Benzodiazepines (Bz)

Bz stimulate specific Bz-receptors

Facilitate GABAA transmission
(Allosteric modification)
Increases Cl- influx
Hyperpolarization
Post-Synaptic Inhibition of
neurons.
 Benzodiazepine receptors are
of TWO types Bz1 & Bz2
(Omega ω1 &ω2).
 (Barbiturates)

C A N D I

Clomipramine Amitriptylin Nortriptyline Desipramine Imipramine

Pharmacokinetics

► Absorbed orally → extensive hepatic first pass metabolism.

►Highly bound to plasma & tissue proteins.
►Highly lipid soluble ➔ Pass easily BBB & Placental barriers.
►Hepatic Metabolism:
1- Stimulate Specific Barbiturate receptor →GABA-mimetic & a- Change of Tertiary amines → Active Secondary amines:

facilitate GABA-A transmission → - Imipramine (Active) → Active Desipramine.

increase Cl- influx→Hyperpolarization → - Amitriptyline (Active) → Active Nortriptyline.

b- Glucuronic acid conjugation → Inactive metabolites.
Post-synaptic inhibition. ►Excretion in urine mainly in conjugated form.
 Tricyclic Antidepressants Mono-Amine Oxidase Inhibitors
(TCA) (MAOI)
Mechanism of Action

►Inhibit Neuronal Uptake1 of Noradrenaline & Serotonin →  NA, 5-HT

Inter-Synaptic

Selective serotonin re-uptake inhibitors Selective NA/5-HT Reuptake Inhibitors

(SSRI) (SNRIs)
 Tetracyclic & Unicyclic Antidepressants Herbal Anti-depressant
St.Jhon’s Wort (Hypericum Perforatum)

Act as SSRI

Used as Alternative medicine

for treatment of

Peri-Menopausal & Pre-

Menstrual Syndromes

Psychic depression
& Anxiety
Seasonal Affective
disorders
Smoking
Cessation

SEROTONIN SYNDROME can occur

with other anti-depressants

Serotonin (5-HT) Receptor Modulators Typical Phenothiazines

Anti-psychotics (Chlorpromazine)
Trazodone , Nefazodone, Vortioxetine, Mirtazapine
C.N.S

Mechanism of Action USES

Antipsychotic Blocks Dopamine
(D2-receptor) in Psychosis e.g. Schizophrenia
limbic system,
Neocortex ➢ Treats mainly the positive signs such
Blocks α-2, 5-HT2C ►Blocks 5-HT2A , 5-HT2B , 5-HT2C → SNRI 5-HT reuptake as: (hallucinations, illusions & delusions.)
and 5-HT3 receptors Release of 5-HT. inhibitor
→  Release of NA &
►Blocks H-1 receptors. (TRAZADONE)  Heat production
5-HT
by  Shivering. USED AS Hypothermic agent
➢  Tissue metabolism during
 Heat loss by cutaneous VD ( cardio-pulmonary surgery
USES HRC,  VMC & -Blocker)

USES
Peri-Menopausal Insomnia
2P Vasomotor ► Anti-emetic EXCEPT motion sickness &
Symptoms pregnancy
 C.T.Z.: Antiemetic
► Hiccough
TRAZADONE
Psychic
depression MAIN USE
Block H1 receptors USES
Preanesthetic medication
 Large doses → Block D2-receptors → LITHIUM CARBONATE
Worsen Parkinsonism

Neurolept-malignant
syndrome (NMS).

Tardive dyskinesia
(abnormal
movements)

SIDE EFFECT
SIDE EFFECT Gynecomastia &
Potent -  Prolactin
Postural Galactorrhea (Non-
blocker hypotension puerperal lactation)
↓
Tachycardia
 FSH &  LH SIDE EFFECT
gonadotrophins Infertility &
Amenorrhea in
Weak H1- SIDE EFFECT females
blocker (Anti-
Histamine) SEDATION
Weak
SIDE EFFECT
ganglion
►Hypotension
blocker
 Appetite & SIDE EFFECT
Weight gain Increased body
weight

Weak Anti- SIDE EFFECT

Muscarinic ►Dry mouth
(Atropine-like) ►Tachycardia

Haloperidol Doconate
(Depot preparation) for
maintenance treatment
 Phenytoin Phenytoin → Hepatic Microsomal Enzyme Inducer:
(Diphenylhydantoin) ❶ Its own metabolism → Tolerance & Failure of its Anti-Epileptic activity.
(KINETIC TOLERANCE)
USES ❷ Metabolism of other drugs as:
Mechanisms of Action
 Other Anti-Epileptic drugs as Carbamazepine & phenobarbitone.
Grand Mal
 Oral contraceptives.
Epilepsy
Block ofNa+-channels (Membrane  Folic Acid & Its intestinal absorption → Megaloblastic anemia
stabilization) → Delay recovery →
Treat Partial & Grand Mal
Partial seizures  Vit. D → Hypocalcemia → Osteomalacia.  Vit. K → Hypoprothrombinemia.
Epilepsy (No Sedation)
HME Inducers as Phenobarbitone & Carbamazepine → Metabolism of
Status Phenytoin.
Epilepticus
HME Inhibitors as Valproate, Cimetidine & Isoniazide → Metabolism of
NOT THE 1ST
LINE Phenytoin.
Class-1 Group-B Anti- Phenytoin displaces Thyroxin & Tricyclic Anti-Depressants from plasma
Arrhythmic→ Useful in
treatment of Ventricular proteins.
arrhythmia with Heart Block→
Arrhythmia Drug of Choice in Digitalis- Aspirin, Sulfa & Valproate → Displace phenytoin from plasma proteins.
Induced arrhythmia.

Adverse effects
Carbamazepine
B–HCG PREGNANCY
Mechanisms of Action USES
Blood: megaloblastic anemia, hypoprothrombinemia
B
First trimester Before labor Grand Mal
Bone: osteomalacia
Block of Na+-channels (Membrane Epilepsy Epilepsy
stabilization) → Delay recovery →
Treat Partial & Grand Mal
Teratogenic → Fetal Hydantoin Syndrome
Hirsutism (Androgenic effect). Partial
H → Hare lip & Cleft palate
seizures
Hepatotoxicity.
Trigeminal
Hypoprothrombinemia in baby
Hypersensitivity → Lymphadenopathy neuralgia
→ Bleeding →Prevented & treated by Vit-K
(Misdiagnosed for Hodgkin’s disease) & Lupus.

Hormones → Release of A.D.H. & Insulin →

Mood stabilizer
Hyperglycemia

CNS:→ Confusion & Hallucinations. Ataxia,

C Nystagmus & Vertigo

GIT: Gastric irritation (highly alkaline) → anorexia, nausea, vomiting → Used after meals.

G
Gum (Gingival) Hyperplasia especially in Children → Irreversible → Consult Dentists.
 Adverse effects Adverse effects

B–HCG PREGNANCY
B–HCG PREGNANCY

Teratogenic → Similar to Fetal Teratogenic → Neural tube defect (Spina bifida)

B Blood: Bone marrow Blood → Thrombocytopenia &
inhibition→Aplastic anemia,
Hydantoin Syndrome B Platelet aggregation →
agranulocytosis Hemorrhage

Hepatitis
H H Hepatotoxicity

Hormones → Release of A.D.H. → Hair Loss (Temporary) → Thin curly

Fluid retention, Hyponatremia hair

C Enzyme inhibitors → Metabolism of Phenytoin,

CNS: Ataxia, Nystagmus & Vertigo C
→ Cerebello-Vestibular C.N.S. → Sedation carbamazepine & barbiturates.

Allergy→ Steven-Jhonson Syndrome Displaces phenytoin from plasma proteins.

G G G.I.T. → Nausea &

GIT: Anorexia, nausea,
Vomiting
vomiting → G.I.T. upset
Hepatic Microsomal Enzyme Inducer (as Phenytoin)

Valproic Acid & Sodium Valproate Ethosuximide

Mechanisms of Action

Block Voltage-dependent T-Calcium

channels.
 L-DOPA ❷ C.N.S.:

a- Dyskinesia e.g. chorea and athetosis →Reduce dose of L-Dopa.

Anti-Parkinsonian Effect:
b- Psychological disturbances
❶L-DOPA (Prodrug) by Central Dopa Decarboxylase (CDD) →
e.g. delusions, hallucinations & aberrant sexual activity.
Dopamine →  D2-receptors.
“Either reduce the dose of L-DOPA or use the atypical antipsychotic Clozapine or use Pimavanserin
❷Best results are obtained in the first few (3-4) years.
5HT2A inverse agonist”
❸Treats all manifestations of Parkinsonism, especially Bradykinesia
→ C.I. in psychological disturbances
→ Tremors by stimulating D2 receptors in basal ganglia.

❸ Eye: a-Mydriasis b- May  IOP.

USES
→ C.I. in CLOSED ANGLE GLUCOMA
❹ C.V.S.:
a-Tachycardia, arrhythmias (due to ↑ catecholamin formation)
b-Postural hypotension or Hypertension
PARKINSONISM: (with the use of Large dose or concurrent use of MAO-I).
→ C.I. in CARDIAC DISEASES
 Used combined with a peripheral decarboxylase inhibitor as carbidopa to ❺ G.I.T.:
 central L-Dopa.
a-Nausea and vomiting that can be treated by Domperidone.
 Start with small frequent doses to be increased gradually
b-Bleeding peptic ulcer (Add Antacids)
→ C.I. in PEPTIC ULCER

❻ Sudden withdrawal → Sever Parkinsonian Rigidity

Adverse effects & C.I. Drug Interactions

❶ Fluctuation in Response: Desirable = Favorable: L-DOPA effect

❶ Peripheral Dopa Decarboxylase Inhibitor (Can NOT pass BBB) → Dose of L-DOPA →
a- At first there is increased sensitivity to L-DOPA → Good response then  response →
Peripheral Adverse effects But Central Adverse effects.
b- Wearing-off → End-of-dose Akinesia. → Related to the timing of L-Dopa intake
Examples:
c- On-off phenomena → Bradykinesia may suddenly worsen and then improve again
a- Carbidopa (10 & 25 mg) + L-DOPA (100 & 250 mg) “1:10” = Sinemet
These fluctuation in response reflect the fluctuating L-dopa b- Benserazide (25 mg) + L-DOPA (100 mg) “1:4” = Madopar.
concentration or due to loss of striatal dopamine nerve endings ❷ MAO-B inhibitor e.g. Selegiline
when the disease progress or destruction by accumulation of reactive
❸ COMT-Inhibitors e.g. Tolcapone&Entacapone.
metabolite as DOPAC & H2O2
❹ Anti-Muscarinic drugs e.g. Benztropine.

Management: Undesirable = Unfavorable: → C.I. to be taken with them

❶L-DOPA effect
 Increase the frequency of intake of L-DOPA.
 Dopamine (D2) receptor blockers:
 Use of slow release preparations (Sinemet CR).
a- Neuroleptics e.g. Phenothiazines & Butyrophenones.
 Add long acting direct dopamine agonists e.g. Bromocriptine & Pergolide.
 Drug-holiday for 3-21 days. b- Anti-emetics e.g. Metoclopramide.

Co-administration of COMT inhibitors (Entecapon)  Pyridoxine (Vit B6)→PDD→Accelerates peripheral decarboxylation → Dopamine.
❷ With Non-selective MAO-I → Severe hypertension.
 Anticholinergic drugs

Synthetic Antiparkinsonian Atropine Substitutes: If one fails try another

❶Benztropine ❷Benzhexol [Trihexyphenidyl]❸Biperiden

 Block muscarinic receptors in basal ganglia→  effect of acetyl choline

Treat mainly tremors, rigidity & Salivation. But no effect on Bradykinesia.

Uses:
Parkinsonism:
a- Add-on to L-DOPA.
b- Used mainly to treat Iatrogenic Parkinsonism induced by neuroleptic drugs.

Adverse effects & Contraindications:

similar to atropine → Glaucoma & Senile BPH.

Direct Dopamine Agonists

Amantadine
Stimulate D2 receptors in BASAL GANGLIA

❶ Antiviral agent in prophylaxis of influenza A.

❷ Acts mainly by Release &Uptake of Dopamine.
❸ Less efficacious than L-Dopa. Its effect wears off within few weeks.
 Analgesic effect of Morphine
CENTERAL ANALGESICS
NOT
Effective in
Narcotic Analgesics Anti-pyretic Analgesics Effective in
(OPIOID) (NSAIDs)

❶ Example Morphine Aspirin all types of pain itching.

especially Deep Morphine is a
visceral pain. Histamine-releaser
❷ Potency Potent, effective in ALL types of pain Less potent, effective in superficial pain
Especially deep visceral But Not itching

Through
❸ Mechanism of Central → Spinal & Supra-spinal - Central on thalamus 3 “In”
Action - Peripheral as anti-inflammatory
Inhibits Release of Substance-P & Inhibits Pain perception
Glutamate in Substantia gelatenosa (SENSORY CORTEX)
❹ With analgesia Stupor & Drowsiness Lowers elevated body temperature to normal Indifference = Alters psychological reaction to
by spinal & supra-spinal pain
mechanisms → Inhibits pain (FRONTAL CORTEX)
transmission.
❺ Long use Tolerance Then Dependence No Tolerance & No Dependence
Narcosis & hypnosis

Mechanism of action of Opiate (Opioid) Receptors Therapeutic uses of Morphine

3 Decrease
4 “P ” Slow respiration.

Decrease cAMP Decrease Release of Decrease

transmitters & mediators Excitation
Pain Primary Preanesthetic Pulmonary Edema due to
Neurogenic medication Acute Left Ventricular
Inhibit Adenylate shock Failure
Block Ca2+- Open K+-Channel →
cyclase Analgesic in
Channel Hyperpolarization. Severe Visceral To provide analgesia,
Pain sedation & amnesia
Venodilator Sedation

↓Sympathetic
Cardiac Cancer Bone ↓Venous
Colic Postoperative → Arterial V.D.
pain pain Fractures return
↓End ↓T.P.R
Myocardial Add Except Biliary
diastolic ↓After-load
infarction Atropine in Except Skull, volume
Morphine is & Eye
Biliary & operations. ↓Preload &
Renal colic. contraindicated
Decreases
in Head injury.
Pulmonary
congestion
 Side effects of Morphine

M O R P H I N E
Histamine
Respiratory Release
Depression

Retention of Bronchospasm Itching

Retention of Stool
urine
= CONSTIPATION

Hypotension

Interfere with
Miosis proper diagnosis of
Head injury & Acute
abdomen
Morphine
Poisoning

Neonatal Nausea &

Acute Chronic = Tolerance & cross- asphyxia Vomiting
Addiction tolerance with other
Opioids

Meperidine Synthetic Morphine Substitutes Fentanyl

(Pethidine) (Non-Phenanthrenes)
❶ Derivative of Meperidine
.
❷ Strong -Agonist → Strong
Pharmacodynamics Analgesic → 80 Times >
Pharmacokinetics
Morphine

Morphine-Like + Atropine- Like ❸ High Lipid solubility: I.V. →

Rapid Onset + Short duration
50% Oral (Redistribution)
Bioavailability
❶Less Analgesia (1/10 Morphine)
❷ Less  R.C. Used as I.V. Anesthesia:
►Quick onset
►Short duration ❸ Less Emetic
❹ Less Addiction a- Fentanyl alone→ Vomiting.
b- Fentanyl + Droperidol (Major
❺Atropine-Like
Metabolized in liver→ tranquillizer) → Neurolept-
❻ No P.P.P. may cause Mydriasis
a-Meperidenic acid→ Inactive→ Analgesia
❼ No Constipation
Conjugated with glucuronic acid c- Fentanyl + Droperidol +
→ Urine. ❽ No Narcosis (No Hypnosis) Nitrous oxide → Neurolept-
b-Nor-Meperidine → Active → ❾ No Antitussive Anesthesia
Excitation & Convulsions. ❿ Local irritant then Local anesthetic. The emetic effect of Fentanyl is
⓫ A.D.H. # Anti-emetic effect of
⓬Antagonized by Naloxone Droperidol.
USES : “Orally or I.M.”
⓭ Large dose → Excitation (Atropine-
❶ Severe Visceral pain e.g.
like + Nor-meperidine). Adverse Effects:
Myocardial infarction.
⓮ Drug Interaction: Meperidine + MAO.I  Vomiting
❷ Alone in Biliary & Renal colic.
→ Severe  RC, excitation & convulsions  Marked inhibition of R.C. &
❸ Pre-anesthetic medication increase Muscle tone →
TTT: IV Hdrocortisone +/- Chloropromazin
(Better than Morphine). Truncal rigidity (It may make
(Mepridine reduce neuronal uptake of
❹ Obstetric Analgesia: Less ventilation in intensive care
“Seretonin , Dopamin , Nor-adrenaline”) difficult.
inhibition of Fetal R.C.
 Narcotic Antagonists

- Opiate receptor antagonist.

- Block all actions (Therapeutic & Toxic) of Morphine & other Opioids.

Naloxone Naltrexone

Pure antagonist. More Pure antagonist. More

selective on -receptors USES selective on -receptors

ONLY IV + SHORT t1/2 USES But :

Stronger, Longer &
Effective orally
❶Acute Morphine poisoning`
→ 0.4 mg I.V. to be repeated due to Short t ½ = 1 hour.
❶Acute Morphine poisoning
❷ Opioid-induced Neonatal asphyxia
❷ Orally to maintain the Opiate-free state of treated addict
→ Mother (IM) or Neonate (Intraumbilical).
❸ Diagnosis of Opioid addiction
→ S.C. → Withdrawal manifestations e.g. Mydriasis

Salicylates
 Treatment of gout Colchicine
Acute Attack

1-N.S.A.I.D (Inhibit PG synthase + Inhibit urate crystal phagocytosis + Inhibit inflammation and pain in Uses:
acute gout flare)

-TREATMENT OF CHOICE for ACUTE attack 1-Acute attacks of gout: (ORALLY)

-Avoid Aspirin,Salicylate & Tolmetin.
For termination of gouty attack especially when NSAIDs &
-OXAPROZIN → Good choice , Effective & Safe like indomethacin
Corticosteroids CONTRAINDICATED or NOT TOLERATED
2-Glucocorticoids (Inhibit activation, proliferation, survival and migration of inflammatory cells +
Inhibit PGs and pro-inflammatory cytokines as IL-1B)
2-Prophylaxis of acute attack of gout (Low dose regimen)
-Good Alternative for patients unable to take NSAIDs in patients initiating urate-lowering therapies
-ORAL : Prednisolone

- Intra-articular: Triamcinolone acetate OR Methyl prednisolone 3-Prophylaxis of Familial Mediterranean fever(polyserositis).

3-Colchicine

-Used IF NSAIDs & Corticosteroids CONTRAINDICATED or NOT TOLERATED.

-LESS favored due to its GIT side effects.

Long term treatment

1-Uricosurics (Probenecid or Benzbromarone)

2-Xanthine-Oxidase Inhibitors (Allopurinol or Febuxostat)

Colchicine Colchicine
Adverse Effects
2. It inhibits 1-Nausea, vomiting (Earliest sign of toxicity) & Diarrhea (often)

of P.M.N.L 4. NO Ruptures
3. NO of P.M.N.L
Phagocytosis of
urate
1.Colchicine binds to 6.NO Precipitation of
2-Bone marrow depression and myopathy
microtubular protein urate
5. NO Release of
lactic acid & 3-Reversible alopecia
(Tubulin) of P.M.N.L chemotactic
factors
Colchicine breaks the cycle of 4-Hepatotoxicity & Nephrotoxicity (Haematuria & Oliguria).
inflammatory response

Colchicine: At higher doses than used to

treat gout has an anti-mitotic effect → Carrying
risk of serious BONE MARROW DEPRESSION
 Uricosuric agent Probenecid
Drugs that increase the excretion of uric acid
Adverse Effects:

1- Formation of renal urate stones

- (To Avoid ...... Alkalinization of urine + plenty fluid intake)

2- GIT disturbances (it is an organic acid) and allergy

3- Probenecid decrease Active tubular excretion of weak acid drugs

a- Penicillin & PASA (anti-TB) …..↑its duration of action.
b- Thiazide & loop diuretics….. antagonize their diuretic effect

Probenecid: Inhibitors Of Uric Acid Synthesis

Large dose > 1 g / day → ↓ Uric acid Reabsorption in Allopurinol (Zyloric)
P.C.T
→ Uricosuric effect. -First-line treatment in hyperuricemia and chronic gout.
Small dose < 1 g / day ↓ Uric Excretion in P.C.T. -Metabolized into alloxanthin (active metabolite)

→ Worsens gout.
N.B: It has NO effect on renal excretion of uric acid.
Uses:
1-As Mono-therapy OR combined with Xanthine oxidase inhibitor.
2-In gouty patients with under-excretion of uric acid when Allopurinol or
Febuxostat CONTRAINDICATED
Allopurinol (Zyloric) Allopurinol (Zyloric)
Actions: Side effects
- Allopurinol is metabolized by
Xanthine Oxidase enzyme (XOE) 1-Acute attack during initial therapy
→ Alloxanthin (Oxipurinol) (so give colchicine/ NSAID prophylactically).
2-Allergy: skin reaction (mainly rash)
Xanthine 3-CNS: Headache and vertigo.
oxidase 4-GIT disturbances & Hepatomegaly
Allopurinol 5-Leucopenia
Occupy 6-Better avoided in children and during lactation (safety issue).
Both & &Inhibit 7-Drug Interaction: (enzyme inhibitor)
Xanthine
Alloxanthine oxidase Inhibit the metabolism of Warfarin, Mercaptopurine, azathioprine,
and Probencide leads to …. Toxicity of these drugs
so their doses should be reduced.
Uric Acid

Allopurinol (Zyloric) Febuxostat

Uses: 1- More selective and potent non-purine inhibitor of xanthine oxidase than
allopurinol.
In chronic gout particularly in: 2- Used as a second-line agent in patients who cannot
tolerate allopurinol.
1- Gouty nephropathy. 3-As with allopurinol, prophylactic treatment with colchicine or NSAID should be
started at the beginning of therapy to avoid gout flares.
2- Recurrent renal urate stones.
4-Extensively metabolized in the liver, Unlike Allopurinol, it is safe in moderate
3- Associated with the use of anticancer drugs. chronic kidney disease.

4- if uricosuric drugs are ineffective or contraindicated.

Side effects
▪ An increase in gout flare after initiation of therapy
▪ Liver function abnormalities.
▪ Nausea , diarrhea and headache.
 Legal medical action Anabolic steroids Diagnosis of Abuse = Urine Sample
Uricolytics:
Pegloticase (Pegylated-uricase) & Rasburicase Increase muscular mass.
The metabolic product (19 –
norandrosterone), is excreted from the body
Enhance puberty to start in urine
1- DNA recombinant form of the enzyme urate oxidase enzyme (uricase)
Can help some males with a genetic
disorder to grow more normally A limit of 2 ng per ml of urine (set by the
It Converts Uric acid Allantoin international Olymphic Committee) is the
more soluble than uric acid and readily excreted in urine. Anabolic effect in osteoporosis, maximum concentration though possible to
anemia and chronic kidney disease occur in human body by natural means and
if this is exceeded the drug test is considered
2- Rasburicase Used by I.V infusion for prevention and treatment of hyperuricemia positive.
in malignant patients at risk of (tumor lysis syndrome), not in chronic gout due to
limited pharmacokinetic parameters (short half-life & Fast acting)
Causes of Abuse anabolic steroids Treatment of steroid abuse
3- Pegloticase is the NEWEST approved uricolytic drug . Given IV in Refractory Treatment in a program that includes
chronic gout Increase muscle mass, strength, and medicines for withdrawal symptoms and
physical attractiveness other health problems

Side effects Treatment in a hospital, if withdrawal

Decrease body fat
1-Gout flare during treatment with pegloticase especially during 1st 3-6 months of treatment symptoms are severe
so give colchicine/ NSAID prophylactically Motivating factors as increasing
2-When used with Methotrexate ( Allergic reactions Abrogated & Efficacy Increased) Individual or family counseling.
confidence and improving mood
3-Risk of Hemolysis in G6PD deficiency patient.

Dose of illegal anabolic steroids is 10 to 100 times higher than the dose a
Drugs Contraindicated in gout: doctor prescribes for medical problems

Reduce sperm count Increased body hair

Side
Men Women
1-Thiazide and loop diuretics, Actazolamide , diazoxide Shrink the testicles
Effects
Skin roughness
Decreased breast
2-Aspirin S.D < 2.6 g/day (it is uricosuric at doses > 3.6 g/day) Infertility size

3-Probenecid S.D < 1 g/ day. Gynecomastia

In both men and women
Deepen the voice

4-Red meat & liver

(Nucleoproteins→ Xanthines→ Uric acid→ Worsen gout) CNS CVS Liver Metabolic Skin

Liver disease and ↑ LDL (bad Oily skin and

Irritability, rage,
possibly liver cholesterol) acne
uncontrolled high Heart attack Hypertension and↓HDL
✓ Coffee & Tea are NOT Contraindicated. energy (mania), or stroke,
cancer. The chance
(good Male – pattern
N.B They are Methyl-xanthines → Methyl-uric acid → Soluble.
or delusions even in a very
of these problems
is higher when cholesterol) hair loss
young person
steroids are taken
as a pill

Withdrawal symptoms: Mood swings, fatigue, anorexia

and craving to steroids.
 2- Intravenous Anesthetics
Blood doping agents
Thiopentone (Ultrashort acting barbiturate): Propofol Ketamine

Anaethesia ►Sedation and hypnosis ►Hypnosis Dissociative anaesthesia (hallucinogen)

stages
►No analgesic or muscle relaxant ►No analgesia ►Has analgesic effect
►Has an amnestic action
►loss of motor activity

onset Rapid induction ►Has rapid onset, short

duration
Has a rapid onset (~ 20 seconds) and a short
duration (5-10 minutes) due to redistribution. ►Faster than thiopental

Adverse ►Profound respiratory depression ►Pain at injection site Bp/HR/COP

effects IOP
►Cough ICP

►Laryngospasm ►Dreams and terrifying hallucination

during recovery occur (emergence
Adverse effects Detection of blood dopers ►Bronchospasm phenomenon which can be controlled by
diazepam)
Kidney damage advantages ►Minimal postoperative nausea and vomiting ►Minimal postoperative ►Potent bronchodilator
Testing the athlete's levels of
hemoglobin nausea and vomiting.
Jaundice ►Accumulate after repeated I.V. administration
uses ► Induction of general anesthesia ►Induction and ►For minor procedures especially in
maintenance of anesthesia infants and children
Blood clots ► General anesthesia for minor short operations
EPO and other blood doping
drugs can be detected in an ► Anticonvulsant
Re-injecting blood from an athlete's
own body can cause blood-borne athlete's system by urine tests
infections and heart problems

1-Inhalation anesthetics Benzodiazepines

(Diazepam, Lorazepam & Midazolam)
Opioids

Nitrous oxide (N2O) Halothane Isoflurane Sevoflurane . Because of their analgesic property,
advantages ►Non–inflammable and ►Non-inflammable, Non-irritant ►Non-inflammable,volatile ►Non-inflammable , ►Produce anterograde amnesia (amnesia for Opioids commonly combined with other
Non-irritant gas. volatile liquid. liquid Non-irritant volatile events occur after drug administered). Anesthetics most commonly fentanyl.
liquid
►Rapid induction and ►Rapid induction & Rapid recovery. ►Rapid induction &Rapid ►When used with opioids : CVS , RES. depression N.B.: Neuroleptanalgesia : produced by
Rapid recovery. recovery. ►Rapid induction and may be severe. combination of Fentanyl and droperidol
►Produces bronchodilatation. So Rapid recovery.
►Good analgesic and useful in patients with bronchial ►Good analgesic and
Sedative effect asthma. Sedative effects. ►With a pleasant ► Analgesia without loss of consciousness.
odor be used in
►Safe on CVS, respiratory ►Produces controlled hypotension. ►No hepatotoxicity. children.
system and vital organs. so useful in plastic surgery to produce Uses ►Useful clinically as IV anesthetics
bloodless area ►No arrhythmias or ►No cardiotoxicity. ►Used in neurosurgery & minor diagnostic &
►Used in dental sensitize the heart to
►Preoperatively for sedation & reduce anxiety. surgical which patients is cooperative
operations & labor catecholamines ►No hepatotoxicity.
( bronchoscopy)
Adverse ►Weak anesthetic ►Weak analgesic. ►Pungent odor ►metabolized by
►Used as anesthetic agents for surgical and
effects ►Weak SK.M Relaxant liver, and compounds
►Weak skeletal muscle ► Less acceptance by formed in the diagnostic procedures e.g endoscopy and cardiac
relaxation ►Cardiotoxic → Bradycardia children anesthesia circuit may catheterization
(vagemimetic), sensitize the heart to be nephrotoxic
► Diffusion hypoxia catecholamine lead to Arrhythmia. ►Associated with dose-
during recovery. So give dependent hypotension,
oxygen during recovery ►Hypotension due to: Inhibition of depression of cardio-
VMC, inhibition myocardium, Direct vascular system.
► Produces postoperative vasodilatation
nausea and vomiting.
►Hepatotoxic.
►Megaloblastic anemia
►Malignant Hyperthermia,
►Teratogenic. Dantrolene given as anesthetic
mixture is withdrawn, and measures
are taken to rapidly cool the patient.
 Pre-anesthetic Medication

Drugs given before the administration of an anesthetic

Local anesthetics
Benefits:
►To produce: sedation, amnesia & analgesia.
►To reduce:
-Amount of anesthetic.
Adverse effects
-Complications after anesthesia.
-Parasympathetic effects on salivary glands, lungs and heart. I-Systemic
So:↓ salivary & bronchial secretions, ↓ bronchospasm & ↓ reflex vagal stimulation.
1. CNS (especially amides)
Drug used:
►Nacrotic (opioid) analgesics: Morphine and meperidine. Central stimulation manifested by restlessness, tremors, and
►Anxiolytics as benzodiazepines.
convulsions >>>>> followed by respiratory depression, coma,
►Neuroleptics as phenothiazines.
►Parasympatholytics as atropine and hyoscine.
and death from respiratory failure.
Hyoscine :
►More depressant on CNS (→sedation, amnesia & potent antiemetic). 2. CVS (especially amides)
►More potent antisecretory→↓salivary & bronchial secretion
Bradycardia and Hypotension (Develop at relatively higher
Anesthetic Adjuvants: plasma levels than do adverse CNS effects)
Drugs used during anesthesia to aid & ensure a safer anesthesia
►Neuromuscular blockers to provide skeletal muscle relaxation,
►Drugs used to produce Controlled hypotension as Trimetaphan and sodium nitroprusside. 3. Allergy (especially esters)
►Hypothermic lytic cocktail (chlorpromazine, promethazine, meperidine).
Allergic reactions include skin rash, edema, and anaphylaxis.

Local anesthetics Local anesthetics

Pharmacodynamics Adverse effects
Mechanism of action: II-Local
1. Pain or hematoma at site of injection
From inside the cell membrane >>>>> blocking sodium
2. Persistent parasthesia
channels >>>>>inhibit sodium influx >>>>> 3. Nerve damage → prolonged sensory & motor
stabilization of cell membrane >>>>> consequent loss
4. Tissue damage → necrosis & sloughing of
prevention of both generation & conduction of nerve tissue due to VC by adrenaline added to LA
impulses 5. Mucosal irritation
 Local anesthetics
Toxicity of spinal anesthesia
I-Systemic toxicity
1. Early
Hypotension (due to veno and arterio dilatation) ttt by
(leg elevation – I.V. fluid – sympathomimetics)

2. Late
– Septic meningitis
– Headache

Aminophylline Pentoxifylline
Uses of Methyl-
Xanthine

Bronchial Asthma -Chronic occlusive arterial diseases e.g.

intermittent claudication:
-Improves RBCs flexibility &↓Plasma
fibrinogen →↓ Blood viscosity, ↓
Caffeine Platelet aggregation.

With Neostigmine in
Myasthenia Gravis.

With Ergotamine → Cafergot in acute

attack of Migraine headache.
Overdose of C.N.S.
With Aspirin or paracetamol in simple depressants e.g. Hypnotics
headache.

Fatigue (Physical or mental)