The document outlines various drugs that affect the central nervous system (CNS), categorized into general and local anesthetics, sedatives, analgesics, and others, detailing their mechanisms and therapeutic uses. It discusses stages of general anesthesia, how anesthetics work at the neurotransmitter level, and the importance of preanesthetic medications. Additionally, it covers intravenous reversal agents and classifications of inhalation anesthetics, highlighting their properties, advantages, and disadvantages.

1. Drugs affecting CNS
(Central Nervous System)

2. 1)General Anesthetics (block pain n conciousness before surgery)
2) Local Anesthetics (block pain n conciousness before surgery)
3) Sedative and Hypnotics ( induce calmness and sleep)
4) Opiod Analgesics (opium plant based analgesics)
5) Antitussive (prevent cough)
6) Antiparkinsonics (prevent rigidity of muscles )
7) CNS stimulants (increase attentiveness)
8) Pshychotropic agents
8.1) Antipsychotics (manage schizophrenia and bipolar disorder )
8.2) Anticonvulsants/ Antiepilepsy (prevent seizures)
8.3) Antidepressants (promotes good mood)
9) Anxiolytics/ Antianxiety (reduces anxiety/fear)
What are the various drugs that target CNS and
what they do?

3. Drugs causing CNS depression
1) General Anesthetics

4. Anesthesia – is a reversible condition of
comfort, stillness and physiological stability in a
patient before, during and after performance of a
surgical procedure
General anesthesia – required for to make the
patient unaware / unresponsive to the painful stimuli
in big surgical procedure e.g. heart, brain surgery. It
effects entire body.
Such drugs are called General Anesthetics eg
cyclopropane, Ether, Nitrous oxide
Local anesthesia - required for to make the patient
unaware / unresponsive to the painful stimuli in small
surgical procedure eg dental surgery. It effect is
limited to the area of application.
Such drugs are called Local Anaesthetics e.g.
Procaine, Lidocaine and Bupivacaine etc.
Anesthetics

5. 1)General Anesthetics
General Characteristics
1) Analgesia (pain relief)
2) Impairment of all skeletal muscle (ie causes
motionlessness and allow smooth surgury)
3) Loss of consciousness (needed to abolish fear and
anxiety in patients during surgury)
4) Loss of motor reflexes
5) Reversible
6) Not therapeutic or diagnostic but facilitates surgery
procedures

6. Side effects of Anesthetics
 May cause short term or long term Amnesia
 Nausea and vomiting after surgery
 Hypothermia (feeling very cold)
 Decreases respiration and heart beat (thus it requires
monitoring during surgery)

7. Stages of GA and its
Mechanism

8. Stages of GA
Stage I: Analgesia
 Starts from beginning of anaesthetic inhalation and lasts
upto the loss of consciousness
 Pain is progressively abolished during this stage
 Patient remains conscious, can hear and see, and feels a
dream like state
 Reflexes, respiration and heart rate remain normal
 use is limited to short surgical procedures eg dental surgery

9. stages of GA – contd.
Stage II: Delirium and Excitement:
 From loss of consciousness to beginning of regular respiration
 Excitement - patient may shout, struggle and hold his breath
 Muscle tone increases, jaws are tightly closed.
 Breathing is jerky; vomiting, involuntary micturition or
defecation may occur.
 Heart rate and BP may rise and pupils dilate due to sympathetic
stimulation.
 No stimulus or operative procedure carried out during this stage.
 This stage is not found with modern anaesthesia due to
preanaesthetic medication, rapid induction to stage 3 etc.

10. stages of GA – contd.
 Stage III: Surgical anaesthesia
 Extends from onset of regular respiration to ending of
spontaneous breathing. This has been divided into 4
planes:
 Plane 1: Roving eye balls. This plane ends when eyes
become fixed.
 Plane 2: Loss of corneal and laryngeal reflexes.
 Plane 3: Pupil starts dilating and light reflex is lost.
 Plane 4: Intercostal paralysis, shallow abdominal
respiration, dilated pupil.

11. stages of GA – contd.
Stage IV: Medullary / respiratory paralysis
 breathing stops and failure of circulation which leads
to death
 Pupils: widely dilated
 Muscles are totally flabby
 Pulse is imperceptible
 BP is very low.

12. Summary
Stage 1: loss of pain
Stage 2: loss of consciousness and excitement
(we want to avoid this stage!)
Stage 3: clam, stable patient. Surgery is done
Stage 4: coma/death
(we want to avoid this stage too!)

13. Mechanism of action
1) Non-specific/ Unified theory of anesthetics/ Meyer-
overton theory
eg all hydrocarbons (ether, cyclopropane)
2) Receptor specific action
 GABA gated Cl- channels
Eg barbiturates, benzodiazepines and propofol
 Glycine gated channels eg Barbiturates, propofol
 NMDA (N – Methyl D- Aspartate) receptors eg Nitrous
oxide and ketamine

14. Mechanism of action of GS
Neurotransmission
/synaptictransmission,
is the process by which
signaling molecules called
neurotransmitters (NT) are
released by a neuron (the
Presynaptic neuron), and
bind to and activate the
receptors of another neuron
(the postsynaptic neuron).
Q) How do neurons communicate with each other?
Ans. Through binding of neurotransmitters eg GABA, Glutamate with their receptors
Physiology Review

15. Many CNS drugs work by influencing
 neurotransmitters release
 neurotransmitters receptor binding sites
 neurotransmitters reuptake
Physiology Review

16. 1) Meyer-Overton Theory
Meyer-Overton proposed a non-specific action
of anesthetic drugs. They concluded:
a) All lipid- soluble substances depress the CNS and act
as anesthetic
b) Increasing partition coefficient increases
activity, regardless the structure
c) The depressant activity occurs mostly in lipid rich
cells

17. Meyer-Overton Theory cont
 Neurons transmit signal across each other when
transmembrane receptor in post-synaptic neuron cell
membrane bind neurotransmitters from pre-synaptic
neuron
 Anesthetics show their effect due to great lipophilicity
 Thus they easily penetrate and dissolve in the
phospholipid bilayer cell membranes of neurons
 This causes increase in volume of the membrane and
alters shape of those transmembrane receptor so that
they can’t bind with their ligands anymore. This
prevents conductance of nerve signals thus effectively
causes anesthesia

18. Receptor based action
 There are receptors present in the neuron cell membrane which
are ligand gated ion channels such as
 glutamate gated Ca+ channels of NMDA receptors.
 GABA gated Cl- channels of GABAA receptor or
 When these ligand bind to their receptors, they allow ion entry
into the cell. This can either
 allow propagation of stimulus in the nerves, as in Ca+ entry
during NMDA opening due to glutamate binding. Glutamate is
thus termed stimulatory neurotransmitter.
 inhibit propagation of stimulus in the nerves, as in Cl- entry
during GABAA opening due to GABA. GABA is thus termed
inhibitory neurotransmitter.
 Drugs show action through direct binding to these receptor in
two ways.
• They can inhibit the binding of glutamate to NMDA receptor
and block its stimulating effect, which brings about CNS
depressing effect
• They can enhance binding of GABA to GABAA receptor and
promote its inhibitory effect, which brings about CNS
depressing effect

19. Preanesthetic medication:
 Definition:
It is the term applied to the use of drugs
prior to the administration of an
anesthetic agent to make anesthesia safer
and more agreeable to the patient.

20.  Aim:
 Relief of anxiety and skeletal muscle relaxation
 Amnesia for pre and post operative events
 Supplement analgesic action so less anesthetic needed
 Decrease salivary and bronchial secretions to prevent any
reflex coughing
 Antiemetic effects
 Decrease acidity and volume of gastric juice

21. Preanaesthetic medication – contd.
 Drugs used:
 Benzodiazepams - diazepam or lorazepam, midazolam,
promethazine (abolish fear and relax skeletal muscle)
Profolol (cause amnesia in addition to anesthesia)
 Opioids – Morphine and its derivatives (analgesic
supplement)
 Anticholinergics – Atropine (inhibit saliva, bronchial
secretion)
 H2 blockers – ranitidine, famotidine (inhibit gastric acid)
Proton pump inhibitors- Omeprazole (inhibit gastric acid)
 Antiemetics – Metoclopramide, domperidone (inhibit
vomitting)

22. Current Intravenous reversal agents
 In some cases drugs are needed to antagonize anesthetic medication
so that patients can be brought back to consciousness after surgury
 Naloxone (reverse opioids),
 Physostigmine (reversal of various sedatives),
 Flumazenil (reversal of benzodiazepine)
 Naloxone is very useful and specific for reversing adverse and life-
threatening respiratory depression caused by narcotic drugs
antagonizing opiod receptors.
 Physostigmime is used for reversing sedative effects in patients who
are depressed after having received
benzodiazepines, droperidol, scopolamine, opioids, and
phenothiazines which prevent metabolic degradation of acetylcholine
and start the parasympathetic NS
 Flumazenil reverses the sedative, respiratory
depressant, anxiolytic, muscle relaxant, anticonvulsant, amnestic, and
anesthetic effects of only benzodiazepine by antagonizing the GABA
receptors

23. Classification of GAInhalation:
1. Gas:
Nitrous Oxide*
2.Volatile liquids:
 Halothane*
 Enflurane
 Isoflurane
 Desflurane
 Sevoflurane
Intravenous:
1. Ultrashort acting
Barbiturates
Thiopental sodium*,
Thiamylal
2. Benzodiazepines
Midazolam
3. Dissociative anesthesia:
Ketamine
4. Narcotic :
fentanyl
5. Micellneous
Propofol and Etomidate

24. Nitrous oxide/laughing gas (N2O)
 Colorless, odorless inorganic gas with sweet taste
 Noninflammable and nonirritating
 Very potent analgesic but weak anesthetic
 Used wit O2 in dental extraction and in obstetrics
 Stored in metal cylinders

25. Mechanism Of Action (MOA)
They antagonize NMDA receptors. This
prevents NMDA from binding to this
receptor which prevents entry of Ca2+ ion
and propagation of action potential. Thus
they block signal transmission between
neurons
NH4NO3 N2O + 2H2O
170 o
C
Synthesis:

26.  Advantages:
- Non-inflammable and
nonirritant
- Rapid induction and
recovery
- Very potent analgesic
(low concentration)
- No nausea and
vomiting
- Nontoxic to
liver, kidney and brain
- doesn’t depress
respiration
 Disadvantages:
 Not potent anasthetic
alone (needs
supplementation)
 If given in high
conc., it causes
Hypoxia
 Inhibits methionine
synthetase (precursor
to DNA synthesis)
 Inhibits vitamin B-12
metabolism
NH4NO3 N2O + 2H2O
170 o
C
Synthesis:

27. Inhalation/Volatile liquids
These are organic compounds that are held by weak
intermolecular forces and hence can transform from liquids to
gas state spontaneously.
They are administered in gas phase by especial equipment
called vaporizer which balance oxygen amount along with
the inhalation
Types: Class Examples
Hydrocarbon Cyclopropane, Ethylene
(2HC=CH2)
Halogenated hydrocarbon Halothane, Ethyl Chloride
(C2H5Cl)
Ether Diethyl Ether (C2H5-O-C2H5)
Vinyl Ether (CH2=CH-O-
CH=CH2)
Alcohol Trichloroethanol (CCl3CH2OH)

28. Anesthetic Vaporizer: A machine that delivers volatile
anesthetic in the right dose while maintaining oxygen
intake too

29. Ideal properties of volatile anesthetics
They should not
 be flammable
 cause irritation to epithelial cells
 cause any physiological response
They should have
 wide margin of safety
 Quick action
 Quick recovery
 Easy to administer
 Good stability in metal containers
 Cheap and easy to manufacture

30. Desflurane
Sevoflurane

31. Halothane
 Fluorinated volatile liquid with sweet odour, non-
irritant non-inflammable and supplied in amber
coloured bottle
 Potent anaesthetic, requires only 2-4% for induction
and 0.5-1% for maintenance
 Boiling point : 50ºC
 Pharmacokinetics: 60 to 80% eliminated unchanged.
20% retained in body for 24 hours and metabolized
Cl
ClCl HF (hydrogen
fluride), 130o
C
SbCl3 (antimony
trichloride),
F
ClF
F
Br2, 450o
C
F
ClF
F Br
Trichloroethylene 2-Chloro-1,1,1
-trifluoro-ethane
Haloethane
Synthesis of Haloethane

32. Halothane – contd.
 Advantages:
- Non-inflammable
and non-irritant
- Pharyngeal and
laryngeal reflexes –
bronchodilatation
- Potent and speedy
induction & recovery
- Controlled
hypotension
- Inhibits intestinal
and uterine
contractions
 Disadvantages:
- Special apparatus
- Poor analgesic and muscle
relaxation
- Respiratory depression
- Decreased urine formation –
due to decreased GFR
- Causes Hepatitis: 1 in 10,000
- Malignant hyperthermia
- Prolong labour

33. Enflurane:
 Non-inflammable, with mild sweet odour and boils at 57ºC
 Similar to halothane in action, except better muscular
relaxation
 Depresses myocardial force of contraction
 Induces seizure in deep anaesthesia and therefore not used
now
 Metabolism is only one-tenth that of halothane ie does not
release high quantity of hepatotoxic metabolites
 But metabolism releases fluoride ion which causes renal
toxicity

34. Isoflurane:
 Isomer of enflurane and have simmilar properties but
slightly more potent and
 Induction dose is 1.5 – 3% and maintenance dose is 1 –
2%
 Needs specialized vapourizer to deliver the patient

35. Isoflurane – contd.
 Advantages:
- Rapid induction and
recovery
- Good muscle relaxation
- Good coronary
vasodilatation
- No renal or
hepatotoxicity
- Low nausea and vomiting
- No seizure and preferred
in neurosurgery
- Uterine muscle relaxation
 Disadvantages:
- Special apparatus
- Pungent and respiratory
irritant
- Special apparatus
required
- Respiratory depression
- Maintenance only, no
induction
- ß adrenergic receptor
stimulation
- Costly

36. Desflurane
 A popular and safe,potent anesthetic
 It has pungent smell, thus first IV anesthetic is used for
induction and this is used for maintenance
 Boiling point is 27 degree (very low)
 Only 0.02% is metabolized, rest expelled unchanged
through lungs
 Induction dose is 3% and maintenance is 2.5% with or
without nitrous oxide

37.  Advantages
- Non- inflammable
- Non-corrosive to metal
- Rapid induction and
rapid recovery
- No hetatotoxicity and
Nephrotoxicity
 Disadvantages
- Pungent smell
- Special vaporizer needed
since BP is so low there is
chance of more drug
delivery as room
temperature fluctuates

38. Sevoflurane
 Potent anesthetic
 BP about 58.6 degree
 About 3% is metabolized, metabolism produces Fluoride
ion
 F ion can cause nephrotoxicity but this effect is negligible
 Dose : 1.4-2.6% alone or 0.7-1.4% with nitrous oxide

39.  Advantage
- Non flammability
- Non-irritating
- Rapid induction and
rapid recovery
- Nephrotoxicity is
negligible
 Disadvantage
- Higher metabolism than
desflurane
- Rxn with sodalime forms
toxic compound

40. “Rxn with sodalime forms toxic compound”.
Explanation:
 The vaporizer machine that delivers the volatile
anesthetic has soda lime (mixture of Ca(OH)2,NaOH,KOH
and water) which is basic in nature
 Its purpose is to react with the exhaled CO2 to form water
soluble salts CO2
 This removes exhaled CO2 , which if not done, then it will
be inhaled again and CO2 toxicity can occur

41. Some terminology defined.
 Maintaining Anesthetic : Volatile anesthetics that are
potent and sustain stage 3 anesthesia long enough to
complete surgery
 Inducing Anesthetic : IV Anesthetics that act rapidly
enough to bypass the 2nd stage of anesthesia which is
needed to prevent choking danger on saliva or vomit
 Minimum Alveolar Concentration : It is defined as the
concentration at 1 atm of anesthetic in the alveoli that is
required to produce immobility in 50% of adult patients
subjected to a surgical incision

42. Intravenous
Delivered by IV injection. Time taken is extremely fast. It
causes anesthesia with 1 min.
 Ketamine
 Profolol
 Etomidate
 Barbiturates (thiopental sodium, thiamylal) &
Benzodiazepam (Midazolam) (lectured in Sedative and
hypnotics)
 Fentanyl (to be lectured in opiod analgesics)

43. Ketamine
 inject able and very potent, rapid acting agent
 Duration of action about 10-25 min
 Advantage: Do not relax skeletal muscle and thus used in
dental surgery
 Disadvantage: After recovery patient is in state of confusion
 Disturbing dreams and hallucinations up to 24 hrs post
recovery
 This long duration action is explained by its metabolic
product norketamine which inhibits NMDA receptors and
is itself a weak anesthetic
 96% is metabolized in this way

44.  MOA:
They antagonize NMDA receptors. This prevents
binding of glutamate/aspartate to this receptor.
Glutamate is the main stimulatory neurotransmitter in
CNS. The lack of any stimulation, causes the CNS to
falls into depression.
 Dissociative effect of ketamine
Ketamine makes patient appear to be awake but his eyes keep
moving here and there and they aren’t aware of their
environment.
The drug disconnects limbic system from the thalamocortical
system. This neural connection is required to feel
consciousness.
Thus patient is alive and well but is not aware about it!

45. Propofol
 Has amnesic property and formulated as a white emulsion. Thus
named “milk of amnesia”
 MOA: It enhances effect of inhibitory neurotransmitter, GABA at the
GABAA receptors and thus promotes CNS depression
 Advantage : Propofol has a fast onset of action and crosses the blood-
brain barrier very quickly. Thus it is a very good inducing anesthesia. Its
short duration of action is due to rapid distribution from the CNS to
other tissues. No vomiting after surgury
 Disadvantage: It has narrow window of safety. High dose can create
cardio-respiratory depression and death. There is no reversal
medication for propofol toxicity. Thus overdose can be lethal.
 The ampoule containing it must be discarded after single use to avoid
risk of sterility breakage
 Dose: 2-2.5 mg/kg produces hypnosis in 1 min lasting upto 5 min

46. Etomidate
 Potent, rapidly acting but short time only (less than 3 min)
hypnotic agent with no analgesic activity
 The anaesthetic induction dose for adult humans is
0.3 mg/kg intravenously, with a typical dose ranging from
20–40 mg
 MOA: It enhances effect of inhibitory
neurotransmitter, GABA at the GABAA receptors and thus
promotes CNS depression
 Advantage: Useful for induction of anesthesia in patients
susceptible to hypotension because of coronary artery
disease
 Disadvantage: Known to inhibit adrenal steroid hormone
synthesis eg aldosterone, testosterone, estrogen etc

47. Thank you
Drug discovery Process
Time taken : 10 years to 15 years
Cost : 5 billion $ as of 2013
Proper study of a disease physiology/pharmacology
is the key to success
There is no cure for type 1 diabetes cause we don’t know what enzyme
or receptor to stimulate or inhibit that will cause insulin secretion

48. Revision
 Anesthetics are drugs that allow painless, fearless and
risk free surgery by depressing signal transfer between
nuerons
 They are not a cure to any disease or manage any
disease symptoms
 Two types
 General Anesthetic- act on full body
 Local Anesthetic – only area of application

49. Summary
Stage 1: loss of pain
Stage 2: loss of consciousness and excitement
(we want to avoid this stage!)
Stage 3: clam, stable patient. Surgery is done
Stage 4: coma/death
(we want to avoid this stage too!)

50. Stages of anesthesia
Match the following
 Stage 1
 Stage2
 Stage 3
 Stage 4
1. Calm, stable patient
2. Excited patient
3. Need maintenance
4. Respiratory failure
5. No pain
6. Surgical stage
7. No consciousness
8. Risk of choking on
vomit and saliva
9. Death

51. Mechanism :Meyer-overturn Theory
•It is a Non-specific mechanism i.e.
drug don’t bind to any receptors but
enters lipid cell membrane and
dissolves in it
•This causes membrane expansion
which alters receptor shape.
NT can’t bind with this altered
receptors

53. How shape of lock/receptor is influenced by just
the lipophilicity of drug?

54. The lipid layer surrounding
the transmembrane protein
have role in maintaining it’s
shape. Both tightening or
loosening of the lipid
membrane alters shape of
protein. Expansion of the lipid
layers as a result of dissolving
of anesthetic drugs squeezes
the protein and alters it’s
shape. In this altered shape it
can’t bind with it’s substrate

55. Mechanism :Meyer-overturn Theory
•Why do inhaled anesthetics enter lipid cell membranes and not just stay in
the blood?
Becoz they have high lipid solubility and high partition coefficient
•What happens when anesthetics enter lipid membranes?
They remain there and dissolve into the lipid membranes , thus increasing
its volume
•What is the result of this increase in volume of membrane?
It alters receptor shape and binding site
•What happens if shape of receptor is altered?
Neurotransmiters can’t bind to this altered receptor’s binding site
•What happens if NT can’t bind to their receptor?
Nuerotransmission between adjacent neurons is stopped. CNS gets
depressed. Person falls into anesthetic stage.

56. Current reversing agents
Naloxone (reverse opioids),
Physostigmine (reversal of
many sedatives),
Flumazenil (reversal of only
benzodiazepine)
Preanesthetic medication Which are not an objective of Preanesthetic medication?
- Remove fear/anxiety after surgery
- Cause memory loss of events before surgery
- Stop urination and defecation during surgery
- Stop salivary secretions/ vomiting/gastric acid
- Supplement analgeisc
- Relax smooth muscles
 Function of Current reversing agents
- Recovery of patients who are extra sensitive to GA
- Counter overdosing of Sedatives/narcotics

57. Inhalation anesthetics :
N2O, Halothane, Enflurane, Isoflurane, Desflurane, Sevof
lurane
 The only truly gas Anesthetic is ______
 The only volatile Anesthetic containing Br is _______
 The halogen not included in volatile Anesthetic is ____
 Which volatile Anesthetic causes seizures during
anesthesia? _______
 Halogen that causes nephrotoxicity is _______
 The weakest anesthetic is ____
 Enflurane and isoflurane are ________ of each other
-Diesteriomer - Conformational isomer
-Geometric isomer - Enantiomer

58. Desflurane Sevoflurane

59. •Why N2O gas can’t be given alone?
a) It is not a potent anesthetic. It requires high dosing to
produce stage 3 anesthesia.
b) If given in such high does, it will reduce O2 intake causing
hypoxia (Hypoxia means lack of O2 in the air we inhale)
•How is N2O stored and delivered to patient?
N2O is stored in pressurized metal gas containers. It is diluted
with oxygen and delivered in gas phase by simple diffusion
process
•What are induction anesthesia?
They are IV anesthetics that rapidly and smoothly bring stage 3
anesthetic stage by avoiding the complications of stage 2 (such
as vomiting, shouting, saliva secretion, irregular
breathing, micturation, defeacation, tight muscles )

60. • Why volatile anesthetics require a vaporizer machine?
They are stored in liquid containers but need to heated to
convert to vapour and then diluted with oxygen gas
properly to allow inhalation to patient in right dose
throughout the entire surgery period
• Why desflurane requires special vaporizer for delivery?
It has very low boiling point of 27oC. Slight increase in room
temp can increase amount of gas inhaled. Thus careful
delivery needs to be done to avoid overdosing as a result of
variation in room temperature .
•Why do vaporizer machine contain soda lime?
To absorb and neutralize the CO2 exhaled by the patient in
a simple acid base rxn so as to avoid inhalation of CO2

61.  Which is false about volatile anesthetics?
 Nitrogen is a volatile anesthetic
 The main route of elimination is by lungs
 They are largely metabolized by liver
 They have rapid action and recovery
 They are non-inflamable and non-irritant
 They require especial equipment to deliver
 They are stored and used in gas form
 Enflurane is not used anymore because it is not potent

62. Intravenous anesthetics
Ketamine, Propofol, Etomidate
 Called inducing anesthetics: Used to cause rapid
anesthesia from stage 1 to stage 3
 Shows analgesic action within 1 min but lasts for short
duration only (10-25 min, 5 min, 3 min)
 Major elimination is through liver and kidney not
lungs
Ketamine Inhibits glutamate at NMDA receptor
Profolol Enhances effect of GABA at GABAa receptor
Etodimate Enhances effect of GABA at GABAa receptor

63.  How ketamine causes bad dreams for upto 24 hrs post
recovery?
It gets metabolized into norketamine, which also has mild
CNS depressing effect
 Etomidate has no analgesic ability ie can’t take away pain.
How can it be used an GA?
It is used because it has good inducing property. The lack of
analgesic activity can be compensated from preanesthetic
medicines. Plus it does not lower BP and has special
advantage in Coronary artery disease
 Why is propofol made into an emulsion?
Because It has poor water/blood solubility

64. Peripheral/Autonomic NS
AdrenalineAcetylcholine

66. Two types of reflex action
a) Jerking of knee when hit by a hammer
b) Drawing hand away from fire when
feeling burnt

67. How agonist differes from antagonist?

68. How allosteric
drugs differ in their
Mechanism from
agonist or
antagonist?