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CS
PHARMACOLOGICA
L ACTIONS
BENZODIAZEPINES
Completely
absorbed from GIT
Erratic absorption if
IM
Can cross BBB and
placenta
Metabolized in liver
CNS
= sedation and
hypnosis, increase
duration of sleep
= decrease anxiety
(alprazolam)
= muscle relaxation
(clonazepam)
= anticonvulsant
= anterograde
amnesia
CVS
= minor effect
= preanesthetic
dose decrease : BP
= preanesthetic
dose decrease :
blood flow
= IV diazepam
increase coronary
flow
GIT
= markedly
decreased nocturnal
BUSPIRONE
CNS
= CNS depression
= sedation, ataxia,
hypnosis
Respiratory
depression
= suppress hypoxic
and chemoreceptor
response to CO2
Enzyme induction
= induce CYP450 in
liver
= diminish action of
many drugs that
depend on CYP450
eg warfarin
BARBITURATES
Rapidly absorbed
from GIT
= high lipid
solubility
Widely distributed
= redistribution to
others in short time
Metabolized in liver
Excreted via renal
route
ETHANOL
Readily absorbed
from GIT
Metabolized via
liver ans excreted
via kidney
CNS depression
= sedation and
hypnosis with
increasing dosage
MOA
USES
gastric acid
secretion
Attach at GABA at
receptor
Opening chloride
ion channels in cells
Anxiolytic
Anticonvulsant
Hypnotic
Muscle relaxant
ROA
ADVERSE EFFECTS
Chronic treatment
of GAD
= efficacy
comparable to Bzs
Lack anticonvulsant and
muscle relaxant
properties
SIDE EFFECTS
Tolerance
Potentiate GABA
action
Bind to receptor at
subunit
Surgical anesthesia
(Thiopentone IV)
Anti-epileptic
Sedative-hypnotic
agent
Treatment of
hyperbilirubinemia
and kernicterus
Similar to Bzs
= dizzy, drowsiness,
amnesia, tolerance,
dependence
Acute toxicity
= respiratory
depression and
circulatory shock
(fatal)
Can cross placental
barrier and excreted
in breast milk
Anxiolytic and
sedation
Oral
Chronic
Overdose coma,
severe respiratory
depression,
hypotension leading
to CVS collapse and
renal failure
DRUG
INTERACTIONS
Dependence
Withdrawal
symptoms
Potentiate effects of
CNS depressants
Cimetidine delays
metabolism of Bzs
Flumazenil (GABA
antagonist)
= IV only
= rapid onset, short
duration of action
(1/2 life 1 hour)
ANTAGONIST
consumption can
lead to liver
disease, gastritis,
and cardiomyopathy
Doesnt potentiate
effcts of CNS
depressants and
alcohol
Potentiate effects of
CNS depressant and
alcohol
Types of Bzs
Long acting
Intermediate acting
Short acting
- Diazepam
- Alprazolam
- Oxazepam
- Flurazepam
- Lorazepam
- Triazolam
During this lengthy period of time, drugs will show up in blood test and drug screens
BENZODIAZEPINES
PSYCHOLOGICAL EFFECTS
TOLERANCE
Relaxation
Drowsy
Distraction from other problems
Physical dependence
WITHDRAWAL SYMPTOMS
EFFECTS IN OVERDOSE
NON BARBITURATES
Chloral hydrate
Paraldehyde
- Relatively safe
- Oral sedative dose
- Induce sleep in hour and lasts in about 6 hours
- Produces action within 15 minutes
- Used when other drugs fails
- Rarely given IV
- Disadvantages = irritant to skin and mucosa
= cyanosis
= unpleasant taste
= cough
= hypotension
- Used in emergency treatment for convulsion of tetanus,
status epilepticus
BENZODIAPINES
Clonazepam
Clorazepate
Flurazepam
Alprazolam
Lorazepam
ADVANTAGE
- Chronic therapy in seizures
-
Less potent
More slowly to be eliminated
= no rebound insomnia upon
discontinuation
DOC for panic disorders
Fewer drug interactions
Safer in patients with hepatic
DISADVANTAGE
- Disturb motor and intellectual
- Potential for dependence
- Withdrawal seizures may occur
impairments
ADVANTAGE
- Useful in long term therapy for
GAD with symptoms of irritability
- Doesnt potentiate CNS
depressants and alcohol
- Low potential for addiction
ADVANTAGE
- Rapid onset of action
BUSPIRONE
Buspirone
BARBITURATES
Phenobarbital
Pentobarbital
Thiopental
TONIC CLONIC
PARTIAL SEIZURE
Valproate
Carbamazepine
Phenytoin
Epileptic Drugs
Uses
Carbamazepine
Phenytoin
Valproate
Pharmacokinetics
Mechanism of action
CLASSIFICATION OF EPILEPSY
PETIT MAL
ATYPICAL
(ABSENCE)
ABSENCE,
MYOCLONIC
Ethosuximide
Valproate
Valproate
Phenytoin
all types of epilepsy
dose : 150-300 mg/day,
gradually increase to
maximal to 600 mg/day
Slow absorption
Inactivated by liver
microsomal enzymes
Inhibition of Na channel
function
DISADVANTAGE
- Slower onset of action
- No muscle relaxation/convulsant
DISADVANTAGE
- Tolerance
- Induce drug-metabolizing
enzymes and physical
dependence
- Severe withdrawal symptoms
STATUS
EPILEPTICUS
TOXAEMIA
(ECLAMPSIA)
Diazepam IV
Clonazepam IV
Lorazepam IV
Paraldehyde IV
Phenobarbiton
e IV
Valproate
Broad spectrum
anticonvulsant
Dose : 600 mg daily
Rapid absorption
Metabolized in liver
Excreted in urine
Similar to phenytoin
Inhibit Na channel function
MgSO4 IV
Carbamazepines
All types of epilepsy
DOC for partial seizures and
tonic clonic seizures
Dose = 100-200 BD
Slow absorption
Metabolized in liver
Excreted in urine
Similar to phenytoin
Inhibit Na channel function
= stabilizes excitables
membranes of neuronal and
cardiac cells
Adverse effects
Drug interaction
CNS
- Cerebello vestibular effects
- Ataxia
- Nystagmus
- Lethargy
- Tremor
- Dystonia
- Confusion
Long term effect
- Gum hypertrophy
- Hirsutism
- Coarsening of facial features
IV route
- Cardiac arrhythmias
- CNS depression
Overdose
- Coma
- Apnea
- Inhibition of phenytoin
metabolism
= valproate
= cimetidine
= cotrimazole
= isoniazid
= chloramphenicol
CARBAMAZEPINE
- Mania
- Trigeminal neuralgia
CNS
- Drowsiness
- Ataxia
- Diplopia
- Headache
- Nystagmus
- Reversible blurred vision
Hypersensitivity reactions
- Rash
- Dyspepsia
Others
- Water retention
- Leucopenia
- Aplastic anemia
VALPROIC ACID
- Mania
- migraine
Carbamazepine
Trigeminal neuralgia
Lamotrigine
Mania
Migraine
Phenytoin
Valproic acid
DEFINITION
ALUMINIUM SALT
- non-systemic
- widely used
MAGNESIUM SALT
- Major salts
= magnedium oxide
= magnesium
hydroxide (MOM)
CALCIUM CARBONATE
- Prompt and prolonged
effect
- Non-systemic
MOA
Can be absorbed
systemically but
rapidly excreted
ADVERSE
EFFECT
Hypophosphatemia
= absorb phosphate
= reduce phosphate
absorption
= increase phosphate
loss
Constipation
Bone fractures
Hypermagnesia
Mg intoxication
Diarrhea
On reaching acididc
environment of
stomach, insoluble
calcium carbonate
turns to calcium
chloride which can be
absorbed
Constipation
Hypercalcemia
Renal calcium stones
Milk-alkali syndrome
= hypercalcemia
+metabolic alkalosis
SODIUM BICARBONATE
- Most common home
remedies for GI upset
- Extremely effective
and prompt acid
neutralizer
- Both sodium and
bicarbonate are freely
absorbed into blood
stream
Hypertension
Systemic alkalosis
USES
IMPLICATIONS
= decrease
phosphate, decreased
calcium
= bone more brittle
Hypercalcemia
= redistribution of
calcium from bone to
blood stream
Hyperphospahtemia :
Al salts
Hypophosphatemia :
Al P
Check patients who
took high dose of
aluminium slats for
hypercalcemia and
hypophosptameia
Encourage person atr
risk of phosphate
deficiency or
osteoporosis
Dont take interacting
medications orally
within 2 hours
Antacids
Laxatives
Antacids
Peptic ulcer
Milk
indigestion/heartburn
phenothiazine
s
chlorpromazin
e
halperidol
Dopamine D2
receptor
antagonist
butyrophenon
es
domperidone
dolperidol
mtaclopramid
e (maxalon)
banzamide
DRUGS
DEFINITION
USES
PHENOTHIAZINES
Potent
Transquilizing
properties and
dopemine antagonist
will inhibit vomiting
(low, non-sedative
dose)
Gastroenteritis
Uraemia
Drug-induced
vomiting (estrogen,
tetracycline,
chemotherapy)
METACLOPRAMIDE
Phenothiazine like
action
Act on CTZ through
dopamine blockage
Oral, IM, IV
Antiemetic in
chemotherapy
ANTIHISTAMINES
Diphenhydramine
Dimenhydrmaine
Doxylamine
Cyclizine
Meclizine
Produce central
anticholinergic action
by blocking action of
H1 subtype of
histamine receptor
Prophylaxis of motion
sickness
Postoperative nausea
and vomiting
ANTICHOLINERGIC
Atropine
Scopolamine
SIDE EFFECTS
Extrapyramidal
symptoms
Dystonia
Hypotension
Agranulocytosis
PHARMACOKINETI
CS
DRUGS
ALKALYTAING AGENTS
-
ADVERSE
EFFECTS
Location
- brain
- spinal cord
CNS depression
Drowsiness and
sedation
Anticholinergic action
ANTIMETABOLITES
Chlorambucil
Cyclophosphamide
IMMEDIATE
-
Receptor type
- (mu)
Extrapyramidal
symptoms
Headache,
drowsiness,
restlessness, fatigue
Rapidly and
completely absorbed
Excreted in urine
Metjotrexate
Florouracil
DELAYED
BM suppression
= immunosuppression
= alopecia
= GIT : stomatitis, mucositis, diarrhea
= infertility and teratogenesis
= skin : pigmentation, edema
= kidney : tubular necrosis
= lung : fibrosis
Effects
- Anelgesia
- Respiratory depression
- Euphoria
(Kappa)
(delta)
brain
spinal cord
brain
Morphine
- Pharmacological effect
Addiction
Decrease GI motility
analgesia
sedation
analgesia , little/no respiratory depression
Explanation
- Analgesia
- Euphoria
- Respiratory depression
- Cough suppression
- Pupillary constriction
- Nausea and vomiting (emesis)
- GIT symptoms
- CVS effects
= no major effects but at larger doses, hypotension and bradycardia
Uses
Route of administration
Duration
BBB
Adverse effects
Caution
Side effects
Abstinence syndrome
Prevention of withdrawal
Drug interactions
= lacrimation
= chills
= muscle ache and jerks
= diarrhea
= vomiting
= yawning
= anxiety
= hostility
= hyperventilation
= hyperthermia
With anpther strong opioid drug
Codeine is not effective
Methadone DOC for maintenance programs
Rare
Enhanced by Phenothiazines and other CNS depressants
DRUGS
PHARMACOKINETICS
HYDROMORPHONE
- Oral
- Onset 15-30 minutes
- IV duration of action (3-4
hours), peak effect (30-60
minutes)
HEROIN
- Greater lipid solubility
- Cross BBB more than
morphine
- Converted to morphine in
body
- Duration of action (1/2 hour)
PROPERTIES AND
EFFECTS
Drugs
General
Potent analgesic
Morphine 8-10X
Used in surgical settings for
moderate to severe pain
Naloxone
Used to reverse opioid receptors by
rapidly displacing all receptor bound
molecules
= 10 fold higher affinity for than
FENTANYL
- Oral, transdermal, IV
- Rapid onset
Oral = 7-15 minutes
transdermal = 12-17 hours
- Duration of action
Oral = 15-30 minues
transdermal = 72 minutes
- Most effective opiate
analgesic
- 80x morphine
10x hydromorphone
Naltrexone
Action similar to naloxone
Longer duration than naloxone
Used in preference than naloxone
Long onset than naloxone
Mechanism of action
Pharmacokinetics
receptors
Rapidly displace all opioid agonist
Antagonist at , , and receptors
IV injection
= onset 30 seconds
= life 30-81 minutes
No pharmacological effects in normal
individuals
No clinical effect with oral but can be
seen with IV
CLASSIFICATION OF
NSAID
-
PROSTAGLANDIN
EFFECTS
EFFECTS OF COX
INHIBITION
ASPIRIN
MOA
MARKED ANTI
INFLAMMATORY ACTION
Salicyclic acid derivatives
(aspirin)
Pyrazolone derivatives
= phenylbutazone
Acetic acid derivatives
= indomethacin
Oxicam derivatives
= piroxicam
COX -1
- Protect mucosa
- Platelet aggregation
- Vasodilatation of kidney
- Gastric ulcers
- Bleeding
- Acute renal failure
Similar to naloxone
MODERATE ANTI
INFLAMMATORY ACTION
Propionic acid
= ibuprofen
Fenamic acid
= mefenamic acid
Non acidic
= nabumetone
COX
-
EXPLANATION
- Inhibitors of COX enzymes
2
Inflammation of peripheral injury site
Modulate pain perception
Promote fever
Reduce inflammation
Reduce pain
Reduce fever
PHARMACOLOGICAL EFFECT
USES
PHARMACOKINETICS
REYES SYNDROME
DOSAGE
ADVERSE EFFECT
Drugs
Properties
Type
= nausea
= vomiting
Bleeding
= prolonged bleeding time
Respiration
= depression and metabolic acidosis at toxic dose
Hypersensitivity
= urticarial, bronchoconstriction, angioedema, anaphylactic shock
Reyes syndrome
= fatal, hepatitis with cerebral edema
Acetaminophen (PAP)
By blocking PG synthesis in CNS
= antipyretic
= analgesic
Less effect on COX in
peripheral tissues, weak
anti-inflammatory action Does not alter platelet
function/increase
clotting time
Not considered NSAIDs
Location
Ibuprofen
Anti-inflammatory,
analgesic and antipyretic
Alter platelet function
and prolong bleeding
time
Widely used for
RHEUMATIC ARTHRITIS
and OSTEOARTHRITIS
because effects are less
intense than aspirin
Function
Celecoxib
COX-2 inhibitor
Uses = RA, osteoarthritis
= acute to
moderate pain
Does not inhibit platelet
aggregration and does
not increase bleeding
time
Similar efficacy to
NSAIDs in treatment of
pain and CVS events
H1 histamine receptor
H2 histamine receptor
H3 histamine receptor
H4 histamine receptor
EXPLANATION
1st gen
2nd gen
Block histamine receptors from histamine
Well absorbed after oral administration
Distributed in all tissues
Plasma half-life = 4-6 hours
Onset = 1-3 hours
THERAPEUTIC USES
ADVERSE EFFECTS
DRUG INTERACTIONS
OVERDOSE
DIFFERENCES
1st GEN H1
- 3-4 daily doses
2nd GEN H1
- 1-2 times daily
Cross BBB (lipophilic, low MW, lack recog of Pglycoprotein efflux pump)
Potentially cause side-effects
Toxicity are possible
Lethal dose identified for yound children
No randomized, double-blind placebo-controlled trials in
children
EXPLANATION
Mediates transmission of nerve impulses across autonomic ganglia in both symphatetic and
parasymphatetic
TYPE
PHARMACOLOGICAL
EFFECT
OTHER CHOLINERGIC
AGENT
PILOCARPINE
ACTIVITY
PHARMACOLOGICAL EFFECTS
ADVERSE EFFECTS
Antagonist