as a side effect.
Define Adverse Drug Event (ADE).
Pt exp's injury from using
Define Adverse Drug Rxn.
Pt exp's injury from drug @ normal dose. Unpredictable. Ie. Allergy
Define Medication Error.
Mishaps that occur during Rx, transcribing, dispensing, admin, monitoring.
Define Near Miss.
Med error stopped before harm could occur to patient.
What's the process of meds getting to the pt (& subsequently the lvls @ which an error can happen)?
MD Rx's order
RN transcribes order
Pharm or MD enters order
Pharm prep's & dispenses med
RN admins med
Define omission error.
Drug wasn't given.
Examples of Rx error?
Handwritting, look alike & sound aline names
Define Unauthorized Error.
Giving something different than what the pt was meant to have.
Define Dosing Error.
Calculation error (ie ped meds need to be adjusted for their weight)
Define Admin Error.
Med given via the wrong route.