عرض تقديمي1

Interpretation of the Prescription

or Medication Order

• By definition, a prescription is an order

for medication issued by a physician,

dentist, or other properly licensed

medical practitioner. Prescriptions

designate a specific medication and

dosage to be prepared by a pharmacist

and administered to a particular patient.

Interpretation of the Prescription or Medication Order

• Prescriptions are usually written on preprinted forms containing the traditional symbol “Rx" (meaning "recipe," "take thou," or "you take"), name, address, telephone number, and other pertinent information regarding the physician or other prescriber


• In hospitals and other institutions,

the forms are somewhat different and

are referred to as medication orders.


Main Street Libertyville, Maryland Phone 333-5555NAME Marv L. SmithDATE January 4, 2001JOHN M. BROWN, M.D. 100

ADDRESS 123 Broad Street

• Rx•

Tetracycline HCI Capsules 500 mgDispense 20 caps

Sig: Take 1 capsule every 12 hours until all are taken


• Slide.6. Components of a typical prescription. Parts labeled are as follows:

• Prescriber information and signature• Patient information• Date prescription was written• symbol (the Superscription) meaning "take thou,"

"you take," or "recipe"• Medication prescribed (the Inscription)• Dispensing instructions to the pharmacist (the

Subscription)• Directions to the patient (the signa)• Special instructions


Interpretation of the Prescription or Medication OrderTable 2.1. Continued

or s.c. or SQ

it should be noted here that when appearing in the Signa, the

symbol, 5 mL, and the abbreviation tsp. are each taken to mean

"one teaspoonful" and the symbol ss, 15 mL, and the abbreviation

tbsp. are each taken to mean "one tablespoonful."

Examples of Prescription Directions to the Pharmacist:

(a) M. ft. ung.

Mix and make an ointment.

(b) Ft. sup. no xii

Make 12 suppositories.

(c) M. ft. cap.. no. xxiv

Mix and make capsules. Give 24 such doses.

• Examples of Prescription Directions to the Patient:• (a) Caps. i. q.i.d. p.c. et h.s.• Take one (1) capsule four (4) times a day after each

meal and at bedtime.• (B) gtt. ii o.d. q.d. a.m.• Instill two (2) drops in the right eye every day in the

morning. • (c) tab. ii Stat tab. 1 q. 6 h. X 7 d.• Take two (2) tablets immediately, then take one (1)

tablet every 6 hours for 7• days.


Abbreviation Meaning • p.r.n. or prn when required• pt. patient• pulv. powder• q- every• q.d. every day• q.h. every hour• q i.d. four times a day• q.o.d. every other day• q.s. or qs. a sufficient quantity• sup. Or supp suppository• susp. suspension• syr. syrup• tab. Tablet• t.i.d. three times a day• t.i.w. three times a week

Abbreviation commonly used in Prescription and

Medication Order

Abbreviation Meaning TPN total parenteral nutrition

tsp. teaspoonful

U or u unit

u.d. or ut. as directed

Ung ointment

URI upper respiratory infection

USP United States Pharmacopeia

UTI urinary tract infection


Abbreviation Meaningaa. or aa. of each

a.c. before meals

ad up to; to make

a.d . right ear

a.m. morning

Amp . ampul

aq. water

a.s. left ear

b.i.d. twice a day

cap. Capsule

d.t.d. Give as such doses

f. or fl . Fluid


Abbreviation MeaningH.s. at bed timeO.d. right eye0.l. left eyeO.u. each eye.O2 both eyesP.c after mealP.o. by mouth


• Schedule 1 includes such drugs as cannabis, lysergide, and mescaline. A licence from the Home Secretary is required to possess, supply, administer, or cause to be administered, any., drugs specified in this schedule.


• Schedule 2 lists those drugs that are used medicinally and are subject to the strictest controls. The list includes amphetamine, cocaine, codeine, dihydrocodeine, dextropropoxyphene, methadone, morphine, pethidine, and many others., these drugs are subject to the full control exercised by the regulations regarding prescriptions, safe custody, and record-keeping.


• Schedule 3 includes the barbiturates and pentazocine. These drugs must fulfil the special prescription requirements for controlled drugs, but not the special requirements for safe custody.


• Schedule 4 includes over 30 benzodiazepines, which are not subject to the strict controls regarding prescriptions, safe custody, or record-keeping indicated for drugs in the previous schedules. The benzodiazepines are prescription only medicines


• Schedule 5 include preparations that, because of their strength are exempt from nearly all the controlled drug requirements. These exempt substances are not preparations for injection. Included in this list are certain preparations of dihydrocodeine or codeine. For instance, dihydrocodeine tartrate 30 mg tablet, because of the strength used, is classed simply as a prescription only medicine, whereas dihydrocodeine for injection is a Schedule 2 drug and therefore strictly controlled. Similarly,


Prescribing in pregnancy and during breastfeeding

Care must be exercised in prescribing drugs in

pregnant patient because of the possibility of

fetal damage. It better not to prescribe drugs to

the pregnant patient at all unless this absolutely

imperative


• MANY FACTOR MAY ALTER THE PATEHNT RESPONSE THE DRUGS IN LIVER DESEASE ALTHOUGH METABOLISM BY THE LIVER IS PROBABLY THE PRINCIPAAL ROUTE WHEREBY DRUGS ARE METABOLISED

• IN LIVER DESEASE DRUGS SHOULD BE USED WITH CARE OR AVOIDED INCLUDE(ANTI-INFLAMATORY OPIOD ANALEGESIC PSYCHOTROPIC DRUGS ANTIMICROBIALS SUCH AS CLINDOMYCIN METRONIDAZOLE AND TETRACYCLINE

PRESCIBING IN LIVER DESEASE

• Cardiovascular system• If a local anesthetic is administered intravenously by

accident it may cause cardiac arrest due to its direct depressant action on the heart, in particular its conduction system. If this occurs it is vital to give external cardiac massage combined with artificial respiration immediately.

• By contrast, if local anesthetic inadvertently injected into a vein is instead distributed in the body, it will produce peripheral vascular collapse, which may require the-administration of vasopressor drugs to restore the blood pressure'.

PrescribingMedication

Medication orders are written for the care of inpatients. Both medication orders and prescriptions may contain the brand or generic name of the drug and may be transmitted electronically. Only prescriptions contain the quantity of medication to be dispensed.

Information provided to the prescriber during a therapeutic intervention should include a description of the problem, reference source, description of the clinical significance, and an alternative. Informing the prescriber that a mistake was made does not encourage cooperation and resolution of the problem.

The prescription number, date of filling, product and quantity dispensed, and pharmacist's initials should be recorded on the prescription. The expiration date of the product being dispensed is not required.

The quantity of medication dispensed, lot number, expiration date of the product, and prescriber's name should be included on the label. The patient's diagnosis, although listed in the patient's profile, is not included on the prescription label.

Auxiliary and cautionary labels are an adjunct to verbal consultation, not a replacement. Appropriate uses for such labels include assuring for proper use, storage requirements, and compliance with statutory requirements; and warning against food and drug interactions.

The patient's name is required to identify each patient. Often the address or room number is required to identify patients with similar names. The patient's allergies, birth date, and instructions for use are required to prevent drug allergies and to assess the appropriateness of the prescription or medication order.

Adverse effects, under-treated conditions, allergic reactions, and drug-drug interaction are all drug-related problems. An undiagnosed condition may lead to a drug-related problem once diagnosed; however, diagnosis is required before the need for medication can be assessed.

28

Antihypertensive drugs

29

Methyldopa Clonidine

Mech. Of action Activate α2 receptors in the medulla→

↓central sympathetic outflow

Adverse effects Sedation, dizziness,

sexual dysfunction,

positive Coombs’

test

Sedation, dry mouth

, edema, severe

rebound

hypertension

Comments Safe in renal

dysfunction and

pregnancy

A-Sympathoplegics

1-Centrally acting Alpha 2 agonist:

30

Reserpine Guanethidine

Mech. of action Destruction of

storage granules→

↓NE

Binds to storage

granules→ inhibit

NE release

Adverse effects Sedation,

depression,

diarrhea.

Orthostatic

hypotension, fluid

retention, sexual

dysfunction

,diarrhea

2-Adrenergic neuron blockers:

31

3-Alpha blockers:

•Mech. of action :

•α1 blocking→ vasodilatation

→↓peripheral resistance

•Selective α1-receptors blockers:

•Prazosin ,

•Terazosin

•Doxazosin.

32

•Adverse effects:

•First-dose orthostatic hypotension,

•Dizziness,

•Headache.

•Used also in benign prostatic

hyperplasia to decrease urinary

retention.

4-Beta blockers:

•Mech. of action: β1 blocking→ ↓cardiac

output & ↓renin secretion.

•Selectivity:

•Nonselective:

• propranolol, timolol, pindolol.

•Cardio selective(β1 selective):

•atenolol, esmolol,metoprolol.

N.B. labetalol (blocks α1 & β receptors-

used in pheochromocytoma)

34

•Adverse effects :

•Impotence,

•Cardiovascular adverse effects

(bradycardia, AV block, CHF),

•CNS adverse effects (sedation, sleep

alterations),

•Non selective drugs may cause

exacerbation of asthma.

35

Hydralazine Minoxidil Diazoxide Nitroprosside

Mech. of

action

arteriolar dilatation

(relax smooth ms.

of arterioles)

arteriolar dilatation

(open K channels in the

arterioles)

Mixed veno-

arteriolar

dilatation

Adverse

effects lupus-like

syndrome,

tachycardia,

fluid retention

Hypertrichosis

, tachycardia,

fluid retention

Hyperglycemia,

tachycardia,

fluid retention

Cyanide

accumulation →

cyanosis, muscle

spasms, psychosis

(with prolonged

therapy),

tachycardia,

fluid retention

Comment

s

Used orally in moderate to severe

cases

Used I.V for hypertensive

emergencies

B-Direct acting vasodilators

36

C-Calcium channel blockers (CCBs)

•Mech. of action:

block Ca channels→↓intracellular Ca.

In cardiac muscle→↓contractility→↓cardiac output.

In blood vessels →vasodilatation.

•Selectivity:

•More selective on heart: Verapamil & Diltiazem

•More selective on blood vessels: Nifedipine & Amlodipine

•Adverse effects:

•Constipation ,

•Nausea.

•Heart failure ,

•Heart block (Verapamil & Diltiazem)

tachycardia , flushing (Nifedipine)

37

D-Drugs affecting angiotensin system

1-Angiotensin converting enzyme inhibitors (ACE

Is):

•Captopril

•Enalapril

•Lisinopril

•Mechanism of action:

•Prevent Angiotensin II formation → prevent

activation of AT-1 receptors→ ↓vasoconstriction

&↓ aldosterone secretion→mixed vasodilatation.

Inhibit the metabolism of

bradykinin→vasodilatation

38

•Adverse effects:

•Cough,

•Angioedema,

•Proteinuria,

•Taste changes,

•Hypotension,

•Pregnancy problems (fetal renal damage),

•Rash, immune reactions,

•Hyperkalemia.

39

2-Angiotensin-1 receptors antagonists (AT-1

antagonists):

•Losartan

•Irbesartan

•Candesartan

•Mech. of action:

Prevent activation of AT-1 receptors→………

•Adverse effects: as ACEIs but without cough .

40

E-Diuretics:

1-Mechansim of action:

- ↓blood volume→↓cardiac output .

- vasodilator effect: direct effect & by ↓vascular

sensitivity to vasopressor agents → ↓peripheral

resistance.

41

2-Selection:

•Thiazide diuretics: initial therapy in most cases, used

in mild to moderate hypertension.

•Loop diuretics: in sever and malignant hypertension

and hypertension of renal failure.

•K-sparing diuretics: in hyperaldosteronism.

42

Indication Suitable drugs

Angina Beta blockers , CCBs

Heart failure ACE Is , AT-1 antagonists

Diabetes ACE Is , AT-1 antagonists

Dyslipidemia

s

Alpha blockers , CCBs

BPH Alpha blockers

F-Antihypertensive drugs in special cases

43

Drugs used in the treatment of

HyperlipidemiaHyperlipidemia is a condition of high levels of cholesterol,

triglycerides, and /or lipoprotein in the blood.

44

DrugEffect on

LDL “bad

cholesterol

”

Effect on

HDL “good

cholesterol”

Effect on

triglyceridesSide effects/problems

Bile acid

sequestrants

(Resins)

e.g.

cholestyramine,

colestipol

↓↓No effect Slight ↑ gastrointestinal upset ,

↓absorption of fat soluble

vitamins, digoxin and

thiazides .

HMG-CoA

reductase

inhibitors (Statins)

e.g. lovastatin,

pravastatin,

simvastatin,

atorvastatin

↓↓↓ ↑ ↓ gastrointestinal upset ,

myopathy

(muscle aches and

weakness)

Nicotinic acid

and its

derivatives

↓↓ ↑↑ ↓ gastrointestinal upset ,

pruritus ,facial redness and

flushing (↓by aspirin or

long-term use) Lipoprotein

lipase

stimulators

(Fibrates)

e.g. gemfibrozil,

clofibrate

↓ ↑ ↓↓↓ gastrointestinal upset ,

myopathy , gallstones,

I-IntroductionA- Transmission of nerve impulse

Most drugs that affect the central nervous

system act by altering some step in the

neurotransmission process.

Drugs affecting the central nervous system may

act presynaptically by influencing the production,

storage, release, or termination of action of

neurotransmitters. Other agents may activate or

block postsynaptic receptors.

B- Blood Brain Barrier

The BBB is semi-permeable; that is,

it allows some materials to cross, but

prevents others from crossing.

1- Functions of the BBB:

•It protects the brain from foreign substances in

the blood that may injure the brain

•Maintains a constant environment for the brain

General properties of the BBB:

•Large molecules do not pass through the

BBB easily

•Low lipid-soluble molecules do not

penetrate into the brain. However, lipid-

soluble molecules rapidly cross through

into the brain.

3- The BBB can be broken down by:

•Hypertension

•Trauma

•Inflammation

•Infection

Sedatives and Hypnotics

A- Introduction

Anxiety is an unpleasant state of tension, apprehension,

or uneasiness-a fear that seems to arise from an

unknown source. Disorders involving anxiety are similar

to those of fear (such as tachycardia, sweating,

trembling, and palpitations) and involve sympathetic

activation.

Because all of the ant anxiety drugs (sometimes called

anxiolytic or minor tranquilizers) cause some sedation,

the same dugs often function clinically as both anxiolytic

and hypnotic (sleep-inducing) agents.

(All sedatives become hypnotics at large doses)

B- Benzodiazepines

Benzodiazepines are the most widely used

anxiolytic drugs. They have largely

replaced barbiturates in the treatment of

anxiety, because the benzodiazepines are

safer and more effective.

The target for benzodiazepines actions are

the GABA receptors.

1- Actions:

•Reduction of anxiety

•Sedative and hypnotic actions

•Amnesia

•Anticonvulsant

•Muscle relaxant

2- Dependence:

Psychological and physical dependence on

benzodiazepines can develop if high doses of the

drug are given over a prolonged period. Abrupt

discontinuation of the benzodiazepines results in

withdrawal symptoms, including confusion,

anxiety, agitation, restlessness, insomnia, and

tension.

3- Adverse effects:

•Drowsiness

•Impaired performance and judgment

•Central nervous system and cardiovascular

toxicity

•Dependence

- Classification of benzodiazepines according to

duration of action:

•Ultra short-acting (4 hours): Midazolam,

Triazolam

•Intermediate-acting (5-20 hours): Lorazepam,

Oxazepam

Long-acting (60 hours): Diazepam, Clonazepam

C- Other anxiolytic and hypnotic

agents

•Zolpidem

•Zaleplon

•Buspirone

D- Benzodiazepines antagonistFlumanezil is a GABA receptor antagonist

that can rapidly reverse the effects of

benzodiazepines. The drug is available for

intravenous (IV) administration only.

Barbiturates

The barbiturates were the mainstay of treatment

used to sedate the patient or to induce and

maintain sleep. Today, they have been largely

replaced by the benzodiazepines, primarily

because barbiturates induce tolerance, drug-

metabolizing enzymes, physical dependence, and

very severe withdrawal symptoms. Foremost is

their ability to cause coma in toxic doses. Certain

barbiturates, such as the very short-acting

thiopental, are still used to induce anesthesia.

1- Actions:

•Depression of the CNS At low doses, the barbiturates

produce sedation (Calming effect, reducing excitement).

At higher doses, the drugs cause hypnosis, followed by

anesthesia, and finally coma and death.

•Respiratory depression

2- Therapeutic uses:

•Anesthesia (Thiopental)

•Anticonvulsant (Phenobarbital)

•Anxiety

-Classification of Barbiturates according to the

duration of action:

•Ultra short-acting (15-30 minutes): Thiopental

•Short-acting (2-4 hours): Pentobarbital, Secobarbital

•Intermediate-acting (4-6 hours): Amobarbital

•Long-acting (6-8 hours): Phenobarbital

F- Nonbarbiturate Sedatives

•Chloral hydrate

•Antihistamines

•Ethanol

V-Antiepileptic drugsEpilepsy is a chronic, usually life-long disorder

characterized by recurrent seizures or convulsions and

usually episodes of unconsciousness and/or amnesia.

Convulsion is a violent involuntary contraction or

series of contractions of the voluntary muscles.

Hydantoins

Phenytoin is a drug of choice for initial

therapy, particularly in treating adults.

B- Carbamazepine

Carbamazepine is highly effective and is

often the drug of first choice.

C- Barbiturates

Phenobarbital has antiepileptic activity.

Primdone resembles Phenobarbital in its

anticonvulsant activity.

D- Valproic acid

Valproic acid has multiple actions and is a broad-

spectrum anticonvulsant, but because of its

hepatotoxic potential, it is a second choice.

E- Succinimides

Ethosuximide is the first choice in absence seizures.

F- Benzodiazepines

Several of the benzodiazepines show antieplipeptic

activity: Diazepam, Lorazepam, Clonazepam,

clonazepate.

G- Newer antiepileptic drugs

•Felbamate

•Gabapentin

•Lamotrigine

•Topiramate

•Tiagabine

VI-Agents used in the treatment of

Parkinson diseaseA- Parkinson disease

Parkinsonism is a movement disorder characterized by

muscle rigidity, tremors and postural instability.

It is due to dopamine deficiency in the basal ganglia

resulting in imbalance of dopaminergic (inhibitory) and

cholinergic (excitatory) influences on the extrapyramidal.

The aim of antiparkinsonian drugs is to increase dopamine

in the basal ganglia.

A- Levodopa and Carbidopa

Levodopa is a metabolic precursor of dopamine.

It restores dopamine levels in the extrapyramidal

centers.

The effects of levodopa on the CNS can be

greatly enhanced by coadministrating carbidopa.

Carbidopa diminishes the metabolism of

levodopa in the gastrointestinal tract and

peripheral tissues.

B- Selegeline

Selegeline selectively inhibits MAO.

By thus decreasing the metabolism of

dopamine, selegeline has been found to

increase dopamine levels in the brain.

C- Dopamine receptor agonists

•Bromocriptine

•Pergolide

•Pramipexole

•Ropinirole

D- Amantadine

It was accidentally discovered that the

antiviral drug amantadine, effective in the

treatment of influenza, has an

antiparkinsonism.

VII-Antipsychotic agents (Neuroleptic drugs)Psychosis (psychotic disorders) are a group of disorders with

more or less severe disturbances of thought, mood and/or

behavior.

Schizophrenia is a particular kind of psychosis characterized

mainly by thought disorders, delusions and hallucinations due to

central dopamine overactivity.

Neuroleptic drugs (also called antischizophrenic drugs,

antipsychotic drugs or major tranquilizers) are used primarily to

treat schizophrenia and manic states and

A- Typical neuroleptic

The typical neuroleptic drugs have several adverse

effects:

•Parkinsonian-like syndrome

•Neuroleptic malignant syndrome (rigidity,

autonomic instability)

•Anticholinergic effects (atropine-like)

•Sedation

•Hyperprolactinemia

•Postural hypotension

Typical neuroleptic (Low potency)

•Chlorpromazine

•Promethazone

- Typical neuroleptic (High potency)

•Fluphenazine

•Haloperidol

•Pimozide

B- Atypical neuroleptic

The newer antipsychotic drugs are referred to

as "atypical", because they have fewer

extrapyramidal adverse effects and

anticholinergic side effects than the typical

antipsychotics.

Atypical neuroleptics:

•Clozapine

•Olanzapine

•Risperidone

VIII-AntidepressantThe symptoms of depression are intense feelings of

sadness, hopelessness, and despair, as well as the

inability to experience pleasure in usual activities,

changes in sleep patterns and appetite, loss of

energy, and suicidal thoughts.

Most clinically useful antidepressant drugs

potentiate, either directly or indirectly, the

actions of epinephrine and/or serotonin in the

brain

A- Selective Serotonin Re-Uptake Inhibitors SSRIs

•Citalopram

•Escitalopram

•Fluoxetine

•Fluvoxamine

•Paroxetine

•Sertraline

- Serotonin/Norepinephrine Re-Uptake Inhibitors

•Venlafaxine

C- Atypical antidpressants

•Bupropion

•Mirtazapine

•Nefazodone

•Trazodone

D- Tricyclic antidpressants

•Amitriptyline

•Clomipramine

•Despiramine

•Imipramine

•Nortriptyline

IX-CNS stimulantsA- Psychomotor stimulants

•Amphetamine

•Atomoxetine

•Caffeine

•Cocaine

•Methylphenidate

•Nicotine

•Theophylline

They have limited therapeutic use.

They can have inhibitory effect on the

appetite.

Amphetamine is used in the Attention

deficit hyperactivity disorder.

- Hallucinogens

•Lysergic acid diethylamide LSD

•Tetrahydracannabinol THC

X-Narcotic analgesicsOpiates are natural alkaloids derived from Papaver

somniferum plant.

Opiods include both naturally occurring opiates and similar

synthetic drugs.

Narcotics are drugs that produce drowsiness with analgesia.

They are usually addictive.

A- Morphine and related opioids:

1- Morphine

It is used in analgesia in severe pain.

Adverse effects:

•Addiction

•Respiratory depression, bronchospasm

•Postural hypotension

•Nausea, vomiting, and constipation

•Urine retention

- Codeine (methylmorphine)

Codeine is less potent than morphine in all

features except in cough suppression.

The clinical use of codeine is as central

antitussive.

B- Meperidine

Meperidine is a synthetic opioid structurally unrelated

to morphine. It is less potent than morphine in al

features. It also has less addiction liability, respiratory

depression and bronchospasm.

Its therapeutic use is as analgesic for acute pain.

Methadone

Methadone is a synthetic, orally effective

opioid that is approximately equal in potency

to morphine but induces less euphoria and has

somewhat longer duration of action.

Methadone is used in the controlled

withdrawal of dependent abusers from heroin

and morphine. Orally administered, methadone

is substituted for the injected opioid.

D-Fentanyl

Fentanyl has 100-fold the analgesic potency of

morphine, and is used in anesthesia.

Three drugs related to Fentanyl – sulfentanil,

alfentanil, remifentanil- are also used as

analgesics.

E- Other analgesic

1- Propoxyphene

It is used as an analgesic to relieve mild to

moderate pain.

2- Tramadol

It is used to manage moderate to moderately

severe pain

F-Antagonists

In patients dependent on opioids, antagonists

rapidly reverse the effect of agonists and

precipitate the symptoms of withdrawal.

•Naloxone

•Naltrexone

Drugs used in migraineA- Pathophysiology of Migraine

The stage of aura: sudden release of serotonin of

unknown cause, which causes vasoconstriction of

cerebral blood vessels, leading to visual, olfactory or

auditory disturbances.

The stage of headache: prolonged vasoconstriction →

accumulation of metabolites → severe vasodilatation

→ perivascular edema and headache.

B- Drugs used during acute attack:

Ergotamine

Sumatriptan

Analgesics

Prophylaxis

Serotonin receptor blockers : methysergide

Beta-blockers : propranolol (unknown

mechanism)

Calcium channel blockers : verapamil

Patient compliance

Learning Objectives

• Describe adherence & co-morbidity

• Identify WHO’s Five Dimensions to

Medication Adherence

• Describe self-management support

strategies for overcoming barriers to

medication adherence.

Patient Adherence to Medications

Adherence

• Mosby’s Medical Dictionary defines adherence as “the process in which a person follows rules, guidelines, or standards, especially as patients follow a prescription and recommendations for a regimen of care”

Co-morbidity

Primary disease

+

One or more diseases

=

Co-morbidity

Self Management Support

• Demonstrating new skills

• Praise & Feedback

Self-Management

Chronic Care Model

Global Medication Adherence is

50%

WHO’s Five Dimensions of

Adherence

1. Social & Economic


• Community Support


• Economic


• Pictures• Use pictures when

giving instructions

• Read Back• Have the patient read

back the instructions

Prescription for Medication

1. Social & EconomicHow to make an Economic Poster

from a PowerPoint Slide

• Go to PowerPoint

• Use Graphics and Make a Poster

• Take a thumb drive or disc to a Print Shop and make a poster.

1. Social & EconomicUse Pictures When Teaching

2. Health Care System

• Provider-Patient

Relationship


• Using two-way communications and asking open ended questions fosters encouragement.

• Shared Decision Making


3. Condition Related

• Chronic conditions, such as hypertension, that lack symptoms highly impact the level of adherence

• People’s belief about the benefits and risks of medications influence whether they abide by a regimen.

3. Condition Related

4. Therapy Related

• Therapy-related factors include the complexity of medication regimen and unpleasant side effects.

• Dosing several times a day may contribute to non-adherence.

4. Therapy Related

• Concern about medication side effects remains a powerful barrier.

4. Therapy Related

5. Patient Related

• Perception of need, medication effectiveness, and safety.

• Follow up Appointments

5. Patient Related

5. Patient Related

• Personalized education and counseling sessions delivered by telephone, intranet, or in person by trained personnel.

Conclusion

QUESTIONS AND

DISCUSSION?

References continued.

• Ruppar, T., Conn, V., & Russell, C. (2008). Medication

Adherence Interventions for Older Adults: Literature

Review. Research and Theory for Nursing Practice: An

International Journal, 22(2) 114-147.

• Sherman, B., Frazee, S., Fabios, R., et al. (2009).

Impact of Workplace Health Services on Adherence to

Chronic Medications. The American Journal of Managed

Care, 15(7), 53-59.

• Simpson, R. (2006). Challenges for Improving

Medication Adherence. The Journal of the American

Medical Association, 296(21), 2614-2616.

• World Health Organization. Adherence to Therapies:

Evidence for Action. Geneva: World Health

Organization, 2003

Drugs acting on the Blood and Blood Forming Agents

I-Drugs for iron deficiency anaemia:

A-Physiology:

Iron is required for haemoglobin production. Absence of adequate iron leads to microcytic hypochromic anaemia (iron deficiency anaemia).

Total body iron: 3.5 gm (2/3 in Hb & 1/3 in ferritin, myoglobin, haemosidren and enzymes).Daily requirement: 10-15 mg of which 10% is absorbed.Main dietary source: meat & liver.

Etiology:↓ intake: starvation,anorexia.↓ absorption: gastrectomy, malabsorption syndrome and excess phytate, phosphate e.g. cereals, tannic acid e.g. tea.↑ requirements: pregnancy, lactation, after hemorrhage.↑ loss: chronic blood loss (e.g. ankylostoma, chronic GIT bleeding

B-Iron therapy:

1-Oral iron (Iron salts): Ferrous sulfate, Ferrous gluconate, Ferrous succinate Ferrous fumarate.

They should be in ferrous form (ferric form is unabsorbable)

Duration of treatment should be 3-6 months to replenish iron store.

Side effects: Nausea, Vomiting, Epigastric discomfort, Abdominal cramps with diarrhea or constipation, Black staining of the teeth & stool.

2-Parenteral iron:Iron dextran complex, Iron sorbitol

They are indicated if patient not tolerated or not absorbing the oral iron.

Side effects: Local pain Brownish discoloration of the tissue at site of injection, Fever, Headache,Arthralgia, Anaphylactic shock

Antidote for toxicity:Desferoxamine.

II-Drugs for Megaloblastic anaemia

A-Physiology:Vitamin B12 and folic acid are essential for normal DNA

synthesis.

Deficiency of either of them results in impaired

production and abnormal maturation of erythroid

precursor cells, giving rise to megaloblastic anaemia.Vitamin B12 deficiency due to a lack of gastric intrinsic factor results in pernicious anemia. This type of megaloblasticanaemia causes neurological damage if it is not treated.

Daily requirement: B12 → 1 mcgm, Folic acid → 1 mg

Main dietary source: B12 → animal products, Folic acid → vegetables

B-Aetiology:

B12 deficiency Folic acid deficiency

↓ intake Vegetarians,

starvation, anorexia

Lack of vegetable intake,

starvation, anorexia

↓ absorption Gastrectomy, pernicious

anemia(absent intrinsic

factor), malabsorption

syndrome

malabsorption syndrome,

drugs: anticonvulsant e.g.

barbitone, folic antagonists e.g.

methotrxate

↓ utilization Lack of transcbalamin II Methotrexate, trimethprim

↑ requirements pregnancy, lactation pregnancy, lactation, hemolytic

anemia, hemodialysis

C-Vitamin B12 therapy:

It is given parenteral.

Cyanocobalamine,

Hydroxycobalamine

D-Folic acid therapy:

Folic acid (Oral),

Folinic acid (Parenteral).

Treatment of Vitamin B12 deficient megaloblastic anemia with folic acid

alone may improve the symptoms; however, neurological damage may still

occur if vitamin B12 intake is not supplemented.

III- Anti-coagulants for Homeostasis

Homeostasis involves the interplay of three phases (vascular, platelet, and

coagulation).

The end result of these phases are, vasoconstriction, platelets aggregation )

platelet plug) at site of injury, and formation of fibrin clot (coagulation) to

prevent blood loss.

The fibrinolytic system prevents propagation of clotting beyond the site of

vascular injury and is involved in clot dissolution, or lysis.

A-Mechanism of Platelets aggregation :

Platelet adhesion to site of vascular injury.

Platelet activation by collagen, ADP, thrombin, TXA2, 5HT →

increase expression of glycoprotein IIb/IIIa receptors on platelets

surface.

Platelets aggregation by a cross-linking reaction due to fibrinogen

binding to glycoprotein IIb/IIIa receptors.

C-Anti-coagulant drugs:

They are drugs which inhibit the development and enlargement of clots by

actions on the coagulation phase.

They do not lyse clots or affect the fibrinolytic pathways.

1-Heparin and LMWH:

Standard heparin: a mixture of sulphated polysaccharides.

Low-molecular-weight heparins (LMWH)

- Enoxaparin,

- Dalteparin,

- Ardeparin,

- Tinzaparin:

Oral Anti-coagulants

Coumarins (warfarin)

Drug interaction with oral anticoagulants:

- Actions increased by aspirin, cimetidine, metronidazole,

sulfonamides.

- Actions decreased by vitamin K, barbiturates, carbamazepine,

cholystramine, rifampin, thiazides

Heparins Warfarin

(oral anticoagulants)

Chemical

nature

Large water-soluble

polysaccharide

Small lipid-soluble molecule

Rout of

administration

Parenteral (IV, SC) Oral

Site of action Blood Liver

Onset of

action

Rapid (seconds) Slow, limited by half-lives of

normal clotting factors

Mechanism of

action

Activates antithrombin III,

resulting in the inactivation

of several clotting factors

(especially IIa & Xa).

Action in vivo & in vitro.

Impairs the hepatic synthesis

of vitamin. K–dependent

clotting factors II, VII, IX,

and X (vitamin K

antagonist). Action in vivo

only.

Duration of

action

Acute (hours) Chronic (weeks or months)

Clinical use Rapid anticoagulation

(intensive) for thromboses,

emboli, stroke, angina,

Myocardial Infarction,

DVT. Used during

pregnancy (does not cross

placenta)

Long-term anticoagulation

(controlled) for ……

Not used in pregnant women

(can cross the placenta).

Monitoring Partial thromboplastin time

PTT (intrinsic pathway)

Prothrombin time PT

(extrinsic pathway)

Toxicity Bleeding,

thrombocytopenia,

hypersensitivity,

osteoporosis.

Bleeding, teratogenic, drug–

drug interactions

Antagonist Protamine sulfate IV vitamin K and fresh

frozen plasma

D-Fibrinolytic drugs

They are also called thrombolytics, drugs which dissolve the thrombus by

formation of the fibrinolytic plasmin from plasminogen.

1-Non-Fibrin selective (Non selective fibrinolytics):

Urokinase.

Streptokinase.

Anistreplase (Anisooylated plasminogen streptokinase activator

complex (APSAC) ).

They Act on both fibrin-bound and free(circulating)plasminogen →

fibrinolysis →dissolve the thrombus,

systemic fibrinogenolysis →generalized hypo-coagulabiliy state .

2-Fibrin selective (Selective fibrinolytics):

Recombinant human tissue-type plasminogen activator (rt-PA):

- Alteplase,

- Reteplase,

- Tenecteplase

Recombinant single chain urokinase plasminogen activator (rscu-PA).

They Act mainly on fibrin-bound plasminogen → fibrinolysis →dissolve

the thrombus

They are less liable to cause coagulation disturbance.

3-Clinical uses of fibrinolytic drugs:

Coronary artery thrombosis in myocardial infarction: they decrease

mortality by >60% if used within 3 hours.

Non coronary thrombosis:

- Deep venous thrombosis,

- Pulmonary embolism,

- Occular thrombosis.

4-Side effects of fibrinolytic drugs:

Bleeding,

Hypersensitivity reaction (streptokinase & APSAC)

5-Antidote in excessive bleeding:

Antifibrinolysins

Aminocaproic acid

Tranxamic acid

E-Anti-platelet drugs

They are drugs which inhibit platelet aggregation and so, inhibit the clot

formation.

1-Aspirin:

The prototype anti-platelet drug.

It irreversibly inhibits COX in platelets→↓ TXA2 →↓activation,

2-ADP receptor blockers:

Ticlopidine

Clopidogrel:

They block ADP receptors on platelets→ ↓activation,

Ticlopidine has risk of causing sever thrombocytopenia & neutropenia

3-Antagonists of Glycoprotein IIb/IIIa:

Abciximab,

Eptifibatide,

Tirofiban:

They are antagonists that bind to glycoprotein IIb/IIIa receptors→

↓aggregation by preventing cross-linking reaction.

4-Dipyridamole:

Inhibition of PDE →↑cAMP in platelets→ ↓aggregation

N.B.: largely ineffective when used alone

5-Clinical uses of anti-platelet drugs:

As a prophylaxis against:

Thrombo-embolism in angina,

Myocardial infarction,

Post angioplasty,

Atrial arrhythmia,

Cerebro-vascular diseases, etc…

F-Fibrinolytic inhibitors (Antifibrinolytics)

Tranexamic acid.

Aminocaproic acid.

They are drugs which inhibit fibrinolysis by inhibition of plasminogen

activation.

Clinical uses:

Antidote for fibrinolytic drugs.

Control bleeding following surgery.

Hemophiliac patients, to control bleeding after minor trauma or

surgery.

DRUG INTERACTION

Defination

• It is the modification of the effect of one drug (the object

drug ) by the prior concomitant administration of

another (precipitant drug).

• Concomitant use of several drug in presence of another

drug is often necessary for achieving a set of goal or in the

case when the patient is suffering from more than one

disease.

• In these cases chance of drug interaction could increase.

• Risk factor• Out come of interaction• Mechanism of interactiona. pharmacokinetic b. pharmacodynamics•

content

Outcomes of drug interactions

1) Loss of therapeutic effect

2) Toxicity

3) Unexpected increase in pharmacological activity

4) Beneficial effects e.g additive & potentiation (intended)

or antagonism (unintended).

5) Chemical or physical interaction

e.g I.V incompatibility in fluid or syringes

mixture

Mechanisms of drug interactions

Pharmacokinetics Pharmacodynamics

Pharmacokinetics involve the effect of a drug on another drug

kinetic that includes absorption ,distribution , metabolism

and excretion.

Pharmacodynamics are related to the pharmacological

activity of the interacting drugs

E.g., synergism , antagonism, altered cellular transport effect

on the receptor site.

Antagonism

When one drug decreases or abolishes the action of

another.

Effect of drug A+ B < Effect of drug A+ Effect of

drug B

Types :

Physical antagonism

Chemical antagonist.

Physiological antagonist.

Pharmacological antagonist.

168

Drug Antagonism

1) Physical Antagonism• Based on physical property.

• No receptor.

Examples

• Charcoal adsorbs alkaloids and can prevent

their absorption used in alkaloid poisoning.

169

Drug Antagonism

2) Chemical Antagonism• Simple chemical reaction.

• No receptor.

Examples

• Antacid & tetracycline.

• Heparin & penicillin

• Tannins & alkaloids.

170

Drug Antagonism

3) Physiological Antagonism • Physiological effect is antagonized.

• Drugs acting on different receptors:

• Noradrenaline → Vasoconstriction → ↑

BP.

• Histamine → Relax vascular smooth →

↓BP.

• Noradrenaline is used in anaphylactic

shock to raise BP.

171

Pharmacokinetic interactions

1) Altered GIT absorption.

•Altered pH

•Altered bacterial flora

• formation of drug chelates or complexes

• drug induced mucosal damage

• altered GIT motility.

a) Altered pH;The non-ionized form of a drug is more lipid

soluble and more readily absorbed from GIT than the

ionized form does.

Ex1., antiacids Decrease the tablet

dissolution

of Ketoconazole (acidic)

Ex2., H2 antagonists

Therefore, these drugs must be separated by at least 2h

in the time of administration of both .

b) Altered intestinal bacterial flora ;

EX., 40% or more of the administered digoxin dose is

metabolised by the intestinal flora.

Antibiotics kill a large number of the normal

flora of the intestine

Increase digoxin conc. and increase its toxicity

c) Complexation or chelation;

EX1., Tetracycline interacts with iron preparations

or

Milk (Ca2+ ) Unabsorpable complex

Ex2., Antacid (aluminum or magnesium) hydroxide

Decrease absorption of

ciprofloxacin by 85%

due to chelation

d) Drug-induced mucosal damage.

Antineoplastic agents e.g., cyclophosphamide

vincristine

procarbazine

Inhibit absorptionof several drugseg., digoxin

e) Altered motility

Metoclopramide (antiemitic)

Increase absorption of cyclosporine due

to the increase of stomach empting time

Increase the toxicity

of cyclosporine

f) Displaced protein binding

It depends on the affinity of the drug to plasma protein.

The most likely bound drugs is capable to displace others.

The free drug is increased by displacement by another drug

with higher affinity.

Phenytoin is a highly bound to plasma protein (90%),

Tolbutamide (96%), and warfarin (99%)

Drugs that displace these agents are Aspirin

Sulfonamides

phenylbutazone

g) Altered metabolism

The effect of one drug on the metabolism of the

other is well documented. The liver is the major site of drug

metabolism but other organs can also do e.g., WBC,skin,lung,

and GIT.

CYP450 family is the major metabolizing enzyme

in phase I (oxidation process).

Therefore, the effect of drugs on the rate of metabolism

of others can involve the following examples.

Stimulation (induction) of drug-metabolizing enzymes (DMEs)

Certain drugs such as phenobarbitone, phenytoin, primidone, carbamazepine, rifampicin, griseofulvin, and ethanol (in chronic use), as well as cigarette smoking, are powerful inducers of DMEs. The result is that the half-life (To?) of some drugs may be reduced substantially. The enzyme induction develops over several weeks and takes about the same time to disappear after the inducing agent has been withdrawn. Drugs with a metabolism likely to be altered by enzyme inducers are anticoagulants and oral contraceptives.

Inhibition of drug-metabolizing enzymes A number of drugs may inhibit DMEs; these include metronidazole, chloramphenicol, phenylbutazone, cimetidine, ethanol (acute intoxication), isoniazid, and MAOIs. The commonest drugs to be affected through this inhibition are phenytoin and anticoagulants. The effects of phenytoin are increased in the presence of isoniazid (in slow acetylators) or chloramphenicol.Unfortunately, despite their name, MAOIs are very unspecific and may also decrease the rate of biotransformation of barbiturates, phenothiazines, and alcohol. It has also been shown in animals that the metabolism of pethidine and other opioids is slowed by MAOIs due to inhibition of pethidine demethylase (Clark 1967),

E.g., Enzyme induction

A drug may induce the enzyme that is responsible

for the metabolism of another drug or even itself e.g.,

Carbamazepine (antiepileptic drug ) increases its own

Metabolism.

Phenytoin increases hepatic metabolism of theophylline

Leading to decrease its level Reduces its action

and

N.B enzyme induction involves protein synthesis .Therefore,

it needs time up to 3 weeks to reach a maximal effect

Eg., Enzyme inhibition;

It is the decrease of the rate of metabolism of a drug by

another one .

This will lead to the increase of the concentration of the

target drug and leading to the increase of its toxicity .

Inhibition of the enzyme may be due to the competition

on its binding sites , so the onset of action is short

may be within 24h.

When an enzyme inducer ( e.g. carbamazepine) is administered

with an inhibitor (verapamil) The effect of the

inhibitor will be

predominant

Ex.,Erythromycin inhibit metabolism of astemazole and terfenadine

Increase the serum conc.

of the antihistaminic leading to

increasing the life threatening

cardiotoxicity

EX., OmeprazoleInhibits oxidative

metabolism

of diazepam

First-pass metabolism:

Oral administration increases the chance for liver

and GIT metabolism of drugs leading to the loss of a

part of the drug dose decreasing its action. This is

more clear when such drug is an enzyme inducer

or inhibitor.

EX., Rifampin lowers serum con. of verapamil level by

increase its first pass . Also, Rifampin induces the

hepatic metabolism of verapamil

Renal excretion:

•Active tubular secretion

It occurs in the proximal tubules.

The drug combines with a specific protein to pass through

the proximal tubules.

When a drug has a competitive reactivity to the protein that is

responsible for active transport of another drug .This will reduce

such a drug excretion increasing its con. and hence its toxicity.

EX., Probenecid ….. Decreases tubular secretion of

methotrexate.

Changes in urinary pH:▪ Alkalization of urine with sodium

bicarbonate ↑ excretion of weak acids▪ Acidification of urine with ammonium chloride ↑ excretion of weak bases

Interactions resulting from alterations in Excretion:

- Reduction in urine elimination:e.g. Probenicid ↓ excretion of penicillin

It means alteration of the dug action without change in its

serum concentration by pharmacokinetic factors.

EX., Propranolol + verapamil Synergistic or additive

effect

Pharmacodynemic interaction

Additive effect : 1 + 1 =2

Synergistic effect : 1 +1 > 2

Potentiation effect : 1 + 0 =2

Antagonism : 1-1 = 0

• Grapefruit juice and Terfenadine• Grapefruit juice and cyclosporin• Grapefruit juice and felodipine

• Grapefruit contains : furanocoumarin compounds that can selectively inhibit CYP3A4

Drug-Food interactions

Severity of interactions is classified in 3 categories:

1• Major (life threating or permenent

damage)

2• Moderate (deteriorating patients

status)

3• Minor ( with little effect)

THANKS TO

ALL

Pharmacokinetics during pregnancy

Maternal drug absorption may be decreased by the combination of delayed gastric emptying and decreased motility. An increase in plasma progesterone level during pregnancy is believed to be responsible for the reduction in intestinal motility

2). There is also a reduction in gastric acid secretions and an increase in mucus secretions, with a consequent increase in gastric ph. These may alter the dissolution and absorption of the drug. Absorption from sites other than the gastrointestinal tract may also be affected. For example, increased pulmonary absorption may result from greater minute ventilation and increased cutaneous absorption as a result of greater surface area and blood flow

3- Excretion. Concomitant changes occur in cardiac output and glomerular filtration rates, which also increase approximately 30 to 50% during pregnancy

4-The expanded apparent volume of distribution, together with an increase in renal clearance leads to lower maternal circulating concentrations of drugs. The drugs which are excreted primarily unchanged in the urine such as amoxycillin, demonstrate enhanced elimination and lower steady-state serum concentrations. Its dose should be doubled for systemic infections (but not for urinary tract infections as penicillins are highly concentrated in the urine)

5-Cholestasis frequently develops during pregnancy and may result in decreased hepatic clearance of drugs that undergo biliary excretion, but their extent can hardly be quantified

Placental drug transfer

The function of the placenta during gestation is protection of the concepts, maintenance of pregnancy, possible prevention of maternal rejection of the pregnancy, transportation of nutrients and wastes, metabolism of endogenous and xenobiotic

substances and endocrine activity. However, any drug or environmental agent that gains access to the maternal bloodstream should be considered capable of crossing the placenta and reaching the fetus unless demonstrated otherwise

In general, lipophilic, unionized, low molecular weight drugs in their free non-protein bound state tend to cross the placenta. A major route of placental drug transfer is a simple diffusion. As with diffusion across other biological membranes lipophilic drugs generally cross the placenta more readily than nonlipophiliccompounds. Drugs which are non-ionized at the physiological pH will diffuse across the placenta more rapidly than more basic or acidic compounds. But this distinction is not absolute, since some drugs which are ionized at physiological pH such as salicylate (aspirin) rapidly and efficiently reach the fetus

The transfer of many substances across the placenta requires energy or special carriers.

Some other agents, such as barbiturates, narcotic analgesics, and local anesthetics, are “flow limited” in their placental transfer because a decrease in maternal blood flow to the placenta may reduce the placental passage of these agents.

Normal uterine contractions during labor, oxytocic drugs, exogenously administered sympathomimetic, or ß-adrenergic receptor blocking agents all affect maternal and fetal hemodynamics and therefore may modify maternal drug distribution and placental transfer.

Adverse effects of drugs on the fetus

Since 1920 it has been known that external agents can affect fetal development, when it was discovered that X-irradiation during pregnancy could cause fetal malformation or death. The drugs as causative agents in teratogens were recognized in 1960 with the shocking affair with thalidomide

Drug or chemical exposure during pregnancy are believed to account for about 1% of all fetal malformations (12).

Drugs may act on the embryo and fetus directly or indirectly. Any drug affecting cell division, enzymes, protein synthesis or DNA synthesis is directly a potential teratogen. Indirectly dangerous

drugs are those acting on the uterus

(vasoconstriction reduce blood supply and cause fetal anoxia; misoprostol /a synthetic analogue of prostaglandin E/ cause uterine contraction leading to abortion) and on the mother’s hormone balance.

The most vulnerable period for major anatomical abnormality is that of organogenesis which occurs during weeks 2-8 of intrauterine life. The adverse actions of drugs taken by the mother at this time may result in permanent birth defects

After the organs are formed abnormalities are less anatomically dramatic, but although developing fetus continues to be vulnerable to drug effects.

The use of drugs during the final weeks of pregnancy may have a damaging effect on the fetus at birth. At that time the newborn has an incompletely developed metabolic system which cannot process and eliminate drugs rapidly and effectively. As a result, over dosage may occur.

Drugs known to be teratogenic, probably or suspected or being teratogenic,

The drugs known to be teratogenic are:

Ethanol in pregnancy causes impaired fetal development, associated with small size, abnormal facial development and other physical abnormalities and mental retardation (14,15, 16).

Cytotoxic drugs can cause malformations when used in early pregnancy, but more often lead to abortion (5).

Retinoides such as isotretinoine and etreti-nate, used by dermatologists to treat different skin diseases (psoriasis, acne etc.), are known teratogens and cause a high proportion of serious abnormalities (skeletal deformities) in exposed fetuses (17).

Anticonvulsant drugs. The incidence of con-genital anomalies among babies born to epileptic women is 2-3 times higher than in the healthy population. None of the major anticonvulsants is to be regarded as free from teratogenic effects and no one drug is clearly safer than any other in this regard. Phenitoin(18) can cause cleft lip/palate, valproate (19) neural tube defects and carbamazepine spinabifida and hypospadias (a malformation of the male urethra)

However a pregnant epileptic woman under anticonvulsant treat-ment has a 90% chance of having a normal child (with regular controle of serum α -feto-protein, uterine ultrasonography and diagnos-tic amniocentois)

Anticoagulant, warfarin administered in the first trimester is associated with nasal hypo-plasiaand various central nervous system abnormalities, affecting roughly 25% of babies. In the last trimester there is as risk of intracranial hemorrhage in the baby during delivery (22

For the drugs under suspicion there has been some reluctance to their use in pregnancy. However, most large-scale controlled studies conclude that these agents can be used safely during pregnancy. But in general the best recommendation is to avoid any drug during the first trimester.The drugs probably teratogenic are: cocaine and sex

hormones. The data suggested that cocaine--exposed infants may be at increased risk for congenital malformations (23,24,25

and for the sex hormones the results of numerous studies have lead to the conclusion that they are slightly teratogenic and that caution is needed (26,27).

The US Food and Drug Administration (FDA) has established five categories for classifying drugs according to the risks they pose to pregnant women and their fetuses (

These categories, labeled A, B, C, D and X are listed below (Table 3) with a description for each. Drugs in category A and B are usually considered safe for use in pregnancy. Drugs in category C may be used despite possible risks. Drugs in category D should usually be avoided and category X is contraindicated because the risks involved clearly outweigh potential benefits. These five categories provide a guide to the relative safety of drugs prescribed to pregnant woman.Selecting drugs for the pregnant dental patient

In the case of a pregnant patient, the dental practitioner must determine that the potential benefits of the dental therapy required for her care outweigh the risks to the fetus.

The most elective dental procedures must be postponed until after the pregnancy is over, although dental treatment for a pregnant woman who has oral pain, advanced disease or infection should not be delayed.

The therapeutic agents commonly used in dental care for pregnant women are local anesthetics, non-narcotic analgesics, antimicrobials and sedatives/ /anxiolytics

Local anesthetics and the admixture

Local anesthetics are considered relatively safe for use during pregnancy. Lidocain (Anelok, Lido-kain) is a widely used local anesthetic agent of the amide type with low toxic potential. Pregnancy risk for lidocaine is B. Lidocaine like all local anesthetics’ can cross the placenta. Within the fetus there is a significant decrease in serum α 1-acid gly-coprotein(the binding proteins for lidocaine and other basic drugs) and therefore the unbound (“free”) drug increases. This could cause fetal depression. The dental practitioner must limit the dose to the minimum required for effective pain control (29).

The adrenaline, a naturally occurring hormone, pregnancy risk C is generally considered to have no teratogenic effects when administered with dental anesthetics. Adrenaline can stimulate cardiovascular functions and its administration demands careful technique and proper dosing (30). Adrenaline may delay the second stage of labor in a pregnant woman because the drug inhibits spontaneous or oxytocin-induced uterine contractions. It may also cause anoxia to the fetus (31).

Non-narcotic analgesics

For management of oral pain during pregnancy, among a number of peripherally acting analgesics, paracetamol (acetaminophen) is considered to be the best choice (32,33). Pregnancy risk for paracetamol is B. The second analgesic is aspirin, pregnancy risk D. Aspirin has widespread use in pregnant woman, and in moderate doses has shown no evidence of teratogenesis in humans. There arevery few reports in which aspirin can be implicated as a human teratogen (34,35,36). Possibly the increased production of prostaglandins during pregnancy overrides the effects of aspirin in the usual dosages. But aspirin and other Nonsteriodal anti-inflammatory drugs (NSAID) such as ibuprofen and naproxen should be avoided particularly during the third trimester of pregnancy because they have the common mechanism of inhibiting prostaglandin synthesis. By blocking synthesis of the prostaglandins’ involved in induction of labor, NSAID may prolong pregnancy. Additionally, prostaglandin inhibitors may cause constriction of the ductus arteriosus in the fetus, resulting in pulmonary hypertension in the infant. The role of aspirin as an antithrombotic agent and its ability to promote bleeding mean that it should be very definitely avoided at parturition, to avoid delivery complications and postpartum hemorrhage in the mother (37).

Antimicrobials

Penicillin G, penicillin V, ampicillin, amoxicillin and cephalosporin’s (all pregnancy risk B) are generally thought to be safe during pregnancy. As remarked above the pharmacokinetic of ampicillin and amoxicillin is altered in pregnant women and this can lead to lower plasma concentrations of the drug when compared with no pregnant women (38).

Pregnancy significantly increases the elimination rate of ampicillin (39). Similar results of the significantly faster elimination rate have also been demonstrated in a pharmacokinetic study on pregnant women and phenoxymethylpenicillin (Peni-cillin V) (40).

Erythromycin (except erythromycin estolate) (41,42), clindamicin - both pregnancy risk C, and metronidazole - pregnancy risk B, are believed to have minimal risk (43).

The greatest concern regarding antimicrobial use is the agents that have limited indications in dentistry: aminoglycosides (gentamycin) cross the placenta and might theoretically cause otological and perhaps nephrological damage to the fetus. No proven cases of intrauterine damage by gentamicin and tobramycin have been recorded (41).

Tetracycline therapy in the second and third trimester of pregnancy have been implicated for causing tooth discoloration and inhibition of bone

development in infants. In view of their effects on the teeth and the bones, as well as in view of an increased risk of potentially fatal fatty liver degen-eration in pregnant women, tetracycline prepara-tions should not be prescribed during pregnancy with the exception of a vital indication (44,45).

Chloramphenicol is contraindicated in preg-nancybecause of maternal toxicity and fetal circulatory failure called gray baby syndrome (46).

Sedatives - anxiolytics

Benzodiazepines (pregnancy risk D) are anx-iolytic drugs commonly prescribed in pregnancy. They readily pass from the mother to the fetus. Pregnant women may have some risk of congenital malformation if exposed to benzodiazepines during the 1 st trimester, although data are contradictory and any real effect would appear to be minimal (47,48). The pregnant women should avoid ben-zodiazepines if possible, during late pregnancy and labour, because floppiness, apnea and withdrawal in the infant can pose obvious clinical problems (49). A single exposure to a clinically acceptable dose of any benzodiazepine, as compared to chronic therapy throughout pregnancy, would have minimal risk (50).

Drugs and breast milk

Breastfeeding of the newborn child has increased during the past ten years in the US and European countries. This, in combination with the explosive growth in the number of new pharmacologic agents concerns over environmental contaminants could be a risk for the breastfeeding infant. Medical pro-fessionals too often simply discourage breastfeeding instead of investigating whether the drug enters breast milk and poses a risk to child or not (51,52).

Human milk represents a complex solution of proteins, carbohydrates, fat, and liquid with a composition similar to that in serum. Its com-position varies during the weeks and the months of lactation as well as during a single feeding. Human milk has a pH of approximately 7.0, which influences the distribution of drugs from the maternal circulation into milk. To enter human milk, a drug leaves the maternal circulation and enters the breastalveolar cells by diffusion across cell membranes or into water-filled channels or through binding to carrier proteins. Since milk is more acidic than plasma basic compouds may be slightly concen-trated in this fluid, and the concentration of acidic compounds in milk is lower than in plasma. Non-electrolites, such as ethanol and urea, readily enter breast milk and reach the same concentration as in plasma, independent of the pH of the milk

For most drugs, the milk concentration is similar to that in the maternal circulation. The usual percentage of the maternal dose transferred to the infant ranges from 0.05% to 2%. Most drugs taken by the mother pose no hazard to the child, but there are exceptions. Practical measures can be used to minimize the passage of drug into milk, e.g., breastfeeding just before the administration of medication so that a significant amount of the drug can be eliminated before the next feeding. Few drugs are considered to be contraindicated during breastfeeding and should be avoided. For some drugs a temporary cessation of breastfeeding is required, some of them must be given with caution during breastfeeding and for some with unknown drug effects care is necessary (Table 4).

When dental treatment is needed to maintain a breastfeeding womans oral health selecting the safest agents is the basic principle of therapy (54). The therapeutic agents most commonly used in dental care are local anesthetics. Low concentrations of lidocaine and its metabolite monoethylglycinexy-lididehave been found in breast milk after a dental procedure, but no risk seems to be involved (55).

Tetracaine (20 times as toxic as procaine) marked serious systemic side effects can develop owing to rapid absorption following topical use (56).

For alleviation of the mother’s oral pain periph-ererally acting analgesic-antipyretic can be used. However salicylates are distributed into breast milk and the use of aspirin should be avoided during breastfeeding (possible association with Reyes syn-drome!) (5). Paracetamol is also excreted into breast milk in low concentrations, but no adverse effects have been reported, so it can be a drug of choice.

Penicillins and cephalosporins are excreted in breast milk and their use, particularly penicillin G and V, in breastfeeding women may sensitize the infant to penicillins

Aminoglycosides are excreted in small amounts in breast milk. An alternative feeding method is recommended during therapy, because the half-life of aminoglycosides is prolonged in neonates owing to the immaturity of their renal system (58).

Tetracycline are excreted in breast milk and should not be used in breast feeding women because of the risk of discoloration of teeth, enamel defects and retardation of the childs bone growth (59).

Chloramphenicol is unsafe. The drug is excreted in milk in low concentrations, posing a risk of bone marrow depression and a slight risk of “gray baby sindrome” (60).

Clindamycin, lincomycin, metronidazole and sulphonamide should be avoided (5).

Erythromicin can be used with cautioun (

Non-Steroidal Anti-

Inflammatory Drugs

Chemical mediators

Inflammatory Process

A normal, beneficial process that begins

immediately after injury to facilitate repair

and return the tissue to normal function

Initiated by stimulus including physical

trauma, radiation, chemicals, heat,

infection, and hypersensitivity

Causes the release of chemical mediators

Arachidonic acid metabolites

Definition:

are compounds released by one cell type that attach to the

receptor of a second cell type to affect the response by that

second cell

Contained in mast cells and basophils

Histamine- increases vascular permeability, increases

blood flow to injured area

Leukotrienes and prostaglandins- pain response, vascular

permeability, and chemotaxis

Phagocytes- neutrophils and macrophages remove debris

Serotonin- increases capillary blood flow and vascular

permeability


Arachidonic acid is an unsaturated fatty acid that is the

substrate for the production of compounds

(metabolites) that contribute to the inflammatory

response

Metabolites of arachidonic acid are also known as

eicosanoids

Arachidonic acid contributes to symptoms of

inflammation, including redness, swelling, and pain

Phospholipase A2 catalyzes the intracellular release of

arachidonic acid from the phospholipids


Follows one of two pathways:

cyclooxygenase (COX)

lipoxygenase (leukotriene)

Pathways lead to four eicosanoid mediators

prostaglandins (PGs)

prostacyclin (PGI2)

thromboxanes (TXs)

leukotrienes (LTs)

The COX pathway leads to the production of TX, PG,and

PGI2

Two forms of COX enzyme, known as isoforms

COX-1- produced in most tissues at a stable rate

COX-2- produced in the brain, female reproductive tract, blood

vessel walls, and kidneys

Production is also induced by tissue injury

Analgesic

Is a drug that selectively relieves pain by acting in the

CNS or on the peripheral pain mechanisms, without

significantly altering consciousness.

Analgesics relieve pain as a symptoms without

affecting its cause.

Analgesics are divided into two groups

1) Opioid /narcotic/ morphine like analgesics.

2) Nonopoid/ non-narcotic/antipyretic/aspirin-like

analgesic or nonsteroidal antiinflammatory

drugs(NSAIDs)

Analgesic

NSAIDs are more commonly employed for dental pain

because tissue injury and inflammation due to tooth abscess,

caries , tooth extraction ,etc…..,is the primary cause of acute

dental pain.

NSAIDs have analgesic , antipyretic and antiinflammatory

actions in different measures.

In contrast to morphine

1) they don’t depress CNS

2) don’t produce physical dependence

3) have no abuse liability

4) are particularly effective in inflammatory pain

classification

1) Nonselective COX inhibitor (conventional NSAIDs)I. Salicylates : aspirin

II. Propionic acid derivatives: Ibuprofine, Ketoprofine

III. Aryl-acetic acid derivatives: Diclofenac

2) Analgesic –antipyretics with poor antiinflammatory

action

Paraminophenol derivative: Paracetamol(Acetaminophen

Beneficial actions due to PG synthesis inhibition:

Book p.316

Shared toxicities due to PG synthesis inhibition:

Book p.316

Adverse effects of NSAIDs

P.318

A- Mechanism of action: They exert their action through inhibition of cyclooxygenase enzyme (COX) causing decrease in the formation of inflammatory mediators (prostaglandins, prostacyclin's and thromboxane's).

There are 2 types of COX:

COX-1: it is the constitutive form, present in many normal tissues.COX-2 : it is the inducible form, produced at site of inflammation (not found in normal tissues)

The pharmacological effects of NSAIDs include: Analgesic, Antipyretic, Anti-inflammatory,Antiplatelet effects .

B-Acetylsalicylic acid (Aspirin)

It is the prototype of the NSAIDs.It is the only NSAIDs that causes irreversible inhibition of both COX-1 and COX-2. Its action is dose dependent.N.B.: Aspirin is available in all forms. Enteric coated aspirin tablets are less gastric irritant but slow in absorption

1-Therapeutic uses of Aspirin:Antipyretic: in feverish conditions.Analgesic & Anti-inflammatory: e.g. headache, toothache, musculoskeletal disorders as rheumatoid arthritis, rheumatic arthritis and osteoarthritis. Anti-platelet: low dose aspirin is used as a prophylaxis against thrombo-embolism in angina, myocardial infarction, post angioplasty, atrial arrhythmia, cerebro-vascular diseases, etc…Keratolytic (local salicylic acid): removal of warts & corns.

2-Adverse effects:Gastrointestinal irritation : gastritis, gastric erosions, ulcers, bleeding.Hypersensitivity: bronchospasm (aggravation of asthma), rhinitis, nasal polyps, skin rash. Bleeding tendency: due to; decrease platelet aggregation & prothrombin synthesis.Renal impairment: analgesic nephropathy(chronic renal failure with prolonged use), fluid retention.Hepatotoxicity.Prolonged labor due to inhibition of uterine contraction.Reye’s syndrome: rare, fatal sever hepatic injury associated with encephalopathy. Occurs if aspirin is used in febrile viral infections in children less than 12 years.Salicylism (low grade aspirin toxicity): vertigo, tinnitus, deafness–often first signs of toxicity.

3-Aspirin overdose (Acute Toxicity): Extensions of the toxic actions described above, plus at high doses:Vasomotor collapse occurs with respiratory, Renal failure, Hyperpyrexia, Dehydration Convulsions.

4- Drug-Drug interactions:

Antagonizes the uricosuric effects of probenecidand the antihypertensive effect of antihypertensive (e.g. ACE inhibitors, beta blockers and loop diuretics).Increases the plasma concentration of anticoagulants.

5-Other salicylic acid derivatives:Non acetylated salicylate ( sodium salicylate, magnesium salicylate ) are less gastric irritants but less effective.

5-aminosalicylic acid ( mesalamine ) is less absorbed and used for treatment of inflammatory bowel disease(local action).Diflunisal: more potent than aspirin, has little antipyretic action, used mainly for osteoarthritis.

C- Other non-steroidal anti-inflammatory drugs: They may be better tolerated than aspirin.1-Non selective COX inhibitors: They inhibit both COX-1 and COX-2 (as aspirin)Acetic acid derivatives:Carboxylic acetic acid: Indomethacin, Sulindac, TolmetinPhenyl acetic acid: DiclofinacPropionic acid derivatives: Ibuprofen, Ketoprofen, Fenoprofen, Naproxen, Ketorolac.Fenamic acid derivatives: Mefenamic acid, Flufenamic acidPyrazolone derivatives: Azapropazone, Phenylbutazone, Oxyphenobutazone.Oxicams: Piroxicam, Meloxicam, Tinoxicam

2-Selective COX-2 inhibitors:

Celecoxib,

Rofecoxib

Their primary differences from other conventional

NSAIDs are:

Less gastrointestinal toxicity.

Less antiplatelet action.

They have been withdrawn from market because

of cardiovascular risk

D- Paracetamol (Acetaminophen):

1- Mechanism of action: Inhibition of cyclooxygenases in CNS not in peripheral tissues.

2- Pharmacological effects: Analgesic, Antipyretic No significant anti-inflammatory effect.

3- Comparison with Aspirin:

No antiplatelet action, No bronchospasm, Gastrointestinal irritation is minimal, Not implicated in Reye syndrome

4- Adverse effects:

Hepatotoxicity,

Nephrotoxicity.

5- Paracetamol overdose (Acute Toxicity):

The toxic metabolites increase causing:

Nausea, Vomiting, Diarrhea, Abdominal pain Hepatic-renal failure.

6- Management of Paracetamol Overdose:

N-acetylcysteine within the first 12 hours can protect against toxicity.

Narcotic AnalgesicsI. Overview of Narcotic Analgesics.

A. Description. They are classified according to their source. Opium, the parent compound, is composed of more than 20 distinct alkaloids including morphine, a pure substance of opium.

B. Action: narcotic analgesics reduced pain by

stimulating opiate receptors in the CNS. In doing this, they mimic the analgesic effect of naturally occurring brain opiates called endorphins.

C. Indications: used for relief of moderate to severe pain.

D. Overview of nursing management. Assess the client’s pain after drug administration.

Assess the client’s respiratory status. Respiratory depression can occur with even small doses of narcotics

because they reduce the sensitivity of the brain stem (respiratory centers)to increases in carbon dioxide tension.

Note that drowsiness and sedation are characteristics features of more potent narcotics and they have a role in their

analgesic effects, so the nurse must know the client’s baseline mental status to evaluate how the drug is affecting the client’s state of mind.

Be aware that nausea and vomiting may occur because

narcotics stimulate the chemoreceptor trigger zone on the medulla. To minimize nausea and vomiting, administer

antiemetics drugs such the phonothiazine or diphenhydramine as prescribed.Narcotics are prescribed to be administered PRN. Analgesia is markedly improved when given around the clock on a regularly scheduled basis

6. Note that a narcotic antagonist(Naloxone( Narcan)) must be available when administering narcotics IV in case respiratory depression becomes life-threatening.

E. Contraindications / cautions.

Narcotics are contraindicated in patients with

hypersensitivity to the drug. Respiratory insufficiency

or depression, severe CNS depression, hart

failure secondary to chronic lung disease;

cardiac arrhythmias, increased intracranial or

cerebrospinal fluid pressure, head injuries, brain

tumors, acute alcoholism and delirium, tremers,

convulsive disorders, post biliary tract surgery,

suspected acute abdomen, and surgical anastomosis.

Clients taking monoamine oxidaze (MAO) inhibitors should not receive

narcotics either together or within 14 days of MAO inhibitor treatment.

Use with caution in clients with excessive respiratory secretions or decreased ventilation because narcotics depress the respiratory center,

decrease ciliary activity, reduce the cough reflex.

Use with caution and in reduced dosage in clients currently receiving other narcotic analgesics, general anesthetics, phenothiazine, other tranquilizers, sedatives, hypnotics, tricyclic antidepressants, and other CNS depressants (including alcohol).

5. Be aware that rapid IV injection of narcotic analgesics increases the possibility of side effects such as hypotension and respiratory depression. F. Side / adverse effects.

CNS: depression of CNS seen as dizziness, sedation, confusion, drug dependence, CV: hypotension and sock.Resp: respiratory depression is a major side effect. Hypercapnia and hypoventilation, resulting in cerebrovascular dilation and increased intracranial pressure may occur.

GI: constipation, nausea and vomiting, spasm in the sphincter of oddi.

GU: can cause spasms in the urinary bladder.

G. Common narcotics analgesics( natural and synthetic)

1.Morphine. ( natural occurring opium alkaloid)2. Codeine: ( has Antitussive effect)3. Fentanyl , Alfenatnil,Sufentanil:( most often used in anesthesia)4. Meperidine (Demerol) : ( frequently prescribed synthetic drug)5.Methadone( Dolophine) : (synthetic)

عرض تقديمي1

Health & Medicine

typical prescription

medication order abbreviation

medication orderprescriptions

specific medication

medication orderslide

medication ordertable

medication orderin hospitals

medication orderby definition