Nervous system

Nervous system   

A. Central Nervous System(CNS)                     b. Peripheral Nervous System(PNS) 

Brain and spinal cord                                            Outside the brain and spinal cord

 

1-Sympathetic	2- Parasympathetic	3- Enteric neurons
(Thoraco-Lumbar outflow) *Preganglionic neurons arise from thoracic and lumbar regions (L1 to L2) of the spinal cord.	(Cranio-Sacral outflow) Preganglionic neurons arise from cranial nerves 24 3rd (Oculomotor) 7th (Facial) 9th (Glossopharyngeal) 10th (Vagus) and from 2nd 3rd and 4th sacral segments.	It is a collection of nerve fibers that innervate the GIT, pancreas, and gallbladder, and it constitutes the "brain of the gut". This system functions independently of the CNS and control the motility, exocrine and endocrine secretions. - It is modulated by both the sympathetic and parasympathetic nervous system.
- Consist of short preganglionic fibers and long postganglionic fibers.	- Consist of long preganglionic fibers and short postganglionic fibers.
Chemical transmitters  - Adrenaline & Nor-adrenaline.  Except: Thermoregulatory (Eccrine) sweat gland & adrenal medulla they release ACh.	Chemical transmitters   - ACh (Acetylcholine).

Most organs in the body are innervated by both divisions of the ANS

(dual innervation)

-Some organs are supplied with one division of ANS:

1.Iris sphincter (pupillary constrictor) muscle (Circular)à Supplied by                       parasympathetic (M3).  

2.Iris dilator (pupillary dilator) muscle (Radial) à Supplied by sympathetic (α1).

3.Arrector pili muscle (pilomotor muscle) Supplied by sympathetic (α 1)àhair erection. The contraction of the muscle is therefore involuntary-stresses  e.g. cold, fear (Goosebumps).

4.Thermoregulatory (Eccrine) sweat gland àSupplied only by sympathetic fibers, but through cholinergic (parasympathetic) receptors (M3).

5.Blood Vessels Vascular smooth muscle is innervated primarily by the sympathetic and indirectly non-innervated by the parasympathetic. 

I.e. Direct acting à innervated sympathetic à α1 receptor (Vasoconstriction).

     Indirect acting Non-innervated parasympathetic M3 receptors (Vasodilatation) via the nitric oxide (NO)/endothelium derived relaxing factor (no direct innervation).

Role of the CNS in the control of autonomic function:

 ANS is provided by streams of afferent impulses, originating in the viscera and other autonomically innervated structures that travel to integrating centers in the CNS, such as the hypothalamus, medulla oblongata and spinal cord. These centers respond to the stimuli by sending out efferent reflex impulses via the ANS.

Reflex arc: A reflex arc is a neural pathway that controls an action reflex. Most of the afferent impulses are involuntarily translated into reflex responses. For example a fall in blood pressure causes pressure- sensitive neurons (baroreceptors in the heart, vena cava, aortic arch, and carotid sinuses) to send fewer impulses to cardiovascular centers in the brain. This prompts a reflex response of increased sympathetic output to the heart and vasculature and decreased parasympathetic output to the heart, which results in a compensatory rise in blood pressure and tachycardia. 

 

 

Chemical transmitters in the ANS:

1.Chemical transmitter for parasympathetic is Acetylcholine (ACh). 

2.Chemical transmitter for sympathetic is mainly Adrenaline (Epinephrine) and Noradrenaline (Nor-epinephrine). 

3.Other transmitters involved: called Non-Adrenergie Non-Cholinergic (NANC) transmitters. Some of the NANC found in peripheral nervous system:

-Nitric Oxide (NO)                                                             -ATP                                 

-Serotonin (5-HT)                                                              -Dopamine                                -Neuropeptide Y (NPY)                                                     -Vasoactive Intestinal Peptide (VIP)

-Gamma-amino-butyric Acid.                   

-Calcitonin gene-related peptide (CGRP) and Substance P. 

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DRUG INTERACTIONS

Types of Agonists

1. Full Agonists

-  If a drug binds to a receptor and produces a maximal response that mimics the response to the endogenous ligand.

2.Partial Agonists

-  Produces a partial response that mimics the response to the endogenous ligand.

3.Inverse Agonists 

-  Produce a response below the baseline response measured in the absence of drug. - Decreases the number of activated receptors.

 

Regulation of receptors:-

•       Continuous stimulation of receptors with agonists à Decrease number of receptors and decrease sensitivity   à    Down regulation. 

•       Continuous blocking of receptors with antagonists à Increase number of receptors and Increase sensitivity à                       Up regulation.

DOSE

-Def. The amount of drug given to the patient at a time.

-Types of dose :- 

ü  Therapeutic dose:                The average dose that produce therapeutic effect.

ü  Maximum tolerated dose:  The largest dose of a drug that can be taken safely.

ü  Initial dose:                            The dose used at start of treatment. 

ü  Maintenance dose:              The dose required to maintain the therapeutic effect.

ü  Lethal dose or Fetal dose:  The dose that produce death.

Therapeutic Index (TI):-

Def. It is the ratio of the dose that produces toxicity in half the population (TD50)  to the dose that produces a clinically desired or effective response in the half of population (ED50).

TI = TD50/ED50                                            

Therapeutic index used for Measure of drug safety.                                         

                                                                                                                                                                           

N.B: Quantal dose response curve gives information about differences in the sensitivity of individuals to increasing doses of drugs.

 

Standard margin of safety (SMS) 

• Def. = The ration of the dosage required to kill 1% of population compared to the dosage that is effective in 99% of population. 

The higher margin of safety the better and safer.

 

Factors affecting the dosage and action of the drug :-

1: Age, weight and body surface area:

 Adult dose (20 - 60 years of age) and weight about 70 kg.

-Elderly required small dose (due to decrease renal excretion and decrease hepatic metabolism). 

-Children required small dose (due to immature kidney and liver and decrease plasma protein).

 

2: Sex: 

Female need smaller dose than male due to :

a.High fat content à Increase fate in the body à Slow rate of oxidation decrease metabolism à Increase drug effect. 

b.Effect of sex hormone (Estrogen) on liver Microsomal enzyme (LME). * Some drug avoided during pregnancy, lactation and menstruation. 3: Routes of administration: • IV > IM > SC > Oral 3: Genetic abnormality.

 

 

 

 

4: Tolerance :-

Def. Failure of responsiveness to the usual dose. 

Types of tolerance: 

a.Congenital Tolerance .

b. Acquired Tolerance 

ü  Cross Tolerance: Between Nicotine and Lobeline (similar). 

ü  Tachyphylaxis  : rapidly diminishing response to successive doses of a drug, rendering it less       effective. e.g. Ephedrine Sudden increase blood Pressure then decrease (Gradually). 

ü  Bacterial resistance to antibiotics.

Mechanism of acquired tolerance (Drug desensitization)

Receptor Mediated	Non-Receptor Mediated
Reduction of receptor numbers. (Down-regulation of receptor)	Physiological adaptation Reduction of receptor-coupled signalling component. Change in kinetics of drugs.

 

 

Drug dependence:-

 It usually occurs with CNS acting drugs. 

It is a phenomena related to tolerance. 

It involves a certain degree of tissue adaptation. 

Withdrawal of the drug could produce certain unpleasant symptoms. Types of dependence:-

Habituation	Addiction
-                      Mild degree of drug dependence.  - Psychic dependence.  -When drug stopped develop some emotional distress for a relative short period.  -                      E.g. Smoking and Coffee.	More serious form of drug dependence. -                      Psychic and physical dependence.  -                      When drug stopped Withdrawal symptoms reverse the normal pharmacological action.  -E.g. Morphine and Heroin.

 

 

DRUG INTERACTIONS

A- Pharmacokinetics Interactions

B-Pharmacodynamics Interactions.

	Increase in drug effects
Addition (Summation) Algebraic sum of the 2 drug effect.  1+1 = 2               E.g. Acetylcholine + Histamine in contraction of intestine.	Potentiation - Drug which increase the effect of other drug.  0 +1 >1   E.g. Physostigmine +Acetylcholine	Synergism  - The combination effect more than algebraic sum .  1 + 1 > 2

 

 

Decrease in drug effect (Antagonism)
Chemical  antagonism   - Chemical interaction between 2 drugs decrease absorption. - E.g. Heparin + Protamine sulfate	Pharmacological antagonism - 2 drugs act on the same receptor but one of them is ü  Non-competitive ü  Competitive	Physiological (Functional) antagonism - 2 drugs act on 2 different receptors Different mechanism of action → Different effect.

 

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Pharmacokinetic parameters & Pharmacodynamics

Pharmacokinetic parameters

1) Bioavailability :-

Def. The amount of administered drug that reaches the systemic circulation.

Oral bioavailability (F) = AUCOral /AUCIV X 100

AUC = Area under curve

> Factors affecting bioavailability:-

• First pass effect  Decrease bioavailability.

• Physicochemical properties of the drug. (Polarity – solubility – Particle size)

 Nature of formulation. (Solution > Suspension > Tablet)

2) Plasma half-life (t1/2) :-

Def. Time needed by the body to decrease a plasma concentration of drug to its half.

(It depend on clearance and Vd)

3) Clearance (Cl) :-

Def. - It is volume of plasma cleared from the drug per unit time (ml/min).

Cl total = Cl hepatic + Cl Renal + CI Pulmonary + Cl others

4) Elimination Kinetics:-

Zero-order elimination First-order elimination

Def. - Elimination of the drug which is

independently of the drug conc.

For example: 1.2 mg are climinated-

every hour.

Elimination of the drug which is

dependently of the drug conc.

For example: increase drug conc. lead

to increase rate of drug elimination.

Elimination

rate

Elimination rate saturates with higher

drug concentration.

Elimination rate is proportional to

drug concentration.

term Non-linear (Saturation) Elimination Linear Elimination

Curve

Log c

time

log c

Example A few substances are eliminated by

zero-order elimination kinetics

- 95% of the drugs in use at

therapeutic concentrations are

eliminated by first order climination

kinetics.

time

Pharmacodynamics

Def. What the drug does to the body (Mechanism of action of drugs).

Drug-Receptor interactions

D+R=DR

D=Drug R=Receptor DR = Drug-Receptor complex

-Biological effect increase when the drug receptor complex increases.

What is a Receptor?

Any biological molecule to which a drug binds and produces response.

Drug or any substance (activate or inactivate receptor) called Ligand.

Major classes of receptors:-

1_Ligand-gated and voltage-gated ion channels ( E.g. cholinergic nicotinic receptors)

2_G-protein-coupled receptors

3_Enzyme linked (Tyrosine kinase-linked) receptors (E.g. insulin receptors)

4_Intracellular receptors (e.g. Steroid receptors)

G-protein-coupled receptors (GPCRS)

G-protein and second messengers:-

• G-protein → Protein located in the cytoplasm between receptor and cell.

Main types:

I. Gs (Stimulatory):- Activate adenylate cyclase  Increase cyclic adenosine monophosphate

(cAMP) that activate protein kinasethen open Calcium channels and Increase Ca* influx

from sarcoplasmic reticulum (SR).

II. Gi (Inhibitory) :- Inactivate adenylate cyclase  Decrease cAMP  Decrease Calcium

influx.

III. Gq (Stimulatory):- Increase phospholipase-C (PLC)  PLC break phosphatidylinositol

bisphosphate (PIP2) into Inositol triphosphate (IP3) and Diacylglycerol (DAG)  IP3 increase

Calcium influx.

Ligand-receptor interaction (Lock and key theory) :-

What is a Ligand? Any substance combines with receptor.

Types of Ligand:-

• Ligand has affinity and efficacy to Receptor  Agonist

• Ligand has affinity and not have efficacy to Receptor  Antagonist or Blocker

Dose Response Curve:

Emax: maximum response) effect ) produced by the lowest dose.

ED50: The conc. of drug producing 50% of the maximum effect. Usually used to determine potency.

Potency:-

 Potency is a measure of the amount of drug necessary to produce an effect of a given

magnitude.

 Drug A is more potent than Drug B, because a lesser amount of Drug A is needed when

compared to Drug B to obtain 50% effect.

Efficacy:-

 Efficacy is the magnitude response a drug causes when it interacts with a receptor.

 Drug A is more potent than Drug B, but both show the same efficacy. Drug C shows lower

potency and lower efficacy than Drugs A and B.

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Metabolism & Elimination

- The kidney cannot efficiently eliminate lipophilic (Non-Polar) drugs that readily cross cell
membranes and are reabsorbed in the distal convoluted tubules. Therefore, lipid-soluble agents are
first metabolized into more polar (hydrophilic) substances.
- The liver is the main site of drug metabolism.
- Drugs can be metabolized by oxidation, reduction, hydrolysis, hydration, conjugation,condensation, or isomerization.

Metabolism

Definition:-

-(biotransformation) usually conversion of drug from non-polar (active) to Polar (less active) 

more polar (not active)  to facilitate excretion.

Classification:-

Phase I

Reactions convert lipophilic drugs into more polar molecules by introducing or unmasking a polar

functional group, such as-OH or -NH.

Phase I Reactions:

1: Oxidation

2: Reduction

3: Hydrolysis

Phase II

This phase consists of conjugation reactions.

Conjugation may be with :

1: Acetic acid (Acetylation) 3: Sulfate

2: Methylation 4: Glycine 5: Glucuronic acid

Metabolism Enzymes:-

Microsomal Enzymes Non-Microsomal Enzymes

Majority Majority of drug biotransformation reaction Some of drug biotransformation reaction

Site Smooth endoplasmic reticulum. Cytoplasm and mitochondria.

Organs Mainly in liver then kidney, lungs,

intestinal mucosa.

Hepatic cells as well as in other

tissues including plasma.

Phase I - Catalyse oxidative(CYP450)

reductive) & hydrolytic reactions

Catalyse few oxidative , reductive &

hydrolytic reactions.

Phase II Glucuronidation reactions only Also conjugation reaction other than

glucuronidation.

Activity Can be induced and inhibited. Can't be induced and inhibited.

Results of metabolism:-

1-Inactivation e.g. Acetylcholine (Active) Choline + Acetic acid (Inactive).

2- Activation e.g. L-dopa(Inactive) Dopamine (Active).

3- Maintain activation e.g. Diazepam (Active) Nor-Diazepam (Active) .

4- Toxification e.g. Methyl alcohol (Non-toxic) Formaldehyde (Toxic-Blindness)

Factors Affecting Metabolism:-

Age:

Deficiency of liver microsomal enzyme especially child prolonged action of drug lead to increase

toxicity e.g. Chloramphenicol when used in babies cause Grey baby syndrome.

Sex differences:

hormonal activity might affect the activity of certain oxidation Sex differences: Metabolic difference

between sexes have been noted for a number of enzymes.

Genetic factor:

Absence of specific gene responsible for synthesis of special enzyme

State of health:

Presence of disease (liver disease) - Alters in the normal metabolism. which essential for normal metabolism

Inhibition of microsomal enzymes:

Certain drugs inhibits the activity of microsomal enzyme (decrease metabolism rate) leading to prolongation the action of other drugs > increase (drug) activity and may leading to toxicity.

Induction of microsomal enzymes:

Certain drugs increase the activity of microsomal enzyme leading to increase metabolism rate decrease activity of drug other drugs.

- Hepatic microsomal enzyme (HME) inducers 

E.g. Carbamazepine, Phenobarbital, phenotoin and Rifampicin.

- Hepatic microsomal enzyme (HME) inhibitors

E.g. Cimetidine, Chloramphenicol, Omeprazole ,Erythromycin and Ketoconazole

Elimination

Def. The process which involve excretion of drug outside of the body.

Routes of drug excretion (elimination):

1-Kidney:-

Through: 1: Glomerular filtration: For water soluble non bound drugs (Most).

2: Proximal (Active) tubular secretion: e.g. Penicillin.

3: Distal (Passive) tubular reabsorption: For lipid soluble drugs.

Reabsorption may affected by pH:-

- Acidification of urine (Vit. C) Increase excretion of basic drugs.

-Alkalization of urine (NaHCo3) Increase excretion of acidic drugs.

2-GIT :- through Saliva and Bile.

3-Skin :- through sweat gland(Rifampecin) and Breast (milk) Nicotine and Morphine.

4-Lung:- e.g. Anesthetic Gases e.g Nitrous oxide & Halothane .

Method used to prolong duration of action of drugs

Decrease Absorption

1) Add Vasoconstrictor(Adrenaline + local anesthesia).

2) Use sparingly soluble complex.

3) Use of drug in oil (Vasopressin in oil).

4) Use of sustand release (slow release) tablets.

5) Use SC pellet implantation.

Decrease Metabolism Use HME inhibitors .

Decrease Excretion  Probenecid with Penicillin .

Increase protein binding Add methoxy group to sulfonamide

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Pharmacokinetics

Def . Effect of the body on the drug .

Consist of 4 process ( ADME )

1 ) Absorption

Def . Transfer of drug from the site of administration to the systemic circulation

Mechanism of Absorption :

1 : Simple diffusion ( Lipid diffusion )

o From high conc . to low conc . ( Along concentration gradient ) .

o Depend on lipid solubility .

o Not needed energy and carrier .

o The drug must be lipid soluble and small in molecular weight ( Mwt . ) .

 Factors affecting simple diffusion :

1: Dose concentration ( Increase dose concentration Increase absorption

2:Molecular weight & size ( Increase Mwt . Decrease absorption ) .

3 : Ionization ( Water soluble drug ( Ionized ) > Decrease absorption )

4 PH at the site of absorption .

Most of drugs are weak acids or weak bases

Weak acid drugs less ionized in acidic medium---decrease ionization --- Increase Absorption

Weak base drugs less ionized in basic medium---decrease ionization--Increase Absorption

2 : Facilitate Diffusion :

- From high concentration to low concentration ( Along concentration gradient . )

- Need carrier and not need energy

3:Active transport :

-From low concentration to high concentration ( Against concentration gradient ) .

- Need carrier and need energy

4 : Pinocytosis or Endocytosis :

- Drugs of exceptionally large size .

- Engulfment of a drug molecule by the cell membrane . - Eg ( Vitamin B1 + intrinsic factor ) complex

► Factors affecting absorption of drugs :

1 : Patient - Related factors :

Route of administration IV > IM > SC > Oral > Skin .

Absorbing surface area Increase surface - Increase absorption .

Systemic circulation Shock and heart failure decrease absorption .

Presence of other drugs Adrenaline SC=Vasoconstriction( VC ) leads to decrease absorption .

Specific factors E.g. intrinsic factor for Vit . B12 .

2: Drug - Related factors:

o Lipid solubility High lipid solubility drug - High absorption .

o Ionization Non - ionized drugs High absorption .

o Valency Ferrous iron ( Fe ) absorbed more than ferric iron ( Fe ) .

o Nature Inorganic ( Small molecules ) > Organic ( Big molecules ) .

o Pharmaceutical preparation Solution > Suspension > Tablet

o PH of the drug .

2) Distribution

Def. The transfer of drug from the blood stream into interstitium(extracellular fluid) and tissue

Distribution of drug Depend on:

1-Blood flow

Increase blood flow---Increase distribution

Blood flow to the vessel-rich organs (brain, liver and kidney) is greater than that to the skeletal

muscles, adipose tissue and viscera

2-Capillary permeability:

 it depend on capillary structure and the chemical nature of the drug.

 In the liver and spleen(high capillary permeability)—large plasma proteins can pass.

 In the brain only lipid soluble drugs can pass through blood brain barrier(BBB).

3-Binding to plasma protiens:

 Albumin is the major drug-binding protein and may act as a drug reservoir.

 Bound fraction of the drug ---not active (not distributed, metabolized and excreted).

 Free fraction of the drug --- active (not distributed, metabolized and excreted)

 The concentration of free drug decrease due to elimination ---the bound drug dissociates

from the protein (to maintain equilibrium between free-drug and bound-drug).

 Amount of free drug can be increase by:

o 1-Displacement by other drugs.

o 2-Decrease in albumin or plasma proteins.

4- Volume of distribution

Def. The apparent volume of fluid into which an administrated drug is dispersed.

Vd ( Volume of distribution ) = Q ( Total amount of drug in the body ) /Cp ( Plasma concentration of the drug )

 Useful to determine the total amount of drug in the body (Q = Cp×Vd)

 Can be used to calculate the amount of drug needed to achieve a desired Cp:

- ( Vd ) ( target concentration = C1 ) = amount of drug initially in the body .

- ( Va ) ( higher conc . = C2) = amount of drug in the body needed to achieve a desired Cp

The additional dosage needed = Vd ( C2- C1 )

- If the drug has high Vd that means The drug has low affinity to binding to PP.

- If the drug has low Vd that means The drug has high affinity to binding to PP.

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What is Pharmacology?

It is the science that deals with the study of chemical substances (drugs).

The study of drug: - How they work?

- What they are?

- What they do?

What is Toxicology?

It is a branch of pharmacology which deals with the undesirable effects of chemicals and drugs on living system.

Drugs (Therapeutic agent):-

Definition (Def.): Any substance other than food can be used in prevention, diagnosis, or treatment of diseases.

Sources of drugs:

1) Natural 2) Synthetic Plant

Plant e.g. Pilocarpine. Chemically e.g. Sulphonamides.

Animal e.g. Heparin. Genetic engineering (rDNA technology)

Microorganisms e.g. Antibiotics. e.g. Human insulin.

Minerals e.g. Ferrous sulfate.

Names of drugs:

1) Chemical name e.g. Acetylsalicylic acid

2) Generic name e.g. Aspirin

3) Trade name e.g. Rivo

ROUTES OF ADMINISTRATION

1: Oral route:-

 Advantage:

-Non irritant

-Palatable

-Most common

-Safer

-Easy of administration

- Economic

 Disadvantage:

- Not suitable for patient suffering from vomiting and diarrhea.

- Not suitable in emergency

- Affected by PH.

- First Pass Effect (Pre-systemic metabolism): (Decrease bioavailability of drug)

Def. of First Pass Effect:

Inactivation or elimination of part or whole of the drug before reaching the systemic circulation.

• Sites:

1) Gut first pass effect:

Gastric acidity.

Digestive enzyme

Mucosal enzyme

2) Hepatic First pass effect:

To overcome hepatic first pass effect:

If partial Increase the dose of the drug.

If complete Use another routes such as IV and sublingual.

Factors affecting oral absorption:-

1: Presence of food and other drugs in the GIT:

Amino acids compete for the same carrier of L-dopa.

-Ca (from milk) decrease absorption of tetracycline.

- Tannic acid (from tea) and tetracycline V absorption of iron.

- Food dilutes drugs and decrease absorption.

* Food is useful in irritant drugs to decrease irritation.

2: State of health of GIT:

Presence of the disease in the GIT decreases absorption.

3: Gastric emptying rate:

May be increase or decrease absorption (depend on the drug):

For Example in high emptying rate

- Increase absorption of Paracetamol (Rapid rate of dissolution and disintegration)

- Decrease absorption of Digoxin (Slow rate of dissolution and disintegration) Atropine decreases

motility of the GIT decrease emptying rate.

4: Motility of GIT:

- Increase Motility (Diarrhea) decrease absorption.

-Decrease Motility (Constipation) Increase absorption.

5: PH of GIT:

- Acidic drugs (Aspirin) - absorbed in acidic medium (Stomach).

Basic drugs (Ephedrine) absorbed in basic medium (Intestine).

6: First pass effect:

= Decrease bioavailability.

7: Related to the drug: (Lipid solubility)

- Lipid soluble drugs Increase absorption.

- Polar drugs (water soluble drug) not totally absorbed (due to high amount of lipid content in the

cells) and not pass through Blood Brain Barrier (BBB).

- Non-polar drugs (Lipid soluble drugs) highly absorbed and Pass BBB.

2: Parenteral routes (injections):

A: Intravenous (IV) injection:

Advantage:

- 100% bioavailability (The amount of drug reached to blood).

- No first pass effect.

- Suitable for irritant drugs.

- Suitable in emergency.

- Suitable for acid labile drugs.

Disadvantage:

- Low safety (May cause allergy or anaphylactic shock).

- Must be sterile (Pyrogenic reaction).

- Spreading of infection (Viral hepatitis).

- Required professional person.

- Not suitable for oily and suspended drugs.

B: Intramuscular (IM) injection:-

- Suitable for solution, suspension and oily drugs.

- Better absorption than SC but less than IV.

C: Subcutaneous (SC) injection:-

- Absorption rate is slower than IV and IM.

- It is suitable for drugs that are non-irritant in aqueous solution or fine suspension.

D: Intradermal (ID) Injection:

- Sensitive tests.

E: Other injection:-

- E.g. - Intra-cardiac -Intra-bone marrow

- Intrathecal - Intra-peritoneal

3: Mucosal route:

- Buccal or Sublingual Systemic delivery of drug

-Ocular Local delivery of drugs

-Vaginal, Nasal and Rectal Systemic or local delivery of drugs

4:Inhalation:-

- Systemic delivery of drugs.

- Highly blood supply and wide surface area.

- Highly absorbed (high bioavailability).

- Many drugs make lung irritants.

5:Topical:-

- Usually local effect but high lipid soluble drugs can be absorbed.

- Transdermal drug delivery system (TDDS) enhance skin absorption e.g. Skin patches of nicotine. 

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