مراجعة فارماكولوجى للخريجين

[اميرة بدينها2]

السلام عليكم ورحمة الله وبركاته
إن شاء الله سوف أنقل لكم بعض تلخيصات الفارما لخريجى صيدلة والموضوع منقول للأمانة من مواقع أخرى نبدأ الآن باسم الله:

The autonomic nervous sysyem
Anatomy

I-Efferent neurons
Carries nerve impulses from the CNS to the effector organs by way
of 2 types of efferent neurons

a) a preganglionic neuron
Its cell body located within the CNS
Emerge from the brain stem or the spinal cord
Make a synaptic connection in ganglia which act as arelay station between the preganglionic neuron and the postganglonic neuron

b) a postganglionic neuron
Its cell body originating in the ganglia
Terminates on effector organ such as
Smooth muscle of the viscera
Cardiac muscle
Exocrine glands

II- Afferent neurons
are important in the reflex regulation of this system
ex: sensing pressure in the carotid sinus and aortic arch and signaling the CNS to influence the efferent branch of the system to respond
Sympathetuc neurons

The preganglionic neurons of sympathetic system
Come from thoracic and lumber regions of the spinal cord
Synapse in 2 cord-like chains of ganglia that run parallel on each side of the spinal cord
Axons of the postganglionic neurons extend from these ganglia to glands & viscera

Special case : (The adrenal medulla) : acts like the sympathetic ganglia
a)receives preganglionic fibers
b)lacking axons
c) if stimulated,it secretes the hormone(epinephrine= adrenaline) + less amount of norepinephrine which influence other organs

Parasympathetic neurons

The preganglionic fibers
arise from the cranial and sacral areas of the spinal cord
synapse in ganglia near the effector organs

In both : postganglionic fibers extend from the ganglia to the effector organs

Function of the sympathetic system
Not essential for life
Has the property of adjusting in response to stressful situations such as

trauma - fear - hypoglycemia - cold - exercise

Effects of stimulation of the sympathetic devision
increase heart rate
increase blood pressure
mobilize energy stores in the body
increase blood flow from the skin to skeletal muscles and heart
diverting flow from the skin and internal organs
stimulation of the pupils and bronchioles
i.e : Fight &Flight response due to
Direct sympathetic response
Stimulation of adrenal medulla to release epinephrine and norepinephrine

Functions of the parasympathetic system
Essential for life
Maintain essential body functions
Usually acts to oppose or balance the actions of the sympathetic division
It is a dominant over the sympathetic division in rest & digest stimulation
Affect specific organs such as stomach and eye

Innervation by the autonomic nervous system

I- dual innervation

Most organs in the body are innervated by both divisions
'ex : the heart has
a) vagal parasympathetic innervation which slows the rate of contraction
b) sympathetic innervation speeds contraction
c)the vagus is the predominant controlling factor for rate

II- Organs receiving only sympathetic
examples
Adrena medulla
Kidney
Pilomotor muscle
Sweat glands

N.B :the control of blood pressure is also mainly a sympathetic activity
Neurotransmitters

Cholinergic and adrenergic neurotransmitters are the primarily chemical signals in the autonomic nervous system
The autonomic nerve fibers can be classified into 2 groups based on the chemical nature of the neurotransmitter released

Acetyl choline
Released from the preganglionic neurons in
both parasympathetic and sympathetic
in adrenal medulla
in neuromuscular junction

Norepinephrine & epinephrine
In sympathetic.it is released from the postganglionic neurons to the
effector organs

يتبع إن شاء الله

[~باغية الجنان العلى~]

أميرة بدينها

جزيتِ خيرا أخيتي
ونفع الله بكِ
هذا لا ينفع الخريجين فقط
بل ايضا يقدم المادة للطلبة بصورة عامةحتى يسهل عليهم
ننتظر جديدكِ ونورتِ قسمنا

[اميرة بدينها2]

جزاك الله خيرا أختى الكريمة ونفع الله بك وسدد خطاك على هدى النبى صلى الله عليه وسلم

[اميرة بدينها2]

Introduction to pharmacology

I- Routes of drug administration : 2 major routes

A- Enteral

Oral
the most common route
the most variable mode in amount of drugs reach the target tissues
some drugs are absorbed from the stomach
most drugs are absorbed from the duodenum
most drugs absorbed from GIT enter the portal circulation and encounter the liver before they are distributed in the general circulation
first pass ****bolism by intestine or liver limits the efficacy of many drugs when taken orally

Sublingual
the drug diffuses to the systemic circulation directly

Rectal
fifty percntage of the drug bypass the portal circulation
Useful if the drug
destructed by the intestinal enzymes
destructed by the low pH of the stomach
induce vomitting or the patient himself is vomitting

B- Parenteral

I.V
the most common parenteral route
drugs avoid first pass ****bolism
permit a rapid effect
permit the maximal degree of control over the circulating levels of drug
the rate of infusion must be carefully controlled

I.M
main route used for depot preparations which dissolves slowly providing a sustained dose over an extended period of time
used also for many aquous solutions of drugs

S.C
as I.M it requires absorbtion
slower than I.V
minimizes the risks associated with I.V injections

Others

Inhalation
provides rapid delivery of drug producing rapid effect almost as that of I.V
Intranasal e.g salmon calcitonin used in osteoporosis
Intrathecal e.g methotrexate in leukemia
Intraventricular
Topical when local effect of the drug is required
Transdermal e.g nitroglycerine when used as antianginal




II- Absorbtion of drugs

the transfer of a drug from its site of administration to
blood streem
the rate and the efficiency of absorbtion depend on the route of administration so in

I.V : Complete absorbtion
Other routes : partial absorbtion which lowers the bioavailability

A- Transport of drugs from GIT

depending on their chemical properities drugs may be absorbed from GIT by


Passive diffusion
Active transport


B- physical factors influencing absorbtion

blood flow to the absorbtion site
total surface area available for absorbtion
contact time at the absorbtion surface


III-Bioavailability

the fraction of administerd drug that reaches the systemic circulation in a chemically unchanged form

ex : if 100 mg of the drug is administrated orally and 70 mg of this drug is absorbed unchanged ..the bioavailability is 70%

Factors that influence bioavailability

first pass hepatic ****bolism
solubility of the drug
chemical instability
the nature of the drug formulation


IV-Drug distribution

the process by which a drug reversibly leaves the blood stream and enters the interstitium (extracellular fluid) and/or the cells of tissues

Factors affect drug distribution

A- blood flow

B- capillary permeability which determined by

Capillary structure
ex : blood brain barrier : lipid soluble drugs readily penetrate to the CNS since they can dissolve in the membrane of its endothelial cells but ionized or polar drugs generally fail to enter the CNS

Drug structure

Binding of drugs to proteins

reversible binding to plasma proteins sequesters drugs in a non diffusible form and slows their transfer out of the vascular compartment



V-Binding of drugs to plasma proteins

Usually albumin

bound drugs are pharmacologically inactive ...only the free unbound drug can act on target sites in the tissues and elicit a biological response
so hypoalbunemia may alter the level of free drug

A- Binding capacity of albumin

binding of drugs to albumin is reversible
albumin may show

Low capacity : one drug molecule per albumin molecule
High capacity : a number of drug molecules per single albumin molecule

albumin has the strongest affinity for anionic drugs(weak acids) and hydrophobic drugs

most hydrophilic drugs and neutral drugs do not bind to albumin

many of drugs are hydrophobic by design since this property permits absorbtion after oral administration

B- Competition for binding between drugs & clinical imprtance of drug displacement

ex : Tolbutamide is normally 95% bound and only 5% free so 95% is inert in its pharmacological action

sulfonamid with higher affinity for albumin if adminiserd it displaces tolbutamide and now 100% of tolbutamide become free in plasma

but note that.... the tolbutamide concentration does not remain elevated since the drug moves out of the plasma into the interstitial fluid and avhievs new equilibrium


VI- Drug ****bolism

drugs are most often eleminated by biotransformation and/or excretion into the urine or bile

The liver is the major site for drug ****bolism

Specific drugs may undergo biotransformation in other tissues

some agents are initially administerd as inactive compounds(prodrugs) and must be ****bolized to thir active forms

[يمامة المسجد]

جزاكم الله خيرا ً

هل ستتناولي أهم الأدوية المتداولة ؟؟؟؟

اليوزيز والمود اوف اكشن والسايد افيكت ؟؟؟

[اميرة بدينها2]

السلام عليكم ورحمة الله وبركاته
إن شاء الله هيكون الكلام عن مرض معين مثلا ال بيصيب الجهاز التنفسى والادوية المستخدمة وإن شاء الله أحاول أجيبلك
mode of action
side effect
وإن شاء الله يعيننى الله على ذلك

[moslma lillah]

وعليكم السلام ورحمة الله وبركاته
بارك الله فيكِ اختنا
هل انتي دكتورة ؟

[اميرة بدينها2]

السلام عليكم ورحمة الله وبركاته
دى محاضرات فارما شرح جزء AUTONOMIC إن شاء الله تستفيدوا منها
ويا رب تكون الروابط صحيحة

http://hotfile.com/dl/103493045/3038c46/Autonomic.1.Dr.Said.Abd.Elhady.mp3.html
http://hotfile.com/dl/103493655/0654856/Autonomic.2.Dr.Said.Abd.Elhady.mp3.html
http://hotfile.com/dl/103494362/d622a0e/Autonomic.3.Dr.Siad.Abd.Elhady.mp3.html

http://hotfile.com/dl/103501147/a967b7b/Autonomic.4.Dr.Said.Abd.Elhady.mp3.html

[اميرة بدينها2]

Drugs affecting the cardiovascular system
Treatment of congestive heart failure CHF

I- Overview of congestive heart failure CHF

it is a condition in which the heart is unable to pump sufficient blood to meet the needs of the body
it can be caused by
impaired ability of the cardiac muscle to contract
an increesed work load imposed on the heart

CHF is accompanied by abnormal increase in blood volume and interstitial fluid
the heart,veins,and capillaries therefore generally dilated with blood.Hence,the term (Congestive) heart failure

Underlying causes of CHF

arteriosclerotic heart disease
dilated cardiomyopathy
congential heart disease
valvular heart disease
left systolic dysfunction secondary to coronary artery disease is the most common cause of CHF

The therapeutic goal for CHF is to increase cardiac output

Three classes of drugs have been shown to be clinically effective in reducing symptoms and prolonging life
Vasodilators: reduce the load on the myocardium
Diuretic agents : decease extracellular fluid volume
Inotropic agents : increase the strength of contraction of
cardiac muscle

these agents
relieve the symptomps of cardiac insufficiency
do not reverse the underlying pathologic condition

Drugs that may preciptate or exacerbate CHF so should be
avoided as possble

non steroidal antiinflammatory drugs
alcohol
B blockers
calcium ghannel blockers
some antiarrythmic drugs


II- Vasodilators
In CHF,the impaired contractile function of the heart is exacerbated by compensatory increase in preload and afterload

Preload
the volume of blood that fills the ventricle during diastole
elevated preload causes overfilling of the heart which increases the work load
Afterload
the pressure that must overcome for the heart to pump blood into the arterial system
elevated afterload cause the heart to work harder to pump
blood into the arterial system

Vasodilators are useful in reducing excessive preload and afterload as follow
dilation of veinous blood vessels increases the venous capacitance by which a decrease in preload occurs
arterial dilators reduce systemic arteriolar resistance by which a decrease in afterload occurs

Classes of vasodilators

A- Angiotensin convertizing enzyme (ACE) inhibitors
ex : captopril - lisinopril - enalapril

Adverse effects

postural hypotension
renal insuffeciency
persistant dry cough
should not be used in pregnant women

B - Direct smooth muscle relaxants
ex: hydrazaline - isosorbide - sodium nitroprusside

III - Diuretics
ex : bu****nide - furosemide - hydrochlorothiazide

relieve pulmonary congestion and peripheral edema
useful in reducing the symptoms of volume overload
Thiazide diuretics are relatively mild diuretics and lose efficacy if patient creatinine clearance is less than 50 ml/min
Loop diuretics are used in patients with renal insuffiency
Overdoses of loop diuretics can lead to profound hypovolemia

IV- Inotropic agents

positive inotropic agents enhance cardiac muscle contractility
and increase cardiac output

although these drugs act by different mechanisms ,in each case the inotropic action is the result of an increased cytoplasmic calcium concentration that enhances the contractility of the cardiac muscle

A-Cardiac glycosides(Digitalis)=digoxin &digitoxin

digoxin(lanoxin) is the most widely used agent

Therapeutic uses

digoxin is indicated in patients with severe left ventricular systolic dysfunction after initiation of diuretic and vasodilation therapy
not indicated in patient with diastolic or right sided heart failure
patients with mild to moderate heart failure will often respond to treatment with ACE inhibitors and diuretics and do not require digoxin

N.B. The digitalis glycosides show only a small difference between a therapeutically effective dose and doses that are toxic or even fatal i.e. have low therapeutic index

Factors predisposing to digitalis toxicity

a) Electrolytic disturbances

hypokalemia can preciptate serious arrythmia
reduction of serum K levels is most frequently observed in patients receiving thiazide or loop diuretics
hypokalemia can be usually prevented by use of a K sparing diuretics or supplementation with potassium chloride
hypercalcemia and hypomagnesemia also predispose to digitalis toxicity

b)Drugs

Quinidine : can cause digitalis toxicity by
displacing digitalis from plasma protein binding sites
competing with digitalis for renal excretion
Verpamil(isoptin) : displace digitalis from( PPBS) and can increase digoxin levels by 50 to 75% which may require a reduction in the dose of digoxin

c)Others

potassium depleting diuretics
corticosteroids
hypothyrodism
hypoxia
renal failure
myocarditis

B- B adrenergic agonists
ex : dobutamine

improves cardiac performance by both
positive inotropic effects

vasodilation
must be given by I.V. infusion and is primarily used in the
treatment of acute heart failure in hospital setting

C- Phosphodiesterase inhibitors : not used clinically

thanks






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