Adrenergic and adergnic blockers Cholinergic and Cholinergic blockers Classification of both the system

1. Drugs acting on
PNS @yogesh2811

3. Imp terms
Receptor =receptors are chemical structures,
composed of protein, that receive and transduce signals that
may be integrated into biological systems. These signals are
typically chemical messengers, which bind to a receptor, they
cause some form of cellular/tissue response.
Affinity =it is the ability of drug to bind the receptor
Efficiency /interinsic activitie=it is the ability of drug to activate the
receptor to produce response

4. Agonists => This are the drugs which bind &
stimulating the receptor & shows efficiency. [I.
E=>both affinity & efficiency ]
Antagonist => this are the drugs that binds &
inhibits the receptor & does not show any
efficiency or p.cologicsl action

5. Classification of ANS
It is derived in two main types
1]parasympatomimetic (agonist action of ACh) (Cholinergic
(Acetylcholine) ACh, drugs)
1]paraympatholytics(break down )(ach Blocking or
Anticholinergic drug)
2]sympathomimetics (Adrenergic drugs)
2] Sympatholytics (antagonist action of Adrenergic drugs) (NA

6. NEURO-HUMORAL TRANSMISSION, CO-
TRANSMISSION AND
CLASSIFICATION OF
NEUROTRANSMITTER
4 turps
(i) Neurotransmission -They are synthesize in persenftic
nerve & Relase in Synaptic claft
Eg-Ach ,Dopa
(ii) Neuromodulation-This are Relase in neuron
reduced pre & post synaptic respond of

7. (ii) Amino acids
The central nervous system contains high concentrations of certain amino acids like
glutamate, Gamma amino butyric acid (GABA). The dicarboxylic acids (glutamate and
aspartate) produce excitation and monocarboxylic ω-amino acids (GABA, glycine,
β-alanine and taurine) produce inhibition.
Classification of Neurotransmitters
Neurotransmitters can be classified in to 4 major
classes as follows:
(i) Acetyl Choline (ACh)
Neurons producing acetyl choline are called as cholinergic neurons. They are present in
cerebral cortex, ascending reticular axcting system, basal ganglia, limbic system,
cerebellum and spinal cord. ACh modulates arousal, respiration, motor activity, vertigo
and memory.

8. (iii) Biogenic amines
Biogenic amine include dopamine, nor-epinephrine/epinephrine, 5-hydroxy tryptamine
and histamine.
(iv) Peptides
Various peptides like vasopressin, oxytocin, tachykinins, neurotensin, vasoactive
intestinal polypeptide (VIP), endogenous opioids like endorphins and encephalins,
cholecystokinin, angiotensin II and neuropeptide Y perform various functions in
different
parts of the body. Some of them act as hormones.

9. Acetylcholine

12. It is derived in two main types
1]parasympatetic (Cholinergic drugs)Acetylcholine
Location-Preganglionic fiber high & postaganglionic fiber is low AC
Receptor - GPCR
Storage--synpetic vesicles (present in post & pre ganglion Fiber)
Synthesis-ACh is synthesised in the axon terminal by
acetylation of choline with acetyl CoA (AcCoA)
Metabolizum-ACh is hydrolysed by the enzyme called as acetyl
cholinesterase to choline and acetic
acid.

13. Cholinergic receptors & it's location

15. SAR for parasympathomimetic OR cholinergic agent
1] Ing's Rule of 5: there should be no more than 5 atoms between the
nitrogen and the terminal hydrogen for muscarinic (or cholinergic) activity
2] The molecule must possess a nitrogen atom capable of bearing a positive
charge, preferably a quaternary ammonium salt
3]For maximum potency, the size of the alkyl groups substituted on the
nitrogen should not exceed the size of a methyl group;
4] molecule should have an oxygen atom, preferably an ester-like oxygen
capable of participating in a hydrogen bond
4] There should be a two-carbon unit between the oxygen atom and the
nitrogen atom.

16. A parasympathomimetic drug, sometimes called a cholinomimetic
drug or cholinergic receptor stimulating agent, is a substance that
stimulates the parasympathetic nervous system (PSNS). These
chemicals are also called cholinergic drugs because acetylcholine
(ACh) is the neurotransmitter used by the PSNS. Chemicals in this
family can act either directly by stimulating the nicotinic or
muscarinic receptors (thus mimicking acetylcholine), or indirectly
by inhibiting cholinesterase, promoting acetylcholine release, or
other mechanisms.

17. Cholinesterase -
After Relase of ACH Is hydrolysed by the
enzyme cholinesterase &choline is
reduced Is
Called cholinesterase
(specific) acetylcholineestrage_AChE or true Choline easterage
(non-specific) Butyrylcholinesterase _BuChE or
pseudocholiestrage
It both are located in Cholinergic sits

18. Anticholinesterases -Cholinesterase inhibitors,
also known as anti-cholinesterase, are chemicals that
prevent the breakdown of the neurotransmitter
acetylcholine or butyrylcholine. This increases the
amount of the acetylcholine or butyrylcholine in the
synaptic cleft that can bind to muscarinic receptors,
nicotinic receptors and others. This group of
inhibitors are divided into two subgroups,
acetylcholinesterase inhibitors and
butyrylcholinesterase inhibitors.

19. 1]cholinergic drugs Also called direct acting drugs
(cholinomimetic, parasympathomimetic )
Its also divided in two main catagory
A] choline easter-ACh, Carbachol,
methacoline ,bethanecol
B] plant alkolides-Atropin, Pilocarine,Nicotine,
Muscarine
2] Anticholinestrages Is also called in directing drugs
(Cholinesterase inhibitor)
It also divided I'm two main catagory
A] Reversible

20. It also divided I'm two main catagory
A] Reversible - its also divided 2 typs
a] carbamates-- Neostigmine ,Physostigmine Pyridostigmine
Rivastigminee
B] non-carbamates - Endrophonium, tacarin,donepezil,galantamine,etc
B] Irreversible- it also divided 2 types
a] carbamates-carbaryl, propoxur *insecticides
B] organophosphates-Eg malathion, Disrobing,
Echothiophate

21. Phaacological action of Acetylcholine
1] M3 receptor => Eye - contractions of circular muscule
of iris result In miosis (miosis-miotics are causes miosis)
The person who can see only any objectives which are
near away but can't see fare away
Contraction of muscle cause Spasm accommodation
reduced intraocular pressure tenshion or increased
aqueous outflow
Or Parasympatetic or Cholinergic stimulation or
cholinomimetic drugs

22. 2] M2 receptor => Heart - ACh hyperpolarization
in SA node decreases Rate of heart is also
called Diastolic depolarization, if it's
Countinouslly depolarization
finally one step called diastolic blocked,
calcium ringer effect, diastolic blocked

23. Heart rate decreased Negative
chronotropic effect
Force of contraction
decreased
Negative inotropic effect

24. M1 Automatic ganglia, gastric
Glands, CNS
INCREASING gastric
secreations bronchial secretion
increasing,
M2 Heart Depressed SA node
Reduced
contraction ,automaticity,
conductivity
M3 Smooth muscle,
Excocrine gland,Eye
Contraction of Pupiles, Miosis,
secreation vascular endothelium
Nn Autonomic ganglia
Adrenal medullla
ACh induce stimulation of
autonomic ganglia which results
in increased output of
acetylcholine and non internal
Nm neuromuscular Junction depolarization of muscle
endplate contraction of skeletal
muscle high dose causes

25. use of anticholinerstrage
1] miotic-Miotic Are miosis (contraction of
Pupile) decreases Pupile size it means the person
can see the object which are near away but can't see
the object fare way.
ACh reduced intraocular pressure by increasing the
drainage of occular fluid especially in GLUCOMA
condition

26. Glaucoma
glaucoma is disease characterized by increase
intraocular pressure which causes damage to optic
nerve thereby producing visual loss.
The damage to optic nerve and visual loss is
probably due to ischemia may be due to direct
pressure on optic nerve

27. Glycoma is classified into
following four types
1]open angle glaucoma
2]closed angle glaucoma
3]drug induced glaucoma
4]congenital glaucoma

28. 2] Mystheniya gravis - Myasthenia
gravis is a neuromuscular autoimmune disease
caused by deficiency of postsynaptic neuromuscular
ACh Myasthenia gravis is disease which
antibodies are found in thymus gland are
targeted on on neuromuscular Junction
treatment is usually started with Neostigamine 15
MG Every 6hr orally, corticosteroids a afford
Improvement in my senior gravis by their
immunosuppressant action

29. anticholinesterase poisoning Or Organic
Phosphorus compound poisoning
causes- *occupational in persons engaged in
spraying insecticides
*accidental
*eating agriculture products Sprayed with
insecticides
*suicidal due to intentional in digestion of
insecticides

30. symptoms
* meiosis
* headache *respiratory depression
*hypertension *bradycardia *failure death
may be occurs
Treatment - 0.6mg Atropine

31. 1]paraympatholytics(ach Blocking or Anticholinergic
drug, muscarinic receptor antagonist,Atropinic)
The drugs which are antagonize or block The
Mascarnic action of acetylcholine are called
parasympatholytic

32. classification of
parasympatholytics
Amino acid derivative
4 nitro atom

33. Pharmacologicl action of Atropine
Organ /part /muscles Pharmacological action
Excocrine gland And secreations Reduced all secretion including
gastric, intestinal, sweat, pharyngeal
Causes dryness ofpharyngeal mouth
Bronchi Relax smooth muscle of bronchi
CVS Increase heart rate m2 receptor
blocker
Tachyacreadia
GIT Reduce tone, MOTALITY, peristalsis
&cause constipation

34. Cns Stimulation of CNS
(RESPIRATORY vasomotor)
high dose cause
hallucinations
Smooth muscle All smooth muscle that
receive
parasympathomimytic motor
innervation are relaxed by
atropin
Body temperature Rise in body temperature
Local anesthetic Atropine is a mild anesthetic action on
the cornea

35. Parasmpatolytic Atropine action
on eye
local installation into eyes atropine produces
mydriasis The ciliary smooth muscle are paralysed
which causes increase in focal length of lens. The
individual can see the object only at long distance
This term aS called cycloplegia Or paralysis of
accumulation
because of Mydrasis & cycloplegia person falls to
respond to bright light this is termed as
photophobia

37. Therapeutical uesof
Parasympathomimytic drugs
*As Antisecratory ⬇️
* As antispasmodic⬇️ (Spasm-sudden contractions of
muscle) *peptic ulcer⬇️
* Bronchial asthma,Asthametic bronchitis,
chronic obstructive pulmonary disease (COPD)
*As mydriatics & cycloplegic
* As cardic vagolytic
* for Parkinson's And motion sickness ( Hyoscine imp)
* Diagnosis of Alzheimer’s disease (AD)

38. 2]sympathomimetics
Adrenergic -epinephrine
Noradrenaline-Norepinephrine
Definition,Synthesis, storage,, Relase,Metabolizum,
Receptors ,Structural activity relationship
Adrenergic receptor classifications It's type or
location & there function, SYMPATHOMIMETICS
DRUG CLASSIFACTION
Agonist

39. Definition - sympathomimetics -
the drugs which produce the action similar to
the stimulation of sympathetic nervous system
is called sympathomimetic
It plays an important role in the fight-or-flight
response by increasing blood flow to
muscles, output of the heart, pupil dilation
response and blood sugar level

40. Synthesis
Synthesis of Adrenaline

41. Synthesis of Adrenaline

43. Catecholamine are synthesize by amino acid
phenylalanine Tyrosine is first oxidized to L-DOPA by
Tyrosine hydroxylase, this is the rate-limiting step.
Then it is subsequently decarboxylated to give
dopamine by DOPA decarboxylase (aromatic L-amino
acid decarboxylase). Dopamine is then converted to
noradrenaline by dopamine beta-hydroxylase which
utilizes ascorbic acid (Vitamin C) and copper. The final
step in adrenaline biosynthesis is the methylation of
the primary amine of noradrenaline. This reaction is
catalyzed by the enzyme phenylethanolamine N-

44. Storage--adrenal glands and a small
number of neurons in the medulla
oblongata

45. A catecholamine (CA) is a monoamine
neurotransmitter, an organic compound that has a
catechol (benzene with two hydroxyl side groups next to
each other) and a side-chain amine.
Catecholamines are derived from the amino acid
tyrosine, which is derived from dietary sources as well
as synthesis from phenylalanine. Catecholamines are
water-soluble and are 50% bound to plasma proteins
in circulation.

46. Relase
Adrenaline-Adernal cortex
Non-adrenaline -postaganglionic part
Dopamine - Basal ganglia(major Neurotrasmettitor)
Binding of receptors - it bind G-protein
couple receptors

47. Metabolizum of adrenaline
Two enzymes are responsible
1]MOA--(momoamine oxidise)
present both inside or out side of
neuroN
2] COMT -- (CATHECHOLE -O-
METHYL TRANSFERASE) present
only outside the neuron

48. Metabolizum pathway

49. SAR OF sympathomimetics
drugs
For maximum sympathomimetic activity, a drug must
1] Amine group 2 carbons away from an aromatic group
2] A OH group at the chiral β-position in the R-configuration
3]-OH groups in the meta & para position of the aromatic ring to form
a catechol which is essential for receptor binding
The structure can be modified to alter binding
. If the amine is primary or secondary, it will have direct action, but if
the amine is tertiary, it will have poor direct action.
If the amine has bulky substituents, then it will have greater beta
adrenergic receptor activity,
The substituent is not bulky, then it will favor the alpha adrenergic
receptors.

50. Adrenergic receptor classifications It's type or
location & there functions
Main two types 1] Alpha α Receptor 2] Beta β Receptor
Receptor α1 α2
Location Eye
Peripheral blood vessels
Uterine smooth muscle
Intestinal smooth muscle
Presyneptic Membrane
Alpha α1& α2 Both are Divided in sub 3 types
α1A, α1B, α1C, & α2A, α2B, α2C.

51. Adrenergic
receptor
β1 β2 β3
Location Heart
JG cells in
kidney
Bronchi
Skeleton blood
vessels
Uterus
Liver, GIT,
URINARY tract
Adipose tissue
Present in outer
covering of organ

52. Organ Effect
Eye Dilates (Mydrasis increase Pupile
size)photophobia
Heartβ2 Increases rate and force of contraction
Lungs Dilates bronchioles via circulating
adrenaline
Blood vessels α1Dilate in skeletal muscle
Digestive system Constricts in gastrointestinal organs
Sweat glands Activates sweat secretion For maintaining body
temperature)
Digestive tract Inhibits peristalsis
Kidney Increases renin secretion

53. Blood vessels
.α 1 periferal vasoconstriction
β2 skeletan muscule blood vessels
α1-Low dose of adrenaline rise systolic
pressure(vasoconstriction)
B2-high dose cause fall in diastolic pressure
(vasodilation)
Metabolizum Adrenalin increases blood sugar levels by
enhancing hepatic glycogenolysis & decreases
utilization of glucose by peripheral tissue
Antiallergic action Adrenalin is a antagonist of Histamine
Cns Therapeutically it's rise restlessness, palpitations,
apprechension

54. Therapeutic uses of adrenaline
Or
CATACOLAMINE
1]choise for treatment in anaphylactic shock
2] used in acute bronchial asthma
3] in dental practices
4] as local vasoconstriction
5] control hemorrhage & applied on locally control capillary bleeding
6] asphyxia--intracardic injection adrenalin to restore heart beat

55. Contraindications
Hypertension *Diabetes
*Arteriosclerosis
Thyrotoxicosis.
Coronary indsufficency
Spinal anesthetics
Pheochromocytoma

56. Therapeutic uses of Non-
catecholamine or amphetamine etc
* Bronchial asthma
* Nasal congestion
* Hypertension
* Narcolepsy
* Heart block= stock Adams syndrome
* Anorectic= loss of appetite
Adverse effects = same as
CATACOLAMINE

57. SYMPATHOMIMETICS DRUG
Classification 1st type
1] Direct acting( Catecholamine)
sympathomimetics
This is a drugs which are direct agonist on α& β Or
Both α& β Adrenoreceptor
Eg- Adrenalin ,nonadrenaline ,isoprenaline,
phenylephrine,methoxamine,xylometazoline,salbut
amol& etc

58. 2 indirect
acting(nonchecholamine)
sympathomimetics
This are the drugs which are act on Adrenergic
neurone to release Noradrenaline
Which they acts on the Adrenoreceptor
Eg- THYRAMINE, amphetamines
3] mixed acting - this are acting both directly or
indirectly
Eg- ephedrine, mephentermine

59. SYMPATHOMIMETICS DRUG Classification 2nd
type
1) catacolamines--Eg- adrenaline and
noradrenaline ,isoprenaline, dobutamine and
dopamine
2] noncatecholamines--
amphetamine ,phenylephrine,Ephedrine,
psudoepherdrine, etc

60. 1] Vasopressor agent Noradrenaline, phenylalanine,
ephedrine, dopa
2i cardic stimulates ADRENALIN, Noradrenaline,
isoprenaline
3] Bronchodilatoras ,Salbutamol, terbutaline,
isoprenaline
Uterine relaxants Isoxsuprine, Ritodrine
Nasal decongestant Xylometazoline, oxymethazoline,
Naphazoline
Cns stimulation Amphetamine,
Dextroamphetamine
Allergic reaction Adrenalin, Ephedrine
8] Anorectics/ Appetite Fenfluramine, Dexfenfluramine,

61. Antiadrenergic Drug (Adrenergic receptor
blockers / Antagonist) & Drugs for
GLUCOMA
Thais are the drugs which are reduces or block the pharmacologicl
action of sympathomimetics drugs
Or
This are the drugs which antagonist the receptor action of
ADRENALINE. They are comparative antagonist at alpha α
&βbeta or both α β adergnergic receptor

62. Classification is Sympatholytics
drugs,
Selective α blockers

63. Selective β Adrenergic blocker

64. Uses of alpha Blockers
1.Pheochromocytoma--its a tumour in adrenal medulla
cells. It's causes bcz excessive CAs are secret in
medulla Pheochromocytoma & dibenamimr
2. Hypertension- alpha blockers like Prazosin
3. Benign hypertrophy of prostate(BHP) Phenoxybenzamine
4. Peripheral vascular diseases - alpha blockers do
increase skin & to some extent muscle blood flow in
normal individual Prazosin

65. β blocker pharmacologicl action
* Heart = decreases heart rate & contractions β-blocker
* blood vessels = block vasodilation & fall BP
* Respiratory tract = increases bronchial resistance
* cns= forgetfulness, dreaming, nightmares
* Local anesthetic = stabilizing Na+ in membrane
* metabolic = Propranolol block Adrenergiically induced
lipolysis & consequent increas in plasma free fatty b
acid level
* skeleton muscle = inhibits provoked tremor

66. Drugs used in GLUCOMA

67. Glaucoma
Definition, type, There periticular
action drugs

68. Definition =>Glaucoma is a group of eye
diseases which result in damage to the optic
nerve and cause vision loss.
Typs=>
1] open angal glyccoma
2] closed angle glyccoma
3]congentisl glaucoma,
4] Drug induced glaucoma

69. 1] open angle glaucoma =in which the
drainage angle for fluid within the eye
remains open Or
It occurs due to degeneration offer
trabeculae leading to diminish
reabsorption offer aqueous humour &
results in increased IOP

70. Treatment
1] Topical beta blockers => Timolol, BETAXOLOL,
levobunolol
2] alpha-adrenergic agonist=>
Brimonidine,dipivefrine
3]carbonic anhydrase inhibitor=> Acetazolamide
250mg oral 6to 12 hourly

71. Closed angle glaucoma Or
normal tenshion Glaucoma
It can present gradually or suddenly. The sudden
presentation may involve severe eye pain, blurred
vision, mid-dilated pupil, redness of the eye, and
nausea. Vision loss from glaucoma, once it has
occurred, is permanent.

72. Risk factors for glaucoma include increased pressure in the eye, a
family history of the condition, and high blood pressure. For eye
pressures, a value of greater than 21 mmHg or 2.8 kPa is often
used, with higher pressures leading to a greater risk. However,
some may have high eye pressure for years and never develop
damage. Conversely, optic nerve damage may occur with normal
pressure, known as normal-tension glaucoma.

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