40 slides that focus on the drugs used to treat epilepsy (anti-epileptic drugs) and their their primary molecular mechanisms of action. Produced by Stephen Kelley (University of Dundee, UK).
Anti-hypertensive agent and Recent developementsnamanjain727
1.To study chemistry, SAR, mechanism of action, side effects, therapeutic uses of various anti-hypertensive drugs.
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Anti-hypertensive agent and Recent developementsnamanjain727
1.To study chemistry, SAR, mechanism of action, side effects, therapeutic uses of various anti-hypertensive drugs.
2.To emphasize on the newer current upcoming drugs for the treatment of hypertension.
This 13-slide slide set created with PowerPoint provides an introduction to antidepressants describing their discovery and development; their modes of action and relationship to the monoamine hypothesis of depression; and their efficacy, latency and unwanted actions. The beginner level introduction is tailored to aid the understanding of individual antidepressants. Contributed by Christopher Fowler, Umeå University, Sweden.
by: Dr. Vishal Pawar, MD Pharmacology
All the recent updates regarding antiepileptics, composed into a single ppt presentation to make researching and learning easier
Lecture 7 from a college level neuropharmacology course taught in the spring 2012 semester by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University.
a presentation on GABA including its synthesis, storage and degradation, types of receptors, and implications in various neuropsychiatric disorder, and finally a small chart on the drugs acting on GABA system.
Lecture slides for Medical Undergraduate teaching in Pharmacology. Study material is based on Essentials of medical pharmacology by KD tripathi and Katzung. Figures are obtained from google image search and above mentioned textbooks.
This 13-slide slide set created with PowerPoint provides an introduction to antidepressants describing their discovery and development; their modes of action and relationship to the monoamine hypothesis of depression; and their efficacy, latency and unwanted actions. The beginner level introduction is tailored to aid the understanding of individual antidepressants. Contributed by Christopher Fowler, Umeå University, Sweden.
by: Dr. Vishal Pawar, MD Pharmacology
All the recent updates regarding antiepileptics, composed into a single ppt presentation to make researching and learning easier
Lecture 7 from a college level neuropharmacology course taught in the spring 2012 semester by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University.
a presentation on GABA including its synthesis, storage and degradation, types of receptors, and implications in various neuropsychiatric disorder, and finally a small chart on the drugs acting on GABA system.
Lecture slides for Medical Undergraduate teaching in Pharmacology. Study material is based on Essentials of medical pharmacology by KD tripathi and Katzung. Figures are obtained from google image search and above mentioned textbooks.
Anticonvulsants are a diverse group of pharmacological agents used in the treatment of epileptic seizures. Charles Locock commented in the Lancet on his use of potassium bromide in 15 cases of "hysterical" epilepsy in young women. The next development was the serendipitous discovery of the anticonvulsant properties of phenobarbital by Alfred Hauptmann in 1912. This predated by more than 20 years the screening of potential therapeutic agents against "electrical seizures" in cats by Houston Merritt and Tracy Putnam. The result was the launching of phenytoin in 1938. Next came primidone, ethosuximide, carbamazepine and valproic acid, all of which can be regarded as first generation antiepileptic drugs (AEDs). Shortly after their synthesis, the benzodiazepines were rapidly recognised as having anticonvulsant activity. The modern era focused on the systematic screening of many thousands of compounds against rodent seizure models under the Anticonvulsant Drug Development Program in the US. This resulted in the global licensing, in chronological order, of vigabatrin, zonisamide, oxcarbazepine, lamotrigine, felbamate, gabapentin, topiramate, tiagabine, levetiracetam, pregabalin and lacosamide.
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anti epileptics drugs is a part of pharmacology. the topic contain information regarding epilepsy and their drug. ppt is short and simple and have correct information
This a is a slide set (42 slides) covering clinically used drugs for lipid lowering. This is an updated version of the lecture series for the 2021-2022 academic year. Suitable for intermediate level learners
A teaching slide set describing the mechanisms of action and clinical use of local anaesthetics. This session is a basic introduction to the pharmacodynamics and pharmacokinetics of local anaesthetics. It is aimed at preclinical medical or dental students, or students in the early years of a pharmacology degree.
This 11-slide slide set created with PowerPoint describes the organic nitrates and their use in the treatment of angina pectoris. Contributed by Christopher Fowler, Umeå University, Sweden.
This set of 17 slides introduces students to the some of the basic physiological processes that are the targets of many analgesic drug classes. It is suitable for beginner/intermediate level learners.
This slide set provides an introduction at new learner to intermediate level to some of the most common drugs that are used clinically to modulate the rate and force of contraction of the heart. Created by Prof. JA Peters, University of Dundee School of Medicine.
This 20-slide slide set created with PowerPoint describes prostanoid synthesis and their effects on the body; mechanisms of action, beneficial and adverse effects of NSAIDS; the difference between the effects of low and high dose aspirin; and the effects and toxicity of paracetamol (acetaminophen). This is an introduction to the topic of NSAIDS which would be appropriate for beginners. Contributed by Christopher Fowler, Umeå University, Sweden.
This 9-slide slide set created with PowerPoint is a short introduction to corticosteroids, in particular, the glucocorticoids, describing their receptor-mediated effects as well as why they exert both wanted and unwanted effects when used as anti-inflammatory and immunosuppressant drugs. This introduction to the topic of corticosteroids would be appropriate for beginners. Contributed by Christopher Fowler, Umeå University, Sweden.
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This is a 16 slide presentation covering the the classes of drugs used in T2DM and their molecular mechanisms of action. Provided by Professor John A Peters, University of Dundee.
Slide set for medical students discussing the physiology and pharmacology of nausea and vomiting. Provided by Professor John A Peters, University of Dundee.
A slide set covering important pharmacokinetic principles, including drug elimination kinetics, drug clearance, dosing, effective and maximum tolerated concentration and the therapeutic ratio. Provided by Professor John A Peters, University of Dundee.
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2. These lectures on epilepsy should help you meet the
following learning outcomes:
• Develop an understanding of the pharmacological
interventions, including knowledge of mechanism of drug
action, for the treatment of epilepsy.
• Develop an understanding of the mechanism of action,
indication, side effects and pharmacokinetics of anti-
epileptic drugs in current clinical use.
2
4. 4
Anti-Epileptic Drugs*
• Drugs that enhance the action of GABA
– Sodium Valproate
– Vigabatrin
– Tiagabine
– Stiripentol
– Phenobarbital (phenobarbitone)
– Benzodiazepines
• SV2A inhibitors
– Levetiracetam
– Brivaracetam
* Grouped according to primary mechanism of action. AEDs may
have multiple MOAs
5. 5
Carbamazepine (Tegretol)
• Derivative of tricyclic anti-depressants
• First discovered to have anti-convulsant properties in
mice
• Indication: focal seizures, secondary tonic-clonic
seizures, primary tonic-clonic seizures. Not
recommended for myoclonic seizures – may worsen
condition!
– Also licensed as an alternative for lithium for prophylaxis of
bipolar disorder and for the treatment of acute mania
• Mechanism of action: Voltage-gated Na+ channel
blocker
ON
N
H
H
6. 6
Carbamazepine (Tegretol)
• Pharmacokinetics: t ½ = 20 - 40 hours first two weeks,
then reduces to 10-20 hours autoinduction of
oxidative metabolism .
• Strong hepatic enzyme-inducing agent- many
interactions with other drugs
– Carbamazepine often lowers the plasma concentration of
clobazam, clonazepam, lamotrigine and phenytoin.
• Cautions: cardiac disease Na+ channels, hepatic
and renal disease
• Side effects include GI upset, sedation, ataxia, rash
(Stevens-Johnson Syndrome, hyponatremia, increase
in vitamin D and folic acid metabolism
ON
N
H
H
7. Stevens-Johnson syndrome
7
Carbamazepine, lamotrigine and phenytoin have
been associated with Stevens- Johnson syndrome.
This is a rare, but severe, form of red or purple rash
that affects the skin and mucous membranes of the
mouth and eyes. This is a serious condition which
requires immediate medical attention.
Further information:
https://www.mayoclinic.org/diseases-conditions/stevens-johnson-
syndrome/symptoms-causes/syc-20355936
https://www.nhs.uk/conditions/stevens-johnson-syndrome
8. • Analogue of carbamazepine
• Indication: Alternative first line treatment or an add-on
therapy for focal seizures
• Mechanism of action: Voltage-gated Na+ channel
blocker
• Pharmacokinetics: t ½ = 5 hours, rapidly metabolises
to is 10,11-dihydro-10-hydroxy-carbazepine
(monohydroxy derivative, MHD) pharmacologically
active metabolite
• Lower frequency of side effects compared to
carbamazepine
• Principal side effects: dizziness, headache,
cytochrome enzyme induction potential failure of
estrogen contraception 8
Oxcarbazepine
9. 9
Eslicarbazepine
• Metabolite of oxcarbazepine
• Indication: Alternative first line treatment or an add-on
therapy for focal seizures
• Mechanism of action: Voltage-gated Na+ channel
blocker
• Pharmacokinetics: t ½ = 10-20 hours
• Dizziness, headache, skin reactions, sleep disorders;
vertigo; vision disorders; GI upset.
10. 10
• First discovered to have anti-convulsant properties in
mice
• Indication: Tonic-clonic, focal seizures,
• Mechanism of action: Voltage-gated Na+ channel
blocker
• Pharmacokinetics: low doses exhibit first order
kinetics, saturation kinetics as therapeutic [D]plasma
(10-20 mg/L) is approached dose increments of
equal size disproportional rise in steady state
[D]plasma that varies between individuals
O
N
H
N
O
HPhenytoin
(Epanutin, Dilantin)
11. 11
Phenytoin
(Epanutin, Dilantin)
• Pharmacokinetics:
– t ½ = 7- 42 hours
– Potent inducer of hepatic enzymes metabolism
of other drugs such as carbamazepine and folic
acid and vitamin D vitamin D deficiency
• Side effects include confusion, gum hyperplasia, skin
rashes, anaemia and teratogenesis
• Phenytoin is not favoured for long term therapy
O
N
H
N
O
H
12. 12
Lamotrigine (Lamictal)
• Indication: Both a first line and adjunct for absence
and tonic clonic seizures, adjunct for focal seizures,
also indicated for bipolar disorder
• Mechanism of action: Voltage-gated Na+ channel
blocker and reduces glutamate release
• Pharmacokinetics: t ½ = 22.8 to 37.4 hours, generally
allows for single daily dose
• Side effects: Rash in 10% of patients
• Cautions for lamotrigine: Myoclonic seizures (may be
exacerbated); Parkinson’s disease (may be
exacerbated) (in adults)
Cl
Cl
N
N
NN
N
HH
H
H
13. 13
Lacosamide (Vimpat)
• Indication: Refractory focal seizures
• Mechanism of action: Voltage-gated Na+ channel
blocker
• Pharmacokinetics: t ½ = 13 hours
• Side effects: dizziness, nausea, headache,
prolongation of PR intervals detected by the ECG
• Cautions: Second- or third-degree AV block
RP
14. 14
Rufinamide
• Indication: Adjunctive treatment of seizures in
Lennox-Gastaut syndrome (without valproate)
• Mechanism of action: Voltage-gated Na+ channel
blocker
• Pharmacokinetics: t ½ = 6-10 hours
• Side effects:
– Anxiety, GI disturbances, dizziness, somnolence,
fatigue, weight loss
• Cautions:
– Individuals at risk of further shortening of QTc interval
15. 15
Ethosuximide
(Zarontin)
• Mechanism of action: Blocks of T-type Ca2+
channels
• Indication: The principal drug used to treat absence
seizures, with little or no effect on other types of
epilepsy
• Pharmacokinetics: t ½ = 53-55 hours
• Side effects: gastric upset, allergic reactions
OO N
H
16. 16
Gabapentin
(Neurotin)
• First discovered to have anti-convulsant properties animal
models
• GABA analogue
• Mechanism of action: Voltage-gated Ca2+ channel blocker,
may also stimulate GAD increasing GABA
• Indication: Monotherapy and adjunctive treatment of focal
seizures with or without secondary generalized seizures, also
peripheral neuropathic pain
• Pharmacokinetics: : t ½ = 5-7 hours, does not induce hepatic
enzymes
• Side-effects: Somnolence, ataxia, dizziness, fatigue
O
O
N
H
H
H
17. 17
Pregabalin
(Lyrica)
• GABA analogue
• Mechanism of action: Voltage-gated Ca2+ channel blocker,
may also stimulate GAD increasing GABA
• Indication: adjunctive therapy for focal seizures with or without
secondary generalization; generalized anxiety disorder
• Pharmacokinetics: t ½ = 6 hours
• Side-effects: Confusion, dizziness, weight gain
18. 18
Topiramate
(Topamax)
• Mechanism of action: carbonic anhydrase inhibitor*
• Also acts as a positive allosteric modulator at GABAA
receptors, a Na+ channel blocker and an antagonist at
ionotropic glutamate (Kainate) receptors.
• Indication: can be given alone or as adjunctive treatment in
generalized tonic-clonic seizures or focal seizures with or
without secondary generalization. Also migraine prevention.
• Pharmacokinetics: t ½ = 19-23 hours
• Side effects: weight loss, cognitive impairment
* The anti-epileptic effect may not be attributed to this MOA
S
O
O
O
O
O O
O
O
NH
H
HH
H
19. 19
Zonisamide
(Zomig)
• Mechanism of action: carbonic anhydrase inhibitor
• Also acts as a Na+ channel blocker and a Ca2+ channel
blocker.
• Indication: monotherapy for the treatment of focal seizures
with or without secondary generalization. Also migraine.
• Pharmacokinetics: t ½ = 63 hours
• Side effects: cognitive impairment, small risk (<1%) of renal
stones
* The anti-epileptic effect may not be attributed to this MOA
20. Dr Kelley 20
Sodium Valproate
• Mono-carboxylic acid, chemically unrelated to other anti-epileptic drugs
• First discovered to have anti-convulsant properties in mice
• Indication: Effective for all forms of epilepsy, including absence
• Also indicated for bipolar disorder as a mood stabiliser
• Multiple mechanisms of action:
(i) Weak inhibitor of GABA transaminase = [GABA]
(ii) Inhibitor of succinic semialdehyde dehydrogenase = (indirectly)
[GABA]
(iii) May stimulate synthesis of GABA by acting at GAD, = [GABA]
(iv) May decrease GABA reuptake by acting at GAT-1 or GAT-3, =
[GABA]
(v) Weak blocker of voltage-gated Na+ channel blocker
(vi) May block NMDA-mediated responses
O
O
H
Valproic acid
21. 21
Sodium Valproate
• Pharmacokinetics: t ½ = 13-19 hours, metabolized
extensively in the liver
– Metabolic inhibitor of its own metabolism and other AEDs
lamotrigine, phenytoin and carbamazepine
– Metabolism of sodium valproate is increased by
carbamazepine
• Side effects: weight gain, impaired glucose tolerance,
teratogenicity, curling of the hair, risk of liver failure
• January 2015: MHRA has strengthened its
warnings on the use of valproate in women of
childbearing potential
O
O
H
Valproic acid
22. 22
Vigabatrin (Sabril)
• GABA analogue
• Mechanism of action: Irreversible inhibitor of
GABA transaminase
• Indication: Effective in patients unresponsive to
conventional drugs
• It should not be used unless all other appropriate
drug combinations are ineffective or have not been
tolerated, and it should be initiated and supervised by
an appropriate specialist. Can be used as a
monotherapy in the management of infantile spasms
in West’s syndrome.
O
O
NH
H
H
23. Dr Kelley 23
• Pharmacokinetics: t ½ = 7.5 hours
– Not metabolized, does not induce hepatic enzymes
• Side effects include sedation and behavioural and
mood changes (e.g., depression)
***visual field defects*** - Gradual withdrawal of
vigabatrin should be considered
• Absence seizures may be exacerbated!
O
O
NH
H
HVigabatrin (Sabril)
24. 24
Tiagabine
• GABA analogue
• Mechanism of action: Inhibits the GABA transporter
(GAT-1)
• Indication adjunctive treatment for focal seizures with or
without secondary generalization that are not satisfactorily
controlled by other AEDs. It should be avoided in absence,
myoclonic, tonic and atonic seizures due to risk of seizure
exacerbation.
• Pharmacokinetics: t ½ = 7-9 hours
• Side-effects: sedation and confusion
S
S
O
O
N
H
H
25. 25
Stiripentol
• Mechanism of action: positive allosteric modulator of
GABAA receptors
• Indication: Adjunct for refractory generalised tonic-clonic
seizures in patients with severe myoclonic epilepsy in
infancy (Dravet syndrome) used in combination with
clobazam and valproate
• Pharmacokinetics: t ½ = 4.5 - 13 hours
• Side effects include appetite and weight loss, sedation,
sleep disorders, irritability; movement disorders
26. 26
Phenobarbital
(Phenobarbitone)
• One of the first barbiturates to be developed
• 1912 first recorded use to treat epilepsy
• Mechanism of action: positive allosteric modulator of
GABAA receptors
• Indication: Adjunct for refractory focal seizures, status
epilepticus
• Pharmacokinetics: t ½ = 53-118 hours. Potent inducer of
liver enzymes - may lower plasma concentrations of other
drugs
• Side effects include sedation, depression, addiction and
withdrawal symptoms
O
O O
N NH H
27. 27
Diazepam
• Mechanism of action: Allosterically binds to the
1 and 2 subunits of the synaptic GABAA
receptor (pKi = 7.8 for both) and increase the
affinity of the receptor for GABA, increasing
the frequency that the GABAA ion channel
switches to the open state. The resulting
increased influx of chloride anions causes
hyperpolarisation of the neuron.
• Indication: Status epilepticus, also severe acute
anxiety, panic attacks, acute alcohol withdrawal.
28. 28
Diazepam
• Pharmacokinetics: t ½ = 20-100 hours
– t ½ for the active metabolite N-desmethyldiazepam, is 36-
200 hours.
• Side effects: sedation, tolerance, addiction and
withdrawal effects
N-desmethyldiazepam
29. 29
Clonazepam
(Rivotril)
Mechanism of action: positive allosteric modulator
of GABAA receptors- identical to diazepam, but
greater affinity for the 1 and 2 subunits of the
synaptic GABAA receptor (pKi = 8.9, 8.8
respectively)
• Indication: status epilepticus and all forms of
epilepsy, anxiety/panic disorder
• Pharmacokinetics: t ½ = 30-40 hours
• Side effects: sedation, tolerance, addiction and
withdrawal effects
30. 30
Lorazepam
Mechanism of action: positive allosteric
modulator of synaptic GABAA receptors-
similar to diazepam
• Indication: status epilepticus
• Pharmacokinetics: t ½ = 14 hours
• Side effects: sedation, tolerance, addiction and
withdrawal effects
31. 31
Midazolam
Mechanism of action: positive allosteric modulator
of synaptic GABAA receptors- similar to diazepam
• Indication: status epilepticus
• Pharmacokinetics: t ½ = 1.8 - 6.4 hours
• Side effects: sedation, tolerance, addiction and
withdrawal effects
32. 32
Clobazam
Mechanism of action: positive allosteric
modulator of synaptic GABAA receptors-
similar to diazepam
• Indication: adjunct in epilepsy, also anxiety (short-
term use)
• Pharmacokinetics: t ½ = 12-60 hours
• Side effects: sedation, tolerance, addiction and
withdrawal effects
33. 33
Levetiracetam
(Keppra)
Mechanism of action: inhibitor of synaptic vesicle
protein 2A
• Indication: monotherapy and adjunctive treatment of focal
seizures, and for adjunctive therapy of myoclonic seizures in
patients with juvenile myoclonic epilepsy and primary
generalized tonic-clonic seizures.
• Pharmacokinetics: Rapid absorption, maintenance dose
reached quickly, metabolized mainly in the kidney,
t ½ = 6-8 hours
• Side effects: psychosis, hallucinations, suicidal ideation
34. 34
Brivaracetam
Mechanism of action: inhibitor of synaptic vesicle
protein 2A
• Indication: Adjunctive therapy of focal seizures with or without
secondary generalization
• Pharmacokinetics: Rapid absorption, maintenance dose
reached quickly, t ½ = 7-8 hours
• Side effects: Anxiety, GI disturbances, cough, depression,
dizziness, drowsiness, fatigue, insomnia, irritability
35. Treatment of focal seizures
First line treatment: carbamazepine, lamotrigine
Alternative first line treatment: levetiracetam,
oxcarbazepine, sodium valproate
Cautions: be aware of potential effect of sodium
valproate in pregnancy
Adjunctive treatment (if first line treatment is not effective
or not tolerated): carbamazepine, clobazam, gabapentin,
lamotrigine, levetiracetam, oxcarbazepine, sodium
valproate, topiramate
• Adjunct Cautions: be aware of potential effect of sodium valproate in
pregnancy
• Action if adjunctive treatment is not effective or tolerated: consider
referral to tertiary epilepsy services (where other AEDs may be tried)
35
2016 NICE guidelines
36. Treatment of generalized tonic clonic seizures
First line treatment: sodium valproate, lamotrigine (if sodium
valproate is not suitable)
Cautions: be aware of potential effect of sodium valproate in
pregnancy. If the person has myoclonic seizures or may have
juvenile myoclonic epilepsy lamotrigine may worsen myoclonic
seizures
Alternative first line treatment: carbamazepine, oxcarbazepine
Cautions for alternates: be aware that these drugs may worsen
myoclonic or absence seizures
Adjunctive treatment (if first line treatment is not effective or not
tolerated): clobazam, lamotrigine, levetiracetam, sodium valproate,
topiramate
• Adjunct Cautions: be aware of potential effect of sodium valproate in
pregnancy. If the person also has absences or myoclonic seizures, or may
have juvenile myoclonic epilepsy do not offer carbamazepine, gabapentin,
oxcarbazepine, phenytoin, pregabalin, tiagabine or vigabatrin
36
2016 NICE guidelines
37. Treatment of absence seizures
First line treatment: ethosuximide, sodium valproate (offer first if
additional tonic clonic seizures are likely)
Cautions: be aware of potential effect of sodium valproate in
pregnancy
Alternative first line treatment: lamotrigine
Adjunctive treatment (if first line treatment is not effective or not
tolerated): consider a combination of ethosuximide, lamotrigine or
sodium valproate.
• Adjunct cautions: be aware of potential effect of sodium valproate in
pregnancy
• Action if adjunctive treatment is not effective or tolerated: consider referral
to tertiary epilepsy services (where other AEDs may be tried)
• Cautions: do not offer carbamazepine, gabapentin, oxcarbazepine,
phenytoin, pregabalin, tiagabine or vigabatrin
37
2016 NICE guidelines
38. Treatment of myoclonic seizures
First line treatment: sodium valproate
Cautions: be aware of potential effect of sodium valproate in
pregnancy
Alternative first line treatment: levetiracetam, topiramate
Alternate cautions: be aware that topiramate has poorer side effects
than sodium valproate or levetiracetam
Adjunctive treatment (if first line treatment is not effective or
not tolerated): levetiracetam, sodium valproate, topiramate
• Adjunct cautions: be aware of potential effect of sodium valproate in
pregnancy
• Action if adjunctive treatment is not effective or tolerated: consider referral
to tertiary epilepsy services (where other AEDs may be tried)
• Cautions: do not offer carbamazepine, gabapentin, oxcarbazepine,
phenytoin, pregabalin, tiagabine or vigabatrin
38
2016 NICE guidelines
39. Treatment of tonic and atonic seizures
First line treatment: sodium valproate
Cautions: be aware of potential effect of sodium
valproate in pregnancy
Adjunctive treatment (if first line treatment is not effective
or tolerated): lamotrigine
• Action if adjunctive treatment is not effective or not tolerated:
consider referral to tertiary epilepsy services (where other AEDs
may be tried)
• Cautions: do not offer carbamazepine, gabapentin, oxcarbazepine,
pregabalin, tiagabine or vigabatrin
39
2016 NICE guidelines
40. Treatment of convulsive status epilepticus
• First line treatment: Intravenous
lorazepam, intravenous diazepam, buccal
midazolam
• Adjunctive treatment (if first line treatment
is not effective or tolerated): Intravenous
phenobarbital, phenytoin
40
2016 NICE guidelines