Pharmacology Exam Components:
NBDE II 1.0. General Principles [5 Qs]
PHARMACOLOGY
EXAM SECTION
[34 Questions]
Dr. Glenn Clark
1.0. General Principles [5 Qs]
1.1. Rx writing, drug laws, and drug abuse
1.2. Toxicity and drug interaction
1.3. Dose response
1.4. Mechanism of action
1.5. Biotransformation
1.6. Absorption, distribution, excretion
1.7. Alternative (herbal) medications
Schedule I: [Use illegal/restricted to research; high abuse
potential; no accepted medicinal use in US]. Examples:
hallucinogens, heroin, marijuana
Schedule II: [Requires prescription; high abuse potential;
no refills or verbal orders allowed; some states require
triplicate Rx]. Examples: amphetamines, barbiturates,
opiates (single entity, some combos)
Schedule III: [Requires prescription; moderate abuse
potential; max 5 refills/6mo; verbal orders allowed].
Examples: anabolic steroids, dronabinol, ketamine, opiates.
Schedule IV: [Requires prescription; low/moderate abuse
potential; max 5 refills/6mo; verbal orders allowed].
Examples: appetite suppressants, benzodiazepines,
sedative/hypnotics.
Schedule V: [Requires prescription or may be OTC with
restrictions in some states; limited abuse potential; max 5
refills/6mo; verbal orders allowed]. Examples: opiate or
opiate-derivative antidiarrheals and antitussives.
2.0. Central Nervous System [4 Qs]
3.0. Autonomic [3 Qs]
4.0. Cardiovascular [4 Qs]
5.0. Local anesthetics [4 Qs]
6.0. Chemotherapy [5 Qs]
7.0. Endocrines/Immunosuppressants [ 2 Qs]
8.0. Analgesics [5 Qs]
9.0. Antihistamines and Autocoids [2 Qs]
Total = 34 questions
Pharmacology is the study of how substances interact with living organisms to
produce a change in function.[1] To protect the consumer and prevent abuse,
many governments regulate the manufacture, sale, and administration of
medication. In the United States , the main body that regulates pharmaceuticals
is the Food and Drug Administration and they enforce standards set by the
United States Pharmacopoeia. The FDA categorizes drugs into six schedules (I
to VI). The safety and effectiveness of prescription drugs in the U.S. is regulated
by the federal Prescription Drug Marketing Act of 1987 .
All drugs have two properties that govern their efficacy. First,
Pharmacokinetics describes the effect of the body on the chemical (e.g. half-life
and volume of distribution), and second pharmacodynamics describes the
chemical's effect (desired or toxic ). The pharmacokinetic properties have 4
properties or characteristics (ADME):
Absorption - How is the drug absorbed (skin, the intestine, the oral mucosa)?
Distribution - How does it spread through the organism?
Metabolism - Is the drug converted chemically inside the body, and into whic h
substances. Are these active? Could they be toxic?
Excretion - How is drug eliminated (through bile, urine, breath, skin)?
Finally drugs have a therapeutic index or therapeutic window which is
the ratio of desired effect to toxic effect. A drug with a narrow therapeutic index
(close to one) exerts its desired effect at a dose close to its toxic dose.
A medical prescription (? ) is an order (often in written form) by a qualified
health care professional to a pharmacist or other therapist for a treatment to be
provided to their patient. Usually on the prescription is text that identifies the
document as a prescription, the name and address of the prescribing provider
and any other legal requirement such as a registration number (e.g. DEA #).
The symbol "Rx" meaning "prescription" is a transliteration of a symbol
resembling a capital R with a cross on the diagonal (? ). Many brand name drugs
have less expensive generic drug substitutes that are chemically equivalent.
Prescriptions will also contain instructions on whether the prescriber will allow
the pharmacist to substitute a generic version of the drug (e.g. substitution
permitted). Some prescriptions will specify whether and how many "repeats" or
"refills" are allowed; that is whether the patient may obtain more of the same
medication without getting a new prescription from the doctor. In the USA,
physicians, veterinarians, dentists, and podiatrists have full prescribing power.
Each state regulates what (if any) prescription powers members o f the above
group are allowed.
There are always 3 elements to a prescription (in addition to patient info,
doctor info and dsignature):
1. Rx: medication (including dosage)
2. Disp.: dispensing instructions (number of pills)
3. Sig.: patient instructions (how to take)
1
Toxicity is a measure to the degree to which something is toxic or poisonous.
The study of poisons is known as toxicology. Toxicity can refer to the effect on a
whole organism, such as a human or a bacterium or a plant, or to a substructure,
such as a cell (cytotoxicity) or the liver. In the science of toxicology, the subject of
such study is the effect of an external substance or condition and its deleterious
effects on living things: organisms, organ systems, individual organs, tissues,
cells, subcellular units. A central concept of toxicology is that effects are dose-
dependent; even water – by itself not toxic – can lead to water intoxication when
taken by a human in large enough doses, whereas for even a very toxic
substance such as snake venom there is a dose for which there is no toxic effect
detectable.
Drug interaction is a situation in which a substance e.g. another drug, affects the
activity of a drug, i.e. the effects are increased or decreased. Typically, interaction
between drugs come to mind (drug-drug interaction). However, interactions may
also exist between drugs & foods (drug-food interactions), as well as drugs &
herbs (drug-herb interactions). Drug interactions may be the result of various
processes that alter the the pharmacokinetics of the drug (ADME). Alternatively,
drug interactions may be the result of the pharmacodynamic properties of the
drug, e.g. via the co -administration of a receptor antagonist and an agonist for the
same receptor.
Metabolism based drug interactions: One notable system involved in metabolic
drug interactions is the enzyme system comprising the cytochrome P450
oxidases. This system may be affected by either enzyme induction or enzyme
inhibition, as discussed in the examples below.
Enzyme induction - drug A induces the body to produce more of an enzyme
which metabolises drug B. This reduces the effective concentration of drug B,
which may lead to loss of effectiveness of drug B. Drug A effectiveness is not
altered.
Enzyme inhibition - drug A inhibits the production of the enzyme metabolising
drug B, thus an elevation of drug B occurs possibly leading to an overdose.
Bioavailability - drug A influences the absorption of drug B. The examples
described above may have different outcomes depending on the nature of the
drugs. For example, if Drug B is a prodrug, then enzyme activation is required for
the drug to reach its active form. Hence, enzyme induction by Drug A would
increase the effectiveness of the drug B by increasing its metab olism to its active
form. Enzyme inhibition by Drug A would decrease the effectiveness of Drug B.

Drug- Route of Administration Key Concepts of Drug Activity

Enteral : GI vs Parenteral : Non-GI
1. Pharmacokinetics: the body’s
Enteral: Oral = stomach = intestines = liver (portal
circulation) = heart = general circulation = target tissues.
effect on a drug.
Sublingual or Rectal = straight into general circulation and 2. Pharmacodynamics: the drug’s
bypasses first-pass liver metabolism.
effect on the body.
Parenteral: Intravascular, intramuscular, subcutaneous
goes straight into general circulation and bypasses first -
pass liver metabolism. Pharmacokinetics (ADME)
Other: 1. Absorption: The onset of action
- Inhalation [i.e. anesthetics, steroids for asthma]
- Intra-nasal [i.e. calcitonin for osteoporosis, cocaine]
of a drug is primarily determined by
- Intrathecal [i.e. analgesics, anti-neoplastics] the rate of absorption
- Topical [i.e. anesthetics, antibiotics, antifungals]

Absorption (continued): 4 factors that affect the absorption of drugs into

the bloodstream:
(1) Bioavailability: The amount (quantity %) that reaches the blood or
plasma. Usually, a drug’s major effect is produced by the amount of
drug that is free in plasma.
(2) Stability: Insulin is unstable in the GI tract, hence the injections for
Diabetics to bypass the enteral route.
(3) Permeability: this is determined by pH (acid-base interactions,
protonation, pKa, Hendersson-Hasselbach) Coated tabs (buffered)
Gastric Emptying, Parasympathetic vs. Sympathetic co-activity, Food in
the stomach (delays gastric emptying and increases acid production to
allow for proper digestion); NOTE: drugs destroyed by acid shoul d be
taken without food when possible. Lipid solubility of drug (hydr ophobic,
non-ionized, i.e. sterols); Water solubility of drug (hydrophilic, ionized or
charged). Transport mechanisms (passive, active, or facilitated)Contact
time, surface area, blood supply.
(4) First -pass hepatic metabolism: For enteral drugs, some are
inactivated by the liver before reaching systemic circulation, thus
decreasing bioavailability; others drugs are activated by the liver,
increasing bioavailabilityIV (intravenous) route of administration
bypasses first-pass liver metabolism, also increasing bioavailability.

2
Category Sample Drug Interaction Information
Nasal -Ask a doctor before use if you: have heart disease, high blood pressure, thyroid disease,
Decongestants diabetes, or difficulty in urination due to an enlarged prostate gland
Nicotine -Ask a doctor before use if you: have high blood pressurenot controlled by medication;
Replacement have heart disease or have had a recent heart attack or irregular heartbeat, since nicotine
Products can increase your heart rate
-Ask a doctor or pharmacist before use if you are: taking a prescription drug for
depression or asthma (your dose may need adjustment);
-Do not use: if you continue to smoke, chew tobacco, use snuff, or use othernicotine-
containing products
Nighttime -Ask a doctor or pharmacist before use if you are: taking sedatives or tranquilizers
Sleep Aids -Ask a doctor before use if you have: a breathing problem such as emphysema or chronic
bronchitis; glaucoma; difficulty in urination due to an enlarged prostate gland
-When using this product: avoid alcoholicbeverages
Pain Relievers -Ask a doctor before taking if you: consume three or more alcohol-containing drinks per
day. (The following ingredients are found in different OTC pain relievers: acetaminophen,
aspirin, ibuprofen, ketoprofen, magnesium salicylate , and naproxen. Important to read the
label of these products to learn about various drug interaction warnings for each ingredient.)
Stimulants -When using this product: limit the use of foods, beverages, and other drugs that have
caffeine. Too much caffeine can cause nervousness, irritability, sleeplessness, and occasional
rapid heart beat; be aware that the recommended dose of this product contains about as much
caffeine as a cup of coffee
Topical Acne -When using this product: increased dryness or irritation of the skin may occur immediate ly
Drugs following use of this product or if you are using other topical acne drugs at the same time. If
this occurs, only one drug should be used unless directed by your doctor
Category Sample Drug Interaction Information
Acid Reducers ( H2 -For products containing cimetidine, ask a doctor or pharmacist before use if you are :
Receptor taking theophylline(oral asthma drug), warfarin (blood thinning drug), or phenytoin
Antagonists) (seizure drug)
Antacids -Ask a doctor or pharmacist before use if you are: allergic to milk or milk products if the
product contains more than 5 grams lactose in a maximum daily dose;
-Ask a doctor before use if you have: kidney disease
Antiemetics -Ask a doctor or pharmacist before use if you are: taking sedatives or tranquilizers
-Ask a doctor before use if you have: a breathing problem, such as emphysema or chronic
bronchitis; glaucoma; difficulty in urination due to an enlarged prostate gland
-When using this product: avoid alcoholicbeverages
Antihistamines -Ask a doctor or pharmacist before use if you are taking: sedatives or tranquilizers ; a
prescription drug for high blood pressure or depression
-Ask a doctor before use if you have: glaucoma or difficulty in urination due to an
enlarged prostate; breathing problems, such as emphysema, chronic bronchitis, or asthma
-When using this product: alcohol, sedatives, and tranquilizers may increase drowsiness;
avoid alcoholic beverages
Antitussives -Ask a doctor or pharmacist before use if you are: taking sedatives or tranquilizers
(Cough Medicine) -Ask a doctor before use if you have: glaucoma or difficulty in urination due to an
enlarged prostate gland
Bronchodilators -Ask a doctor before use if you: have heart disease, high blood pressure, thyroid disease,
diabetes, or difficulty in urination due to an enlarged prostate gland;
Laxatives -Ask a doctor before use if you have: kidney disease and the laxative contains
phosphates, potassium, or magnesium; stomach pain, nausea, or vomiting

A dose-response curve is a simple X-Y graph relating the amount of a drug
or toxin given to the response of the organism to that drug. The curves are
usually qualitative , though they can use quantitative information.
The measured dose (usually in [[milligrams, micrograms , or grams per
kilogram of body-weight) is generally plotted on the X axis and the response
is plotted on the Y axis. Commonly, it is the logarithm of the dose that is
plotted on the X axis, and in such cases the curve is typically sigmoidal , with
the steepest portion in the middle. The first point along the graph where a
response above zero is reached is usually referred to as a threshold -dose.
For most beneficial or recreational drugs, the desired effects are found at
doses slightly greater than the threshold dose. At higher doses still, undesired
side effects appear and grow stronger as the dose increases. The stronger a
particular substance is, the steeper this curve will be. In quantitative
situations, the Y-axis usually is designated by percentages, which refer to the
percentage of users registering a standard response (which is often death,
when the 50% mark refers to LD50).
Phase I and Phase II reactions are biotransformations of chemicals that
occur during drug metabolism.
Phase I metabolism usually precedes Phase II, though not necessarily.
During these reactions, polar bodies are either introduced or unmasked,
which results in (more) polar metabolites of the original chemicals. Phase I
reactions may occur by oxidation, reduction or hydrolysis reactions. If the
metabolites of phase I reactions are sufficiently polar, they may be readily
excreted at this point. However, many phase I products are not eliminated
rapidly and undergo a subsequent reaction in which an endogenous
substrate combines with the newly incorporated functional group to form a
highly polar conjugate.
Phase II reactions — usually known as conjugation reactions (e.g., with
glucuronic acid, sulfonates (commonly known as sulfation) , glutathione or
amino acids ) — are usually detoxication in nature, and involve the
interactions of the polar functional groups of phase I metabolites.

Examples of some commonly used herbal medicines:

Artichoke and several other plants reduced total serum cholesterol levels.[9]
Black cohosh and other plants that contain phytoestrogens have some benefits
for treatment of symptoms resulting from menopause.[10]
Echinacea extracts limit the length of colds in some clinical trials, although some
studies have found it to have no effect.[11]
Garlic lowers total cholesterol levels, mildly reduces blood pressure, reduces
platelet aggregation, and has antibacterial properties.[12]
2.0. Central Nervous System [4 Qs]
Grapefruit seed extract as a natural antimicrobial has minimal effectiveness as 2.1. Sedatives - hypnotics & alcohols
an anti-bacterial, anti-parasitic, and anti -fungal herb.[13][14][15][16][17]
Nigella sativa (Black cumin) is a general medicinal plant used for cough, 2.2. Antianxiety & conscious sedation drugs
pulmonary infections, asthma, influenza, allergy, hypertension and stomach
ache. The seeds are considered carminative, stimulant, diuretic and 2.3. Anticonvulsants & anti-Parkinson
galactogogue. Seed powder or oil is externally applied for eruptions of skin.
Peppermint tea for problems with the digestive tract , including irritable bowel
2.4. Psychotropics (antipsychotic &
syndrome and nausea. antidepressant )
Rauvolfia Serpentina, used extensively in India for sleeplessness, anxiety, and
high blood pressure.
St John's wort, has yielded positive results, proving more effective than a
placebo for the treatment of mild to moderate depression.[18]
Valerian root can be used to treat insomnia .

3
A sedative is a substance that depresses the central nervous system (CNS), resulting
in calmness, relaxation, reduction of anxiety, sleepiness, slowed breathing, slurred
speech, staggering gait , poor judgment, and slow, uncertain reflexes. Sedatives may be Hypnotic drugs are a class of drugs that induce sleep (which differentiates
referred to as tranquilizers, depressants, anxiolytics, soporifics, sleeping pills, them from the sedative category), used in the treatment of severe insomnia
downers, or sedative-hypnotics. At high doses or when they are abused, many of and in surgical anesthesia. Often the treatment of insomnia will not begin
these drugs can cause unconsciousness (see hypnotic) and death. with drugs at all, however, as many (not all) hypnotic drugs are habit forming.
A physician will usually recommend alternative sleeping patterns and
exercise before prescribing medication for sleep. These drugs include:
Examples of sedatives Uncategorized sedatives Barbiturates
Antidepressants eszopiclone (Lunesta®) Benzodiazepines
mirtazapine (Remeron®) ramelteon (Rozerem®) Zolpidem
trazodone (Desyrel®) methaqualone (Sopor®, Quaalude®) Zaleplon
Barbiturates ethchlorvynol (Placidyl®) Zopiclone
secobarbital (Seconal®) chloral hydrate (Noctec ®) Eszopiclone
pentobarbital (Nembutal ®) meprobamate (Miltown ®)
amobarbital (Amytal ®) chloral hydrate
glutethimide ( Doriden ®)
Benzodiazepines ("minor tranquilizers") methyprylon (Noludar ®) Chlormethiazole
alprazolam (Xanax®) gamma-hydroxybutyrate (GHB) Antihistamines
diazepam (Valium®) ethyl alcohol (alcoholic beverage) Doxylamine
lorazepam (Atavan ®) diethyl ether (Ether) Promethazine
Herbal sedatives methyl trichloride (Chloroform) diphenhydramine.
catnip zopiclone (Imovane®, Zimovane ®)
Valerian (plant) chloral hydrate (Noctec ®)
Mandrake Alcohol is often tried as a hypnotic drug but it is not particularly effective.
zaleplon (Sonata®)
Kava Kava zolpidem (Ambien®)

Anti-Convulsants Antipsychotics are drugs used to treat psychosis (e.g. schizophrenia, mania
1 Aldehydes and delusional disorder. Antipsychotics also have some effects as mood
The anticonvulsants, sometimes also called
2 Aromatic allylic alcohols stabilizers , leading to their frequent use in treating mood disorder (particularly
antiepileptics, belong to a diverse group of
3 Barbiturates bipolar disorder) even when no signs of psychosis are present. Antipsychotics
pharmaceuticals used in prevention of the
4 Benzodiazepines are also referred to as neuroleptic drugs. The word neuroleptic is derieved
occurrence of epileptic seizures. The goal of
5 Bromides from Greek. 'Neuro ' refers to the nerves and 'lept' means 'to take hold of'. Thus
an anticonvulsant is to suppress the rapid and
6 Carbamates the word means 'taking hold of one's nerves' which implies their role in mood
excessive firing of neurons that start a
7 Carboxamides stabilization. There are currently two main types:
seizure. Failing this, a good anticonvulsant
8 Fatty acids 1. Typical antipsychotics ("major tranquilizers")
would prevent the spread of the seizure within
9 Fructose derivatives fluphenazine (Prolixin®)
the brain and offer protection against possible
10 Gaba analogs haloperidol (Haldol ®)
excitotoxic effects that may result in brain
11 Hydantoins thiothixene (Navane®)
damage. An excellent anticonvulsant would
12 Oxazolidinediones trifluoperazine (Stelazine®, Trifluoperaz®)
have few serious side effects. However, no
13 Propionates loxapine succinate (Loxitane®)
such drug exists.
14 Pyrimidinediones perphenazine (Etrafon®, Trilafon®)
15 Pyrrolidines prochlorperazine (Compazine®)
Many anticonvulsants block Sodium (Na+)
16 Succinimides 2. Atypical antipsychotics
channels , Calcium (Ca2+) channels, AMPA
17 Sulfonamides clozapine (Clozaril®)
receptors or NMDA receptors . Some
18 Triazines quetiapine (Seroquel®)
anticonvulsants inhibit the metabolism of
19 Ureas risperidone (Risperdal ®)
GABA or increase its release.
20 Valproylamides (amide ziprasidone (Geodon®) (some become tired, some get insomnia)
derivatives of valproate) olanzapine (Zyprexa®)

Anti-depressants
An antidepressant is a medication designed to treat or alleviate the
Monoamine oxidase inhibitors (MAOI) Harmaline, Iproclozide, Iproniazid , Isocarboxazid , Nialamide,
symptoms of clinical depression. Some antidepressants, notably the
Phenelzine, Selegiline, Toloxatone, Tranylcypromine
tricyclics , are commonly used off-label in the treatment of neuropathic pain,
whether or not the patient is depressed. Smaller doses are generally used for Reversibleinhibitor of monoamineoxidase A
Brofaromine, Moclobemide
(RIMA)
this purpose, and they often take effect more quickly. Many antidepressants
Dopamine reuptake inhibitor(DARI) Amineptine, Phenmetrazine, Vanoxerine, Modafinil
also are used for the treatment of anxiety disorders , and tricyclic
antidepressants are used in the treatment of chronic pain disorders such as Norepinephrine-dopamine reuptake inhibitors Bupropion
chronic functional abdominal pain (CFAP), myofascial pain syndrome, and
Norepinephrine reuptake inhibitor(NRI) or
post-herpetic neuralgia. (NARI)
Atomoxetine, Maprotiline, Reboxetine, Viloxazine
The main classes of antidepressants have similar efficacy, but the newer
Serotonin -norepinephrine reuptake inhibitor
types are generally regarded to have a more benign side -effect profile and (SNRI)
Duloxetine, Milnacipran , Venlafaxine
less risk of lethality if taken in overdose.
Selective serotonin reuptake inhibitor(SSRI) Alaproclate , Etoperidone, Citalopram, Escitalopram, Fluoxetine,
Mechanism of action: The therapeutic effects of antidepressants are Fluvoxamine, Paroxetine, Sertraline, Zimelidine
believed to be related to an effect on neurotransmitters , particularly by
Selective serotonin reuptake enhancer (SSRE)
inhibiting the monoamine transporter proteins of serotonin and Tianeptine

norepinephrine. SSRI’s specifically prevent the reuptake of serotonin Tricyclicantidepressants (TCA) Amitriptyline, Amoxapine, Butriptyline, Clomipramine,
(thereby increasing the level of serotonin in synapses of the brain), whereas Desipramine, Dibenzepin , Dothiepin , Doxepin , Imipramine,
earlier monoamine oxidase inhibitors (MAOIs) blocked the destruction of Iprindole, Lofepramine, Melitracen , Nortriptyline, Opipramol,
Protriptyline, Trimipramine
neurotransmitters by enzymes which normally break them down. Tricyclic
Tetracyclic antidepressants
antidepressants (TCAs ) prevent the reuptake of various neurotransmitters , Maprotiline, Mianserin , Nefazodone, Trazodone
including serotonin, norepinephrine, and dopamine. Noradrenergic and specific serotonergic
antidepressant (NaSSA) Mirtazapine

4
 Adrenergic Agents bind with adrenergic receptors (or adrenoceptors),
which are a class of G protein-coupled receptors that are targets of the
catecholamines. Adrenergic receptors specifically bind their endogenous
3.0. Autonomic [3 Qs] ligands , the catecholamines adrenaline and noradrenaline (also called
epinephrine and norepinephrine in the USA), and are activated by these. Many
cells possess these receptors, and the binding of an agonist will generally
3.1. Adrenergics cause the cell to respond in a fight-or-flight manner. For instance, the heart rate
will increase and the pupils will dilate, energy will be mobilized, and blood flow
3.2. Cholinergics diverted from other organs to skeletal muscle.

3.3. Blocking agents

(adrenergic, cholinergic, etc) Direct
Albuterol – Clonidine – Dobutamine – Dopamine - Epinepherine
- Formoterol - Isoproterenol - Metaproterenol - Methoxamine -
Acting: Norepinephrine - Phenylephrine - Piruterol - Salmeterol -
Tamsulosine - Tamsulosine – Terbutaline

Indirect
Amphetamine – Tyramine
Acting
Mixed Ephedrine
Action:

A synapse is cholinergic if it uses acetylcholine as its neurotransmitter.

Anticholinergic Drugs
Cholinergic means "related to the neurotransmitter acetylcholine". The
parasympathetic nervous system is entirely cholinergic. A substance is Unclassified benztropine (Cogentin®)` Nicotinic receptor antagonists
cholinergic if it is capable of producing, altering, or releasing acetylcholine. Muscarinic receptor antagonists Ganglionic Trimethaphan
A cholinergic, also known as a cholinergic agent or a blocking agents
Belladonna Scopolamine (L-Hyoscine)
parasympathomimetic , is any chemical which functions to enhance the alkaloids
effects mediated by acetylcholine in the central nervous system, the Nondepolarizing Atracurium
Atropine (D/L-Hyoscyamine) neuromuscular
peripheral nervous system, or both. These include acetylcholine's precursors
Synthetic and Dicyclomine blocking agents
and cofactors , acetylcholine receptor agonists (such as muscarine and
Semisynthetic
nicotine), as well as cholinergic enzymes such as the anticholinesterases. Doxacurium
----------------------------- Flavoxate
Mivacurium
An anticholinergic agent is a member of a class of pharmaceutical Ipratropium
Pancuronium
compounds which serve to reduce the effects mediated by acetylcholine in Oxybutynin
the central nervous system and peripheral nervous system. Tubocurarine
Pirenzepine
Anticholinergics are typically reversible competitive inhibitors of one of the Vecuronium
two types of acetylcholine receptors , and are classified according to the Tiotropium
Depolarizing Suxamethonium chloride
receptors that are affected: antimuscarinic agents operate on the Tolterodine (Detrusitol®) neuromuscular
muscarinic acetylcholine receptors , and antinicotinic agents operate on the Tropicamide blocking agents
nicotinic acetylcholine receptors . The majority of anticholinergics are
Solifenacin (Vesicare®)
antimuscarinics .
Darifenacin (Enablex®)

Beta blockers are a class of drugs used for various indications, but
Alpha blockers (also called alpha-adrenergic blocking agents) constitute a particularly for the management of cardiac arrhythmias and cardioprotection
variety of drugs which block a1 -adrenergic receptors in arteries and smooth after myocardial infarction.
muscles. Beta blockers block the action of endogenous catecholamines, epinephrine
(adrenaline) and norepinephrine (noradrenaline) in particular, on ß-adrenergic
receptors , part of the sympathetic nervous system which mediates the "fight
Indications: These drugs may be used to treat: or flight" response. There are three known types of beta receptor, designated
•benign prostatic hyperplasia (BPH) ß1, ß2 and ß3. ß1-Adrenergic receptors are located mainly in the heart,
•high blood pressure (hypertension). This is not typically the drug of choice kidney, and adipose tissue. ß2-Adrenergic receptors are located mainly in the
unless the patient also has BPH. heart, lung, GI tract, liver, pancreas, and skeletal muscle. The role and
•symptoms of non inflammatory chronic pelvic pain syndrome, a type of location of ß3-receptors is less well-defined.
prostatitis. As a side effect they may reduce blood pressure and result in
lightheadedness. Indications for beta blockers include:
Hypertension
Examples of alpha blockers: Alpha blockers include: Angina
•Doxazosin (Cardura) Cardiac arrhythmia
•Prazosin (Minipress ) Congestive heart failure
•Phenoxybenzamine Myocardial infarction
•Phentolamine (Rogitine) Glaucoma
•Tamsulosin (Flomaxtra/Flomax) Migraine prophylaxis
•Alfuzosin (Uroxatral) Symptomatic control (tachycardia , tremor) in anxiety and hyperthyroidism
•Terazosin (Hytrin) Essential tremor
Phaeochromocytoma, in conjunction with a-blocker

5
 Beta-Blocking Drugs
Non-selective agents ß1-Selective agents
Alprenolol Acebutolol
Carteolol
Levobunolol
Atenolol
Betaxolol
4.0. Cardiovascular [4 Qs]
Mepindolol
Metipranolol
Bisoprolol
Esmolol
4.1. Cardiac glycosides
Nadolol
Oxprenolol
Metoprolol
Nebivolol
4.2. Antiarrhythmics
Penbutolol
Pindolol
Mixed a1/ß-adrenergic antagonists
Carvedilol
4.3. Antihypertensives - diuretics
Propranolol
Sotalol
Celiprolol
Labetalol
4.4. Anti-anginal agents
Timolol ß2-Selective agents
Butoxamine (weak a-adrenergic
4.5. Anticoagulants, coagulants &
agonist activity) antihyperlipidemics

Cardiac glycosides are drugs used in the treatment of congestive heart failure
and cardiac arrhythmia. These glycosides are found as secondary metabolites
in several plants, but also in some animals. Some of these compounds
(ouabain and some frog poisons) are used in Africa as arrow-poisons for
hunting. Cardiac glycosides work by inhibiting the Na+/K+ pump. They do this
by stabilizing the E2-P transition state of the Na+/K+ pump. This inhibition
increases the amount of Ca++ ions available for contraction of the heart
muscle, improves cardiac output and reduces distention of the heart. T hey
have an antiarrhythmic effect by prolonging the refractory period of the AV
node (Atrioventricular node), reducing the number of impulses reaching the
ventricles. Cardiac output is restored but atrial fibrillation or atrial flutter are not
abolished. Examples of plants producing cardiac glycosides:
- Strophanthus - ouabain g/k/e-strophanthin
- Digitalis lanata and Digitalis purpurea - digoxin, digitoxin
---------------------------------------------------------------- ----------------------------------------
Digoxin is a cardiac glycoside extracted from the foxglove plant, digitalis. Its
corresponding aglycone is digoxigenin. Digoxin is widely used in the treatment
of various heart conditions, namely atrial fibrillation, atrial flutter and congestive
heart failure that cannot be controlled by other medication. Digoxin
preparations are commonly marketed under the trade name Lanoxin.
Antiarrhythmic agents are used to suppress fast rhythms of the heart (cardiac
arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and
ventricular fibrillation. Suppression is often done to relieve the symptoms that may
be associated with the loss of the atrial component to ventricular filling (atrial kick )
that is due to atrial fibrillation or flutter. In individuals with ventricular arrhythmias,
antiarrhythmic agents are often still in use to suppress arrhythmias. If these drugs
fail it may lead to implantation of an implantable cardioverter-defibrillator (ICD).
---------------------------------------------------------------- --------------------------------------------
5 main classes in the Vaughan Williams system of antiarrhythmic agents:
Class I agents interfere with the sodium (Na+) channel.
Class II agents are anti-sympathetic nervous system agents (all: beta blockers ).
Class III agents affect potassium (K+) efflux.
Class IV agents affect the AV node.
Class V agents work by other or unknown mechanisms.
---------------------------------------------------------------- --------------------------------------------
class Ia:Ajmaline , Disopyramide, Prajmaline, Procainamide, Quinidine, Sparteine
class Ib: Aprindine, Lidocaine , Mexiletine, Tocainide
class Ic:Encainide, Flecainide, Lorcainide, Moricizine, Propafenone
class II: various Beta blockers
class III:Amiodarone, Bretylium tosilate, Bunaftine, Dofetilide, Ibutilide
class IV: various Calcium channel blockers
class V:Adenosine, Digoxin

Antihypertensives:
1.1 Diuretics Anti-anginal agents: for treatment of angina pectoris, a symptom of ischaemic
heart disease. Drugs used are:
1.2 Anti-adrenergics
1.3 Calcium channel blockers 1. nitrates such as nitroglycerin (glyceryl trinitrate) or pentaerythritol tetranitrate
1.4 ACE inhibitors These drugs cause vasodilation of the venous capacitance vessels by simulating
the endothelium-derived relaxing factor (EDRF). Used to relieve both exertional and
1.5 Angiotensin II receptor antagonists
1.6 Aldosterone antagonists vasospastic angina by allowing venous pooling, reducing the pressure in the
ventricles and so reducing wall tension and oxygen requirements in the heart.
1.7 Vasodilators
1.8 Centrally acting adrenergic drugs Short-acting nitrates are used to abort angina attacks that have occurred, while
longer-acting nitrates are used in the prophylactic management of the condition.
1.8.1 Adrenergic neuron blockers
1.9 Herbals provoking hypotension ---------------------
2. beta blockers , either cardioselectives such as acebutolol or metoprolol , or non-
1. Diuretics: help the kidneys eliminate excess salt and water from the body's cardioselectives such as oxprenolol or sotalol
These drugs are used in the prophylaxis of exertional angina by reducing the work
tissues and blood. There are several types including:
-Loop diuretics: (bumetanide, ethacrynic acid, furosemide, torsemide) the heart is allowed to perform below the level that would provo ke an angina attack.
They cannot be used in vasospastic angina and can precipitate heart failure.
-Thiazides: (chlortalidone, epitizide, hydrochlorothiazide & chlorothiazide)
----------------------
-Thiazide-like diuretics: (indapamide, metolazone)
-Potassium-sparing diuretics : (amiloride; triamterene) 3. calcium channel blockers , either Class I agents (e.g., verapamil), Class II agents
(e.g., amlodipine, nifedipine), or the Class III agent diltiazem.
(NOTE: evidence suggest that by lowering blood pressure. Evidenc e suggests that These drugs are Calcium ion antagonists and are used for treatment of exertional &
vasospastic angina. In vitro, they dilate coronary & peripheral arteries. T hey have
reduction of the blood pressure by 5-6 mmHg can decrease the risk of stroke by
40%, of coronary heart disease by 15-20%, and reduces the likelihood of dementia, negative inotropic & chronotropic effects, decreasing afterload, improving
myocardial efficiency, reducing heart rate & improving coronary blood flow.
heart failure, and mortality from cardiovascular disease.)

6
 Acenocoumarol, Clorindione, Dicumarol
Vitamin K
(Dicoumarol}, Diphenadione, Ethyl biscoumacetate,
antagonists:
Phenprocoumon, Phenindione, Tioclomarol, Warfarin

An anticoagulant is a substance that prevents coagulation; that is, it stops Heparin group Antithrombin III, Bemiparin , Dalteparin, Danaparoid,
(Platelet aggregation Enoxaparin, Heparin, Nadroparin, Parnaparin ,
blood from clotting. Anticoagulants are given to people to stop thrombosis
(blood clotting inappropriately in the blood vessels). This is useful in primary and inhibitors): Reviparin, Sulodexide, Tinzaparin
secondary prevention of deep vein thrombosis , pulmonary embolism, Abciximab, Acetylsalicylic acid (Aspirin), Aloxiprin,
myocardial infarctions and strokes in those who are predisposed. Beraprost, Ditazole, Carbasalate calcium,
1. Vitamin K antagonists: Oral anticoagulants are a class of pharmaceuticals Other platelet
Cloricromen, Clopidogrel, Dipyridamole,
aggregation
that act by antagonizing the effects of vitamin K. It is important to note that they Epoprostenol , Eptifibatide, Indobufen, Iloprost,
take at least 48 to 72 hours for the anticoagulant effect to develop fully. In cases inhibitors:
Picotamide, Prasugrel , Ticlopidine, Tirofiban,
when an immediate effect is required, heparin must be given concomitantly. Treprostinil, Triflusal
The most important oral anticoagulants are Warfarin (Coumadin). Heparin and Alteplase, Ancrod, Anistreplase, Brinase, Drotrecogin
derivative substances: Heparin is a biological substance, usually made from Enzymes: alfa, Fibrinolysin, Protein C, Reteplase, Saruplase ,
pig intestines. It works by activating antithrombin III, which blocks thrombin from Streptokinase, Tenecteplase, Urokinase
clotting blood.
2. Direct thrombin inhibitors: Another type of anticoagulant is the direct Direct thrombin Argatroban, Bivalirudin, Dabigatran, Desirudin,
thrombin inhibitors . Current members of this class include argatroban, lepirudin, inhibitors: Hirudin, Lepirudin, Melagatran, Ximelagatran
and bivalirudin. Other Dabigatran, Defibrotide, Dermatan sulfate,
antithrombotics: Fondaparinux, Rivaroxaban
Non-medicinal: Citrate, EDTA , Oxalate

Product Description Indications and features

The coagulation of blood is a complex process during which blood forms solid
clots. It is an important part of hemostasis (the cessation of blood loss from a
damaged vessel) whereby a damaged blood vessel wall is covered by a fibrin
clot to stop hemorrhage and aid repair of the damaged vessel. Disorders in
coagulation can lead to increased hemorrhage and/or thrombosis and
embolism.
In a normal individual, coagulation is initiated within 20 seconds after an injury
occurs to the blood vessel damaging the endothelial cells. Platelets
immediately form a haemostatic plug at the site of injury. This is called primary
haemostasis . Secondary haemostasis then follows —plasma components
called coagulation factors respond (in a complex cascade) to form fibrin strands
which strengthen the platelet plug. Contrary to popular belief, coagulation from
a cut on the skin is not initiated by air or drying out, but by platelets adhering to
and activated by collagen in the blood vessel endothelium. The activated
platelets then release the contents of their granules, these contain a variety of
substances that stimulate further platelet activation and enhance the
haemostatic process.
Many different hemostatic agents!!!! (need table)
Gelfoam Absorbable gelatin sponge made from purified gelatin
solution. Absorbs in 3 -5 days.
Instat Absorbable collagen made from purified and
lyophilized bovine dermal collagen. Can be cut or
shaped. Adheres to bleeding surfaces when wet, but
does not stick to instruments, gloves, or gauze sponges.
Surgicel, Oxidized regenerated cellulose. Exerts physical effect
Oxycel rather than physiologic. Swells upon contact with
blood, with resulting pressure adding tohemostasis.
Thrombin ineffective with these agents because of
inactivation as a result of pH factors.
Avitene, Microfibrillar collagen hemostat (MCH). Dry, sterile,
Helistat fibrous, water insoluble, HCl acid salt purified bovine
corium collagen. MCH attracts platelets and triggers
aggregation in fibrous mass.
Colla-Cote,, Absorbable dressings from bovine collagen. Can be
Tape, Plug sutured into place, used understents, dentures, or
alone. Fully resorbed in 10 -14 days.
Thrombostat, Topical thrombin. Directly converts fibrinogen to
Thrombinar , fibrin. Derived from bovine sources.
Thrombogen
Cyklokapron Tranexamic acid. Works as a competitive inhibitor of
plasminogen activation. Used as a rinse.
Beriplast Fibrin/tissue glue.
Useful for most patients taking anantithrombotic agent.
Helpful to place topical Thrombin onGelfoam . For
extensive or invasive surgery, oneshould consider
placing inside a splint.
Mild -to -moderate bleeding is usually controlled in 2 -5
min. More expensive thanGelfoam .
After 24-48 h, it becomes gelatinous. Can be left in place
or removed. Useful to control bleeding when other agents
ineffective.
Thrombin ineffective with these agents due to
inactivation as a result of pH factors. Moderate-to -severe
bleeding.
Shaped according to intended use; Cote 3 /4 in× 1.5 in,
Tape 1 in× 3 in, Plug 3/8 in× 3/4 in. All are superior
hemostats for moderate-to -severebleeding.
One5000 -unit vial dissolved in 5mL of saline solution
can clot equal amount of blood in less than 1 sec. For
severebleeding.
Useful in short term (2-8 d) for preventing hemorrhage
following dental extractions.
Not available in the United States at this time.

There are several classes of hypolipidemic drugs (a.k.a. anti-hyperlipidemics ).

Some lower lower bad cholesterol (low density lipoproteins) and others may
increase high density lipoprotein (HDL), "the good cholesterol".
1. statins are good at lowering LDL, which is strongly linked to cardiovascular
diseases. The studies show they lower LDL-C by 18% to 55%, depending on
the specific statin being used. Risk of severe muscle damage (myopathy & 5.0. Local anesthetics [4 Qs]
rhabdomyolysis) with statins.
2. fibrates are indicated for hypertriglyceridemia . Fibrates typically lower 5.1. Basic pharmacology
triglycerides by 20% to 50%. Level of the good cholesterol HDL i s also
increased. Fibrates may decrease LDL, though generally less than statins. Risk
of severe muscle damage (myopathy & rhabdomyolysis) with fibrates.
5.2. Vasoconstrictors
3. nicotinic acid, like fibrates , is also well-suited for lowering triglycerides by 20-
50%. It may also lower LDL by 5-25% and increase HDL by 15-35%. Nicotinic
acid may cause hyperglycemia, and may also cause liver damage.
4. bile acid sequestrants (resins) are particularly effective for lowering LDL -C by
sequestering the cholesterol-containing bile acids released into the gut and
preventing their reabsorption. This decreases LDL by 15-30% and raises HDL
by 3-5%. It has little effect on triglycerides. Risk with resins is G.I. problems, and
may also reduce the absorption of other drugs and vitamins from the gut.
5. ezetimibe (Zetia) is a selective inhibitor of dietary cholesterol absorption.
6. phytosterols may be found naturally in plants. Similar to ezetimibe,
phytosterols reduce the absorption of cholesterol in the gut. Hence, they are
most effective when consumed with meals.

7
A local anesthetic is a drug that reversibly
inhibits the propagation of signals along
nerves. When it is used on specific nerve Amino esters
pathways, effects such as analgesia (loss of
pain sensation) and paralysis (loss of muscle
power) can be achieved. Clinical local
anesthetics belong to one of two classes:
aminoamide and aminoester local
Amino amides
anesthetics. These so-called synthetic local
anesthetics are structurally related to cocaine .
Local anesthetic drugs act mainly by inhibiting
sodium influx through sodium-specific ion
channels in the neuronal cell membrane, in
particular the voltage-gated sodium channels.
When the influx of sodium is interrupted, an
action potential cannot arise and signal
conduction is inhibited. Local anesthetics are
weak bases and are usually formulated as the Combinations
hydrochloride salt to render them water-
soluble. Acidosis such as caused by wound
infection partly reduces the action of local
anesthetics because of reduced ability to
cross the cell membrane.
Adverse reactions to local anesthetics are not infrequent, but true
Benzocaine
allergyis very rare. Non-allergic reactions may resemble allergy in
Chloroprocaine
their manifestations. In some cases, skin tests and provocative
Cocaine
Procaine challenge may be necessary to establish a diagnosis of allergy. There
are also cases of allergy to paraben derivatives, which are often
Bupivacaine added as preservatives to local anesthetic solutions.
Levobupivacaine ---------------------------
Lidocaine Methemoglobinemia: The systemic toxicity of prilocaine is
Mepivacaine comparatively low, however its metabolite, o-toluidine, is known to
Prilocaine cause methemoglobinemia. As methemoglobinemiareduces the
amount of hemoglobin that is available for oxygen transport, this side
Ropivacaine
effect is potentially life-threatening. Therefore dose limits for prilocaine
Septocaine
should be strictly observed. Prilocaine is not recommended for use in
Lidocaine/prilocaine (EMLA) infants.

A vasoconstrictor , also vasopressor

and simply pressor , is any substance or Vasoconstrictors
that acts to cause vasoconstriction Antihistamines
(narrowing of the lumena of blood vessels)
Adrenaline
and usually results in an increase of the
Asymmetric dimethylarginine
blood pressure. The opposite process,
vasodilation, is the opening of blood ATP 6.0. Chemotherapy [5 Qs]
Cannabis
vessels. Many vasoconstrictors act on
specific receptors, such as vasopressin Catecholamines 6.1. Antibacterials
Cocaine
receptors or adrenoreceptors .
Vasoconstrictors are also used clinically to Decongestants 6.2. Antifungals
increase blood pressure or to reduce local Endothelin
blood flow. Exposure to moderately high Phenylephrine 6.3. Antivirals
levels of stress also induces
Pseudoephedrine
vasoconstriction. Vasoconstriction also
occurs in superficial blood vessels of Neuropeptide Y 6.4. Antineoplastics
warm -blooded animals when their ambient Norepinephrine
environment is cold; this process diverts Tetrahydrozoline hydrochloride
the flow of heated blood to the center of Thromboxane
the animal, preventing the loss of heat.

Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics

Brand
An antibiotic is a drug that kills or slows the growth of bacteria . They have no Class Generic Name Common Uses Side Effects
Names
effect against viruses, fungi, or parasites. Antibiotics are generally small
molecules with a molecular weight less than 2000 kd. They are not enzymes. Aminoglycosides Amikacin Amikin
Some antibiotics have been derived from mold, for example the penicillin
Gentamicin Garamycin
class. Antibiotics can be categorized based on their target specificity: 'narrow-
spectrum' antibiotics target particular types of bacteria, such as Gram- Kanamycin Infections caused by Hearing loss
negative or Gram-positive bacteria, while 'wide -spectrum' antibiotics affect a Gram-negative bacteria, Vertigo
Neomycin
larger range of bacteria. The effectiveness of individual antibiotics varies with such as Escherichia coli Kidney
Netilmicin and Klebsiella damage
the location of the infection, the ability of the antibiotic to reach the site of
infection, and the ability of the bacteria to resist or inactiva te the antibiotic.
Streptomycin
Some antibiotics actually kill the bacteria (bactericidal), whereas others
merely prevent the bacteria from multiplying (bacteriostatic ). Antibiotics can Tobramycin Nebcin
also be classified by the organisms against which they are effec tive, and by Carbacephem
the type of infection in which they are useful, which depends on the Loracarbef Lorabid
sensitivities of the organisms that most commonly cause the infection and the
Carbapenems Ertapenem
concentration of antibiotic obtainable in the affected tissue.
Imipenem/
Primaxin
Cilastatin

Meropenem

8
 Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics
Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics
Brand
Class Generic Name Common Uses Side Effects
Names
Cephalosporins Cefadroxil Duricef Class Generic Name Brand Names Common Uses Side Effects
Gastrointestinal upset and diarrhea
(First generation)
Cefazolin Ancef Nausea (if alcohol taken concurrently)
Allergic reactions Glycopeptides
Cephalexin Keflex Teicoplanin

Cephalosporins Cefaclor Ceclor

(Secondgeneration ) Vancocin
Cefamandole Mandole Vancomycin
Gastrointestinal upset and diarrhea
Cefoxitin Nausea (if alcohol taken concurrently)
Allergic reactions Macrolides Zithromax ,
Cefprozil Cefzil Azithromycin
Sumamed
Cefuroxime Ceftin
Clarithromycin Biaxin
Cephalosporins Cefixime
(Third generation)
Cefdinir Omnicef Dirithromycin
Streptococcal infections, Nausea, vomiting, and
Cefditoren syphilis, respiratory diarrhea (especially at
Cefoperazone Cefobid Erythromycin infections , mycoplasmal higherdoses)
Gastrointestinal upset and diarrhea infections , Lymedisease Jaundice
Cefotaxime Claforan
Nausea (if alcohol taken concurrently)
Cefpodoxime Allergic reactions Roxithromycin
Ceftazidime Fortum
Ceftibuten Troleandomycin
Ceftizoxime
Ceftriaxone Rocephin Monobactam
Aztreonam
Cephalosporins Gastrointestinal upset and diarrhea
(Fourthgeneration) Cefepime Maxipime Nausea (if alcohol taken concurrently)
Allergic reactions

Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics

Brand
Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Class Generic Name Common Uses Side Effects
Names
Bacitracin Mupirocin Eye, ear or bladder
Kidney and
infections; usually applied
Brand Colistin nerve damage
Class Generic Name Common Uses Side Effects Polypeptides directly to the eye or inhaled
Names (when given by
into the lungs; rarely given
Polymyxin B injection)
Amoxicillin Novamox by injection
Ampicillin Ciproxin,
Quinolones Ciprofloxacin
Ciplox
Azlocillin
Carbenicillin Enoxacin
Gastrointestinal
Cloxacillin upset and diarrhea Gatifloxacin Tequin
Wide range of Allergy with
Dicloxacillin infections; penicillin
serious Levofloxacin Levaquin
Penicillins used for streptococcal Urinary tract infections,
Flucloxacillin anaphylactic
infections, syphilis, and bacterial prostatitis, bacterial Nausea (rare)
reactions Lomefloxacin
Mezlocillin Lyme disease diarrhea, gonorrhea
Brain and kidney
Nafcillin Moxifloxacin Avelox
damage (rare)
Penicillin Norfloxacin
Piperacillin
Ofloxacin Ocuflox
Ticarcillin
Trovafloxacin Trovan

Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics
Brand
Class Generic Name Common Uses Side Effects
Names Class Generic Name Brand Names Common Uses Side Effects
Sulfonamides Mafenide Others Chloramphenicol Chloromycetin

Prontosil (archaic) Clindamycin Cleocin

Sulfacetamide Ethambutol
Nausea, vomiting, and
diarrhea Fosfomycin
Sulfamethizole
Urinary tract infections Allergy (including skin Furazolidone
Sulfanilimide (archaic) (except sulfacetamide rashes)
and mafenide); Crystals in urine Isoniazid
Sulfasalazine mafenide is used Kidney failure Linezolid Zyvox
Sulfisoxazole topically for burns Decrease in white blood
cell count Metronidazole Flagyl
Trimethoprim Sensitivity to sunlight Nitrofurantoin Macrodantin
Trimethoprim- Platensimycin
Sulfamethoxazole Bactrim
(Co-trimoxazole ) Pyrazinamide

Tetracyclines Demeclocycline Quinupristin/

Gastrointestinal upset Syncercide
Syphilis, chlamydial Dalfopristin
Doxycycline Vibramycin Sensitivity to sunlight
infections, Lyme Rifampin
Staining of teeth
Minocycline disease, mycoplasmal
Potential toxicity to Spectinomycin
infections, acne
Oxytetracycline mother and fetus during
rickettsial infections
pregnancy
Tetracycline Sumycin

9

Use or misuse of antibiotics may result in the development of antibiotic
resistance by the infecting organisms, similar to the development of pesticide
resistance in insects. Evolutionary theory of genetic selection requires that as
close as possible to 100% of the infecting organisms be killed off to avoid
selection of resistance; if a small subset of the population survives the
treatment and is allowed to multiply, the average susceptibility of this new
population to the compound will be much less than that of the original
population, since they have descended from those few organisms which
survived the original treatment. This survival often results from an inheritable
resistance to the compound which was infrequent in the original population
but is now much more frequent in the descendants thus selected entirely
from those originally infrequent resistant organisms.
An abscess caused by methicillin-resistant Staphylococcus aureus bacteria
(MRSA). By 1984 half of the people with active tuberculosis in the United
States had a strain that resisted at least one antibiotic. In certain settings,
such as hospitals and some child-care locations, the rate of antibiotic
resistance is so high that the normal, low cost antibiotics are virtually useless
for treatment of frequently seen infections. The situation is worsened by the
fact that genes coding for antibiotic resistance can be transferred between
bacteria, making it possible for bacteria never exposed to an an tibiotic to
acquire resistance from those which have.
Antiviral drugs are a class of medication used specifically for treating
viral infections. Most of the antivirals now available are designed to help
deal with HIV, herpesvirus, which is best known for causing cold sores but
actually covers a wide range of diseases, and the hepatitis B and C
viruses, which can cause liver cancer. Researchers are now worki ng to
extend the range of antivirals to other families of pathogens.
The emergence of antivirals is the product of a greatly expanded
knowledge of the genetic and molecular function of organisms, al lowing
biomedical researchers to understand the structure and function of
viruses, major advances in the techniques for finding new drugs, and the
intense pressure placed on the medical profession to deal with the human
immunodeficiency virus (HIV), the cause of the deadly acquired
immunodeficiency syndrome ( AIDS) epidemic. Though no one could
sensibly claim that AIDS has been a benefit to humankind, it has certainly
done much to advance the state of antiviral technology.
Antineoplastics (or "antitumor antibiotics", or "noncovalent DNA-
binding drugs", or "cytotoxic antibiotics", see also neoplastics) are drugs
that inhibit and combat the development of tumors.
Modes of action: antineoplastics work by inhibiting topoisomerase II
which stops DNA being unwound, which is required for both DNA
replication and RNA/protein synthesis.
Examples
actinomycin.
dactinomycin
anthracyclines
doxorubicin
daunorubicin
epirubicin which also inhibit topoisomerase II)
other cytotoxic antibiotics
Bleomycin. This agent forms free radicals, which induce damage
and chromosomal aberrations.
plicamycin
mitomycin
Antifungals work by exploiting differences between mammalian and fungal cel ls
to kill off the fungal organism without significantly harming the host. Unlike
bacteria, both fungi and humans are eukaryotes. The basic structure of fungal
cells and human cells is nearly identical. This means it is more difficult to find a
target for an antifungal medication to attack that does not also exist in the
infected organism. Consequently, some of the side-effects of systemic anti -
fungals can be life -threatening. Classes include:
1. Polyene antibiotics: bind with sterols in the fungal cell wall, principally
ergosterol and this causes the cell's contents to leak out and the cell di es. Animal
cells have cholesterol instead of ergosterol and are less susceptible: Nystatin ;
Amphotericin B; Natamycin ; Rimocidin; Filipin; Pimaricin.
2. Imidazoles and triazoles: inhibit the enzyme cytochrome P450 14a-
demethylase. This enzyme converts lanosterol to ergosterol, and is required in
fungal cell wall synthesis and block steroid synthesis in humans. Imidazoles:
Miconazole; Ketoconazole; Clotrimazole ; Econazole; Mebendazole; Bifonazole ;
Butoconazole ; Fenticonazole; Isoconazole; Oxiconazole ; Sertaconazole;
Sulconazole; Thiabendazole; Tiaconazole. Triazoles: Fluconazole; Itraconazole;
Ravuconazole; Posaconazole; Voriconazole.
3. Allylamines: inhibit enzyme squalene epoxidase, an enzyme required for
ergosterol synthesis: Terbinafine (Lamisil ); Amorolfine; Naftifine ; Butenafine.
4. Echinocandin: inhibit the synthesis of glucan in the cell wall, probably via the
enzyme 1,3-ß glucan synthase: Anidulafungin; Caspofungin ; Micafungin
5. Others: Flucytosine is an antimetabolite; Griseofulvin binds to polymerized
microtubules and inhibits fungal mitosis; Fluocinonide; Gentian Violet
Aciclovir, Cidofovir, Docosanol, Famciclovir, Fomivirsen, Foscarnet,
Anti-herpesvirus
Ganciclovir, Idoxuridine, Penciclovir, Trifluridine, Tromantadine,
agents Valaciclovir, Valganciclovir, Vidarabine
Anti-influenza agents Amantadine, Oseltamivir, Peramivir, Rimantadine, Zanamivir
Abacavir, Didanosine, Emtricitabine , Lamivudine, Stavudine,
NRTIs
Zalcitabine, Zidovudine
NtRTIs Tenofovir
Anti-
retroviral
drugs NNRTIs Efavirenz, Delavirdine, Nevirapine
Amprenavir, Atazanavir, Darunavir, Fosamprenavir, Indinavir,
PIs Lopinavir, Nelfinavir, Ritonavir, Saquinavir, Tipranavir
Fusion
inhibitors
Enfuvirtide
Adefovir, Fomivirsen, Imiquimod, Inosine,Interferon,
Other antiviral agents
Podophyllotoxin, Ribavirin, Viramidine
Chemotherapeutic agents/Antineoplastic agents
Nitrogen mustards: ( Chlorambucil, Chlormethine, Cyclophosphamide,
Ifosfamide, Melphalan). Nitrosoureas: ( Carmustine, Fotemustine,
Alkylating
Lomustine, Streptozocin). Platinum: ( Carboplatin, Cisplatin, Oxaliplatin,
agents:
BBR3464). Busulfan, Dacarbazine, Mechlorethamine, Procarbazine,
Temozolomide, ThioTEPA, Uramustine
Folic acid: ( Methotrexate, Pemetrexed, Raltitrexed). Purine: ( Cladribine,
Antimetabolites: Clofarabine, Fludarabine, Mercaptopurine, Tioguanine). Pyrimidine: (
Capecitabine). Cytarabine, Fluorouracil, Gemcitabine
Taxane: ( Docetaxel, Paclitaxel). Vinca: ( Vinblastine , Vincristine,
Plant alkaloids:
Vindesine, Vinorelbine).
Cytotoxic/antitu Anthracycline family: (Daunorubicin, Doxorubicin, Epirubicin, Idarubicin,
mor antibiotics: Mitoxantrone, Valrubicin). Bleomycin, Hydroxyurea, Mitomycin
Topoisomerase
inhibitors:
Topotecan, Irinotecan, Podophyllum: ( Etoposide, Teniposide).
Monoclonal Alemtuzumab, Bevacizumab, Cetuximab, Gemtuzumab, Panitumumab,
antibodies: Rituximab, Trastuzumab
Photosensitizers: Aminolevulinic acid, Methyl aminolevulinate, Porfimer sodium, Verteporfin
Alitretinoin, Altretamine, Amsacrine, Anagrelide, Arsenic trioxide,
Asparaginase , Bexarotene, Bortezomib, Celecoxib, Dasatinib, Denileukin
Other:
diftitox, Erlotinib, Estramustine , Gefitinib, Hydroxycarbamide, Imatinib,
Pentostatin, Masoprocol, Mitotane, Pegaspargase , Tretinoin
10

7.0. Endocrines and
Immunosuppressants [2 Qs]
Immunosuppressive drugs or immunosuppressants are drugs that are used
in immunosuppressive therapy to inhibit or prevent activity of the immune
system. Clinically they are used to:
prevent the rejection of transplanted organs and tissues (e.g. bone marrow,
heart, kidney, liver)
treatment of autoimmune diseases or diseases that are most likely of
autoimmune origin (e.g. rheumatoid arthritis , myasthenia gravis, systemic lupus
erythematosus, Crohn's disease, and ulcerative colitis).
These drugs are not without side effects and risks. Because the majority of them
act non-selectively, the immune system loses its ability to successfully resist
infections and spreading of malignant cells. There are also other side effects,
like hypertension, dyslipidemia, hyperglycemia, peptic ulcers , liver and kidney
injury. The immunosuppressive drugs also interact with other medicines and
affect their metabolism and action.
Immunosuppressive drugs can be classified into four groups and others:
glucocorticoids
cytostatics
antibodies
drugs acting on immunophilins
other drugs
Cytostatics: inhibit cell division. And include the alkylating agents and antimetabolites. In
immunotherapy, they are used in smaller doses than in the treatment of malignant diseases.
They affect the proliferation of both T cells and B cells.
1. Alkylating agents: are used in immunotherapy are nitrogen mustards
(cyclophosphamide), nitrosoureas, platinum compounds and others. Cyclophosphamide is
probably the most potent immunosuppressive compound. In small doses, it is very efficient in
the therapy of systemic lupus erythematosus, autoimmune hemolytic anemias, Wegener's
granulomatosis and other immune diseases. High doses cause pancytopenia and
hemorrhagic cystitis.
2. Antimetabolites: interfere with the synthesis of nucleic acids. These include:
folic acid analogues, such as methotrexate; purine analogues such as azathioprine and
mercaptopurine; pyrimidine analogues and protein synthesis inhibitors.
(1) Methotrexate: is a folic acid analogue. It binds dihydrofolate reductase and prevents
synthesis of tetrahydrofolate. It is used in the treatment of autoimmune diseases (for exampl e
rheumatoid arthritis) and in transplantations.
(2) Azathioprine and Mercaptopurine: are is extensively used to control transplant rejection
reactions. It is nonenzymatically cleaved to mercaptopurine, that acts as a purine analogue
and an inhibitor of DNA synthesis. Mercaptopurine itself can also be administered directly.
By preventing the clonal expansion of lymphocytes in the induction phase of the immune
response, it affects both the cell and the humoral immunity.
(3) Cytotoxic antibiotics
Among these, dactinomycin is the most important. It is used in kidney transplantations. Other
cytotoxic antibiotics are anthracyclines, mitomycin C, bleomycin, mitramycin.
The endocrine system consists of several glands, that secrete hormones directly
into the blood rather than into a duct system. To be classified as a hormone, a
chemical must be produced by an organ, be released (in small amo unts) into the
blood, and be transported by the blood to a distant organ to exe rt its specific
function. This definition holds for most ‘classical ’ hormones, but there are also
paracrine mechanisms (chemical communication between cells within a tissue or
organ), autocrine signals (a chemical that acts on the same cell), and intracrine
signals (a chemical that acts within the same cell). Three class es of hormone:
1. Amines: such as norepinephrine, epinephrine, and dopamine, are derived from
single amino acids, in this case tyrosine. Thyroid hormones such as 3,5,3’-
triiodothyronine (T3) and 3,5,3’,5’-tetraiodothyronine (thyroxine, T4) make up a
subset of this class because they derive from the combination of two iodinated
tyrosine amino acid residues.
2. Peptides and Proteins: consist of three (in the case of thyrotropin-releasing
hormone) to more than 200 (in the case of follicle-stimulating hormone ) amino acid
residues and can have molecular weights as large as 30,000. All hormones
secreted by the pituitary gland are peptide hormones, as are leptin from
adipocytes , ghrelin from the stomach, and insulin from the pancreas.
3. Steroids: are derivatived from cholesterol and are subdivided into those with an
intact steroid nucleus (gonadal and adrenal steroids) and those with a broken
steroid nucleus (vitamin D). Steroid horomones include estrogen and
progesterone from the ovary, testosterone from the testes, and cortisol and
aldosterone from the adrenal gland.
Glucocorticoids: glucocorticoids are used to suppress various allergic,
inflammatory, and autoimmune disorders. They are also administered as
posttransplantory immunosuppressants to prevent the acute transplant rejection
and graft-versus-host disease. Nevertheless, they do not prevent an infection and
also inhibit later reparative processes. These drugs suppress the cell-mediated
immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3,
IL-4, IL-5, IL-6, IL-8 and TNF-?, the most important of which is the IL-2. Smaller
cytokine production reduces the T cell proliferation. Glucocorticoids also suppress
the humoral immunity, causing B cells to express smaller amounts of IL-2 and of
IL-2 receptors . This diminishes both B cell clone expansion and antibody synthesis.
Antiinflammatoryeffects
Glucocorticoids influence all types of inflammatory events, no matter what thei r
cause. They induce the lipocortin-1 (annexin-1) synthesis, which then binds to cell
membranes preventing the phospholipase A2 from coming into contact with its
substrate arachidonic acid. This leads to diminished eicosanoid production. The
cyclooxygenase (both COX -1 and COX -2) expression is also suppressed,
potentiating the effect.
Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space,
where it binds to the leukocyte membrane receptors and inhibits various
inflammatory events: epithelial adhesion , emigration, chemotaxis , phagocytosis ,
respiratory burst and the release of various inflammatory mediators (lysosomal
enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from
neutrophils , macrophages and mastocytes .
Antibodies: are used as a quick and potent immunosuppression method to prevent the acute
rejection reaction.
1. Polyclonal antibodies: Heterologous polyclonal antibodies are obtained from the serum of
animals (e.g. rabbit , horse) and injected with the patient's thymocytes or lymphocytes. The
antilymphocyte (ALG) and antithymocyte antigens (ATG) are being used. They are part of the
steroid-resistant acute rejection reaction and grave aplastic anemia treatment. However, they are
primarily added to other immunosuppressives to diminish their dosage and toxicity. They also
allow transition to cyclosporine therapy. These agents inhibit T lymphocytes and cause their lysis,
which is both complement mediated cytolysis and cell-mediated opsonization followed by removal
of reticuloendothelial cells from the circulation in the spleen and liver]]. In this way, polyclonal
antibodies inhibit cell-mediated immune reactions, including graft rejection, delayed
hypersensitivity (i.e. tuberculin skin reaction), and the graft-versus-host disease (GVHD), but
influence thymus-dependent antibody production. Because of a high immunogenicity of polyclonal
antibodies, almost all patients have an acute reaction to the treatment. It is characterized by fever,
rigor episodes and even anaphylaxis. Later during the treatment, some patients develop serum
sickness or immune complex glomerulonephritis. Serum sickness arises 7-14 days after the
therapy has begun. The patient suffers from fever, joint pain and erythema that can be soothed
with the use of steroids and analgesics. Urticaria (hives) can also be present. It is possible to
diminish their toxicity by using highly purified serum fractions and intravenous administration in
the combination with other immunosuppressants, for example calcineurin inhibitors, cytostatics
and cortisteroids. The most frequent combination is to simultaneously use antibodies and
cyclosporine. Patients gradually develop a strong immune response to these drugs, reducing or
eliminating their effectiveness.
2. Monoclonal antibodies: are directed towards exactly defined antigens. Therefore, they cause
fewer side effects. Especially significant are the IL-2 receptor (CD25) and CD3 directed
antibodies. They are used to prevent the rejection of transplant ed organs, but also to track
changes in the lymphocyte subpopulations. It is reasonable to expect similar new drugs in the
future.
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 3. T-cell receptor directed antibodies
OKT3 (R) is presently the only approved anti-CD3 antibody. It is a mouse anti-CD3 monoclonal
antibody of the IgG2a type that prevents T-cell activation and proliferation by binding the T-cell
receptor complex present on all differentiated T cells. As such, it is one of the most potent
immunosuppressive substances and is clinically used to control the steroid and/or polyclonal
antibodies resistant acute rejection episodes. For acting more specifically than polyclonal
antibodies, it is also used preventively in transplantations. Presently, the OKT3's action
mechanism is not yet sufficiently understood. It is known that the molecule binds TCR/CD3, the T-
cell receptor complex. During the first few administrations, this binding non-specifically activates T
cells, leading to a serious syndrome 30 to 60 minutes later. It is characterized by fever, myalgia,
headache and artralgia. In some cases, it progresses to a life-threatening reaction of the
cardiovascular system and the central nervous system needing a lengthy therapy. Past this
period, CD3 (R) blocks the TCR - antigen binding and causes conformation change or the
removal of the entire TCR3/CD3 from the T-cell surface. This lowers the number of T cells,
perhaps by sensitising them for the uptake by the reticular epithelial cells. The cross-binding of
CD3 molecules also activates an intracellular signal, causing the T cells' anergy or apoptosis,
unless they receive another signal through a costimulatory molecule. CD3 antibodies also shift the
balance from Th1 to Th2 cells.
IL-2 receptor directed antibodies: is an important immune system regulator necessary for the
clone expansion and survival of activated lymphocytes T. Its eff ects are mediated by the trimer
cell surface receptor IL-2a, consisting of the a, ß and ? chains. The IL-2a (CD25, T-cell activation
antigen, TAC) is expressed only by the already activated T lymphocytes. Therefore, it is of special
significance to the selective immunosuppressive treatment and the research has been focused on
the development of effective and safe anti-IL-2 antibodies. By the use of the recombinant gene
technology, the mouse anti-Tac antibodies have been modified leading to the presentation of two
himeric mouse/human anti-Tac antibodies in the year 1998: basiliximab (Simulect (R)) and
daclizumab (Zenapax (R)). These drugs act by binding the IL-2a receptor's a chain, preventing
the IL-2 induced clonal expansion of activated lymphocytes and shortening their survival. They
are used in the profilaxis of the acute organ rejection after the bilateral kidney transplantation,
Drugs acting on immunophilins
Cyclosporin: Together with tacrolimus, cyclosporin is a calcineurin inhibitor. It has been in use since
1983 and is one of the most widely used immunosuppressive drugs. It is a fungal peptide, composed
of 11 amino acids. Cyclosporin is thought to bind to the cytosolic protein cyclophilin (an immunophilin)
of immunocompetent lymphocytes, especially T-lymphocytes. This complex of ciclosporin and
cyclophilin inhibits calcineurin, which under normal circumstances induces the transcription of
interleukin-2. The drug also inhibits lymphokine production and interleukin release, leading to a
reduced function of effector T-cells.
Cyclosporin is used in the treatment of acute rejection reactions, but has been increasingly
substituted with newer immunosuppressants, as it is nephrotoxic.
Tacrolimus (Prograf(TM): is a bacterial product (Streptomyces tsukubaensis). It is a macrolide
lactone and acts by inhibiting calcineurin. The drug is used particularly in the liver and kidney
transplantations, although in some clinics it is used in heart, lung and heart/lung transplants. It binds
to an immunophilin, followed by the binding of the complex to calcineurin and the inhibition of its
phosphatase activity. In this way, it prevents the passage of G0 into G1 phase. Tacrolimus is more
potent than cyclosporin and has less pronounced side effects.
Sirolimus (Rapamune(Tm), Rapamicin): Sirolimus is a macrolide lactone, produced by the
actinomycetes Streptomyces hygroscopicus. It is used to prevent rejection reactions. Although it is a
structural analogue of tacrolimus, it acts somewhat differently and has different side effects. Contrary
to cyclosporine and tacrolimus that affect the first phase of the T lymphocyte activation, sirolimus
affects the second one, namely the signal transduction and their clonal proliferation. It binds to the
same receptor (immunophilin) as tacrolimus, however the produced complex does not inhibit
calcineurin, but another protein. Therefore, sirolimus acts synergistically with cyclosporine and, in
combination with other immunosuppressants, has few side effects. Indirectly it inhibits several T
lympohocyte kinases and phosphatases, preventing the transmission of signal into their activity and
the transition of the cell cycle from G1 to S phase. Similarly, it prevents the B cell differentiation to the
plasma cells, which lowers the quantity of IgM, IgG and IgA antibodies produced. It acts
immunoregulatory.

Other drugs
Interferons: IFN-ß suppresses the production of Th1 cytokines and the activation of
monocytes. It is used to slow down the progression of multiple sclerosis. IFN-? is able to trigger
lymphocytic apoptosis.
Opioids: Prolonged use of opioids may cause immunosuppression by inhibiting the migration
of leukocytes.
TNF binding proteins: A TNF -a (tumor necrosis factor alpha) binding protein is a monoclonal
antibody or a circulating receptor such as infliximab (Remicade®), etanercept (Enbrel ®), or 8.0. Analgesics [5 Qs]
adalimumab (Humira®) that binds to TNF - a and prevent it from inducing the synthesis of IL- 1
and IL- 6 and the adhesion of lymphocyte activating molecules. They are used in the treatment
of rheumatoid arthritis, ankylosing spondylitis, Crohn's disease and psoriasis.
8.1. Opioids
TNF or the effects of TNF are also suppressed by various natural compounds, including
curcumin (an ingredient in turmeric) and catechins (in green tea). 8.2. Non-opioids, NSAIDs
These drugs may raise the risk of contracting tuberculosis or inducing a latent infection to
become active. Infliximab and adalimumab have label warnings stating that patients should be
evaluated for latent TB infection and treatment should be initiated prior to starting therapy with
them.
Mycophenolate: Mycophenolic acid acts as a non-competitive, selective and reversible
inhibitor of inosine monophosphate dehydrogenase (IMPDH), which is a key enzyme in the de
novo guanosine nucleotide synthesis. In contrast to other human cell types, ly mphocytes B and
T are very dependent on this process.
[edit] Small biological agents
FTY720 is a new synthetic immunosuppressant, currently in phase 3 of clinical trials. It
increases the expression or changes the function of certain adhesion molecules ( a4/ß7
integrin) in lymphocytes, so they accumulate in the lymphatic tissue (lymphatic nodes) and their
number in the circulation is diminished. In this respect, it dif fers from all other known
immunosuppressants.

Non-steroidal anti-inflammatory drugs

Morphine is an extremely powerful opiate analgesic drug and is the

principal active agent in opium. Like other opioids, e.g. heroin, morphine Arylalkanoic acids Diclofenac, Indometacin, Sulindac
acts directly on the central nervous system (CNS) to relieve pain. Side
2-Arylpropionic Carprofen , Flurbiprofen , Ibuprofen , Ketoprofen , Ketorolac,
effects include impairment of mental performance, euphoria, drowsiness, acids (profens) Loxoprofen , Naproxen , Tiaprofenic acid,
lethargy, and blurred vision. It also decreases hunger, inhibits the cough
reflex, and produces constipation. Morphine is highly addictive when N-Arylanthranilic Mefenamic acid
acids (fenamic
compared to other substances, and tolerance and physical and
acids)
psychological dependence develop quickly. Morphine is an opioid receptor
agonist – its main effect is binding to and activating the µ-opioid receptors Pyrazolidine Phenylbutazone
derivatives
in the central nervous system. Activation of these receptors is associated
with analgesia, sedation, euphoria, physical dependence and respiratory Oxicams Meloxicam, Piroxicam
depression. Morphine is also a ?-opioid receptor agonist, with this action
associated with spinal analgesia and miosis. The effects of morphine can Coxibs Celecoxib , Etoricoxib , Parecoxib, Rofecoxib, Valdecoxib
be countered with naloxone or naltrexone.
Morphine is primarily metabolized into morphine-3-glucuronide and Sulphonanilides Nimesulide
morphine-6-glucuronide. High doses of morphine may be fatal due to
respiratory depression.

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 Analgesics
Opioids : Buprenorphine, Butorphanol , Codeine,
Dextropropoxyphene, Dihydrocodeine, Fentanyl , 9.0. Antihistamines and
Diamorphine (Heroin), Hydrocodone,
Hydromorphone, Ketobemidone, Morphine,
Autocoids [2 Qs]
Nalbuphine, Oxycodone, Oxymorphone,
Pentazocine, Pethidine (Meperidine), Tramadol
Salicylic acid Aspirin (Acetylsalicylic Acid), Diflunisal,
and Ethenzamide
derivatives:
Pyrazolones: Aminophenazone, Metamizole, Phenazone
Anilides: Paracetamol (acetaminophen), Phenacetin
Others: Ziconotide, Tetrahydrocannabinol

Autocoids and Antihistamines Pharmacologic effects: H1-agonists produce

Autocoid agonists or antagonists include: vasodilation, increased capillary permeability,
-H1 and H2 receptor antagonists bronchoconstriction, pain or itching. H2-agonist effect
-Eicosanoids (prostaglandins) includes increased gastric acid secretion.
-Thromboxanes
-Leukotensin Adverse effects includes: Anaphylaxis – serious and
-Serotonin agonists sometimes fatal, difficulty breathing, convulsions, lapses
-Angiotensin inhibitors into unconsciousness, vasodilation and increased
-Cytokinins capillary permeability, if high levels of histamine
-Histamine released, this will decrease BP severely causing shock
NOTE: Histamine is released during allergic reactions, and CV collapse.
immune reactions, or after admin. of certain drugs and
amount released determines effects. Uses include: diagnosis of achlorhydria and
pheochromocytoma. Drug of choice to counteract
histamine rxn is epinephrine.

Antihistamines (H1 receptor antagonists): Widely used for hay fever, mild
allergic reactions and additive with other CNS depressants
Four common: Dipheniramine (Benedryl ); Chlorphenhydramine (ClorTrimeton);
Promethazine (Phenegan); Loratidine (Claritin)
Pharmacologic effects: H1 blocking effects include: Capillary permeability is
blocked producing reduced edema; Blocks dilation of vascular smooth muscle;
Blocks some bronchoconstriction; Suppresses the itching and pain
The End
&
Other effects: CNS depression (Sominex, Nytol); Anticholinergic ; Antiemetic
(Dramamine, Bonine);
Adverse reactions: Undesirable CNS depression. Sedative effect cancelled out
when combined with decongestant (adrenergic agonist). CNS stimul ation can
occur in a few cases. More common in children, elderly with larger doses.
Newer nonsedating H1 blockers (Clariton) produce less sedation. Xerostomia
Toxicity: More common due to easy accessibility in OTC preparations
Death can result.
Uses: Control seasonal hay fever; Relieve itching, edema and erythema
Some topical anesthetic effect; To prevent and treat motion sickness
Preop sedation and antiemetic effects; OTC sleep aids.
Good Luck

13
 The conjugation of glucuronic acid
to a drug by the liver is an example
of a:
A. Cytochrome P450 reaction
B. Transformation reaction
C. Phase I activation reaction
D. Phase II inactivation reaction

Drugs showing zero-order kinetics of

elimination: Question: Why or
A. Are more common than those
showing first-order kinetics
When do we use
B. Decrease in concentration
exponentially in time
drugs (clinically)?
C. Have a half-life that is independent
of dose Answer: To control, cure,
D. Show a plot of drug concentration
versus time that is linear or prevent disease

Question: What can

Question: Who can you Rx? Answer: Drugs
prescribe drugs, and within the scope of your
Where? practice
Answer: Licensed doctors, Answer: Drugs within
requires DEA registration the scope of your
and is state specific.
practice

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