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Definition of Pharmacology
science of the interaction of chemicals with living systems at the molecular level
Definition of Toxicology
Branch of pharmacology that deals with UNDESIRABLE EFFECTS of chemicals on living systems
Definition of Drugs
Chemicals that alter the function of living systems by interactions at the molecular level
Definition of Pharmacogenomics
-the relation of the individuals genetic make up to his/her response to specifc drugs

*future clinicians may be able to screen every patient for a variety of such differences before prescribing a drug-- DNA profiling to predict responses to drugs
Definition of Pharmacokinetics and Pharmacodynamics
Pharmacokinetics
-WHAT THE BODY DOES TO THE DRUG
-the actions of biological system on drugs including absorption, distribution, and elimination

Pharmacodynamics
- WHAT THE DRUG DOES TO THE BODY
-describes the detailed actions of drugs on living systems
Name the three types of chemical forces or bonds and describe each type
1) Covalent: very strong; NOT reversible under biological conditions; longer acting

2) Electrostatic: more common than covalent; varies between strong and weak linkages (weaker than covalent)

3) Hydrophobic: quite weak; shorter acting
Weaker drug receptor bonds usually are more _______.
highly selective

*weaker bonds required a very precise fit of the drug to its receptor if an interaction is to occur
*if you want a highly selective drug that is short acting, you would avoid a covalent bond.
How can a drug interact with one receptor type and not with others?
A receptor and drug is analogous to a lock and key. Just as only those keys with the proper fit a particular lock..

Only those drugs with the proper size, electrical charge, shape, and anatomic composition will interact with a specific receptor.
what is constitutive activity?
even in the absence of agonist, there is some activity at receptor site
what are agonist drugs?
Agonist drugs activate the receptor
what are partial agonist drugs?
drugs that bind to receptors but do not evoke a full response
What are inverse agonists?
drugs that reduce the constitutive activity, opposite effects of agonist activity
What are antagonist drugs?
drugs that block the receptor
(prevent binding by other molecules)
what are the 2 types of allosteric modulators.
Positive allosteric modulators (PAM)
-boost what the neurotransmitter does

Negative allosteric modulators (NAM)
-block what the neurotransmitter does

*these allosteric molecules have little or no activity when the neurotrasmitter is absent
what are the different mechanisms of drug permeation?
1) passive diffusion
2) aqueous diffusion
3) lipid diffusion
4) special carriers
5) endocytosis/exocytosis
If a drug is in lipid soluble form during passage down renal tubule, a big fraction will be reabsorbed by passive diffusion. How do you excrete the drug?
Adjust the urine ph to get drug in ionized state.

Weak acids excrete faster in alkaline urine

Weak bases excrete faster in acidic urine
Name 2 drugs that are antagonists to both beta and alpha receptors.
Labetalol and carvedilol

B1=B2 >/= A1 >A2

(review selectivity of antagonists for adrenoceptors pg 152)
what are the beta adrenoceptor antagonists that are equally selective to B1 and B2
Propranolol, Carteolol, Penbutolol, Pindolol, Timolol
(review selectivity of antagonists for adrenoceptors pg 152)
what drugs are used for the management of aortic dissection?
Sodium nitroprusside dilates both arterioles and venules, favoring venous pooling and afterload reduction. The reduced blood pressure would typically cause a reflex increase in myocardial rate and contractility--NOT desired in this case. The addition of a beta-blocker reduces the beta adrenergic receptor mediated cardiac effects.
what beta adrenoceptor antagonist drugs are more beta1 selective, ?

(important to know if you are deciding to give a beta blocker to a diabetic patient-- b/c if you block beta2 receptors then you are blocking glycogenolysis-- which is bad for diabetics who are prone to hypoglycemia)
metoprolol, acebutolol, alprenolol, atenolol, betaxolol, celiprolol, esmolol, nebivolol
what is the antidote for beta blockers?
Glucagon stimulates the heart via glucagon receptors, which are not blocked by B antagonists.
TRUE OR FALSE.

Antihypertensive properties of beta-blockers may be reduced by concurrent administration of nonsteroidal anti-inflammatory drugs.
True
Name Potassium sparing diuretics.
Spirnolactone

Amiloride

Eplerenone

Traimterene
site of action of carbonic anhydrase inhibitors--- diamox, acetazolamide, dazamide, diamox sequels
Proximal Convoluted Tubule (PCT)
site of action of Osmotic diuretics-- mannitol
Proximal tubule
Descending limb of Loop of Henle
site of action of loop diuretics-- furosemide, bumetanide, torsemide, ethacrynic acid
Thick Ascending limb of loop of henle
site of action of Potassium sparing diuretics--spirnolactone, triamterene, eplerenone, amiloride
distal tubule
site of action of thiazide diuretics-- hydrochlorothiazide, chlorithalidone, metolazone, etc
distal convoluted tubule
what antihypertensive drug group is beneficial for diabetics?
ACE inhibitors--are useful in treating diabetics b/c it improves intrarenal hemodynamics, with decreased glomerular efferent arteriolar resistance and a resulting reduction of intraglomerular capillary pressure (see pg182).

Also extremely useful for kidney disease, heart failure, and after an MI.
what is sodium nitroprusside used for?
hypertensive emergencies and severe heart failure

it is a powerful parenterally administered vasodilator that dilates both arterial and venous vessels-- decreased PVR, BP and venous return
what antihypertenisve drug is associated with lupus-like syndrome?
hydralazine
what are some adverse effects of thiazide diuretics?
-elevated serum uric acid levels (gout)
-increased LDL and total chol (hyperlipidemia)
-decreased insulin secretion and glucose tissue utilization (hyperglycemia)
-hyponatremia
what part of the renal tubular transport system is considered to be the major site of reabsorption for filtered organic solutes and water.
-85% NaHCO3, 60% H20, and over 60% K+, Ca2+, and Na+.
PCT- proximal convoluted tubule
what is the MOA of Carbonic Anhydrase Inhibitors?
Diuretics: Carbonic Anhydrase Inhibitors-- (diamox, actetazolamide, dazamide, diamox sequels)

-MOA: inhibit reabsorption of NaHCO3, NaCL, H20
major indications/uses of Carbonic Anhydrase Inhibitors
diuresis (rarely)
lower IOP for glaucoma pts
renal alkalization
correct alkalosis
cerebral edema
lower seizure threshold
altitude sickness
side effects of Carbonic Anhydrase Inhibitors
-significant HCO3- loss
-acidosis
-decreased urinary excretion of NH4+ (converts to NH3+ and reabsorbed)--> hyperammonemia + hepatic encephalopathy in pts with cirrhosis
Contraindications/Caution of Carbonic Anhydrase Inhibitors
-Sulfonamide derivative
-electrolyte imbalance
-severe renal or hepatic disease (cirrhosis)
Toxicity of Carbonic Anhydrase Inhibitors
metabolic acidosis
renal stones formation
renal potassium wasting
drowsiness and paresthesias
MOA of Loop Diuretics-- furosemide, bumetanide, torsemide, ethacrynic acid
MOA: inhibit the Na+/K+/2CL- NKCC 2 transport system in the thick ascending limb in the loop of henle
indications of loop diuretics
-edema (pulmonary edema, heart failure)
-hyperkalemia
-hypercalcemia
-acute renal failure
-toxic ingestions (bromide, fluoride, and iodide)
Side effects of loop diuretics
-hypokalemia
-hypocalcemia
-hypomagnesemia
-volume depletion
-metabolic acidosis
-renal stones
-hyperammonemia (pts with cirrhosis)
-ototoxicity (reversible)
What drugs will interact with loop diuretics?
anticoagulants
antihypertensives
aminogycosides
lithium
Considerations/Caution of loop diuretics
-sulfa allergy cross-sensitivity
-cirrhotic pts resistant to loop diuretics due to high aldosterone levels.
If a patient has a sulfa allergy, which loop diuretic drug can be used?
ethacrynic acid (not a sulfaonamide)
MOA of Osmotic Diuretics (mannitol)
MOA: inhibit passive reabsorption of water by increasing the osmolarity of the glomerular filtrate in the proximal convoluted tubule and descending limb of loop of henle
Test dose for Osmotic Diuretic Mannitol
12.5mg IV test dose before continuous administration
indications of Osmotic Diuretic
-induce osmotic diuresis to prevent renal failure in hyperosmolar conditions (tissue damage/ rhabdomyolysis).
-reduce ICP in cerebral trauma
-opthalmic surgical procedures
-reduce IOP (glaucoma)
Effects/Toxicity of Osmotic Diuretic
Marked diuresis
nausea/vomiting
headache
MOA of K+ sparing diuretics-- spironolactone, traimeterene, eplerenone, amiloride
Triameterene and amiloride-- are Na+ inhibitors (fast onset)

Spironolactone and eplerenone-- directly inhibit mineralcorticoid receptors (aldosterone receptor antagonist)-- slow onset
Indications of K+ sparing diuretics
-primary aldosteronism due to hypersecretion (conn's syndrome), ectopic production
-secondary hyperaldosteronism-- induced by heart failure, hepatic cirrhosis
-nephrotic syndrome
Side effects/ toxicity of K+ sparing diuretics
-hyperkalemia
-gynecomastia, impotence, BPH
-hyperchloremic metabolic acidosis
-triametere precipitation-- renal stone formation
Drugs interactions with K+ sparing diuretics
Drugs that reduce or inhibit renin or angiotensin II activity (BB, ACEI, NSAIDS, aliskiren(tekturna)-- increase likelihood of hyperkalemia
Contraindications/Caution of K+ sparing diuretics
-renal insufficiency
-liver disease
-CYP3A4 inhibitors (ketocanozole) will increase blood levels of eplerenone
MOA of thiazide diuretics
-inhibit NaCl absorption in the DCT
-block NaCl (NCC) transporter
-enhance Ca2+ reabsorption
Indications of Thiazide diuretics
-hypertension
-heart failure
-hypercalciuric nephrolithiasis
-nephrogenic diabetes insipidus
Side effects/toxicity of thiazide diuretics
-elevate serum uric acid levels
-worsen hyperlipidemia
-decrease insulin secretion and glucose tissue utilization
-hyponatremia
Drug interactions of Thiazide diuretics
NSAIDS may inhibit action of thiazide
Considerations/Caution of Thiazide diuretics
-sulfonamide derivative
-avoid excessive use in hepatic cirrhosis, renal failure,
-diabetes
-hyperlipidemia
what are centrally acting sympathoplegics (alpha 2 agonists) ?

MOA?
Clonidine and Methyldopa
Clonidine--reduce sympathetic and increase parasympathetic tone-- decrease BP through reduction of PVR and HR
Methyldopa- reduces renal and PVR resistance; mainly used in pregnancy
Side effects/Contraindications/Caution of centrally acting sympathoplegics (alpha 2 agonists)-- methyldopa and clonidine?
-sedation
-do not Rx clonidine to pts at risk for depression, stop if depression occurs
clonidine should be gradually discontinued while other agents are started- sympathetic response can be life threatening
Beta Blockers-"lols"

MOA?
-reduce stimulation of renin production
-reduce sympathetic tone, decrease PVR
-decrease heart rate and cardiac output
Indications of beta blockers
useful in mild to mod HTN, S/P MI, heart failure
Side effects/Caution/Contraindications of beta blockers
non-cardio selective formulations can precipitate asthma exacerbations
(propanolol, nadolol, pindolol, nebivolol, etc)
-even the cardio selective drugs are non-cardio selective at high doses
-adjust dose in renal insufficiency
-do not d/c abruptly after prolong used--> results in tachycardia, HTN, angina, MI
what drug is used to block both alpha 1 and alpha 2 for the management of HTN in pheochromocytoma?
Phenoxybenzamine
what are Alpha 1 blockers?

MOA?
"ozins"
-prazosin, terazosin, doxazosin, etc
- selective blockade of alpha 1 receptors in arterioles and venules-- dilation decreases PVR- lowers BP in upright more than supine
-dilates vessels in bladder, prostate, improve urine flow in BPH
Indications of alpha 1 blockers ("ozins")?
mil to mod HTN, esp good for men with BPH
Side effects/Contraindications/Caution of alpha 1 blockers
orthostatic hypotension and reflex tachycardia common with first dose, when initiating therapy-- give first dose at night
Name Parenteral agents used for HTN emergencies
Nitropusside
Diaxozide
Fenoldopam
MOA of Nitropusside
-venous and arteriole dilation--decreased PVR, BP, and venous return
-relax vascular smooth muscle via release of nitric oxide
-very short duration
-sensitive to light
- toxicity: signs of cyanide accumulation-- metabolic acidosis, arrythmias, profound hypotension, death
MOA of diaxozide
-long acting, dilates arterioles
-structure similiar to thizide but has no diuretic effect
-opens K+ channels and stabilizes membrane potential at resting.
-Toxicity: profound hypotension, reflex tachycardia
MOA fenoldopam?
-activates D1 receptors resulting in dilation of arterioles and natriuresis
-used in hypertensive emergencies and post op HTN
-increases IOP (no to glaucoma pts)
MOA of Calcium channel blockers?
-non-dihydropyridines: verapamil and dilitizem-- nonselective block of L-type calcium channels

-Dihydropyridines: amlodipine, isradipine, felodipine, nifedipine--block vascular calcium channels > cardiac calcium channels

-reduce PVR and BP
-African americans respond better to CCBs and diuretics than other meds
MOA of ACE inhibitors?
"prils"- benazepril, captopril, fosinopril, ramipril

MOA: block formation of angiogensin II- a potent vasoconstrictor; also increases bradykinin (a vasodilator) levels-- decreases PVR through vasodilation, reducing Na and H20 retention
Indictions of Ace inhibitors?
-mild to mod HTN, heart failure, S/P MI
-recommended for most pts with DM, unless contraindicated
-good response in asians
Side effects/contraindications/caution of ACE inhibitors
-ACEIs are teratogenic
- severe hypotension in pts on diuretics
- dry cough-- then switch to ARBs
-hyperkalemia, angioedema (rare), rash
- do not use K+ sparing diuretics
MOA of ARBs?
Angiogensin Receptor Blockers- "sartans"

-MOA: block angiotensin II type 1 receptors
-less bradykinin activity or no activity compared to ACEI
-indications/side effects is same as ACEI
Name a renin inhibitor
aliskiren
MOA of renin inhibitors
inhibits enzyme activity of renin

-reduces angiotensin I and II and aldosterone
what drug used for treatment of heart failure is contraindicated in wolff parkinson white syndrome?
Cardiac glycosides (Digoxin)
Fill in the blank

Protanated form of weak ____ is neutral lipid-soluble

Unprotonated form of weak____ is neutral lipid soluble.
Protanated form of weak acid is neutral lipid-soluble

Unprotonated form of weak base is neutral lipid soluble.
Define desensitization.
after reaching an initial high, the response diminishes over seconds to minutes even in continued presence of agonist.
Define down regulation
repeated or prolonged exposure of receptors to agonist causes cellular changes that cause destruction of receptors
what is therapeutic index?
toxic dose/ effective dose
what is volume of distribution?
amount of drug in the body/ concentration
what is clearance?
factor that predicts the rate of elimination in relation to the drug concentration
what is rate of elimination?
clearance x concentration
what is half-life?
the time required to change the amount of drug in the body by 1/2 during elimination (or during a constant infusion)
how many half lives must elapse before full effects will be seen by the drug?
4 half-lives
What is bioavailability
the fraction of unchanged drug reaching the systemic circulation following administration of any route?
Bioavailability of different routes of administration.
IV 100%
IM 75 to <100%
SC 75 to <100%
PO 5 to < 100%
PR 30 to < 100%
Inhalation 5 to < 100%
Transdermal 80 to <100%
what is the target concentration approach?
a rational dosage regimen is based on the assumption that there is a target concentration that will produce the desire therapeutic effect.
what is maintenance dose?
the dose to keep a steady state.

just enough to replace what has been eliminated
ADSL
Asymmetrical Digital Subscriber Line
Asymmetric Digital Subscriber Line (ADSL) is one form of the Digital Subscriber Line technology, a data communications technology that enables faster data transmission over copper telephone lines than a conventional voiceband modem can provide. It does this by utilizing frequencies that are not used by a voice telephone call.[1] A splitter, or DSL filter, allows a single telephone connection to be used for both ADSL service and voice calls at the same time. ADSL can generally only be distributed over short distances from the central office, typically less than 4 kilometres (2 mi),[2] but has been known to exceed 8 kilometres (5 mi) if the originally laid wire gauge allows for further distribution.

At the telephone exchange the line generally terminates at a Digital Subscriber Line Access Multiplexer (DSLAM) where another frequency splitter separates the voice band signal for the conventional phone network. Data carried by the ADSL are typically routed over the telephone company's data network and eventually reach a conventional Internet Protocol network.
what are the steps of obtaining a target concentration?
1. choose target concentration
2. predict volume distribution and clearance
3. give loading dose or maintenance dose
4. measure patient's response and drug concentration (ie labs)
5. Revise based on measure concentration
6. Repeat steps 3-5, adjusting dose to achieve target concentration
what is the single most important factor determining drug concentration?
clearance
AMR
Audio Modem Riser
The audio/modem riser, also known as an AMR slot, is a riser expansion slot found on the motherboards of some Pentium III, Pentium 4, Duron, and Athlon personal computers. It was designed by Intel to interface with chipsets and provide analog functionality, such as sound cards and modems, on an expansion card.

[edit] Design goalsOne of the design goals of Intel for AMR was to allow motherboard manufacturers a way to implement analog I/O (audio and modem functionality) on an expansion card for U.S. Federal Communications Commission (FCC) certification. Potential cost-savings could then be realized by reusing the card on multiple motherboards and skipping FCC certification for those motherboards.

[edit] TechnologyPhysically, it has two rows of 23 pins, making 46 pins total. Three drawbacks of AMR are that it eliminates one Peripheral Component Interconnect (PCI) slot, it is not plug and play, and it does not allow for hardware accelerated cards (only software-based).

Technologically, it has been superseded by the Advanced Communications Riser (ACR) and Intel's own Communications and Networking Riser (CNR). However, riser technologies in general never really took off. Modems generally remained as PCI cards while audio interfaces were integrated on to motherboards.

Recently motherboard manufacturer Asrock has resurrected this concept, introducing the High Definition Multimedia Riser (HDMR) slot on most of its motherboards. Little information is available, but drivers on the Asrock website indicate the existence of V.92 modem cards for this standard. It is not clear how HDMR differs from AMR, if indeed at all.
Describe phase 1 and phase 2 biotransformation reactions.
Phase 1--> involves one of members of a large family of hepatic enzymes called cytochrome P450 enzymes that catalyze oxidation, reduction, and hydrolysis.

Phase 2--> conjugation of a polar group (sulfate, acetate, glucuronate) to the drug molecule
an example of a drug with phase 2 biotransformation preceding phase 1.
INH
which p450 isoform is the most common and responsible for 50% of the metabolism of prescription drugs metabolized by the liver?
CYP3A4
what is enzyme induction?
repeated administration of certain substrates/drugs induces (stimulates) p450

enhanced rate of p450 synthesis or reduced rate of degradation (substrate stabilization).

accelerated substrate metabolism and a decrease in pharmacological action (unless drugs metabolized into active metabolites)
what is enzyme inhibition?
reduced substrate metabolism

in some cases there can be irreversible inhibition of p450
what p450 isoform and phase 2 pathway is involved in more than 75% of drugs in use?
CYP3A4/5 and UGT
what occurs in acetaminophen overdose?
Acetaminophen normally undergoes glucuronidation and sulfation to the corresponding conjugates, which together make up 95% of the total excreted metabolites. The alternative p450 dependent GSH conjugation pathway accounts for 5%. When acetaminophen exceeds therapeutic doses, the glucuronidation and sulfation pathways are saturated, and the p450 dependent pathway becomes impt. Little hepatotoxicty will occur as long as GSH is available. However, with time, GSH becomes depleted faster than it can be generated, and a reactive toxic metabolite accumulates. The reactive metabolite (N-acetylbenzoiminoquinone) reacts with nucleophilic groups of cellular proteins resulting in hepatoxicity.
what is the antidote for acetaminophen overdose?
cysteamine and N-acetylcysteine.

Adminstration of N-acetylcysteine withing 8-16 hrs following overdose has shown to protect from hepatotoxicty and death
what is succinylcholine?
a depolarizing blockade,

an agonist that causes prolonged depolarization of the neuromuscular end plate, blocking impulse conduction into the muscle membrane, which results in paralysis.

Major use: intubation
what is pralidoxime?
an antidote in severe cholinesterase inhibitor poisoning caused by organophosphate insecticides

it is a cholinesterase regenerator
what is physostigmine?
a cholinesterase inhibitor

used to reverse the central and peripheral signs of muscarinic blockade (from atropine or TCA intoxication)
*can produce dangerous CNS effects-- use only in emergency for pts with high fever or rapid SVT
what is Atropine used for?
anti-muscarinic

used to treat cholinomimetic drug overdose (organophosphates)
What is autoinjection syringes Pyridostigmine and atropine used for?
Pyridostigmine: cholinesterase inhibitor
Atropine: Anti-muscarinic

Used as a preventative therapy for cholinesterase inhibitors used in chemical warfare
What is Erdophonium?
a nicotinic agonist

treats Myasthenis gravis

*Erdophonium-- used to diagnose the condition
*Pyridostigmine-- for long term treatment
what is Neostigmine & Erdophonium used for in anesthesia?
Cholinesterase inhibitors

used as a reversal of nondepolarizing muscle relaxants
what are side effects of atropine? and what systems in the body?
CNS: sedation, reduction of motion sickness, and reduction of parkinsonian tremor
Eye: mydriasis, cycloplegia, increase IOP
Airway: reduce bronchospasm
Gi tract: reduce hypermotility and secretion of gastric acid, salivation is reduced
Gu tract: relax bladder muscle and may precipitate urinary retention
CV: HR and AV conduction increase due to vagal blockade