• The degree of ionization is the degree to which ions are less able to move passively.
• In similar evironments drugs are less ionized which increases chance of absorption into cell.
• acids: less ionized @ low environmental pH. bases: less ionized @ high pH

• Potency: amount of drug necessary to procduce a given pharmacologic effect: note: has nothing to do with the maximum aeffect a drug can produce.
• Efficacy: Maximum effect produced by a drug. I.E. how effective it is at producing a given pharmacologic effect. Note: has nothing to do w/the dose needed to achieve this effect.

Define:

Official Name

Chemical Name

Generic Name

Trade Name

• Official Name: name used in the official drug reference, the U.S.P.
• Chemical Name: name describing exact chemical composition of the drug.
• Generic Name: for older drugs its the name handed down from antiquity. For newer drugs its usually the "code" name given during testing phase thats based upon the chemical name. The generic name will become official name if drug is included in U.S.P
• Trade Name:copyrighted name whose use is restricted to a single company. it maybe renewed so it remains w/1 co.

What are the advantages of the major drug reference books?

U.S.P, N.F., AMA Drug Evaluations, Physician's Desk Reference, DF&C,

American Hospital Formulary

• U.S.P: Single drugs are listed. older drugs deleted in favor of newer drugs. Very Authoritative: avg. dose, toxicity, methods of admin & also shows how to prepare drugs.
• N.F.: 1888-1975- now w/USP. Single drugs & formulas for drug mixtures. Often included deleted drugs from USP. Standards for Tablet disintegration.
• AMA Drug evaluations: Drugs grouped according to use & general discussion provided for each group. favorable & unfavorable judgements expressed.
• PDR: manufacturers buy space. Also for non-prescription meds. info sim. to drug inserts. Cross referenced to generic & chem names which is a useful section on drug ID & dosage forms. off-labe uses NOT listed.
• DF&C: Drugs grouped according to use. comparison of various drug forms including cost. color photos. lists off label usage.
• AHFMS: similar to DF&C

Local: Drug action occuring only @ site of app.

Systemic: action of a drug thats absorbe then distributed throughout the body

1)action maybe on whole body or only on a specific target organ.

2) toxic effects may occur when local admin becomes systemically absorbed.

• Can be ordered with a prescription; physician must renew registration number yearly with DEA in Dept of Justice.
• Record kept for 2 years
• DEA sets quotas for amoutm anufactured & distributed through pharmacies & health care agencies.  Monitors distribution and sales of all controlled substances and can request records at any time from physician, pharmacists, & manufacturers

• The DEA monitors distribution and sale
• will include "signature drugs" (no prescription necessary). Amt or concentration of narcotic is controlled. (i.e. codeine in cough syrup). Pharmacy keeps record of purchaser for 2 years.
• CA law does not permit schedule V drugs to be dispensed without a prescription.

schedule II: may be for 30 day supply. May not be refilled but reordered. In case of ER or managed care setting, prescriptions may be renewed by phone but a written prescription must follow w/in 72 hours.

Schedule III: must renew prescriptions for schedule III & IV meds after 6 mo or 5 refills. May be renewed by telephone of FAX.

Schedule IV: same as for schedule III bt can be differ in penalties for illegal possesion.

Whats the difference btwn sympathetic vs parasympathetic nervous systems?

Study the responses of both PNS &CNS on the different systems of the body on page 41.

Sympathetic Nervous System:

• short preganglionic neurons & long postgang
• mimics "fight or flight" response.
• stimulates adrenergic receptors by NE or e

Parasympathetic Nervous System:

• long preganglionic neurons & short postgang
• stimulates cholinergic receptors by Ach

Nicotinic Receptors:

What are they?

What is the transmitter for the receptors?

What happens when they are stimulated?

• nicotinic receptor is a cholinergic receptor
• stimulated by AcH
• They are found in ganglia, neuromuscular jucnt, & adrenal medulla.
• when they are stimulated it may:

stimulate both the sym & para simultaneusly @ ganglia

stimulates adrenal medulla

stimulates skeletal muscle- volutary sys

Muscarinic receptors:

What are they?

What neurotransmitter stimulates it?

Where are they found?
What happens when they are stimulated?

• cholinergic receptor
• stimulated by AcH
• chiefly found at effector after postganglionic neuron but also found esp in smooth muscle of hollow organs
• what happens when stimulated:

contracts smooth muscle including the eye sphinter causing pupil to constrict. (except gi & urinary spinchters & blood vessels)

stimulates exocrine glands

decreases heart rate & sometimes contractility

adrenergic receptors:

What are they?

what neurotransmitters that stimulate them?

where can they be found?

what do they do when stimulate?

Neurotransmitter: NE or epinephrine

alpha: contracts smooth muscle(vasulature)

beta 1: stimulates heart rate, strength (major location is heart) 

beta 2: relaxes smooth muscle(bronchioles) and increases metabolic rate.

adrenergic agonists:

Therapeutic uses

side effects

toxicity

contraindications

Therapeutic uses:

• can cause vasoconstriction & reduce edema
• hypotention like that caused in spinal anesth
• nasal congestion
• delays absorption with local anesthetics so it can be longer acting
• topical hemostatic
• dilates pupil for eye exam

Side Effects:

• anxiety, tremulousness
• awareness of rapid heart beat

Toxicity:

• photophobia
• headaches
• substernal pain
• acute pulmonary edema
• tissue necroisis

Contraindications:

• angina
• hypertension

alpha antagonists:

indications & contraindications

beta agonists:

indications & contraindications

beta antagonists:

indications & contraindications

INDICATIONS: 1)cardiac arrythmias 2)prevention of angina by decreasing workload 3)hypertension 4)controlling signs of thyrotoxicosis-counteracts (tachycardia, high b/p increase) 5)Prophylaxis of migraine headaches and, perhaps treatment of acute attacks.

CONTRAINDICATIONS:

Asthma

Hypotension (unless with arrhthmisa requiring treatment)

Congestive heart failure, heart block

caution: Diabetes

What is postural hypotension?

What drugs cause it?

postural hypotention: dizziness & weakness upon standing.

drugs that cause postural hypotention: Nitrates(treat angina), alpha adrenergic blockers, & anit-depressants (tricyclics, MAO's) 

Antihypertensives: Beta Blockers

What are they?

MOA?

Who do they work best for?

Common side effects?

• propranolol, timolol, metoprolol, atenolol
• MOA: decreases H.R. & hearts force of contraction, therefore, decreases cardiac output, also inhibits renin release decreasing B.P. & decreasing vasoconstriciton
• most useful in patients under 40
• side effects: G.I.-nausea, vommiting, diarrhea
• heart: uncommon bt can cause av-block
• bronchioles-constricts airway

Antihypertensive agent: ACE inhibitors

what are they

MOA

who are they most useful for

common side effects

• drugs ending in "pril"
• MOA: less vasoconstriction &less aldosterone secretion so less fluid retention. Work well. Becoming more popular.
• less effective in black patients
• side effects: persistent cough, rash, proteinuria, headache, myalgia, dyspepsia, diarrhea. Sever: bone marrow depression & renal damage.

Antihypertensives: calcium channel blockers

what are they?

MOA

who do they work best for?

common side effects?

• MOA: causes vasodilation (usually a reflex tachycardia ocurs)
• choice for black patients. patients over 60 respond better to calcium channel blockers
• side effects: peripheral edema, dizziness, fatigue, flushing, constipation, nausea, diarrhea

antihypertensives: diuretics

what are they

MOA

best for?

side effects

• mainstay of antihypertensive therapy; if use onlyone drug, it is usually a diuretic. esp useful w/other agents as well since therapy tends to cause fluid retention. Thiazide types are used.
• MOA: prevents hypervolemia, causes increased NA secretion & water follows, relaxes blood vessels
• side effects: potassium depletion (causes arrythmias)
• may affravate diabete mellitus(seem to inhibit insulin secretion)

Angina:

What is it? How is it treated?

angina is heart pain caused by oxygen supply of to heart is insufficient to meet hearts demands.

Treatments:

beta blockers-used to prevent attack

calcium channel blockers- blocks movement of extracellular calcium into cells, decreasing contractility of heart.

nitrates/nitrites- drug of choice: relaxes smooth muscle, decreases workload of heart by decreasing b.p., increase O2 supply by dilating coronary arteries

• any disorder of heart rate, impulse formation, or conduction of heart.
• bradycardia- slow arrhythmia, tachycardia (100-200 impulses/min), flutter (200-300 impulses/min), fibrilation (>300 impulses/min), AV block(<50-60/min), P.V.C.
• treatment:

quinidine: MOA: cardia depressant, anticholinergic(action on av node: prevents cardiac slowing. therapeutic uses: 1)atrial fibrillation 2)atrial flutter-used if digitalis doesnt work 3) ventricular tachycardia 4)P.V.C.

Cardiac glycosides: atrial flutter & fibrillation

Lidocaine: given only IV in ER's. rapid onset & short duration

beta blocker: treats atrial fib & flutter

couteracts digitalils toxicity

calcium channel blockers: claimed to stop 90% of supraventricular tachycardias w/a single iv dose.

adrenergic agents or anticholinergic agents: temp. treatment only. stimulates beta activity of heart or blocks muscarinic slowing. treats av block and bradycardia

Anticoagulant: slows/retards blood clotting but doesn't work once clot is formed

Types of anticoagulants: 

1. Heparin:must be admin parenterally. Interferes w/conversion of prothrombin to thrombin & fibrinogen to fibrin
2. Coumarin Derivatives: interferes w/vit K, preventing formation of prothrombin liver. activates p450 enzymes. 
3. Asprin: decreases platelet aggregation. treats coronary thrombosis. discontinue 7 days be4 surgery because long lasting.
4. NSAIDS: minor anticoagulant & nt as long lasting as aspirin. 99% protein bound

MOA: replace missing factors for blood formation

types: 

1. Iron-microcytic-necessary component of hemoglobin (most common cause of anemia)
2. vitamin b12- macrocytic-coenzyme for synthesis of DNA & other cell component
3. folic acid-macrocytic-needed fo amino acid & dna synthesis
4. rbc, whole blood- erythropoitin now available as a drug epoetin alfa for rbc deficiency

epilepsy:Gabba

parkinsons disease: decrease in dopamine therefore Ach dominates dopamine.

depression: low levels of Norepi

anxiety: high levelss of norepi

schizopreniza:dopamine

manic-depressive episode:Norepi

1)amphetamines

• narcolepsy-uncontrollable urge to sleep
• weight control
• AD-HD (RITALIN-increases NE which seems to increase attention span in child

salycitates vs aniline type

uses?

side effects?

         salicylates          vs.         aniline type

uses:1) relief of pain-       1)same bt not 

        headache,dysmenorreha       for arthritis

        arthritis

        2)antipyretic       2)antipyretic

        3)antiinflam:      3) none

           a. rheumatiod arth.

           c. rheumatic fever- decr. scarring of heart 

              valve.

        4)anticoagulant- effects    4)none

         for venous or coronary

         thrombosis. helped to prevent stroke after

         myocardial infarction.

SE:   1) gi irritation & decreased         1)none

          coagulation w/cont use, gastric

          mucosa usually heals in 3 days

          caution: black stools

       2) cns stim; resp stim to point     2)none

           resp alkalosis

MOA of barbituates & benzos?

uses & side effects:

MOA:

Barbituates: mech unclear. depresses all areas of brain-inhibits reticular activating sys. Enhances gaba complex. Gaba independent.

Benzos: binds to special receptors that decrease activity of the brain. Also increases activity of GABA but GABA dependent. When GABA decrease so does degree of depression. Safer than barbs

Uses & side effects:

Clinical uses:

• relieves anxiety (most common use) 2kinds of anxiety: 1-situational anxiety(exam, new job etc) 2-neurotic anxiety- no rational reason
• sleep disorders-use temporarily. if trouble sleeping use drug w/quick onset. if trouble staying asleep use drug w/slow onset & longer duration like benzos.
• anticonvulsant- eg treat epilepsy (barbs &benzos)

Side effects:

• drowsiness- less likelyh w/benzos
• impaired performance or decreased perception & judgement. often w/long term use
• hangover effect- less w/ benzos cause doesnt repress REM sleep
• hyperalgesia(only barbs) increase sensitivity to pain. benzos are better sleep aid
• overdose-depress resp. main cause of od death. benzos are less likely to be fatal only if no other depresants are combined

antieleptic agents:

treatment goal

adverse effects

some are general depressants & others are selective agents (dilantin)

treatmet goal: control seizures w/out adverse side effects to cns.

adverse effects:

1)sedation-locomotar & mental activity depressed

chronic use can cause:

2) kidney & liver damage

3)blood disease- anemia, depresses wbc production

each agent has own adverse effects:

dilantin-blurred vision, excess hair on face & arms, hyperkalemia, thickened brow ridges, gum hyperplasia

what is parkinsons disease?

main neurotransmitter involved?

treatment of parkinsonian's disease

Parkinsonism is a nerological disorder of CNS -Occurs later in life (after age 50) due to deterioration of cells in brain. -Lose neurons that produce dopamine in brain. -Symptoms:motor- ridgity, tremors of hands. indiv moves slowly & stiffly. advanced stages: drooling,speech slurring, face mask- like, shuffling walk - symptoms may be caused by environment: brain damage (lack of O2). genes 5%, drugs. Main transmitter involved: dopamine (lack of)

2 ways parkinsonism is treated: 1) INCREASE DOPAMINE a. amantadine- increa. release of dopamine in brain. chiefly antiviral med. Must take 2 wks be4 assuming ineffective. b.LEVADOPA-almost dopamine - drug of choice. Lrg amts orally, replenish stores of dopamine in brain. c. bromocriptine & permax stim. postsynaptic dopamine receptors d. selegiline- beta inhibitor. decreases breakd of dopamine. can delay need 4 L-dopa 6-9mo 2)DECREASE AcH w/ ANTICHOLINERGIC DRUGS Brings Ach in balance w/dopamine- blocks muscarinic receptors in brain. Some anti- histamines are used for their anticholinergic effect cause they are less likely to cause confusion or insomnia. good for mild cases or in com. useful as adjucnt anytime during treatment.

Uses: to prevent nonproductive coughing that is exhausting & painful to patient

Narcotic anttussives:

MOA-depresses cough center in medulla of CNS

Side effects: potetial for abuse, constipation, depress resp, drug dependency

non narcotic antitussives:

MOA- Peripherally-reduces activity of lung stretch receptors, also topical anesthetic

Centrally-acts on medulla- DEXTROMETHORPHAN (half as potent as codeine)

side effects: not serious-sometimes atropine like

H1 agonists?

what are they, therapeutic uses, side effects & cautions

H1 agonists: known as classical "antihistamines"

• 1st generation bind peripherally & centrally. More sedating & more useful as a sedative, for motion sickness & in treating parkinson's
• 2nd generation: less drowsy but produce adverse cardiovascular effects
• therapeutic uses: antagonize allergic reactions (hives, watery eyes, stuffy nose-NOT ASTHMA!)Prevents further symptoms from occuring but will not stop what has already happened. Epi is better at counteracting reaction that has already occured. Motion sickness.

Side effects:

• antipsychotic like- drowsiness, sedation, dizziness. hallucinations, sedating 
• antimuscarinic: dryness of mouth blurred vision

cautions:

• potentiator of other sedatives
• avoid use in asthmatics
• do periodic blood tests for blood dyscrasias

H2 agonists?

what are they, therapeutic uses, & side effects?

H2 agonist block second type of histamine receptors found in the stomach

therapeutic uses:

1) decrease gastric secretion (ulcer patients)

2) unapproved use- to treat heartburn.

side effects:

minimal. occasionally causes diarrhea, muscle pain, rash, dizzines. also p450 enzymes so it can delay metabolism of other drugs in liver. breast enlargement in men(rare0

Local: (w/inhaler use) hoarseness, drym mouth, local infections in mouth & pharynx

Systemic: (minimized by inhaler)

irreversible- osteoporosis, cataracts, stunting of growth in children

Reversible- proness to infections. Poor wound healing (including proness to ulcers)(vit C helps), salt & h20 retention, signs of CNS stim (restlessnes, insomnia, & manic states including depredssive episodes in some individuals)

Define resp & digestive terms below:

demulcents

expectorants

digestants

emetics

antiemetics

cathartics

antidiarrheics

absorbents

astringgents

sedatives & antispasmodics

carminatives

Demulcents: agents w/a soothing effect for cough & throat irritation

expectorants: drugs that increase secretion of mucus in bronchi or modify it to reduce viscosity (asthma, brochitis, pneumonia, coughs)

Emetics: cause vomiting

antiemetics: decreases vomitting reflex in GI or CNS irritation

Cathartics: laxatives for constipation, surgery, worm infestations, chem poisoning

Antidiarrheics:

demulcents

absorbents-agsor gas or irritatitin sub

astringents- precipitate protein & cover surface of membrate

antiinfectives-if micro org present

sedatives & antispasmodics- opium preparations & antimuscarinic

carminatives: increase motility to help expel gas

Bactericidal:

beta lactams-Penicillin, cephalosporins, carbapenems, monobactams, glycopeptides

Protein synthesis inhibitors: aminoglycocydes including streptomicin

DNA inhibitors: quinolones & fluoroquionolones

Bacteriostatic:

Protein systhesis inhibitors:Macrolides including erythoromycin, tetracyclines, lincosamides, chloramphenicololic

folic acid synthesis inhibitors: sulfonamides

trimethoprim

Narrow Spectrum:

Penicillins

Cephalosporins

glycopeptides (vancomycin, bacitracin)

macrolides (erythromycin)

monobactams

broad spectrum:

carbapenems

aminoglycosides

quinolones/flyuoroquinnolones

tetracycline

chloramphenicol

sulfonamides

trimethoprim

lincosamides

MOA of Antiinfectives?

Cell wall synthesis inhibitors:

Beta-lactams (penicillins, cephalosporins, carbapenems, monobactams)

glycopeptides(bancomysin, bacitracin)

Protein synthesis inhibitors:cidals

aminoglycosides (streptomycin)

DNA inhibitors:

quinolones & fluoroquinolones

protein systhesis inhibitors: statics

macrolides (erythromycin)

tetracyclines

licosamides

chloramphenicol

folic acid synthesis inhibitors:

sulfonamides

trimethoprim

Topical:

• tretinoin- skin is more susceptible to sunburn & UV light. Might accelerate carcinogenic effect of UV radiation

Systemic

• Tetracycline- can get gastric upset & vaginitis, skin, fungal infections. decreases effectiveness of oral contraceptives. contraindicated with pregnancy.
• erthromycins- can get gastric upset & vaginitis, skin, gungal infections. Can be used w/caution in pregnancy
• oral 13-cisretinoic acid (acutane)- TERATOGENIC, dry cracked skin, alopecia, hypertrigllyceridemia, hepatits, acute pancreatitis, pseudotumor ccerebir, joint & muscoskletal pain including back, snd skeletal hyperstoses. all charac of vit A toxicity.

1)congenital glaucoma: born with

2)Primary glaucoma:

Narrow angle- poor drainage because position of iris is displaced.

Wide angle- poor drainage most probably due to abnormal blood vessel permeability

3) Secondary glaucoma: develops secondary to other eye disease or catarct surgery.

Steroids are used for ocular inflammation. NOT FOR INFECTION! reduces scarring, impaired vision, inflammation.

therapeutic uses:

allergic reactions of eye

severe injury

non-pus producing inflammations

Emollient: fatty or oily substances that may be used to soften or soothe irritated skin & mucous memebrane

Keratolytic: keratin dissolvers, i.e. softern scale and loosen the outer horny layer of the skin. (examples: salicylic acid found in wart removers, topical Vitamin A more specific to blackhead, noninflammatory acne)

Define:

filtration

reabsorption

secretion

filtration: both nutrients & wastes moved from glomerulus to Bowman's capsule by high pressure in glomerulus

reabsorption: chiefly nutrients moved from tubule back to blood; often done by active transport

secretion-chiefly waste products of foreign materials moved from blood into tubule at any point after Bowman's capsule; often done by active transport

To correct alkalosis the kidney helps eliminate excess bicarbonate ion by reabsorbing less bicarbonate & more chloride. Helps retain H+ by secreting less H+ and more K+.

To correct an acidosis the kidney reabsorbs more bicarbonate ion in the proximal tubule. the kidney actively secretes H+ instead of K+ in the distal tubule takes two days to reach max effect.

The kidney may alleviate acid/base imbalance if cause is from another source.

the kidney may cause acid/base imbalance if malfunction or diuretic given

What is a diuretic?

What is the mechanism of action of most diuretics?

A diuretic is an agent that increases the rate of urine flow. Diuretics ofthe alter the pH and the ionic composition of both the urine and the blood.

Direct or indirect inhibition of ion reabsorption (Na+, Cl-, or HCO3)3) is the primary mech of action of all diuretics. all result in decreased Na+ reabsorption.

• ER drung when rapid effective diuretic needed
• CHF, often results in pulmonary edema
• acute pulmonary edema (vasodilator effect)
• acute hypertension only (vaso effect)
• chronic renal failure

• withdraw water from overhydrated cells (especially in brain or eye)
• maintains high vol of urine- prevent renal failure after hemolytic reaction, shock, hemorrhage, or surgery. helps eliminate drug OD such as barbs, salicylates, etc

What are the types of immunity?

Natural Immunity: (inborn) microbe-causeing disease will not live in individual's tissue.

acquired immunity: Immunity resulting from antibodis & ability to produce them

1. Active: body forms antibodies in response to antigen. Exposure to disease.