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38 Cards in this Set

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What is first order elimination?
rate of elimination is proportional to the concenration.

the higher the concentration of drug the greater amount of drug is eliminated per unit time.

this is the more common type of elimination
What is zero-order elimination?
the rate of elimination is constant

independent of concentration

this is the less common type of elimination
What is Vd?
Vd describes how large a blood volume would be required to contain the entire ADMINISTERED dose at the measured concentration of drug in the blood
What is the Henderson-Hasselbalch Eq.?
pKa= pH + log [RH]/[R-] for acids

pKa= pH + log [BH+]/[B] for bases
How does ionization affect solubility?
At low pH, weak bases are in ionized form which makes them less lipid soluble and cannot cross membranes.
For ex. a drug that is a weak base cannot cross the membrane of the stomach because the pH of the stomach is really low and the weak base will be predominantly in it's ionized form.

Weak Acids are in the ionized form at high pH. For ex., in the high pH environment of the small intestines a drug that is a weak acid will predominantly in its ionize form therefore it will not cross the membrane of the small intestine.

ionized forms of drugs are less lipid soluble
Name some factors that influence the distribution of absorbed drug?
1. regional diff in blood flow (eg. brain vs. kidney?)
2) tissue mass
3) transport mechanism
4)permeability charachteristics
5) ion-trapping
6) nonspecific binding
What is the difference between drugs that exhibit one compartment vs two compartment distribution?
One Compartment Distribution
- rapid equilibrium is achieved btwn plasma and tissue distribution following a drug administration.
Two compartment
-rapid distribution to a central compartment (plasma) followed by slow distribution to other tissues/binding sites (2nd compartment).

causes a biexponential [plasma] time profile

repetitive administration, steady-state concentrations are achieved only after 5-6 elimination half-lives.

Ex. Digoxin, Lidocaine, Phenytoin

An administered dose is given and when steady state is achieved distribution continues and elimination starts.
Volume of Distribution?
volume of distribution (Vd) is a measure of how evenly the drug is distributed in the body

Vd= Dose/Cο
Vd= total drug in the body÷plasma concentration of the drug

Vd tells us the ability of drugs to distribute into the tissues. A large Vd signifies that most of the drug is being sequestered in some organ or compartment
What is bioavailability?
the fraction of the administered dose that reaches the systemic circulation unchanged

drug may have imcomplete bioavailability if it undergoes first-pass metabolism
What is drug elimination half-life?
the time required to eliminate one-half of the body content of a drug.

dependent on Vd and Clearance of Elimination

t1/2 = 0.69 x Vd x CL

When Vd is constant t1/2 is proportional to CL
What is steady-state concentration?
Steady-State Concentration, Css =
Dosing Rate/Elimination Clearance

There is a direct proportionality btwn dosing rate and steady-state plasma concentration

This is true for most drugs used in medicine because most drugs follow first-order kinetics of elimination.

** First-Order Kinetics of Elimination:
the rate of drug elimination is protoprtional to the amount of drug present in the body.
Describe the steps in Phase I Reactions
parent drug is converted to a more POLAR metabolite by introducing or unmasking a functional group on the molecule so that it can then be usually excreted.
Describe the steps in Phase II Reactions
some phase I metabolites are not eliminated rapidly & subject to phase II

endogenous substrate combines w/ the functional group derived from phase I rxns

result: high polar conjugate which is easily eliminated by the body
What is the role of Cytochrome P450?
Plays a critical role in Phase I reactions

-microsomal oxidation reaction

RH--> cyp 450 + oxidation steps --> ROH

remember Phase I rxn convert a parent drug (RH) to a more polar electrolyte by introducing or unmasking a functional group (in this case OH) so it can be excreted.
What factors affect drug metabolism?
1. Drug-age interaction
neonates and elderly have slow biotransformation

2. Drug-drug interactions
induction- pharmacokinetic tolerance enzyme inducer may stimulate metabolism simultaneously administered drug- decrease therapeutic effectiveness

3. Drug-endogenous substance interactions
2 drugs compete for same substrate eg. glucuronic acid for conjugation

4. Drug-disease interactions
liver disease (eg. cirrhosis and cancer) can impair microsomal oxidation ->slow metabolism
heart disease can limit blood flow to the liver can slow down the hepatic metabolism of a drug.

5. Drug-genetic interactions
mutation in genes coding for enzymes that metabolize drugs
How does protein binding affect drug distribution?
low protein binding generally leads to a large volume of distribution (drug being sequestered in some tissue or organ)

high protein binding = low Vd
what is the function of administering a loading dose?
loading dose can be used with certain medications to achieve an immediate therapeutic response

especially for drugs with long half-lives and for patients with critical disease states

is usually higher than maintenance dose

LD(mg) = Css x Vd(L/kg) x Wt(kg)

NOTE: Loading Dose does not bring you to steady state any FASTER
what is the function of administering a maintenance dose?
maintains desired concentration

MD(mg)= Vd (L/kg) x Wt(kg) x (Cmax-Cmin)
Detail some drug-drug interactions that affect absorption

Sucralfate + digoxin
Ciprofloxacin + Aluminum hydroxide
Tobramycin in an ascitic pt
●Sucralfate + digoxin
-Sucralfate coats stomach so digoxin is not absorbed
drug administration must be spaced
●Ciprofloxacin+ AlOH
-Chelation decreases absorption
-drug administration must be spaced
●Itraconazole + raniditine
-raniditine decreases stomach pH which decreases absorption of Itraconazole
Describe the neurochemistry of Autonomic nerves

what neurotransmitter is released by
Neurochemistry of Autonomic nerves
Pre-ganglionic cells release Ach
Post-ganglionic parasympathetic release Ach

Post-ganglionic sympathetic release NE

Adrenal gland releases EPI and NE

Exceptions: sympathetic fibers innervating sweat glands and some skeletal muscle vascular smooth muscle release Ach
Functional Effects of Parasympathetics on

GI tract
Eye: Pupillary Constriction (miosis)
Heart: Negative Chronotropy (decr. in hr)
Bronchioles: Constriction
GI tract: Increased Motility
Bladder: Stimulates Emptying (a lot of muscarinic receptors on the bladder)
Functional Effects of Sympathetics on

blood vessels
GI tract
metabolic functions
Eye: Pupillary Dilation
Heart: Increased Chronotropy and Inotropy
Bronchioles: Relaxation
Blood vessels: Constriction and Relaxation
GI: Decreased Motility
Bladder: Inhibits Emptying
Metabolic functions: Increased Blood Sugar
calcium funny current of the SA node leads to faster depolarization??? review
Describe the Autonomic influences on the eye
Sphincter (para)
Dilator (symp)
Ciliary Muscle (para)
Ciliary Body (symp)
sphincter cells are circular shaped cells that are innervated by para
dilators are innervated by sym nerves and its response is mediated by alpha receptors
ciliary m. changes shape of lens to accomodate for near objects, these express muscarinic receptors (para)
the ciliary body produces aqueous humor and is mediated by beta receptors (symp)
Types of adrenoreceptors, some of the peripheral tissues in which they are found and the major effects of their activation
tissue: most vascular smooth muscle, pupillary dilator muscle
actions: increase vascular resistance, contracts pupil

tissue: adrenergic and cholinergic nerve terminals, some vascular sm. muscle
action: inhibits transmitter release and contracts some vascular smooth muscle

tissue: heart, JG cells
Actions: stimulates heart rate and force of contraction, stimulate renin release from JG cells (leads to angiontensin II which increases Blood Pressure and can cause hypertension)

tissues: Respiratory, uterine and vascular smooth muscle, liver, pancreatic B cells, somatic motor nerve terminals (voluntary)
actions:relaxes resp., uterine, and vasc. sm. muscle, stimulates glycogenolysis, stimulates insulin release (cells are able to take the glucose in )and causes tremor in voluntary muscle.

Dopamine 1 acts on renal and other splanchnic blood vessels to relax them and reduce resistance

Dopamine 2 acts on nerve terminals to inhibit adenylyl cyclase
Beta 3 receptors are found on fat cells and stimulate lipolysis
Describe the alpha 1 signal cascade

α1 adrenergic signaling, e.g. in vascular smooth muscle
agonist binds alpha-1 receptor which causes the GDP to be phosphorylated to GTP.

Phospholipase C cleaves releases IP3 and DAG
IP3 acts to free stored Calcium which stimulates Ca-dependent protein kinase to become activated protein kinase which produces biological effects in vascular smooth muscle you have actin and myosin interaction leading to contraction.
DAG stimulates protein kinase C to become actived PKC
Describe the alpha 2 signal cascade
when an agonist bind to an alpha-2 receptor(alpha-i) GDP is phosphorylated to GTP which inhibits adenylyl cyclase--> ATP is not cleaved to cAMP and biological effect is inhibited
MLCK when phosphorylated becomes inactive

MLCK is needed to phosphorylate myosin-LC so that Myosin-LC-PO4 can become activated and actin can bind to it leading to contraction
α2 signaling e.g. in adrenergic in nerve terminal
agonist binds to alpha-2 receptor in the noradrenergic nerve terminal, this inhibits NE release. This is a form of Negative Feedback..when NE is release some is recycled by reuptake and soem NE binds to the alpha-2 receptor to inhibit NE release.
α2 signaling e.g. in vascular smooth muscle constriction
alpha-2 agonist inhibits ATP being cleaved to cAMP which would stimulate MLCK phosphorylation

MLCK then goes down another pathway to stimulate myosin light chain by phosphorylation which leads to myosin light chain phosphorylation (actin binds and muscle contracts) and Myosin Light Chain relaxation
β1 receptor signaling in cardiac pacemaker cells
agonist binds beta receptor which phosphorylates Gs GDP to GTP this stimulates adenylyl cyclase so that ATP is cleaved to cAMP

Biological effect is phosphorylation of L-type calcium channels and increased calcium current during phase 4 depolarization
cAMP can bind to If funny current channels which causes increase opening time of that current and more current generated during hyperpolarization. This increases the heart rate.
β1 receptor signaling in cardiac myocyte
Biological effect is phosphorylation of calcium channel that increases open probability time, leads to increased SR calcium release
β2 receptor signaling in smooth muscle
β2 stimulates ATP cleavage to cAMP

cAMP stimulates phosphorylation of MLCK

some MLCK is timulated to bind actin and produce contraction
opposite of alpha-2
What are some Direct Acting Sympathomimetics:
Endogenous Compounds
Relative Potency of Direct Acting
α1-receptors EPI≥NE>>Iso
α2-receptors EPI≥NE>>Iso
β2-receptors Iso>Epi>>NE
β1-receptors Iso>Epi=NE
Cardiovascular effects of direct acting sympathomimetics
need notes
Endogenous Adrenergic Agents
Epinephrine (stimulates α1, α2, β1 and β2)
Physiological effects:
Low rates
lower diastolic BP
Increase CO
Higher rates
Increase TPR and CO

Cardiac Arrest

Cerebral hemorrhage
Cold extremeties
Pulmonary Edema

Later term pregnancy
Norepinephrine (stimulates α1, α2 and β1 receptors)
Physiological effects:
Increase diastolic BP
Increase CO
Increase TPR
Decrease HR (baroreflex)
Overall increase MAP

Limited to shock


Late term preganancy and pre-existing vasoconstriction
Dopamine (stimulates D1,D2, β1, α1 and α2)
Physiological effects:
Low rates
Decreases TPR (D1 receptor)
Increases CO (β1)
Higher rates
Increases MAP and TPR (α1)

Low BP (at low infusion rates)
Ischemia (high infusion rates)

Cardiogenic Shock

Ventricular fibrillation
Synthetic Sympathomimetics
Isoproterenol (stimulates β1 and β2 receptors)
Physiological effects:
Decrease TPR (β2 receptor)
Increase CO (β1)
Small increase in MAP
Bronchodilation (β2)


Bradycardia/heart block
when TPR is high
Bronchospasm w/ anesth