A PowerPoint presentation on Anti Muscarinic drugs it has a broad information on different drugs like Anti-Muscarinic drugs Anti-Nicotinic drugs and some information on Ganglionic blocking drugs with their general information including different brands, different generics, their pictures, dosage, side effort and treatment measures etc.
May this information may be helpful to you.
Regards.
SYED MASOOD AHMED QUADRI
The current slide include the pharmacology og cephalosporins.
Contents
Introduction to Cephalosporins
Classification of Cephalosporins
Cefazolin
Cephalexin
Cefuroxime
Cefuroxime axetil
Cefotaxime
Cefixime
Cefpodoxime proxetil
Cefepime
Adverse effects of Cephalosporins
Uses of Cephalosporins
The current slide include the pharmacology og cephalosporins.
Contents
Introduction to Cephalosporins
Classification of Cephalosporins
Cefazolin
Cephalexin
Cefuroxime
Cefuroxime axetil
Cefotaxime
Cefixime
Cefpodoxime proxetil
Cefepime
Adverse effects of Cephalosporins
Uses of Cephalosporins
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
An overview of muscarinic receptor agonists and antagonists. This presentation was delivered to 2nd year pharmacy students enrolled in a pharmacology & toxicology class and accompanies Goodman & Gilman's (12e) chapter 9.
Parasympatholytics are the drugs that block or inhibit the actions of acetylcholine at postganglionic nerve endings and cholinergic receptors. They are also referred to as anticholinergics or cholinergic blocking agents or antispasmodics.
Anticholinergic drugs include atropine and related drugs- atropine is the prototype. Atropine is obtained from the plant Atropa belladonna. Atropine and scopolamine (hyoscine) are the belladonna alkaloids. They compete with acetylcholine for muscarinic receptors and block this receptors-they are muscarinic antagonists.
Cholinergic antagonists and blockers-Dr.Jibachha Sah,M.V.Sc,LecturerDr. Jibachha Sah
Dr. Jibachha Sah,M.V.Sc( Veterinary pharmacology, TU,Nepal),posted lecturer notes on AUTONOMIC AND SYSTEMIC PHARMACOLOGY for B.V.Sc & A.H. 6 th semester veterinary students of College of veterinary science,Nepal Polytechnique Institute, Bharatpur, Bhojard, Chitwan, Nepal.I hope this lecture notes may be beneficial for other Nepalese veterinary students. Please send your comment and suggestion .Email:jibachhashah@gmail.com,moble,00977-9845024121
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
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Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
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Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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3. Characteristics of important
subtypes of Muscarinic receptor
By pharmacological as well as molecular cloning techniques,
muscarinic receptors have been divided into 5 subtypes M1, M2, M3,
M4 and M5.
The major subtype that are present on effector cells as well as on
prejunctional nerve endings, and are expressed both in peripheral
organs as well as in the CNS.
The M4 and M5 receptors are present mainly on nerve endings in
certain areas of the brain and regulate the release of other
neurotransmitters.
Most organs have more than onesubtype, but usually one subtype
predominatesin a given tissue.
4. Three main types of
Muscarinic receptor
M1 :-
The M1 is primarily a
neuronal receptor
located on ganglion
cells and central
neurones, especially
in cortex,
hippocampus and
corpus striatum. It
plays a major role in
mediating gastric
secretion, relaxation
of lower esophageal
sphincter (LES) on
vagal stimulation and
in learning, memory,
motor functions, etc.
M2 :-
Cardiac muscarinic
receptors are
predominantly M2
and mediate vagal
bradycardia.Autorece
ptors on cholinergic
nerve endings are also
of M2 subtype.
Smooth muscles
express some M2
receptors well which,
like M3,media
contraction.
M3 :-
Visceral smooth
muscle contraction
and glandular
secretions are elicited
through M3 receptors,
which also mediate
vasodilatation .
Together the M2 and
M3 receptors mediate
most of the well-
recognized muscarinic
actions including
contraction of LES.
8. Muscarinic drugs mechanism
of action
competitively block muscarinic receptors. Atropine
and scopolamine block all M receptors. Other
antimuscarinic drugs are selective.Tertiary
antimuscarinics don't block Nn. Quarernary block
muscarinic but also Nn.
9. Anti-muscarinics on CNS
Antimuscarinic onCNS high dose :-
Amnesia, malaise, restlessness, irritability, disorientation, halluciations, delirium.
Coma.
Antimuscarinics on CNS intermediate dose :-
Mild vagal stimulation. Fatigue, sedation, drowsiness, depression of vestibular,
reduction in parkinsonian tremor and rigidity.
10. Antimuscarinics on Heart
Antimuscarinics on heart intermediate dose :-
Tachycardia. Many types of reflex vagal cardiac slowing can be abolished. Atria -
increase in automaticity and contractility. AV node - increase in conduction and
automaticity, decrease in refractoriness. Ventricles - minimal direct effect.
Antimuscarinics on heart low dose :-
Decrease in heart rates (due to blockade of M2 presynaptic autoreceptors and to
central vagal stimulation.
11. Antimuscarinics on
Cardiovascular (CV) vessels
Antimuscarinics on CV vessels after high dose :-
Dilation of cutaneous blood vessels (unknown mechanism) in children can cause
atropine flush.
Antimuscarinics on Cardiovascular vessels therapeutic dose :-
Negligible effects (but vasodilation and hypotension caused by choline esters are
antagonized).
12. Antimuscarinics on
GASTROINTESTINAL TRACK
Antimuscarinics on GIT :-
Decreased gastric secretion, decreased tone, contractions, peristaltic activity.
Relaxation of LES, gallbladder, bile ducts.
13. Antimuscarinics on Genitourinary
System
Antimuscarinics on Genitourinary system :-
Relaxation of pelves, calyces, ureters. Decreases peristalsis, relaxation of detrusor
muscle (increased capacity).
14. Antimuscarinics on respiratory
system
Antimuscarinics on respiratory system :-
Bronchial relaxation, decreased secretions, decreased mucociliary clearance
(except ipratropium).
15. Antimuscarinics on eyes
Antimuscarinics on eyes :-
Relaxation of sphincter of iris (mydriasis), relaxation of ciliary muscle (cycloplegia,
accommodation is lost) hinders outflow of aqueous humor thru schlemm's canal.
When atropine is given locally, these effects last for 3 days. Decreased lacrimal
gland secretion.
16. Antimuscarinics on skin
Antimuscarinics on skin :-
Decreased sweat. Raises body temperature. Infants and children are prone to
atropine fever.
17. Antimuscarinic toxicity
Antimuscarinic toxicity :-
Skin rashes, urticarial, fever. Therapeutic index >100 adults, but a dose of 5mg
can be lethal to children. Serious atropine poisoning appears in 30 minutes, lasts
for 2-7 days. Death due to respiratory failure may follow coma and collapse.
Poisoning by antimuscarinics :-
mydriasis, blurring of vision, dryness conjunctiva, difficulty speaking, dyspnea,
respiratory depression, dry hot red skin, dryness of mouth, difficulty swallonging,
no bowel sounds, difficulty in micturition, tachycardia, arrhythmias, fatigue,
ataxia, restlessness, delirium, hallucinations, coma.
18. Diagnosis of antimuscarinic
poisoning
Diagnosis of antimuscarinic poisoning :-
IM injection of physostigmine. If signs of muscarinic activation do not occur,
poisoning with antimuscarinic drug is almost always certain.
19. Treatment for poisoning
Antimuscarinic treatment :-
maintenance of vital signs, alleviation of convulsion with diazepam, temp control
with ice bag and alcohol sponges.
20. Contraindications of
Anti-Muscarinics
Contraindications of antimuscarinics :-
glaucoma, prostatic hypertrophy, urinary tract obstruction, GI tract obstruction, a
dynamic ileus, gastric ulcer, infectious diarrhea, UC, chron's disease,
tachyarrhythmia’s, coronary artery disease, hyperthyroidism, children, elderly.
21. Therapeutic uses of antimuscarinics
Therapeutic uses of antimuscarinics :-
Funduscopic exam (mydriasis), measurements of refractive errors, iritis,
chroiditis. IBS diahrea, renal colic, enuresis, urinary incontinence (to
reduce frequency), preoperative lung surgery to reduce secretions,
bronchial asthma and copd (ipratropium), cardio resuscitation (when
vagal hyperactivity is the cause of cardiac arrest), sinus or nodal
bradycardia, AV block due to increased vagal tone. CNS - prevention of
motion sickness (scopolamine), parkinsons (triexyphenidyl).To
counteract parasympathomimetic effects of neostigmine in myasthenic
patients. Poisoning by AchE inhibitors or mushrooms containing
muscarine.
27. Acetylcholine is the main contractile neurotransmitter of the
detrusor muscle – it stimulates the muscarinic receptors. Anti-
muscarinic medications are, therefore, used to treat overactive
bladder, to :-
• reduce intravesical pressure,
• reduce uninhibited contractions.
28. Available Medication’s
The available medications are:
• listed:
oral oxybutynin IR (Ditropan), propantheline (Pro-
Banthine), imipramine (Tofranil) and, as a second-line,
the oxybutynin transdermal patch (Oxytrol).
• private script:
tolteridine IR (Detrusitol), solifenacin (Vesicare),
darifenacin (Enablex), and the oxybutynin transdermal
patch (Oxytrol).
30. Oxybutynin IR ( Ditropan XL,
Urotrol )
1. This is an anticholinergic,
antispasmodic and local
anaesthetic.
2. It is more selective for the salivary
gland than the bladder, so dry
mouth and constipation are
common.
3. However, most side effects are
caused by an active metabolite
from first pass mechanism in the
gut.
4. It has well-documented
effectiveness at doses of 2.5–5mg
up to 4 times a day
31. Oxybutynin patch (oxytrol )
1. This has no more systemic side effects than placebo, with minimal
discontinuation due to dry mouth.
2. It releases oxybutynin 3.9 mg/day and the patch is changed twice a
week.
3. There may be redness at the application site.
32. Solifenacin
Brand Name(s):
India : Soliten (5 mg) | Bispec (10
mg) | Solicept (5mg) | Bispec (5 mg) | Soliten
(10 mg) |Vesiact (5mg)
Foreign Names : VESIcare
1. Solifenacin is more selective for
M3 receptors in the bladder than
in the salivary glands, so there are
low rates of dry mouth and a low
discontinuation rate.
2. Again, there is well-documented
effectiveness with doses of 5–10
mg once a day.
33. Darifenacin ( Enablex )
1. Darifenacin is a relatively selective M3 receptor antagonist with low
discontinuation rates and good effectiveness.
2. It is given as a once daily oral dose of 7.5–15 mg.
34. Tolterodine IR ( Detrol LA )
1. Tolterodine in a nonselective muscarinic receptor antagonist with
more affinity for the bladder than the salivary gland.
2. It is effective at 1–2 mg twice a day.
35. Propantheline (Spastheline )
Foreign Names
• Propanthelini Bromidum (Latin)
• Propanthelin bromid (German)
• Propanthéline bromure de (French)
• Propantelina, bromuro de (Spanish)
1. Propantheline is a nonselective muscarinic receptor antagonist with
poor GIT absorption, a short half-life, a poor side-effect profile, and
varying effectiveness.
36. Imipramine (Tofranil )
1. Imipramine has systemic
antimuscarinic actions and
blocks reuptake of serotonin
and noradrenaline.
2. It therefore has cardiovascular
side effects and can cause
drowsiness in therapeutic
antidepressant dosages.
3. Use low dosage to benefit
nocturnal enuresis and
nocturia
37. Side Effects
The side effects of antimuscarinic drugs include:
dry mouth with difficulty swallowing and thirst
dilation of the pupils with difficulty accommodating and sensitivity to
light - i.e. blurred vision
increased intraocular pressure
hot and flushed skin
dry skin
bradycardia followed by tachycardia, palpitations and arrhythmias
difficulty with micturition - urinary retention
Constipation
More rarely:
fever
confusion, mania, hallucinations
rashes
39. For many years, antimuscarinic drugs have been the first-line
pharmacological treatment for urgency, frequency, and urge
incontinence, all symptoms of the disorder termed overactive
bladder.
Antimuscarinic treatment is not always effective and is associated
with side-effects that limit its clinical use.
They may not be the perfect treatment for all patients with this
disorder, but their value for individual patients should not be
underestimated.
Further clinical trials with improvement in quality of life as the
primary endpoint are needed and may give a fair reflection of the
clinical value of antimuscarinic drugs.
41. Nicotinic receptors are selectively activated by
nicotine and blocked by tubocurarine or
hexamethonium.
They are rosette-like pentameric structures
which enclose a ligand gated cation channel;
their activation causes opening of the channel
and rapid flow of cations resulting in
depolarization and an action potential.
On the basis of location and selective agonists
and antagonists two subtypes NM and NN
(previously labelled N 1 and N 2) are recognized.
42. Two types of Nicotinic
receptors
NM:
These are present at skeletal
muscle end plate are
selectively stimulated by
phenyl trimethyl ammonium
(PTMA) and blocked by
tubocurarine.They mediate
skeletal muscle contraction.
NN:
These are present on
ganglionic cells (sympathetic
as well as parasympathetic),
adrenal medullary cells
(embryologically derived from
the same site as ganglionic
cells) and in spinal cord and
certain areas of brain.They are
selectively stimulated by
dimethyl phenyl piperazinium
(DMPP), blocked by
hexamethonium, and
constitute the primary
pathway of transmission in
ganglia.
44. About NEUROMUSCULAR BLOCKERS
Neuromuscular junction blocking agents
(NMBA’s) act on cholinergic receptors on the
skeletal muscle endplate to produce muscle
paralysis.
They are used during anaesthesia to facilitate
endotracheal intubation and provide surgically
required muscle relaxation.
47. Atracurium (Tracrium ® )
May be given undiluted by IV bolus.
Dosing (Adults):
initially 0.4 to 0.5 mg/kg IV bolus, followed by 0.08 to 0.1
mg/kg every 20 to 45 minutes after initial dose.
Continuous infusion: initially 0.4 to 0.5 mg IV bolus,
followed by 9 to 10 mcg/kg/min. Maintenance infusion
rates of 5 to 9 mcg/kg/min are usually adequate. (Range:
2 to 15 mcg/kg/min).
Toxic metabolite (laudanosine) may accumulate in
renal failure.
[Supplied: 50 mg/5 ml ; 100 mg/10ml vial]
48. Cisatracurium (Nimbex ® )
Dosing (Adults):
Intermittent: initial dose: 0.15 to 0.2 mg/kg IV bolus
followed by 0.03 mg/kg IV every 40 to 60 minutes.
Continuous infusion: 0.15 to 0.2 mg/kg IV bolus followed
by 1 to 3 mcg/kg/min.The average infusion rate for long
term use in the ICU is at 3 mcg/kg/min (range: 0.5 to 10.2
mcg/kg/min). In some cases, re-administration of the
bolus dose may be req'd while titrating. Dosage
reductions are not required in renal or hepatic failure.
Drug of choice in the following cases:
(1) hemodynamically significant increases in HR (eg
>20%) while paralyzed with pancuronium or MAP>110.
(2) Concurrent corticosteroid administration (>72hrs)
(3) Significant renal dysfunction (CRCL < 30 ml/min)
(4)History of asthma or bronchospasm.
49. Doxacurium (Nuromax OD ® )
Dosing (Adults): (usual)
Anesthesia adjunct: initial, 0.05 mg/kg and 0.08
mg/kg IV to provide neuromuscular block for an
average 100 min and 160 min, respectively.
Maintenance, 0.005 mg/kg and 0.01 mg/kg IV to
provide neuromuscular blockage for an average of
30 min and 45 min, respectively.
Endotracheal intubation: 0.05 mg/kg IV.
Endotracheal intubation: (with succinylcholine)
initial, 0.025 mg/kg IV.
[ Supplied: 1 mg/ml Solution]
50. Mivacurium (Mivacron ® )
Short-acting arizing neuromuscular blocking
agent.
Dosing (Adults)
Endotracheal intubation: 0.15 mg/kg IV bolus. For
extended neuromuscular block, IV average infusion
rates of 6 to 7 mcg/kg/min are used. Recovery from
muscular paralysis occurs within 15 to 30 minutes.
51. Pancuronium (Pavulon ® )
Non-depolarizing skeletal muscle blocker--
competes with acetylcholine at the
neuromuscular junction.
Dosing (Adults)
Intermittent dosing: 0.1 to 0.2 mg/kg (usually 0.1)
every 1 to 3 hours (range: 0.04 to 0.2 mg/kg).
Continuous infusion: Loading dose: 0.04 to 0.10
mg/kg , followed by 1 to 1.7 mcg/kg/min or 0.06 to
0.1 mg/kg/hr
52. Rocuronium (Zemuron ® )
Dosing (Adults) (usual):
Intubation(rapid sequence intubation): initial, 0.6-
1.2 mg/kg IV. tracheal intubation: initial, 0.6 mg/kg
IV. Maintenance, 0.1-0.2 mg/kg IV repeated as
needed.
Maintenance (continuous IV infusion): 0.01-0.012
mg/kg/minute.
Skeletal muscle relaxation: initial, 0.6 mg/kg IV.
Maintenance: 0.1-0.2 mg/kg IV repeated as needed.
Alternatively: maintenance (continuous IV infusion):
0.01-0.012 mg/kg/minute
53. Succinylcholine
Depolarizing skeletal muscle blocker. Indications:
procedures of short duration such as endotracheal
intubation.
Dosing (Adults):
Intermittent: 0.6 mg/kg (0.3 to 1.1) over 10-30
seconds, up to 150mg total dose. Maintenance: 0.04
to 0.07 mg/kg every 5-10 minutes as needed.
Continuous infusion: 2.5 mg/min (0.5 to 10
mg/min).
Dilute to 1-2 mg/ml.
54. Vecuronium (Norcuron ® )
Dosing (Adults)
Intermittent dosing: initially 0.08 to 0.1 mg/kg IBW
IV bolus. (Higher initial doses-up to 0.3 mg/kg-may
be used for rapid onset. Maintenance: 0.01 to 0.015
mg/kg every 25 to 45 minutes as needed.
Continuous infusion: initial IV bolus (0.08 to 0.3
mg/kg), followed by (after 20-40min), 1 mcg/kg/min
infusion (usual range: 0.8 to 1.2 mcg/kg/min).
Dosage reductions are not req'd in renal failure.
56. Pharmacology of Ganglionic
Blocker’s
A ganglionic blocker (or ganglioplegic) is a type of
medication that inhibits postganglionic transmission,
primarily by acting as a nicotinic antagonist .
Because ganglionic blockers block the parasympathetic
nervous system and sympathetic nervous system, the
effect of these drugs depends upon the dominant tone in
the organ system.
57. Ganglionic blockers on CVS :-
Moderate HR increase, decreasedCO (b/c of
peripheral venous pooling decreases preload),
marked decrease in venous tone and peripheral
resistance (hypotension in upright position), skin
blood flow is decreased, spanchnic and renal
blood flow are decreased.
58. Ganglionic blocker on heart
Ganglionic blocker on heart effect :-
Tachycardia (M2).
Ganglionic blocker on arterioles:-
vasodilation, orthostatic hypotension .
Ganglionic blocker on veins :-
vasodilation, venous pooling, decreased cardiac
output.
59. Ganglionic blocker on eye
Ganglionic blocker on iris :-
Mydriasis.
Ganglionic blocker on ciliary muscle :-
Cycloplegia.
60. Ganglionic blocker on GI
tract
Ganglionic blocker on GI tract:-
Decreased motility and tone, constipation.
63. Ganglionic blocker on sweat
glands
Ganglionic blocker on sweat glands:-
reduced secretion (anhydriosis).
64. Therapeutic Uses
- Ganglionic blockers are used less frequently now than
they were in the past, because more selective agents are
now available. However, they are still used in some
emergency situations, such as aortic dissection
or autonomic dysreflexia.
65. Drug’s Available
The first ganglion-blocker to be used clinically
wasTetraethylammonium, although it was
soon superseded by better drugs.
Other examples include :-
Hexamethonium, Pentolinium, Mecamylamine,
Trimetaphan, and Pempidine.
66. Hexamethonium (Methium)
It was formerly used to treat disorders, such
as chronic hypertension, of the peripheral
nervous system, which is innervated only by
the sympathetic nervous system.The non-
specificity of this treatment led to
discontinuing its use.
67. Pentolinium (Ansolysen)
Is a ganglionic blocking agent which acts as
a nicotinic acetylcholine receptor antagonist. It can
be used as an antihypertensive drug during surgery
or to control hypertensive crises. It works by binding
to the acetylcholinereceptor of adrenergic nerves
and thereby inhibiting the release of noradrenaline
and adrenaline. Blocking this receptor leads
to smooth muscle relaxation and vasodilatation.
Pentolinium can be given orally,
injected intramuscularly or
administered intravenously.
68. Mecamylamine
A nicotinic antagonist that is well absorbed from
the gastrointestinal tract and crosses the blood-
brain barrier. Mecamylamine has been used as a
ganglionic blocker in treating hypertension, but,
like most ganglionic blockers, is more often used
now as a research tool.
70. Trimetaphan camsilate or trimethaphan
camsylate (USA), trade name Arfonad, is a drug
that counteracts cholinergic transmission at
the ganglion type of nicotinic receptors of
the autonomic ganglia and therefore blocks both
the sympathetic nervous system and
the parasympathetic nervous system. It acts as a
non-depolarizing competitive antagonist at the
nicotinic acetylcholine receptor, is short-acting,
and is given intravenously.
71. Pempidine
Is a ganglion-blocking drug, first reported in
1958 by two research groups working
independently, and introduced as an oral
treatment for hypertension.
72. Pharmacokinetics of ganglionic blocker’s:-
Hexamethonoium is quaternary ammonium,
mecamyalamine is secondary amine (active by
oral and enters CNS).
73. Side Effects
Cardiovascular: Orthostatic(postural) hypotension,
Tachycardia,
GIT: Dry-mouth, GIT atony,urine retention, digestive
problems,
Sexual Dysfunction: Failure of erection and ejaculation.
Blocks baroreceptor reflex.
Blocks parasympathetic mediated pupil contraction and
accommodation.