practical pharmacology

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Practical Pharmacology

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Dr.Gulala



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Practical Pharmacology Dr.Gulala

f) Sublingual tablet: it is usually uncoated specially produced to de suitable for absorption

from sublingual mucosa to get rapid action and avoid destruction by first pass

metabolism, e.g: Angised.

g) Effervescent tablet: this is relatively large tablet containing large dose of the drug , it is

producing by mixing the drug with citric acid and sodium bicarbonate to form granules

these granules are compressed to form the tablet, this type of tablet appear to have rapid

action, disintegration and dissolution occur in water inside the glass , e,g: Vitamin C

tablet.

h) Chewable tablet: this is ordinary uncoated tablet specially manufactured to be sucked or

chewed usually have a good taste, e.g: Antacid.

i) Lozenges tablet: this is a sugar flavoured tablet with different shape and attractive color

it is usually sucked to treat simple tonsillitis and relief cough, it is usually contain

volatile oil, antiseptic, antibiotics, e.g: Vicks.

2- Pill:

Is the spherical body containing the drug in a solid or liquid form given by mouth, a pill

should not weight more than (0.3 gm), it is sometime coated when the drug has a bitter taste

or liable to oxidation, e.g: Contraceptive pill.

3- Capsule (ordinary capsule, spansule capsule, and capsule for inhalation):

a) Ordinary capsule: it is a small oval or rounded shape made of gelatine, it is either:

v Hard containing powdered drug, e.g: Tetracycline.

v Soft contain liquid form of drug, e.g: Adalat.

The capsule shell will dissolve in stomach used for the following purpose:

Ø to mask the bad taste of drug.

Ø prevent oxidation of drug.

Ø to get accurate dose of drug.

b) Spansule capsule: containing different granule each with different disintegration and

dissolution rate , this will prolong duration of action and decrease frequency of

administration, e,g: Stelazine.

c) Capsule for inhalation: it is ordinary capsule which contain a drug which is usually

unabsorbed from the bowel,it is intended to be inhaled to get local action in the lung

using certain instrument manufactured for that purpose, e,g: Cromoglycate.



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z Liquid preparations :

1. Syrup: the drug is water soluble usually dissolved in already prepared simple syrup with

good taste particularly for children, e.g: Samilin ,Ampicillin. The antibiotic syrup

usually supplied by pharmaceutical company as a powder mixed with sugar and

prepared by adding sufficient quantity of water before use because antibiotics hydrolysis

in the aqueous solution to other compound which has no antibacterial activity or causing

allergic reaction.

2. Aqua: it is a watery solution contain volatile substance used as flavoured (flavored)

vehicle,e.g: Chloroform water.

3. Elixir: it is syrup containing 25% alcohol, e.g: hypnoral.

4. Suspension: a solution contain indiffusibe solid which does not distributed evenly to

get a uniform mixture so, it should be shacked before use, e.g: Methoprim.

5. Extract: the solid or semisolid preparation of active principle obtained from plant by

mixing with a suitable solvent, after evaporation we get the extract. different solvent are

used such as ( water, alcohol, ether and chloroform ).it is named according to the

solvent, e.g: watery extract of Cascara, Alcoholic extract of Belladonna. The evaporation

done under low pressure otherwise it will destroy the active drug.

6. Liquor: it is a solution containing chemical substance dissolved in water if it is for

internal use and alcohol if it is for external use.

7. Emulsion: is a mixture of two immiscible liquid such as water and oil in which one of

the liquid is broken up and surrounded by a film emulsifying agent to be dispersed

through the other liquid.

8. Mixture: is a combination of drug in liquid form , e.g: white mixture of Magnesium

sulphate (which is used as purgative).

9. Decoction: solution of drug obtained from plant by boiling for 10 min, and then strained.

10. Infusion: a dilute solution of active principle obtained from plant by adding hot or cold

water shacked from time to time and then strained.

z Powder preparation:

1. Ordinary powder: contain the drug as a fine powder in which specific quantity of the

powder is mixed with sufficient water before use, e.g: Gastrogel (used for heart burning)

2. Effervescent powder: it is an ordinary powder mixed with sodium bicarbonate and citricacid to de prepared by mixing with sufficient water before use, e.g: Citrogran powder.



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z Drop for internal use:

This type of preparation is most convenient for infant, in which the drug is concentrated into

a few drops to facilitate swallowing and minimize the loss of drug, e.g: paracetamol, Digoxin.

z Aerosol:

A pressurized liquid form of the drug intended to be inhaled by puff each puff contain a

specific dose, e.g: Ventolin (sulbutamol).

z Implant:

A minute disc preparation inserted under the skin which is usually contain hormone, it is

slowly metabolized or absorbed to give a prolonged duration of action, e.g: Stilbestrol.

z Parenteral:

a. Ampoule: is a thin glass container for single injection,it is usually sterile to be

injected (IV, IM, SC) e.g: Buscopan. The ampoule which contains hormone usually

mixed with oil and should not be used IV because of fat embolism sometime put in

separate ampoule (the solvent and the drug ) ,e.g; Pregnyl.

b. Vial : a thick container with a rubber cap contains powder or solution for single or

multiple injection , e.g: Procaine Penicillin (for 1 injection ) , Xylocaine

(for multiple injection ) .



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External preparations

1) Suppository:

a. Rectal: is conical or turbido shaped preparation inserted into the rectum for local (e.g :

Antihemorrhoid) or systemic action (e.g:Aminophylline). The active drug is mixed with

a fatty base which is melt at body temperature and should not exceed (4 gm) to facilitate

the entry and prevent proctitis, the reason of manufacturing of this preparation :

Ø to avoid irritation of stomach , e.g: Indomethacin.

Ø to get local action in the intestine, e.g: Laxative (Bisacodyl).

Ø in uncooparable patient (children, unconscious ‘coma case patient’ ). e.g: Revanin.

Ø in patient with repeated vomiting (pregnant women), e.g: Plasil.

Ø to get full dose during night, e.g: Aminophylline.

b. Vaginal: it is called ovule or pessary due to its shape, the active drug is mixed with a

fatty base melt at vaginal temperature and its miscible in vaginal secretion, inserted into

the vagina by a certain applicator. e.g: Mycostatine (antifungal drug), Flagyl.

2) Ointment:

The semisolid preparation consist of a fatty base, e.g: Paraffin, Ovile, Wax, andVaseline. Containing the active drug and the base is immiscible with water therefore it is

suitable to be applied on dry surface.

3) Cream:

It is a semisolid preparation containing the drug mixed with the fatty base which is

miscible with water applied to wet surface, e.g: Nystacort, Clotrymazole ( vaginal

cream), Estrogen.

4) Liniment:

It is a semisolid or liquid preparation containing irritant substance applied to the skin by

friction . e.g: Rheumalgin. 5) Lotion:

Is a liquid preparation applied to the skin without friction , it usually containing cooling

substance , e.g: Calamine. sometime contain drug like steroid or antiseptic.

6) Enema:

It is a solution intended to be injected into the rectum for local (e.g: watery solution of

soap’ as a laxative’) or systemic (e.g: Prednisolone ’ Predsol Retention Enema’ for the

treatment of ulcerative colitis).



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7) Drop:

ü Eye: watery sterile isotonic solution instilled into the eye by a dropper, it contains

one of the following:

1. Antiseptic, e.g: Boric acid.

2. Antibiotic, e.g: Chloramphenicol.

3. Decongestant, e.g: phenylephrine.

4. Antihistamine, e.g; Mepyramine.

5. Steroid , e.g: Betamethasone.

6. Mydriatic, e.g: Atropine. Miotic, e.g: Pilocarpine.

ü Ear: is a watery solution instill into the ear contain antihistamine, steroid,

substance that solubilise the wax.

ü Nasal: is a watery solution instill into the nose contains decongestant,

antihistamine, steroid.




Prescription writing

It is a term applied to the formula

medication and to the patient for t

1) Superscription: consists of:

a) Name, address, and telephone No.

b) Name, age, and sex (gender) of

c) Date of prescription and registra

d) Diagnosis.

e) Symbol (R).

2) Inscription: consists of :

a) Name of the drug.

b) Strength of the drug.

c) Amount of the drug.

d) Pharmaceutical form.

3) Subscription: it comprises the d

is usually applied when there is

4) Transcription: include direction

frequency of administration and

Compound prescription: it is a ty

pharmacist at the time of dispensin

The reason of compound prescrip

1) To mask a well known drug from t

2) In case of unavailability of small d

e.g:Phenobarbital.

3) When the combination of drug are

available as whole drug.

4) In case of unavailability of certain

ritten by the physician to the pharmacist fo

e use of the drug, it consists of :

of the physician. written at the upper right han

he patient. written at the left hand corner.

tion.

rection to the pharmacist for preparation o

ompound prescription.

to the patient for the use of the drug, consi

time around meal and amount to be used.

e of prescription, include preparation of dr

by mixing tow or more drugs in a various

tion:

e patient.

ses,

not

ngredient.

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Dr.Gulala

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corner.

the drug. It

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dosage form.




Prescription Abbreviati

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Dr.Gulala



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Drug Elimination (excretion)

Drugs are eliminated from the body after being partly or wholly converted to water soluble

metabolites or in some case without being metabolised.

Renal elimination :

The following mechanisms are involved :

1. Glomerular filtration : the rate at which a drug enters the glomerulus filtrate depend on

the concentration of free drug in the plasma and on its molecular weight .substances that

have molecular weight in excess 50,000 are excluded from the glomerular filtrate, while

those of M.W less than 10,000 pass easily through the pores of the glomerular

membrane.

2. Active tubular secretion: cells of the proximal tubules activily secrete acid and base by

tow transport systems.thus acid like Penicillin, Salicylic acid, Probenecid, Frusemidand

base like amphetamine and histamine are so secreted. Drugs may compete for the same

transport system resulting in prolongation of action of each other, eg: Penicillin and

Probenecid.

3. Passive tubular reabsorption : passive diffusion of drug molecule can occur in either

direction in the renal tubules depending on the drug concentration, lipid solubility and

Ph. As highly lipid soluble drugs are largely reabsorbed, there excretion is slow. acidic

drug get ionised in alkaline urine and are easily excreted while base are excreted faster in

acidic urine .This property is useful in the treatment of poisoning .

In the poisoning with acidic drugs forced alkaline dieresis is employed to hasten drug excretion

Faecal and Biliary elimination :

unabsorbed portion of the orally administered drugs are eliminated through the faeces.

Liver transfer acids, base and unionized molecule into bile by specific acid &base transport

system. Large water soluble conjugates are excreted in the bile. Some drugs may get

reabsorbed in lower portion of the gut and carried back to the liver. Such recycling is called

(enterohepatic circulation) it prolong the duration of action of the drug, e.g:

Chloramphenicol, tetracycline, oral contraceptive and erythromycin.




Pulmonary excretion:

The lungs are the main route of eli

alcohol, and has legal implication i

Other routes:

small amount of some drugs are eli

saliva may result in a unique taste o

taste with metronidazole.

The excretion of drugs in the milk i

mother , but for the sucking infant i

immature metabolic excretory mec

mination for gases and volatile liquids (ana

medico-legal practice.

inated through the sweat and saliva .Excr

f some drug like Phenytoin, clarithromycin

s in small amount and is of no significance

may be important especially because of th

anisms.

10

Dr.Gulala

sthetics) and

tion in

metallic

to the

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Histamine and antihistamine drugs ( Lippincott :Page 520-524 and 330-332)

I.Histamine

Histamine is a chemical messenger that mediates a wide range of cellular responses,

including allergic and inflammatory reactions, gastric acid secretion, and neurotransmission

in parts of the brain. Histamine has no clinical applications, but agents that interfere with the

action of histamine (antihistamines) have important therapeutic applications.

A. Location, synthesis, and release

z Location: Histamine occurs in practically all tissues, but it is unevenly distributed, with

high amounts found in lung, skin, and the gastrointestinal tract (sites where the inside of

the body meets the outside). It is found at high concentration in mast cells or basophils.

Histamine also occurs as a component of venoms and in secretions from insect stings.

z Synthesis: Histamine is an amine formed by the decarboxylation of the amino acid

histidine by histidine decarboxylase,2 an enzyme that is expressed in cells throughout the

body, including central nervous system (CNS) neurons, gastric mucosa parietal cells,

mast cells, and basophils. In mast cells, histamine is stored in granules as an inactive

complex composed of histamine and the polysulfated anion, heparin, along with an

anionic protein. If histamine is not stored, it is rapidly inactivated by amine oxidase

enzymes.

Release of histamine: The release of histamine may be the primary response to some

stimuli, but most often, histamine is just one of several chemical mediators released.

Stimuli causing the release of histamine from tissues include the destruction of cells as a

result of cold, bacterial toxins, bee sting venoms, or trauma. Allergies and anaphylaxis

can also trigger release of histamine.

B. Mechanism of action

Histamine released in response to various stimuli exerts its effects by binding to one or

more of four types of histamine receptorsH1, H2, H3, and H4 receptors. H1 and H2 receptors

are widely expressed and are the targets of clinically useful drugs. H3 and H4 receptors areexpressed in only a few cell types, and their roles in drug action are unclear. All types of

histamine receptors have seven transmembrane helical domains and transduce extracellular

signals by way of G protein mediated second-messenger systems. Some of histamine's wide

range of pharmacologic effects are mediated by both H1 and H2 receptors, whereas others

are mediated by only one class. For example, the H1 receptors are important in producing

smooth muscle contraction and increasing capillary permeability. Histamine promotes

vasodilation by causing vascular endothelium to release nitric oxide.3 This chemical signal

diffuses to the vascular smooth muscle, where it stimulates cyclic guanosine

monophosphate production, causing vasodilation. Histamine H2 receptors mediate gastric

acid secretion. The two most common histamine receptors exert their effects by different



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second-messenger pathways. The actions of H1 antihistamines occur through at least two

mechanisms. Antiallergic activities of H1 antihistamines, such as inhibition of the release of

mediators from mast cells and basophils, involves stimulation of the intracellular activity of

the polyphosphatidylinositol pathway.4 Other actions of H1 antihistamines involve the

down-regulation of nuclear transcription factors that regulate the production of

proinflammatory cytokines and adhesion proteins. In contrast, stimulation of H2 receptorsenhances the production of cyclic adenosine monophosphate (cAMP) by adenylyl cyclase.

C. Role in allergy and anaphylaxis

The symptoms resulting from intravenous injection of histamine are similar to those

associated with anaphylactic shock and allergic reactions. These include contraction of

smooth muscle, stimulation of secretions, dilation and increased permeability of the

capillaries, and stimulation of sensory nerve endings.

Role of mediators: Symptoms associated with allergy and anaphylactic shock result

from the release of certain mediators from their storage sites. Such mediators include

histamine, serotonin, leukotrienes, and the eosinophil chemotactic factor of anaphylaxis.

In some cases, these cause a localized allergic reaction, producing, for example, actions

on the skin or respiratory tract. Under other conditions, these mediators may cause a full-

blown anaphylactic response. It is thought that the difference between these two

situations results from differences in the sites from which mediators are released and in

their rates of release. For example, if the release of histamine is slow enough to permit

its inactivation before it enters the bloodstream, a local allergic reaction results.However, if histamine release is too fast for inactivation to be efficient, a full-blown

anaphylactic reaction occurs.

II. H1 Antihistamines

The term antihistamine, without a modifying adjective, refers to the classic H1-receptor

blockers. These compounds do not influence the formation or release of histamine; rather,

they block the receptor-mediated response of a target tissue. [Note: This contrasts with the

action of cromolyn and nedocromil, which inhibit the release of histamine from mast cellsand are useful in the treatment of asthma.] The H1-receptor blockers can be divided into

first- and second-generation drugs. The older first-generation drugs are still widely used

because they are effective and inexpensive. However, most of these drugs penetrate the

CNS and cause sedation. Furthermore, they tend to interact with other receptors, producing

a variety of unwanted adverse effects. By contrast, the second-generation agents are specific

for H1 receptors, and because they do not penetrate the blood-brain barrier, they show less

CNS toxicity than the first-generation drugs. Among these agents desloratadine ,

fexofenadine, and loratadine show the least sedation. [Note: The histamine receptors are

distinct from those that bind serotonin, acetylcholine, and the catecholamines.]



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A. Actions

The action of all the H1-receptor blockers is qualitatively similar. However, most of these

blockers have additional effects unrelated to their blocking of H1 receptors; these effects

probably reflect binding of the H1 antagonists to cholinergic, adrenergic, or serotonin

receptors.

B. Therapeutic uses

Allergic and inflammatory conditions: H1-receptor blockers are useful in treating

allergies caused by antigens acting on immunoglobulin E antibodyâ€“sensitized mast

cells. For example, antihistamines are the drugs of choice in controlling the symptoms of

allergic rhinitis and urticaria, because histamine is the principal mediator. However, the

H1-receptor blockers are ineffective in treating bronchial asthma, because histamine is

only one of several mediators of that condition. [Note: Epinephrine has actions on

smooth muscle that are opposite to those of histamine, and it acts at different receptors.

Therefore, epinephrine is the drug of choice in treating systemic anaphylaxis and other

conditions that involve massive release of histamine.] Glucocorticoids show greater anti-

inflammatory effects than the H1 antihistamines.

Motion sickness and nausea: Along with the antimuscarinic agent scopolamine, certain

H1-receptor blockers, such as diphenhydramine, dimenhydrinate , cyclizine , meclizine ,

and hydroxyzine, are the most effective agents for prevention of the symptoms of motion

sickness. The antihistamines prevent or diminish vomiting and nausea mediated by boththe chemoreceptor and vestibular pathways. The antiemetic action of these medications

seems to be due to their blockade of central H1 and muscarinic receptors.

Somnifacients: Although they are not the medication of choice, many first-generation

antihistamines, such as diphenhydramine and doxylamine, have strong sedative

properties and are used in the treatment of insomnia. The use of first-generation H1

antihistamines is contraindicated in the treatment of individuals working in jobs where

wakefulness is critical.

C. Pharmacokinetics

H1-receptor blockers are well absorbed after oral administration, with maximum serum

levels occurring at 1 to 2 hours. The average plasma half-life is 4 to 6 hours except for

meclizine, which has a half-life of 12 to 24 hours. H1-receptor blockers have high

bioavailability and are distributed in all tissues, including the CNS. All first-generation H1

antihistamines and some second-generation H1 antihistamines, such as desloratadine and

loratadine, are metabolized by the hepatic cytochrome P450 system. Cetirizine is excreted

largely unchanged in the urine, and fexofenadine is excreted largely unchanged in the feces.

After a single oral dose, the onset of action occurs within 1 to 3 hours. The duration of

action for many oral H1 antihistamines is at least 24 hours, facilitating once-daily dosing.



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They are most effective when used prophylactically before allergen exposure rather than as

needed. Tolerance to the action of H1 antihistamines has not been observed.

D. Adverse effects

First-generation H1-receptor blockers have a low specificity; that is, they interact not only

with histamine receptors but also with muscarinic cholinergic receptors, ±-adrenergic

receptors, and serotonin receptors. The extent of interaction with these receptors and, as a

result, the nature of the side effects vary with the structure of the drug. Some side effects

may be undesirable, and others may have therapeutic value. Furthermore, the incidence and

severity of adverse reactions for a given drug varies between individual subjects.

1) Sedation: First-generation H1 antihistamines, such as chlorpheniramine,

diphenhydramine, hydroxyzine, and promethazine, bind to H1 receptors and block the

neurotransmitter effect of histamine in the CNS. The most frequently observed adverse

reaction is sedation. Other central actions include tinnitus, fatigue, dizziness, lassitude (a

sense of weariness), uncoordination, blurred vision, and tremors. Sedation is less

common with the second-generation drugs, which do not readily enter the CNS. Second-

generation H1 antihistamines are specific for H1 receptors and penetrate the CNS poorly.

They show less sedation and other CNS effects.

2) Dry mouth: Oral antihistamines also exert weak anticholinergic effects, leading not

only to a drying of the nasal passage but also to a tendency to dry the oral cavity. Blurred

vision can occur as well with some drugs.

3) Drug interactions: Interaction of H1-receptor blockers with other drugs can cause

serious consequences, such as potentiation of the effects of all other CNS depressants,

including alcohol. Persons taking monoamine oxidase (MAO) inhibitors should not take

antihistamines, because the MAO inhibitors can exacerbate the anticholinergic effects of

the antihistamines. In addition, the first-generation antihistamines (diphenhydramine and

others) have considerable anticholinergic (antimuscarinic) actions. These actions would

decrease the effectiveness of cholinesterase inhibitors (donepezil, rivastigmine, and

galantamine) in the treatment of Alzheimer's disease.

4) Overdoses: Although the margin of safety of H1-receptor blockers is relatively high and

chronic toxicity is rare, acute poisoning is relatively common, especially in young

children. The most common and dangerous effects of acute poisoning are those on the

CNS, including hallucinations, excitement, ataxia, and convulsions. If untreated, the

patient may experience a deepening coma and collapse of the cardiorespiratory system.



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III. Histamine H2-Receptor Blockers

Although antagonists of the histamine H2 receptor block the actions of histamine at all H2

receptors, their chief clinical use is to inhibit gastric acid secretion, being particularly

effective against nocturnal acid secretion. By competitively blocking the binding of

histamine to H2 receptors, these agents reduce the intracellular concentrations of cyclicadenosine monophosphate and, thereby, secretion of gastric acid. The four drugs used in the

United Statescimetidine, ranitidine, famotidine, and nizatidine potently inhibit (greater than

90 percent) basal, food-stimulated, and nocturnal secretion of gastric acid after a singledose.

Cimetidine is the prototype histamine H2-receptor antagonist; however, its utility is limited

by its adverse effect profile and drug interactions.

Actions: The histamine H2-receptor antagonists cimetidine, ranitidine, famotidine, and

nizatidine act selectively on H2 receptors in the stomach, blood vessels, and other sites,

but they have no effect on H1 receptors. They are competitive antagonists of histamineand are fully reversible. These agents completely inhibit gastric acid secretion induced

by histamine or gastrin. However, they only partially inhibit gastric acid secretion

induced by acetylcholine or bethanechol.

Therapeutic uses: The use of these agents has decreased with the advent of the PPIs.

Peptic ulcers: All four agents are equally effective in promoting healing of duodenal

and gastric ulcers. However, recurrence is common after treatment with H2

antagonists is stopped (60-100 percent per year). Patients with NSAID-inducedulcers should be treated with PPIs, because these agents heal and prevent future

ulcers better than H2 antagonists.

Acute stress ulcers: These drugs are useful in managing acute stress ulcers

associated with major physical trauma in high-risk patients in intensive care units.

They are usually injected intravenously.

Gastroesophageal reflux disease: Low doses of H2 antagonists, recently released for

over-the-counter sale, appear to be effective for prevention and treatment of

heartburn (gastroesophageal reflux). However, about 50 percent of patients do not

find benefit, and PPIs are now used preferentially in the treatment of this disorder.

Because H2-receptor antagonists act by stopping acid secretion, they may not relieve

symptoms for at least 45 minutes. Antacids more efficiently, but temporarily,

neutralize secreted acid already in the stomach. Finally, tolerance to the effects of H2

antagonists can be seen within 2 weeks of therapy.



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Pharmacokinetics:

Cimetidine: Cimetidine and the other H2 antagonists are given orally, distribute

widely throughout the body (including into breast milk and across the placenta), and

are excreted mainly in the urine. Cimetidine normally has a short serum half-life,

which is increased in renal failure. Approximately 30 percent of a dose of cimetidineis slowly inactivated by the liver's microsomal mixed-function oxygenase system

and can interfere in the metabolism of many other drugs; the other 70 percent is

excreted unchanged in the urine. The dosage of all these drugs must be decreased in

patients with hepatic or renal failure. Cimetidine inhibits cytochrome P450 and can

slow metabolism (and, thus, potentiate the action) of several drugs (for example,

warfarin, diazepam, phenytoin, quinidine, carbamazepine, theophylline, and

imipramine;), sometimes resulting in serious adverse clinical effects.

Ranitidine: Compared to cimetidine, ranitidine is longer acting and is five- to ten-fold more potent. Ranitidine has minimal side effects and does not produce the

antiandrogenic or prolactin-stimulating effects of cimetidine. Unlike cimetidine, it

does not inhibit the mixed-function oxygenase system in the liver and, thus, does not

affect the concentrations of other drugs.

Famotidine: Famotidine is similar to ranitidine in its pharmacologic action, but it is

20 to 50 times more potent than cimetidine, and 3 to 20 times more potent than

ranitidine.

Nizatidine: Nizatidine is similar to ranitidine in its pharmacologic action and

potency. In contrast to cimetidine, ranitidine, and famotidine, which are metabolized

by the liver, nizatidine is eliminated principally by the kidney. Because little first-

pass metabolism occurs with nizatidine, its bioavailability is nearly 100 percent. No

intravenous preparation is available.

Adverse effects: The adverse effects of cimetidine are usually minor and are associated

mainly with the major pharmacologic activity of the drug namely, reduced gastric acid

production. Side effects occur only in a small number of patients and generally do notrequire discontinuation of the drug. The most common side effects are headache,

dizziness, diarrhea, and muscular pain. Other central nervous system effects (confusion,

hallucinations) occur primarily in elderly patients or after intravenous administration.

Cimetidine can also have endocrine effects, because it acts as a nonsteroidal

antiandrogen. These effects include gynecomastia, galactorrhea (continuous

release/discharge of milk), and reduced sperm count. Except for famotidine, all these

agents inhibit the gastric first-pass metabolism of ethanol. Drugs such as ketoconazole,

which depend on an acidic medium for gastric absorption, may not be efficiently

absorbed if taken with one of these antagonists.

Thank You

practical pharmacology

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