Lymph Notes - Pharmacology (2nd Term)

LY M P H N O T E S
PHARMACOLOGY
TABLE OF CONTENTS
Blood · 
CNS · 
GIT · 
Endocrine · 
Chemotherapy · 
Lymph Notes in Pharmacology | 2
CHAPTER ONE
Blood
Enumerate
1. Ten Examples of systemic anti-Coagulants & Mechanism Of Action of One Of

them.
1. Vitamin K
2. Thromboplastin
3. Vitamin C in Scurvy
4. Antihemophilic Globulin IV in Hemophilia
5. Protamine Sulphate: Antidote for Heparin Overdose
6. Amino Caproic Acid & Tranexamic Acid
7. Fresh Blood Transfusion
8. Fresh Frozen Plasma
9. Desmopressin Acetate
10. Cryoprecipetate: Plasma Protein Fraction Obtained From Blood Very Rich in
Fibrinogen, Used to treat Patients with Factor VIII Deficiency, Von Willibrand Disease
and Diseases related to Abnormalities Of Fibrinogen as : Disseminated Intravascular
Coagulation.
2. Three Drugs used As Sclerosing Agents.

1. Sodium Morphuate.
2. Sylnasol.
3. Sodium Ricinoleate.
Compare
1. Between Hypolipidemic Drugs.

P.O.C Statins Niacin

1. Competitive Inhibition Of
1. MechanismOf - In Adipose Tissue:
HMG-CoA Reductase, So
Action Binds to Niacin Receptors →
they
↓Mobilization Of Fatty Acids To
↓ Intracellular Synthesis Of Liver → ↓ TG, VLDL Synthesis.
Cholesterol → ↑ Number of
- In Liver: Inhibits DAG
LDL Receptors On Liver
Acyltransferase, So it ↓TG &
Cells → ↓Plasma LDL
VLDL Synthesis.
Cholesterol.
- In Plasma : ↑↑LPL Activity,
2. ↑ Plasma HDL Levels.
↑↑ Clearance Of VLDL &
3. ↓ Plasma Triglycerides.
Chylomicrons.
Absorbed Orally, taken at Orally.

2. Ph. Kinetics
bed time because of Diurnal
Rhythm Of Cholesterol
Synthesis except
Atrovastatin & Rosuvastatin
as they have long ½ Life.
All Types Of Hyperlipidemia Mixed Hyperlipidemia.
3. Uses
1. Hepatotoxic → ↑ Serum 1. Cutaneous Flush & Peruritis.

4. Side Effects
Transaminase. 2. Nausea, Abdominal Pain,
2. Myopathy: ↑ Gastric Motility & Acid
Rhabdomyolysis →Cola Production.
Colored Urine. 3. Hyperurecemia.
3. ↑Plasma CK 4. ↑ Aminotransferases.
Potentiate Action Of Potentiate actions Of

5. Interactions
anticoagulant Drugs & Antihypertensive drugs.
antidiabetic Drugs.
a. Pregnancy a. Gout.
6. Contraindications
b. Lactation. b. Peptic Ulcer.
Lovastatin, Atrovastatin Niacin (nicotinic acid).
7. Members Of this
Rosuvastatin, Fluvastatin
Group.
Simvastatin.
P.O.C (Fibric Acid Derivatives) bile acid binding resins.

Fibrates
a. Bind To PPAR α receptors a. Bind To Bile Acids preventing
1. Mechanism Of
on Muscle & Liver Cells. their Reabsorption, increase
Action
their Excretion & ↓ their
b. Activation Of PPAR leads
Enterohepatic Circulation.
To:
b. Cause Liver to scavenge more
- ↑LPL Activity →↑Hydrolysis Of
Cholesterol From The Body To
TG→↓VLDL
form Bile salts.
- ↓Hepatic Triglyceride Secretion.
c. Upregulate LDL Receptors in
a. Inhibits Lipolysis →↓Fatty Liver →Clearing more LDL from
Acids To The Liver & ↓TG the Blood.
Synthesis.
b. ↑ HDL Levels
due to ↓their catabolism.
1. Hypertriglyceridemia. Only treat 1ry
Uses
Hypercholesterolemia.
2. Mixed Hyperlipidaemia.
1. GIT Upsets. 1. GIT upsets especially

Adverse Effects
Constipation.
2. Arrhythmia.
2. at High Doses ↓ Absorption of
3. Hypokalaemia.
Fat Soluble Vitamins (A,D,E,K) .
4. Cholesterol Gall Stones.
5. Myopathy, Myositis.
6. Cholecystitis.
7. ↑Liver Enzymes.
4. Contraindications 1. Pregnancy, Lactation. ______

2. Gall Bladder Diseases.
3. Hepatic & Renal Dysfunction.
______ ↓ Absorption Of Other Drugs As :

5-Drug Interactions
1. Cardiac Glycosides.
2. Thiazides.
3. Warfarin ….etc.
N.B
Colesevelam doesn`t bind to
Warfarin, Digoxin & Reductase
Inhibitors.
Gemfibrozil. Colestipol
6-Examples
Fenofibrate. Cholestyramine
Colesevelam.
Inhibitors Of Intestinal Sterol Absorption CETP Inhibitors

Inhibit Absorption Of Dietary & Biliary Cholesterol. Anacetrapib
Examples: Ezetimibe. Dalcetrapib
Currently Under Trial.
Discuss
1. Give 4 Examples of Fibrinolytic Drugs & Mention The Mechanism Of Action Of

One Of Them.
- Streptokinase.
- Urokinase.
- Antistrestreptase.
- Tissue Plasminogen Activator.
- Urokinase: Human Synthasized By The Kidney & Directly Converts Plasminogen To
Active Plasmin which breaks down fibrin and fibrinogen into fragments as well as
interfering with platelet functions, thrombin activity and fibrin polymerization.
2. What Are The Therapeutic Uses & Drug Interactions Of Warfarin?

Therapeutic Uses: See comparison between Heparin & Warfarin.
Drug Interactions:
Enhance The Action Of Warfarin Inhibit the action of warfarin
Ph. kinetics Ph. Dynamics. Ph. kinetics Ph. Dynamics.

Liver Enzyme Inhibit Platelet Enzyme increase
Inhibition: Aggregation: induction: synthesis of
clotting factors:
- Amiodarone - Aspirin. - Barbiturates.
- Vit. K.
- Cimetidine - Rifampin.
- Disulfiram.
- Metronidazole
- Fluconazole.
- Cotrimoxazole
Displacement Potentiate Inhibition Of Decrease

From Plasma Antithrombin GIT Absorption: Turnover Of
Proteins: III: Clotting Factors:
- Cholestyramine.
- Phenylbutazone. Heparin. - Hypothyroidism
- Sulfinpyrazone.
Increase Increase Clotting

Turnover Of Factor Conc. :
Clotting Factors: - Diuretics.
-hyperthyroidism
- hepatic Disease
Inhibit Vit. K
Synthesis:
Cephalosporins
3rd Generation
3. Enumerate One Drug That Targets Thromboxane A2 & Inhibits It & Mention Its
Therapeutic Indication?
Aspirin “ COX Inhibitor “ and (Thromboxane Synthase inhibitor)

Therapeutic Indications:
They Are Only Considered For Arterial Or Intracardiac Thrombi Because They are
Rich In Platelets.
4. Compare Between ADP Receptor Antagonist & Glycoprotein IIb / IIIa Receptor
Antagonist
(Compare Between Clopidogril & Eptifibatide) .
ADP Receptor Antagonist Glycoprotein IIb/IIIa Antagonist

(Clopidogril) (Eptifibatide)
- It Blocks Irreversibly ADP Binding to ADP Abciximab: one of drugs that
Receptors On Platelets → ↓ Activation Of GP antagonize GP IIb/IIIa Receptors, it
IIb/IIIa Receptors That leads to ↓↓their consists of Monoclonal Antibodies
Binding to Fibrinogin and to each others. which bind to Receptors.
- Administrated Orally Eptifibatide: is Analogue to Delta
Chain Of Fibrinogen which mediates
- Maximum Effect After 3-6 days.
Binding Of Fibrinogen to GP IIb/IIIa
- Clopidogril is a prodrug that must be Receptors on Platelets.
activated in liver by cytochrome P450
- Taken By IV Infusion,
enzymes.
- Oral Drugs Are Too Toxic.
- Major Interactions with Drugs that
inactivate Liver Microsomal Enzymes as - Is an active drug
PPIs. - Bleeding may occur especially If used
- IPs approved in Myocardial Infarction, with Anticoagulants.
Stroke & Unstable Angina.
5. Write A Short Account On Phosphodiesterase Inhibitors.

Dipyridamole & Cilostazole
Dipyridamole acts through :

- ↓↓ Of Platelets Phosphodiesterase Enzyme →↑ c-AMP.
- ↓↓ Of Uptake Of Adenosine into Platelets →↑Local Concentration Of Adenosine →
Stimulating Platelet Cyclase →↑ c-AMP.
- Via these mechanisms platelet aggregation is inhibited.
- Dipyridamole is used in Combination with Aspirin, Ineffective If used alone.

Cilostazole is used in ttt of intermittent Claudication.
They are Coronary Vasodilators.
6. Compare Between Warfarin & Heparin.
C.O.P Heparin Warfarin

- Not Effective Orally - Absorbed Orally,
Ph. Kinetics
Given IV / SC. - Bound To Plasma
Proteins. passes The
- Metabolized By The Liver &
placenta But Not secreted
Reticuloendothelial System.
in Milk.
- Excreted in Urine Partly
-Metabolized By The Liver.
Unchanged.
- Excreted in Urine &
- Don`t Cross The Placenta &
Stool.
Not Secreted in Milk.
- Potentiates Anti-thrombin - Prevents Reductive

Mechanism Of Action
III which inhibits The Action Metabolism Of The
Of Several Clotting Factors Inactive Vitamin K
particularly Factor Xa, IIa. Epoxide back to its Active
Hydroquinone Form.
- Vit K activates many
Clotting Factors.
TTT of:
Uses
1. DVT.
2. Pulmonary Embolism.
3. Myocardial Infarction.
4. Cerebral Thrombosis.
- Prophylactic to prevent Postoperative Thrombosis &
Pulmonary Embolism.
- (Heparin Only) to prevent Blood Clotting during
Transfusion & Dialysis.
Hyperlipidaemia (Heparin only)
- Haemorrhage. - Haemorrhage
Side Effects
- Hypersensitivity - Hypersensitivity that
leads to Skin Rash & Skin
- Heparin –induced
Necrosis.
Thrombocytopenia
- Teratogenic
- Thrombosis
- GIT Upset.
- Hyperkalaemia
- Transient Alopecia
- Osteoporosis
- Hypersensitvity.
Contraindications
- Bleeding Disorders: Haemophilia, Intracranial
Haemorrhage.
- Surgery.
Some Diseases as: Subacute Bacterial Endocarditis, TB &
Ulcers Of GIT.
- Liver and kidney Diseases
- Pregnancy (Warfarin only)
Explain The Pharmacological Basis Of:
1. Low Molecular Weight Heparin (LMWH) as Enoxaparin have replaced

Unfractionated Heparin.
- LMWH are administrated SC (Heparin Mainly given IV).
- Once daily (Longer Half Life than Heparin).
- No need for Laboratory Monitoring due to:
- Predictable Pharmacokinetics & Pharmacodynamics As it doesn`t bound to Plasma
Proteins.
- Less likely to cause Thrombocytopenia.
- LMWH is Effective, Safer, less Frequent Haemorrhage than Heparin.
2. Oral Anticoagulant Drugs should be Stopped 3-4Days Before Operations.

- Due To Long Half Life (20-50)hours, to avoid much Problems As Bleeding in The
Operation.
3. Protamine Sulphate is used as Antidote For Heparin Toxicity.

- Heparin is Strongly Acidic & Carries Strong Electronegative Charge Which Is Very
Important For Its Action.
- Protamine Sulphate is Strongly Electropositive Charged, Combines Ionically with
The Strong Electronegative Heparin Forming Inactive Stable Complex.
4. Clopidogrel Is Better Than Ticlopidine.

CLOPIDOGREL HAS FEWER SIDE EFFECTS THAN TICLOPIDINE WHI CH CAUSES
NEUTROPENIA INCREASING THE RISK OF I NFECTION.
CHAPTER TWO
Central Nervous
System
Enumerate:
1. Mixed agonist- antagonist narcotic opioids. Mention their mechanism of action on

receptors.
Mixed agonist-antagonist narcotic opioids:
Pentazocine- Butorphanol- Nalbuphine- Buprenorphine.
Mechanism of action:
Their action on receptor depends on Morphine addiction:
-If No Morphine Addiction →Kappa Agonist →Analgesic.
-If Morphine Addiction →M-Antagonist→ Withdrawal manifestations.
2. Uses of:
A. Ethyl Morphine:
Eye drops in corneal ulcer s& iritis (counter-irritant).
B. Apomorphine:
Central emetic.
C. Papaverine:
Spasmolytic (colic)/ VD (coronary, pulmonary & peripheral thrombosis).
D. Narcotine:
Non narcotic central antitussive.
E. Methadone:
- Analgesic in sever visceral pain e.g. Terminal cancer.
- To substitute Morphine, Heroin during their withdrawal.
F. Naltrexone:
- Orally to maintain opiate- free state of treated addict.
- Acute Morphine poisoning.
G. Diclofenac:
- Inflammation esp. Arthritis.
- Colic as in dysmenorrhea.
- Ocular inflammation (eye drops).
3. Uses & adverse effects of Indomethacin.

Uses:
1. Potent antipyretic analgesic.
2. Potent anti-inflammatory, anti-Rheumatic.
Adverse effects:
1. CNS: confusion, psychosis.
2. Allergy: bronchial asthma.
3. GIT: irritation, peptic ulcers and liver and kidney damage.
4. Teratogenic.
5. Bone marrow inhibition: leukopenia.
6. Corneal opacity and blurred vision.
7. Displace other drugs from plasma proteins- increase their free form- increase
activity and toxicity.
Explain:
1. Methadone is used in treating Morphine addicts.

As it is similar to morphine but less withdrawal manifestations so it is used for gradual
substitution of morphine.
2. Loperamide and Diphenoxylate are better than Morphine in treating diarrhoea.

Loperamide doesn't pass BBB → No CNS actions. While Diphenoxylate partially → has
some CNS actions (some narcosis).
So they don't have adverse effects of Morphine on CNS as inhibition of RC.
Compare:
1. Morphine & Meperidine (Pethidine).
Morphine Meperidine
Kinetics
Low (25-30%) oral 50% oral bioavailability.
Absorption:
bioavailability.
Better absorbed after SC &
IM injection.
In shock: slow dil. IV.
Distributed all over the

Distribution:
body.
Extensive (70-75%) hepatic In liver.
1st pass metabolism.
Metabolism: Meperidinic acid → inactive
Conjugated with → conjugated with
glucuronic acid glucuronic acid → urine.
Morphine 6 glucuronide → Nor-meperidine → active →
more active. excitation & convulsions.
Morphine 3 glucuronide →
inactive.
Morphine stimulates a Like morphine + atropine
Dynamics:
specific opioid receptors in like.
CNS & periphery
Therapeutic uses: 4Ps: 1. Alone in biliary and renal

1. Severe visceral pain + add colic.
atropine in biliary and renal 2. Obstetric analgesia:
colic. Meperidine +Hyoscine
2. Pulmonary edema due to twilight sleep –less fetal
R.C depression.
left ventricular failure
3. Pre anaesthetic
3. Primary neurogenic
medication (better than
shock
4. Pre anaesthetic morphine).

medication 4. Severe visceral pain: as
MI.
2. Morphine & Codeine (Methyl morphine).
Morphine Codeine (methyl-

morphine)
Kinetics
Low oral bioavailability Similar to Morphine but
Absorption:
(25-30%). better oral bioavailability
(50%).
Better absorbed after S.C&
IM
Shock: slow dil. IV.
Distribution:
All over the body.
Metabolism:
Extensive hepatic first pass
metabolism.
Excretion:
Saliva , stomach , bile , milk

, urine
Duration (6-8hourse ) Shorter duration.
Dynamics:
Mechanism of action: Stimulates specific opioid Similar to morphine But:

receptors in CNS & - Weaker than morphine as
periphery. analgesic, constipation &
addiction.
- As potent as morphine as
antitussive.
- Large dose → -- R.C , --
V.M.C & excitation epilepsy

in children.
4Ps:
Therapeutic uses:
1. Severe visceral pain. Antitussive in dry useless
cough & dangerous cough.
2. Pulmonary edema due to
acute left ventricular Analgesic in mild
failure. &moderate visceral pain
+aspirin &paracetamol
3. Primary neurogenic
(APC).
shock.
4. Pre anaesthetic
medication.
3. Paracetamol and Diclofenac.
Diclofenac Paracetamol
1. -- COX both central 1. -- COX-3 in CNS
and peripheral (both mainly:
COX-1 & COX-2). anti pyretic –analgesic
2. Increase incorporation 2. Almost no peripheral
of arachidonic acid into action:
triglycerides. almost no anti
3. Decrease both PG and inflammatory action.
LT. 3. Almost no effect on
respiration and CVS.
1. Inflammation Anti pyritic analgesic
Uses:
e.g. arthritis and especially in patient who
myositis. can not tolerate aspirin
2. Colic e.g. e.g. allergy to aspirin and
dysmenorrhea. bronchial asthma.
3. Eye drops to treat
ocular inflammation.
1. GIT irritation (used as 1. Toxic dose of
Adverse effects:
Enteric coated tablets). paracetamol:
2. Hepatotoxicity Depletion of Glutathione
(increased serum –SH leading to
transaminase). hepatotoxicity and
nephrotoxicity.
2. Allergy
(Hypersensitivity).
3. Aspirin and Paracetamol.
Aspirin Paracetamol
Aspirin→ Acetylation Previously Mentioned.
Mechanism of Action
(Irreversible inhibition
of COX enzyme).
Previously Mentioned.
Uses Local Uses:
Salicylic acid:
1. Keratolytic in corns &
warts.
2. Fungi-static in Tinea
of skin.
3. Anti-septic in
Hyperhidrosis.
Methyl salicylate:
Counter irritant in
myositis & arthritis.
Systemic Uses:
1. Anti-pyretic→ Non-
specific & Non-causal.
2. Analgesic in mild
superficial pain e.g.
Headache and
Neuralgia.
3. Common cold: Treat
Fever, headache,
muscle and joint pain.
4. Rheumatic fever.
5. Rheumatoid arthritis.
6. Chronic gout.
7. Anti-platelet.
8. Prophylaxis against
cancer rectum.
Give an account on:
Adverse effects of Aspirin.

ASHGAR TIN
1. Acute toxicity:
Manifestations:
- Hyperreflexia & excitement.
- Hyperpyrexia & hyperventilation.
- Hyperacidity & irritation with nausea and vomiting.
- Hyperglycemia.
- Hypotension.
- Hypoprothrombonemia.
- Acid/ base imbalance.
2. Salicylism (Large doses for long time):
Manifestations:
- Tinnitus & blurring of vision
- GIT upset & hyperventilation.
3. Hypoprothrombinemia.
4. GIT irritation:
Nausea & vomiting and pain.
5. Allergy:
Rash, urticarial & bronchial asthma.
6. Reye's syndrome:
Encephalopathy & hepatotoxicity in some children with viral infection.
7. Teratogenicity.
8. Idiosyncrasy:
Hemolysis in patient with Glucose 6-phospate dehydrogenase deficiency (favism).
9. Nephropathy.
Enumerate:
1. Advantages of Fosphenytoin over Phenytoin.

It is a prodrug of Phenytoin with the following Advantages:
1. Less Vascular Irritation .
2. Ability to be injected faster.
3. Greater Physical Compatibility with I.V & I.M Solutions used to dilute it.
4. Can be given I.M.
2. Drugs used in: Grand mal Epilepsy-Petit mal Epilepsy.

Grand mal Epilepsy:

1. 1st Choice: Carbamazepine & Phenytoin.
2. Alternative : Valproate .
3. Phenobarbitone .
Petit mal Epilepsy:
1. 1st Choice: Ethosuximide.
2. Alternative: a- Valproate. b- Clonazepam. c- Lamotrigine as add- on.
3. Uricolytic drugs & mention their mechanism of action, uses & route of
administration.
Uricolytics:
Rasburicase & PEGylated uricase.
DNA recombinant form of the enzyme urate oxidase (uricase) that converts uric
acid to allantoin which is more soluble than uric acid and excreted in urine.
Route of administration & uses:
Used I.V in hyperuricemia associated with tumor lysis syndrome.
4. Drugs contraindicated in gout (hyperuricemia).

1. Probenecid (small dose)
2. Diuretics as Thiazide & loop diuretics.
3. Aspirin (small dose).
4. Diazoxide (thiazide like).
5. Adverse effects of Probenecid.

1. Formation of renal urate stones:
Can be avoided by alkalization of urine & fluid intake.
2. GIT disturbance and allergy.
Mention:
1. Mechanism of action, uses and adverse effects of Ethosuximide.

Block Voltage Dependent T-Calcium Channels.
Uses:
Drug of Choice in Absence Seizures = Petit Mal Epilepsy.
Adverse effects:
1. CNS: Drowsiness, Lethargy & Behavioural Changes.
2. GIT: Anorexia, Nausea & Vomiting.
3. Blood: Leukopenia & Thrombocytopenia.
2. A drug used in all types of Epilepsy and mention its action, uses and adverse
effects.
Valproate.
Action:
1. Block Na Channels → Similar to Phenytoin Effective in Partial & Grand Mal Epilepsy.
2. Block T-Ca2+-Channels → Similar to Ethosuximide, effective in absence of Seizures.
3. ↓ GABA Transaminase Enzyme → ↑ GABA.
4. Antagonize Excitatory Transmitters e.g. Aspartate.
Uses:
1. Broad spectrum anti-epileptic useful in Grand mal epilepsy, partial seizures & petit
mal epilepsy (Not Drug of Choice → Sedation & Hepatotoxic).
2. Drug of choice in patients with:
a. Mixed Petit Mal + Grand Mal Epilepsy.
b. Myoclonic Epilepsy.
3. Mood stabilizer in manic depressive disorders.
4. Migraine headache.
Adverse effects:
1. CNS: Sedation.
2. GIT: Nausea & Vomiting.
3. Blood → Thrombocytopenia & ↓ Platelet Aggregation → Hemorrhage.
4. Hepatotoxicity.
5. Temporary Loss Of Hair →Thin Curly Hair.
6. Teratogenic → Spina Bifida.
7. Allergy.
3. Adverse effects of Phenobarbitone.

1. CNS: Sedation, Ataxia, Nystagmus & Vertigo.
2. GIT: Anorexia & Nausea.
3. Blood → Megaloblastic Anaemia & Hypoprothrombinaemia.
4. Bone: Osteomalacia.
5. Tolerance & Dependence (Addiction).

6. Drug interactions:
Hepatic Microsomal Enzyme Induction (As Phenytoin)
a. ↑ Its Own Metabolism → Tolerance & Failure Of Anti-epileptic Activity.
b. ↑ Metabolism Of Other Drugs as:
- Anti-epileptic Drugs e.g. Phenytoin & Carbamazepine.
- Oral Contraceptives.
- Folic Acid → Megaloblastic Anaemia.
- Vit D → Hypocalcaemia → Osteomalacia.
- Vit K → Hypoprothrombinaemia.
Compare:
1. Colchicine and Allopurinol: adverse effects, uses & actions.
Colchicine Allopurinol
I. Anti gout effect: 1. Allopurinol is
Actions
1. Effective in treatment metabolized by xanthine
of acute attack of gout. oxidase enzyme –give
2. Not effective in other alloxanthine.
type of arthritis. 2. Both allopurinol
3. Not affect uric acid and alloxanthine
synthesis. occupy and decrease
4. No rupture of O.X.E.
leukocytes. 3. Lead to decreased
5. No release of lactic synthesis of uric acid.
acid, no inflammatory 4. It has no effect on
acidity. renal excretion of uric
6. No release of acid.
chemotactic factors e.g.
Glycoprotein.
7. It binds to
microtubular protein →
no migration of
neutrophils.
II. Antimitotic:
Inhibit cell division.

1. Prophylaxis of gout. Hyperuricemia and
Uses
2. Prophylaxis of familial Chronic Gout, especially
Mediterranean Fever. in:
3. Acute attacks of gout: - Associated with the use
useful when NSAID & of Anti-cancer drugs
Corticosteroids are - Gouty nephropathy and
contraindicated. urate renal stones.
- If uricosuric drugs are
ineffective or
contraindicated.
1. GIT: Nausea and 1. CNS: Headache.
Adverse effects
vomiting. 2. Allergy.
2. Hepatotoxicity. 3. GIT disturbance.
3. Nephrotoxicity and 4. Acute Attack of gout
Hematuria. during initiation of
4. Bone marrow treatment.
depression. 5. Hepatomegaly.
5. Myopathy. 6. Leukopenia.
6. Reversible Alopecia. 7. Better avoided in
lactation & in children.
8. Drug interaction: --
metabolism of
Probenecid &
Mercaptopurine (Anti-
cancer) leading to
toxicity.
2. Phenytoin and Carbamazepine (Mechanism of action, Uses and Adverse Effects).
Phenytoin Carbamazepine
Block Na+ Channel Block Na+ Channel
Mechanism of Action
(Membrane Stabilization). (Membrane Stabilization).
1. Grand Mal Epilepsy & 1. Grand Mal Epilepsy &
Uses
Partial seizures. Partial seizures.
2. Trigeminal neuralgia. 2. Trigeminal neuralgia.
3. Status Epilepticus. 3. Mood stabilizer.
4. Class 1 Group B anti-
arrhythmic: DOC in
Digitalis-induced
arrhythmia (ventricular
arrhythmia with heart
block).
1. CNS: Ataxia & Vertigo. 1. CNS: Ataxia & Vertigo.
Adverse Effects
2. GIT: Gastric Irritation. 2. GIT: Gastric Irritation.
3. Anemia & 3. Bone marrow inhibition
Hypoprothrombinaemia. (Aplastic Anemia).
4. Bone: Osteomalacia. 4. Anti-diuretic → Fluid
5. Hirsutism. retention.
6. Hepatotoxicity. 5. Hepatitis.
7. Hypersensitivity. 6. Teratogenic.
8. Hormones: Decrease the 7. Allergy.
release of ADH & Insulin.
9. Gum Hyperplasia →
Consult Dentists.
10. Teratogenic (hare lip &
cleft palate).
11. Hypoprothrombinaemia
in baby before labor.
Explain
21. The Mechanism of action of L-Dopa and adverse effects

I. Dynamics of L-Dopa: (anti- Parkinsonism)
𝐶𝐶𝐶𝐶𝐶𝐶
L-Dopa �⎯⎯⎯⎯⎯⎯⎯⎯� Dopamine
Treat all manifestation of Parkinsonism especially BradyKinesia and Tremors By ++ D2
Receptors in Basal Ganglia.
II. Adverse effects of L-Dopa:
1•Fluctuation in Response:
•Good response then ↓↓ in response
•Wearing off → DOPAC + H2O2
•End of dose Akinesia → destroy dopamine vesicles
•ON-OFF phenomena → rapid ↑ then rapid ↓ in dopamine levels in CNS
2•CNS:
Dyskinesia, chorea, athetosis and psychic disturbances e.g. Delusions, hallucinations
and aberrant sexual activity
* Use atypical antipsychotic clozapine.
3•Eye:
Mydriasis &↑ IOP
4•CVS:
Tachycardia, arrhythmias, postural hypotension and hypertension especially with
MAO inhibitors
5•GIT:
•Nausea, vomiting, can be treated by Domperidone
•Constipation, sometimes bleeding Peptic ulcer.
6•Sudden withdrawal:
Severe Parkinsonism rigidity
22. Drug interactions of L-DOPA

I. Favorable interactions: ↑ L-DOPA effect
1•Peripheral DOPA decarboxylase inhibitors:
•Carbidopa
•Benserazide
2•MAO-B inhibitors:
Selegiline
3•COMT inhibitors:
Tolcapone, Entacapone
4•Anti-Muscarinic:
Benztropine
II. Unfavorable combinations: ↓ L•DOPA effect
1•D2 Blockers:
•Neurolepticsphenothiazines, Butyrophenones
•Anti-emetics Metoclopramide
2•Pyridoxine:
↑Peripheral decarboxylase  accelerates peripheral decarboxylation.
3•Non selective MAO inhibitors:
Severe hypertension
23. Action, uses, adverse effects and drug interactions of chlorpromazine

Action depends on blocking dopamine receptors
Actions:
I. CNS:
1•Antipsychotic→ block dopaminergic D2 receptor in limbic system, neocortex and
hypothalamus
2•Basal ganglia→ large dose→ blocks D2 receptor→ worsen Parkinsonism
3•Hypothalamus:
•hypothermia→ ↑heat loss by cutaneous VD+ ↓heat production by ↓shivering
•↑appetite
•↑prolactin
4•↓C.T.Z: antiemetic in all vomiting except motion sickness
5•Potentiate other CNS depressant
6•Lowers seizure threshold
II. Endocrine:
1•Dec. ACTH
2•Dec. FSH and LH gonadotrophins→ infertility and amenorrhea in female
3•Inc. prolactin→ Gynecomastia and Galactorrhea
III. Receptors:
(6 anti: 3 potent and 3 weak)
1•Potent anti-serotonin
2•Potent anti-dopamine
3•Potent anti-alpha
4•Weak anti-ganglion
5•Weak anti-muscarinic
6•Weak anti-histaminic (H1)
IV. Skeletal muscle:
Muscle relaxation
V. Local Anesthetic
VI. CVS:
1•Hypotension and postural hypotension due to:
•Inhibition of VMC
•Ganglion and alpha blocker effect
•Direct vasodilation and myocardial depression
2•Tachycardia→ atropine like action + reflex from Dec. blood pressure
3•Increase coronary flow
Uses
1•Psychosis e.g. Schizophrenia mainly signs like hallucinations and delusions
2•Pre-anesthetic medication
3•Hypothermic agent→ Dec. tissue metabolism during cardio pulmonary surgery
4•Hiccups (hiccoughs)
5•Anti-emetic except in motion sickness and pregnancy
Adverse effects:
1•CNS:
•Sedation
•Extra pyramidal manifestation:
1•Acute dystonia
2•Akathisia
3•Parkinsonism
* Treat by decrease dose of neuroleptic and use anti-cholinergic anti-
Parkinsonism drug
•Neuroleptic malignant syndrome (NMS):

Idiosyncratic reaction, similar to malignant hyperthermia
* Treat by I.V Dantrolene
•Tardive dyskinesia (abnormal movement):
Occurs after long use of neuroleptic, due to up regulation of D-receptor
* No treatment but can be prevented by lithium
2•Inc. body weight
3•Opacity of the cornea and lens
4•Dry mouth
5•Allergy: dermatitis, photosensitivity and Agranulocytosis
6•Tachycardia
7•Endocrine disturbance e.g. Gynecomastia and Galactorrhea
8•Allergic obstructive cholestatic jaundice
9•Teratogenic, don't use in vomiting of pregnancy
10•Postural hypotension
Drug interactions:
1•Chlorpromazine potentiates:
•Sedatives (alcohol)
•Hypotensives (VD)
•Anti-cholinergics (atropine)
•Muscle relaxants (curare)
2•It Dec. neuronal uptake of Guanethidine→ antagonize its hypotensive effect
3•Chlorpromazine→α- blocker→ reverses pressor effect of adrenaline
Compare
Fluoxetine & TCA regarding uses and adverse effects
P.O.C Fluoxetine TCA

1•Psychic Depression
1•Psychic Depression 2•Panic attack
2•Panic Disorders 3•Chronic Pain
Therapeuti 3•Obsessive compulsive 4•Obsessive compulsive
c uses disorders disorders
4•Bulimia Nervosa 5•Nocturnal enuresis in
children
1•Anorexia, Nausea, 1•Delayed onset of action
Diarrhea. 2•CNS:
2•Anxiety, Insomnia, Mania
3•↑↑ aggression, violence Sedation, seizures, tremors,
and suicide. confusion
4•Fluoxetine +MAOI → 3•CVS:
serotonin syndrome (fatal).
Postural hypotension,
tachycardia, cardio-toxicity
→ fatal arrhythmia.
4•Atropine like effects:
Dry mouth, Blurred vision,
tachycardia, constipation
Side and urine retention.
Effects
5•Weight gain
6•Allergy:
Obstructive jaundice,
Agranulocytosis.
7•Acute toxicity:
Common & fatal.
Manifestations:
•Excitement, seizures,
arrhythmia, atropine
like.
TTT:
•ICU + Diazepam +
Phenytoin
+Physostigmine.
ENUMERATE
1. Five new anti-epileptic drugs

1•Lamotrigine
2•Gabapentin
3•Pregabalin
4•Topiramate
5•Tiagabin
2. Advantages of Bromocriptine over L•DOPA

1•Does not need synthesizing enzyme
2•More specific on D2 receptors
3•No active transport system, so no competition with amino acids
4•No toxic oxidative metabolites
5•Longer t1/2  less fluctuation in response
3. Five drugs of Atypical Anti-psychotic drugs

1•Pimozide:
Selective D2-blocker specific on limbic system
2•Sulpiride:
Selective D2-blocker specific on limbic system
3•Clozapine:
Blocks D4 and 5HT2 receptor
4•Risperidone:
Block D2 and D4=5-HT2 receptor
5•Ziprasidone:
Blocks 5-HT2 >D2 receptor
6•Olanzipine:
Blocks 5-HT2 >D2 receptor
7•Quitiapine:
5•HT1A partial agonist
8•Aripirazole:
D2 and 5-HT1A partial agonist
4. Pharmacological actions of TCA

[5 Anti, L, S]
1•Anti-depressant effect
2•Anti-cholinergic = Atropine like
3•Anti-Histaminic
4•Anti-serotonin
5•Alpha blocker effect
6•Lower seizure threshold
7•Sedation
Give an account on:
Therapeutic uses, pharmacological actions & adverse effects of Benzodiazepines.

Actions:
I. CNS:
1. Anti Anxiety:
Action on limbic system → less anxiety and sedation (taming in animals).
2. Hypnosis:
Action on reticular system
Uses depend on their duration of action:
- Long acting → induce and maintain sleep.
e.g. Flurazepam & Nitrazepam.
- Intermediate → maintain sleep.
e.g. Temazepam.
- Short acting → induce sleep.
e.g. Traizolam.
3. Anterograde amnesia:
Triazolam.
4. IV anaesthesia:
Diazepam as Inducer.
Midazolam is better (quicker, shorter & less irritant).
5. Anticonvulsant:
Diazepam is drug of choice in status epilepticus.

Clonazepam → broad spectrum anti epileptic.
6. Anti depressant:
Alprazolam ONLY.
II. Peripheral:
1. Smooth muscles relaxant:
Diazepam and clonazepam.
:‫ﻣﻦ ﺗﺤﺖ ﻟﻔﻮق‬
2. NO Hepatic microsomal Induction.
3. NO CVS depression.
4. NO Respiratory depression.
5. NO extra-pyramidal manifestations.
6. No Autonomic manifestations.
Therapeutic uses:
I. Sleep-related:
1. Anxiety.
2. Insomnia (initiate by short acting, maintain by intermediate and long acting).
3. Anesthesia (consider it sleep): by Diazepam and Midazolam.
4. Preanesthetic.
II. Seizures-related:
1. Antispasticity (Diazepam and Clonazepam).
2. Anti convulsant and anti epileptic:
Dia-, Lora-, Clona-zepam for status epilepticus.
Clona → broad spectrum anti epileptic.
III. Psychiatry-related:
1. Anxiety.
2. Diagnostic for some cases in neurology and psychiatry
3. Alcohol withdrawal; due to cross dependence.
4. Alprazolam → anxiety, psychic depression, panic and phobic disorders.
Adverse effects:
I. Allergy.
II. Personal life-related:
1. Increased appetite
2. Dependence and addiction
3. Affect sexual function.
III. CNS-related:
1. Daytime sedation (long acting) or Anxiety (short acting)

2.Amnesia.
3. Mental confusion of elderly.
4. Ataxia.
5. If + alcohol →toxicity → severe CNS depression (+ Resp & CVS).
Compare between:
1. Diazepam and Buspirone.
Benzodiazepines Buspirone
(Clonazepam)
Stimulates a specific Bz Partial agonist on
Mechanism of action
receptor → increase in presynaptic 5HT1A
GABAA transmission → ++ receptor.
Cl- influx →
hyperpolarization.
- Normal BZ family - Anxioselective + minimal
Advantages
characters + undergoes sedation.
decarboxylation by - No hypnosis → No effect
stomach HCl → active on skills like driving.
metabolite (rapidly - No sk. ms. relaxation.
absorbed). - No tolerance or cross
- Skeletal ms relaxant. tolerance.
- Broad spectrum anti- - Little dependence.
epileptic.
1. Delayed onset (1-2
Adverse effects I. Allergy.
weeks).
II. Personal life-related:
2. GIT distress.
1. Increased appetite
2. Dependence and 3. Tachycardia.
addiction 4. Nervousness.
3. Affect sexual function.
III. CNS-related:
1. Daytime sedation (long
acting) or Anxiety (short
acting)
2.Amnesia.
3. Mental confusion of
elderly.
4. Ataxia.
5. If + alcohol →toxicity →
severe CNS depression (+
Resp & CVS).
2. Barbiturates & Benzodiazepines.
Barbiturates Benzodiazepines
Marked REM decrease: Less REM decrease:
Sleep
- Hangover. - Less.
- Rebound insomnia. - Less.
Induction: No induction:
HME
:‫ﻛﴪ ﻧﻔﺴﻪ وﻛﴪ ﻏﲑه‬
- Tolerance & cross
- Less.
tolerance.
- Less.
- Dependence.
- Less.
- Drug interactions.
Low (-- RC). High (Safer on RC).
Therapeutic index
No. Flumazenil (competitive
Specific antidote
inhibitor).
4. Morphine and Salicylates.
Morphine Salicylates
Act on opiate receptors Inhibit COX enzymes

Mechanism of action
(Mu, Kappa, Delta & (Aspirin → irreversible
Sigma). inhibition) → less PGs .
Actions
Organs from above downwards
Mainly depressant. Mainly depressant.
CNS
1. Analgesic (all types of 1. Analgesic (superficial
pain, esp. visceral, except pain mainly) via ++ pain
itching). threshold in thalamus & --
2. Narcosis. sensitivity of pain
3. Euphoria. receptors.
4. ++ VMC & CIC. 2. Antipyretic via
5. Excitation in females & readjustment of

some animals. hypothalamic heat
6. ++ CTZ. regulatory center,
7. Miosis. peripheral VD, sweating &
8. -- HRC → hypothermia. mobilization of fluids from
9. -- ACTH, FSH & LH. tissues to plasma.
10. ++ Monosynaptic but --
Polysynaptic reflexes.
11. Lower seizures
threshold.
12. Trunkal rigidity due to
++ hippocampal pyramidal
cells.
SD → No effect. SD → No effect.
CVS
LD (IV mainly) → LD → VD.
hypotension. Never use salicylates' salts
in edema caused by HF.
-- RC. SD → No effect.
Respiratory
-- Cough center LD → ++ RC.
(antitussive). In adults: hyperventilation
Histamine release → → CO2 wash → resp.
bronchospasm esp. in alkalosis.
asthmatic patient. In children: Impaired CHO
metabolism → metabolic
acidosis.
May cause asthma by
shifting arachidonic acid to
LOX pathway.
Spasmogenic → Salicylate release (local) →
GIT
constipation. irritant.
Decreases all secretions. Less PGs (systemic) →
Spasmogenic on biliary hyperacidity.
tract & sphincter of Oddi. Liver → hydrocholeretic
effect.
Hepatotoxic (Reye's
syndrome).
++ Glycogenolysis.
Spasmogenic on ureter & -- PGs → renal VC →
Kidney
sphincters → retention of nephropathy in LD.
urine. Uricosuric in LD.
++ ADH → oliguria.
No effect on uterus but Tocolytic.
Uterus
causes neonatal asphyxia at
labor.
-- ESR.
Blood
-- Leukocytosis.
Hypoprothrombinemia in
LD (Warfarin-like).
-- Platelet aggregation.
Hemolysis in favism.
Methyl-salicylates →
Local
counter-irritant.
Salicylic acid → keratolytic,
fungistatic & antiseptic.
-- PGs (inflammatory
Anti-inflammatory
mediators).
++ ACTH (LD) → ++
Cortisol.
-- Kallikrein → less pain &
edema.
-- PMNs & macrophage
migration + lysosomal
membrane stabilization +
uncoupler in LD (less ATP
in phagocytic cells).
Histamine release →
Skin
itching.
-- BMR. ++ BMR in LD.
Metabolism
Therapeutic uses 4P Local:

1. Pain: 1. Salicylic acid:
- Cardiac pain. - Keratolytic in warts.
- Cancer pain (esp. terminal - Fungistatic in tinea of
stages). skin.
- Colics (add Atropine in - Antiseptic in
biliary & renal colics). hyperhiderosis.
- Bone fractures (except 2. Methyl-salicylate:
skull). - Counter irritant in
- Post operative (except eye myositis & arthritis.
& biliary). Systemic:

2. Pulmonary edema due to 1. Antipyretic:
acute left ventricular HF: Non-causal, non-specific.
Venodilator + sedation + 2. Analgesic:
slow resp. Mild pain.
3. Primary neurogenic 3. Common cold:
shock. Treat fever, headache,
4. Pre-anaesthetic muscle & joint pain.
medication: 4. Rheumatoid arthritis.
Analgesia + sedation +
amnesia. 5. Rheumatic fever
(arthritis).
6. Blood related:
Anti-platelet.
7. Chronic gout:
In LD + urine alkalization +
fluid intake.
Adverse effects Organs from above ASHGAR TIN

downwards: 1. Acute toxicity:
1. Head injury: Convulsions, hyperpyrexia,
Miosis interferes with hyperventilation,
proper Dx. hyperhiderosis,
hyperacidity, hypotension,
2. -- RC → more CO2 → VD →
hypoprothrombinemia.
++ CSF → ++ intracranial
tension → more -- RC. 2. Salicylism:
LD for long time → tinnitus,
3. ++ Epilepsy.
blurred vision, GIT upset,
4. In myxoedema → -- BMR hyperventilation.
may cause coma.
5. Respiratory:
4. GIT irritation:
Asthma & COPD.
Nausea, vomiting &
6. GIT: iatrogenic ulcer.
- Analgesia interferes with
5. Allergy:
proper Dx of acute
Rash, asthma or
abdomen.
angioedema.
- Constipation.
- Never alone in biliary 6. Reye's syndrome:
colic. Hepatotoxicity &
encephalopathy in virally-
7. Liver diseases or old age: infected children.

Incomplete metabolism. 7. Teratogenic.
8. Urinary: 8. Idiosyncrasy:
- Urine retention. Hemolysis in favism
- Never alone in renal colic.
9. Nephrotoxicity.
9. Uterus:
Addict fetus & neonatal
asphyxia.
10. Itching.
11. Tolerance & cross
tolerance.
Contraindications From above + 1. Allergy.

2. Blood-related:
1. Allergy.
Favism & bleeding
2. History of opiate
tendency.
addiction.
3. Gout (esp. in SD).
4. GIT & liver-related:
Peptic ulcer & Reye's
syndrome.
5. Resp. - related:
Asthma.
6. Children are more
susceptible to adverse
effects & toxicity.
Mention
Manifestations and lines of treatment of:
1. Acute Morphine poisoning.

2. Chronic Morphine poisoning.
3. Acute Aspirin toxicity.
I. Acute Morphine poisoning:
Manifestations:
1. Coma.
2. Miosis.
3. Hypoventilation and hypoxia.
4. Hypotension.
5. Hypothermia.
6. Cause of death: respiratory failure.
Treatment:
1. Artificial respiration, but not pure O2 as it causes apnea.
2. Stomach wash in all cases even after parenteral poisoning (use K-permanganate +
Charcoal + MgSO4).
3. Specific morphine antagonist, e.g. Naloxone.
II. Chronic morphine poisoning:
Causes & manifestations:
1. Tolerance →psychic and physical dependence (due to ↓endogenous endorphin
and enkephalin).
2. The addict → PPP, constipation, psychosis and moral deterioration.
3. Sudden stop of morphine or usage of morphine antagonist → withdrawal or
abstinence →psychic craving for morphine, anxiety, yawning, lacrimation,
rhinorrhea then reversal to all action of morphine → excitation, severe pain, fever,
mydriasis, hyperventilation, hypertension, tachycardia, diarrhea and urination.
Treatment:
1. Hospitalization+ psychotherapy.
2. Gradual withdrawal of morphine till the stabilizing dose.
3. Gradual substitution with Methadone → similar to morphine but less withdrawal
manifestations.
4. Gradual withdrawal of Methadone.
5. Clonidine → control withdrawal symptoms.
6. Acupuncture→↑release of endogenous endorphin and enkephalin.
7. Oral Naltrexone →µ-antagonist →antagonize euphoria; causing dysphoria.
III. Acute aspirin toxicity:
Manifestations:
1. Hyperreflexia, excitation, convulsion then coma.
2. Hyperpyrexia.
3. Hyperventilation.
4. Hyperhidrosis → dehydration.
5. Hyperacidity and irritation →nausea, vomiting, pain, ulcer, and bleeding.
6. Hyperglycemia.
8. Hypotension.
Treatment:
1. Acid base imbalance.
2. Symptomatic.
3. Stomach wash by sodium bicarbonate.
4. ↑urinary excretion by alkalization of urine, forced diuresis (hemodialysis may be

needed).
5. Anti-convulsants.
6. Cooling.
7. Correct dehydration & acid base imbalance.
8. Vitamin K + fresh blood transfusion.
1. Sedatives, hypnotics, anxiolytic.

2. Analgesia.
3. Anti-epileptics.
4. Anti-parkinsonism.
5. Anti-psychotic.
6. Anti-depressant.
7. CNS stimulants.
1. Anxiolytic.
a. BZ
b. propranolol
c. buspirone.
2. Sedatives
1. Benzodiazepines.
2. Bz-1.
3. Chloral Hydrate.
4. Anti-histaminic.
3. Analgesia
opioid NSAID
I. Agonist: I. Non selective COX

a. Natural (4) 1. salicylates.
2. Pyrazolone Derivatives.
- morphine
3. Indol Derivatives.
- codeine
4. Phenyl-acetic acid dervatives.
- papaverine.
5. Oxicams.
-narcotine.
6. Propionic acid dervatives.
b. synthetic. (5) 7. Fenamates.
- meperidine.
II. selective COX:
- fentanyl
1. Celecoxib.
- methadone
- dextro-propoxyphene. 2. Rofecoxib.
3. Meloxicam.
- tramadol
c. semisynthetic. (5) III. selective COX 3:
- paracetamol.
- Di-acetyl-morphine “”heroine”
- Di-hydro-morphine.
- Di-hydro-codeinone.
- Apomorphine.
- EthylMorphine
II. Antagonist: (2)
- naloxone
- naltrexone.
III. Mixed: (4)
- pentazocine.
- nalbuphine
- buprenorphine.
- butorphanol.
4. Gout.
Acute Prophylaxis ( ↓ uric acid)
I. Anti-inflammatory (1st line) I. inhibit production

- steroidal - allopurinol
- non steroidal - febuxostat
II. colchicine (2nd line) II. ↑ Excretion
due to 1st side effects. - probenecid
- benzbromarone.
III. break down
- pegylated uricase
- Rasburicase
5. Adverse effects of gout drugs:
Allopurinol Colchicine probenecid
Disturbance. Nausea, vomiting & Disturbance.

GIT
diarrhea.
## adverse Allergy. ‫ــــــــــــــــــــــــــ‬ Allergy.
- CNS. - Hepatotoxicity. - urate stone.

Cytotoxic.
- Hepatomegaly. - nephrotoxicity.
- leucopenia. - bone marrow
depression.
- Myopathy.
- reversible
alopecia.
6. Actions of Gout drugs:
Colchicine Probenecid Allopurinol

- acute and prophylaxis of gout - Hyperuricemia &
chronic gout
- gouty nephropathy
& urate stones.
- after failure of
uricosuric
- with anticancer drug.
- not with acute attack
(add colchicine)
7. Anti-epileptics
Block Na+ Block T-Ca+2 ↑ GABA ↓ Excitatory

transmitter
- Phenytoin. - Ethosuximide. - Benzodiazepine. - Valproate.
- Carbamazepine. - Valproate. - Valproate.
- valproate.
New: New: New: New:

- zonnisamide - lamotrigine - Gabapentin. - levetircetam.
-topiramate. - pregablin.
- lamotrigine. - tiagabin.
- levetircetam.
8. Parkinsonism.
Dopaminergic Anti-cholinergic.
- Benztropine.
I. L-Dopa: - Benzhexo
- Peripheral dopa decarboxylase - Biperidine.
inhubitors.
II. COMT inhibitor:

- Tolcapone.
- Entacapone.
III. MAO inhibitor:

- selegiline.
IV. Direct dopamine agonists

a. Ergoilines
- Bromocriptine
- pergolide
- lisuride.
b. Non Ergot
- pramippexole
- Ropinirole
V. Amantadine
CHAPTER THREE
GIT
Enumerate
Central anti-emetics and mention the mechanism of action, therapeutic uses and side
effects of metoclopramide.
Central Anti-emetics:
MG FHD PNK ‫ﻣﺞ ﻓﻬﺪ ﺑﻨﻚ‬
I. Muscarinic Receptor Blockers:
HYOSCINE:
•Blocks M-receptors in vomiting centre.
•Effective in ALL vomiting including Motion Sickness
•Short Acting → Useful in Air Sickness
II. Glucocorticoids:
Dexamethasone:
•Used in vomiting due to cancer chemotherapy.
III. 5-HT3 (Serotonin) Receptor Blockers:
ONDANSETRON, GRANISETRON:
•Block 5-HT3 receptors in CTZ.
•Used in vomiting due to cancer chemotherapy.
IV. H1 Receptor Blockers (Anti-histaminic):
•Block H1-Receptor in Vomiting Centre.
•Effective in ALL Vomiting including Motion Sickness
•Long Acting→ useful in Sea Sickness
•e.g.: Dimenhydrinate, Diphenhydramine, Promethazine, Meclizine, and Cyclizine
V. D2 (Dopamine) Receptor Blockers: Block D2 in CTZ.
Effective in all vomiting EXCEPT Motion Sickness
E.g.: Metoclopramide, Domperidone, Phenothiazines, Butyrophenones.
VI. Pyridoxine (Vit-B6):
Effective in vomiting of Pregnancy
VII. Neurokinin Receptor Blockers:
Aprepitant
Used in vomiting due to cancer chemotherapy
VIII. Cannabinoids:
Dronabinol
Used in vomiting due to cancer chemotherapy
METOCLOPRAMIDE:
Mechanism of Action:
Acts by Dual Mechanism:
•Centrally: by blocking D2 receptor in CTZ.
•Peripherally: stimulate 5-HT4 Receptors in Enteric Ganglia→ release A.Ch.→
↑Gastric Motility → ↑Gastric Emptying → Prokinetic agent.
Therapeutic Uses:
1•ALL vomiting EXCEPT Motion Sickness
2•Gastric Hypo-motility, e.g. diabetic gastroparesis
3•GERD (Gastro-Esophageal- Reflux-Disease)
4•Hiccup
Side Effects:
1•Dizziness& Nervousness
2•Extrapyramidal Manifestations e.g. Parkinsonism and Ataxia
3•Hyperprolactinemia→ Galactorrhea in Females
4•↑Absorption Of Concomitantly administrated Drugs e.g. Paracetamol, BUT NOT
digoxin
Compare Between
1. Metoclopramide and hyoscine in treatment of vomiting
Metoclopramide Hyoscine
Central & Peripheral Actions: •Blocks M-receptors in vomiting
center.
•Centrally:
•Effective in ALL vomiting including
By blocking D2 Receptor in CTZ.
Motion Sickness.
•Peripherally: •Short Acting → Useful in Air
Stimulate 5-HT4 Receptors in Sickness.
Enteric Ganglia→ release A.Ch.→
↑Gastric Motility → ↑Gastric
Emptying → Prokinetic Agent.
•ALL vomiting EXCEPT Motion

Sickness.
2.
Purgatives Mech. Of Action & Disadvantages

•Softens & Lubricates Hard Fecal Masses & Mucosa
Liquid Paraffin =
Of Large Intestine.
Paraffin Oil.
•Useful In Chronic Constipation.
(Physical)
Disadvantages:
1•Bad Consistency, use either Fruit Juice or
use an emulsion.
2•↓ Absorption Of Fat Soluble Vitamins.
•↓ Vitamin D → ↓ Ca Absorption → ↓
Growth & Teething In Children.
•↓ Vitamin K→ Hypoprothrombinemia →
Potentiate Oral Anticoagulants
3•↓ Absorption Of Other Drugs.
4•If reaches Lung → Lobar Pneumonia.
5•Uncontrolled Leakage From Anal
Sphincter→
•Pruritis Ani
•Anal Polyp
•Delay Healing Of Anorectal Operation.
6•If Absorbed Orally → Foreign Body
Reaction In Liver.
(Moderate Irritant) E.g.: Aloe, Cascara & Senna.

Anthracine •In Large Intestine they release → Emodine &
Crysophanic Acid → Absorbed.
Derivatives
Or Disadvantages:
1•Colicky Pain
2•Excreted In Milk → Diarrhea In Suckling
Baby.
3•Excreted In Urine → Red Discoloration In
Alkaline Urine.
Disadvantages:
1•Cumulation.
2•Liver Damage
3•Skin Rash.
Phenolphthalein 4•Red Discoloration Of Alkaline Urine.
3. H2 Blockers& PPI & PG Analogues.
P.O.C H2 Blockers PPI PG Analogues
Pharmacodynamics •Active •Prodrug •Active

& Mechanism Of •Compete with •Block Activity •Act On PG
Action Histamine for its Of Proton Pump Receptors → ↓C-
H2 Receptors Irreversibly. AMP.
•↓Gastric Cell •↓Acidity Up To •↓HCL Secretion.
Secretory Activity 100% (Block Of
represented by: Activity).
1•↓Pepsin
2•↓Intrinsic
Factor.
3•↓Acidity
(↓Vol. & H
Conc.)
•No Effect On •No Effect On •↑Mucous
Gut Motility. Gut Motility. •↑HCO3
•Selectivity isn`t •↑Gastrin. •VD → Nutrition
Absolute, I.e. it & Healing.
blocks H1
Receptors of
affected Blood
Vessels → VC.
•Stress, NSAIDs, •Zollinger •NSAIDs mainly.

Therapeutic Uses
Zollinger Ellison Ellison
The Drug Of Choice in Syndrome. Syndrome.
Peptic Ulcer Induced •GERD . •GERD.
By: •Pre-anesthetic
in Emergency
Cases .
•TTT of Systemic
Mastocytosis
•IM / IV in
Upper GIT
Bleeding.
•Mental •Headache •Nausea and

Adverse Effects:
Confusion in Dizziness Abdominal pain
elderly. Drowsiness.
•Rash, Itching, •Nausea, colic, •Oxytocic Effect.
Allergy. Diarrhea.
•Constipation, •↑Gastrin
Diarrhea. Carcinoid Tumor
•↑Prolactin → in Female Rat.
Galactorrhea. •↑Bacterial
•↓Androgen→ Infections
Gynecomastia •Bacterial
•Blood Colonies in Stock.
Dyscrasias
(↓Granulocytes,
Aplastic Anemia,
↓Platelets).
•↓Kidney
Functions →
↑Creatinine in
Serum.
•↓Liver
Functions by:
↓ Blood Flow,
↓Cytochrome
P450 Activity.
•↓HR.
•Recurrence in
Sudden Stop.
Explain why
Diphenhydramine is better than metoclopramide in treatment of vomiting in patients

with Parkinson’s disease.
I. Metoclopramide can cross BBB and causes Extrapyramidal manifestations as

Parkinsonism & Ataxia.
So, it is contraindicated in Parkinson`s patient
II. Diphenhydramine has limited passage to BBB → rare Extrapyramidal manifestations.
So, it is better in this patient.
Mention
Different mechanisms of action with example of anti-emetics

See question 1
What is the TTT of Diarrhea?

Specific TTT for the Cause:
E.g.
•Ciprofloxacin for Shigella Bacterial Infection Causing
Bacillary Dysentery
•Metronidazole for ameba Causing amebic Dysentery
Non Specific (Symptomatic) TTT:
•Correction of Dehydration
•GIT Protectives
•Anti-motility Drugs
I. Correction of Dehydration:
The Main Stay of Therapy in Cases of Dehydration
1. In Mild & Moderate Cases use Oral Rehydration Therapy (ORP):
•ORP doesn`t cure Diarrhea but only corrects Dehydration, Acid / Base Balance
& Electrolyte Imbalance.
•Powder containing Glucose (4g) + NaCl (0.7g) +KCl (0.3g) +Na Citrate (0.51g) to
be dissolved in 200ml Water
The Presence of H2O Facilitates the Absorption of Na with Subsequent Absorption
of Cl & H2O.
2. In Severer Cases use Parenteral Rehydration Therapy.
II. GIT Protectives:
Absorb Toxic Substances & Provide Coating for The Intestine.
1•Adsorbent:
Kaolin, Bismuth, Chalk & Charcoal
2•Absorbent:
Pectin which presents In Rice, Carrots & Apple

3•Astringents:
Tr. Catechu →release Tannic Acid in Intestine, precipitate Surface Proteins
III. Anti-motility Drugs:
1•Parasympatholytics:
Atropine, Propantheline for pain relief of intestinal colic
2•Opiates:
Diphenoxylate & Loperamide for symptomatic control of Diarrhea
Classify with Examples
The Different Anti-secretory Drugs used in TTT of Peptic Ulcer & mention the side
effect of one of them.
Anti-secretory Drugs
I. Anti-muscarinic Drugs:
1•Pirenzepine & Telenzepine → M1 Blocker → ↓ Acidity > Motility
2•Propantheline, Oxyphenonium & Oxyphencyclamine → ↓ Motility > Acidity
II. Gastrin Antagonists:
1-Proglumide: Receptor Blocker
2-Somatostatine & Octreotide → ↓ Release of Gastrin
III. Prostaglandins:
Misoprostol: TTT of NSAID-Induced Peptic Ulcer.
IV. H2 Blockers:
1•Cimetidine: Competitive Blocker on H2 receptor
2•Ranitidine
3•Nizatidine
4•Famotidine
Side Effects of Cimetidine:
1•Sudden Stop → Recurrence of the Ulcer & Bleeding
2•GIT Upsets → Constipation / Diarrhea
3•Hypersensitivity Reactions
4•Affect Liver & Kidney
5•↓Hepatic Blood Flow → ↓ Metabolism of Lidocaine & Propranolol
6•Hepatic Microsomal Enzyme Inhibitor
7•Males → Gynecomastia & ↓ Spermatic Count
8•Females → ↑ Prolactin → Galactorrhea & Infertility
9•Elderly → Mental Confusion
10•Muscle Pain
11•Blood Dyscrasias: Aplastic Anaemia & Thrombocytopenia.
True or False with Explanation
1. Anti-secretory Effect of Omeprazole outlasts its Plasma T½ .

•True
As it acts via Irreversible Inhibition of Proton Pump
So, The Effect lasts till New Pump Synthesis.
2. Misoprostol is given safely in Ulcer TTT in Pregnant Women .

•False
Due to its oxytocic Effect
3. Itopride is Serotonin Agonist used in GERD .

•True
As it increases Tone of Lower Oesophageal Sphincter
:‫ ﺑـ‬side effects of H2 Blocker‫ﻣﻤﻜﻦ ﻧﺤﻔﻆ اﻟـ‬

:(‫)ﺟﺮاﻟﻚ ﻫﺒﻪ‬
G→ GIT Upset
R→ Rebound Activity
A→ Allergy
L→ ↓Liver Activity
K → ↓Kidney Activity
H→ ↓Hepatic Bl. Flow
P→ ↑Prolactin
B =BBB → CNS Confusion
A→ Anti-androgen
CHAPTER FOUR
Endocrine
Insulin secretagogues Insulin sensitizers Alpha glucosidase
inhibitors
1. Sulphonylurea: 1. Biguanides: 1. Acarbose

Members
Tolbutamide Metformin 2. Miglitol
Glipizide 2. Glitazones
2. Others: (Thiazolidenediones):
Meglitinides: Repaglinide Rosiglitazone
D-phenylalanine: Nateglinide Pioglitazone
↓ α-glucosidase on brush
Mechanism 1. They depend on presence of 1. Biguanides:
endogenous insulin (30% a. They do not stimulate border of intestinal
functioning B cells): release of insulin. mucosa → ↓ absorption
a. Block ATP-sensitive K+ b. ↓ glucose absorption of complex carbohydrate
channels of B cells of pancreas from intestine. → ↓ postprandial
→ depolarization → influx of c. ↑ Glucose uptake by hyperglycemia.
ca++ → exocytosis → ↑ release skeletal muscle.
of insulin d. ↓ Hepatic
b. sensitizes B cells to effect of gluconeogenesis.
glucose → ++ release of insulin e.↑ metabolic glycolysis
c. inhibits release of in peripheral tissue → ↑
catecholamine(anti-insulin) → removal of glucose from
++ release of insulin. blood → but increase
lactic acid production.
2. ↓ release of glucagon (directly
f. ↓ release of glucagon.
or through ↑ insulin &
g. ↑ sensitivity of tissues
somatostatin).
to insulin by ↑ binding to
3.extra-pancreatic effect: its receptors.
++ no. & sensitivity of insulin
2. Glitazones
receptors → potentiate
Binds to PPAR α nuclear
peripheral action of insulin.
receptors in sensitive
tissues to insulin (e.g.
adipose, skeletal, liver) →

gene expression →
synthesis of cellular
molecules important for
insulin signalling e.g.
Glut-4 &lipoprotein
lipase enzyme.
Indication 1. NIDD (type II): Biguanides 1. Control post prandial

a. non-obese 1. Obese NIDD hyperglycemia in NIDD.
b. non-complicated diabetes 2. Can be combined with 2. used alone or with
c. no stress, major organ disease, insulin or sulfonylurea.
sulfonylureas.
history of diabetic ketoacidosis. Glitazones 3. not used with
2. Chloropropamide → anti- monotherapy or with
metformin.
diuretic →treat hypothalamo- sulfonylurea or
pituitary diabetes mellitus metformin in NIDD.
3. other group of drugs: control
postprandial hyperglycemia.
Adverse 2A B 2C D E F G 2H & T 1. flatulence
Biguanides
effects 1.↑Appetite → weight gain. 1. GIT→ anorexia, 2. diarrhoea
2. Allergy: hypersensitivity & nausea, vomiting & 3.↓absorption pf
cross allergy with diarrhoea. metformin.
sulphonamides e.g. thiazides. 2. lactic acidosis
especially in patient with:
3. Bone marrow inhibition.
* hepatocellular failure
4. Cholestatic jaundice. * renal insufficiency
5. CNS manifestations: * hypoxic status
headache, confusion, vertigo & * chronic alcoholism
ataxia. * advanced ages
3. long use →↓absorption
6. Edema due to antidiuretic of vit B12.
effect.
Glitazones
7. Failure:
Primary in 10-15%NIDD 1. Moderate weight gain,
Secondary due to exhaustion of edema & mild anaemia.
B cells. 2. ++ Risk of MI & sudden
death.
8. GIT disturbances: heart burn, 3. hepatotoxicity.
nausea, vomiting & diarrhoea. 4. increase incidence of
9. Heart disease: osteoporosis.
↑ the incidence of coronary 5. ++ Risk of bladder

heart disease. cancer.
6. teratogenic
10. Hypoglycaemia:
specially → overdose, elderly, or N.B produce euglycemia
liver or kidney disease. not hypoglycemia.
11. Teratogenic.
12. Disulfiram like action:
Alcohol Intolerance.
N.B the other group of drugs is
less liable to produce
hypoglycaemia & weight gain.
Glucocorticoids Actions Side Effects Contraindication Precautions Therapeutic uses

1. Metabolic 1. Iatrogenic Cushing's 1. Cushing’s 1. Addison’s disease.
Mein
disease. disease
a. CHO:
�‫ﻣ‬
Gluconeogenesis.
Glycogenesis. 2. Hyperglycemia. 2. Diabetes 1. Sugar in
↓ Glucose uptake. mellitus. urine.
b. Fat:
Lipolysis
Lipemia
Redistribution 3. Moon face & Buffalo
hump
c. Protein:
Most tissues → 4. osteoporosis 3. Osteoporosis 2- X-ray spine, 2. Lymphoma &
catabolic ↑protein in diet Leukemia
& Anbolics.
2. Electrolytes 5. Edema & Hypertension 4. Heart failure,

→ Mineral 3. Weight, Bl.p.
Hypertension&
a. Na+ & Water Digitalis toxicity Digital toxicity
retention
↓NaCl & ↑K+
b. k+ depletion
*NB: ↑ free water
clearance
(glucocorticoids)
3. Anti-Inflammatory 6. Mask infections bacterial 5. Untreated
& Anti-Rheumatic and Viral infections. infections 3. Inflammations
4.Gastric: ↑ HCl & 7. Peptic ulcer 6. Peptic ulcer

GAB
↓mucin
‫ﺟﺎب‬
5.↓Antibody 4. Allergy
formation &
↓Antigen/Antibody 8. ↓immunity & ↑infection 5. Auto-immune
reaction 6. Tissue graft
6.Blood
a. ↑ RBCs & ↑PMNL
b. ↑Platelets
c. ↑Coagulation 9. Thrombosis 7. Thrombo-
d. ↓Lymphocytes embolism
e. ↓Eosinophils
7. Euphoria 10. Psychological 8. Psychological
EUP
disturbances. Disturbances
‫اﻳﻮب‬
8. ↓Pituitary A.C.T.H 11. Sudden stop→ Addison’s 9. Sudden

Crisis withdrawal
4. Gradual 7. Adreno-genital
withdrawal syndrome
9. Wound healing 12. Delay healing 8. Keloid formation
W‫و‬
10. Uricosuric 9. Gout
U
S
V 11. Anti-Shock & 5. ↑Dose in
Anti-stress stress 10. Shock
‫ﻳﻮﺳﻒ‬
12. Anti-Vitamin D 13. Hypocalcemia 6. ↑Ca+2 11. Hypervitaminosis

14. Retard growth in D (Hypercalcemia)
children
15. Myopathy
16. Sublaxation of joints 10. Repeated
intra-articular
17. teratogenic 11. Pregnancy

18. Cataract & Glaucoma 12. Glaucoma

DM:
Metabolic disorder due to ↓ ] insulin: absolute or relative
- ↑ Glucose (on blood):
- ↑ glycogenolysis / gluconeogenesis
- ↓ Uptake
↓
Hyperglucosuria
↓
Polyuria
↓
Polydipsia.
↑ lipid (blood) :
- ↑ lipolysis
- ↓ lipogenesis
↓
Hyperketonemia
↓
Hyperketonuria
↑ protein catabolism → azotemia → azoturia
Due to ↑ catabolism → polyphagia → ↓ weight → weakness → ↓ immunity →
infections.
Types of DM
Type 1 Type 2 Type 3 Type 4
Absolute Relative Other causes Pregnancy

Deficient Resistant Drug- endocrine-
pancreatic- non
pancreatic
• Insulin • Non-insulin • Kill cell: • Insulin /
• Non-obese • Obese - Alloxan metformin
• Ketosis • No - Streptozotocin
• Autoimmune • No • Inhibit synthesis
• less than 30 years →
immunosuppresive
• More than 40 • Inhibit release:

years - α2 agonist
- β2 antagonist
- Thyazied &
diazoxide
- Phenytoin
• Counteraction:
- Glucagon
- Catecholamines
- Cortisol
- GH & Thyroxin
- contraceptives
Non-insulin drugs
Inhibit glucose Insulin New drugs Insulin

absorption sensitizers secretagogues
• Acarbose • Biguanides • GLP-1 receptor • Sulphonylureas

agonist
• Miglitol • Glitazones • Meglitinides
• Exenatide
• DPP-IV
inhibitor
• Sitagliptin
• Amylin
analogue
Pramlintide
Insulin given to:

• type 1: → always
• type 2:
- failure of therapy
- Stress
- Pregnancy
- Renal impairment
- DKA: hyperosmolar
• Hyperkalemia.
• Anorexia nervosa.
Insulin
Weight gain Hypoglycemia
Resistance Hypersensitivity
- Reactive hyperglycemia
• local: somogyi effect.

- redness –itching.
- lipodystrophy.
• systemic (to
animals/protamine):
- rash- urticarial.
- angioedma-
anaphylaxis.
Insulin Types:
1. Onset:
About 10 min 30 min About 3 hours
rapid Short acting - Intermediate
- long
2. Duration:
3 hours Half a day 1 day

- rapid
intermediate long
- short
3. Peak:
2 hours 4 hours Peakless

rapid
intermediate long
short
Insulin:
• ↓ glucagon
• ↓ lipid & ketone bodies
• Anabolic / ↑ nucleoproteins
• ↓ K+
Non-insulin drugs:
• Secretagogues: ↑ insulin
Sulfonylureas & others:
- ↑ Insulin ( sensitivity / block ATP-K+ channel ).
- ↓ Glucagon & catecholamines.
- ↑ number & sensitivity to insulin receptors
- ^ somatostatin
• Sensitizers:
Metformin:
↓ Blood glucose:
- ↓ Absorption / gluconeogenesis /glucagon.
- ↑ Uptake /glycolysis.
↑ Sensitivity.
Glitazones:
- Bind to PPAR-γ → ↑ sensitivity .
- Gene expression → ↑ Glut-4 / lipoPtn lipase
• α Glucosidase inhibitor:
• GLP-1:
• ↓ gastric emptying
• ↑ insulin release
• ↓ glucagon / appetite
• DPP-4: like GLP-1
• Amylin: affects brain
• ↓ gastric emptying
• ↑ appetite
• ↓ glucagon
Members:
1. Inhibitors of glucose absorption:
• Acarbose
• Miglitol
2. Sensitizers:
• Metformin : (Biguanides)
• Glitazones: (Thiazolidinediones)
• Rosi (glitazones)
• Pio (glitazones)
3. Secretagogues:
a. Sulfonylureas :
• First:
- Tolbutamide : 4 amide
- Acetohexamide : 6 amide - COOH
- Chlorpropamide : 3 amide- Cl
• Second:
- (Gli) benclamide = Glyburide.
- (Gli) pizide.
- (Gli) clazide.
- (Gli) mepiride.
b. Meglitinides / D –phenylalanines
• Repa (glindine)
• Nate (glindine)
4. GLP agonist:
• Exanatide
• liraglutide
5. DPP-IV inhibitirs:
• Sita (gliptin)
• Vilda (gliptin)
• Saxa (gliptin)
6. Amylin: Pramlintide
Sulfonylurea Glitazones Metformin Alpha GLP-1 Di-peptidyl

(secretagogue) glucosidase analogues transferase
inhibitors inhibitors
(-gliptin)
1. Allergy. 1. Hepatotoxic. 1. GIT. 1. Flatulence. 1. Nausea. Acute
2. Bone 2. Osteoporosis. 2. Lactic 2. Diarrhea. 2. Delayed pancreatitis.
marrow 3. Bladder acidosis. 3. – Metformin gastric
inhibition. cancer. 3. Vit. B12 absorption. emptying (--
3. Cholestatic 4. Edema. deficiency. absorption of
jaundice. 5. Infarction. rapidly
4. Disulfiram- 6. Teratogenic. disintegrated
like. drugs).
5. Edema.
6. GIT
disturbances.
7.
Heart/Hypogly
cemia.
8. Teratognic.
Adverse effects of NI (From largest to smallest):
Uses of corticosteroids:
Aldosterone DOC/Fludrocortison ACTH Glucocorticoids

e
- Rarely used. - Addison's disease. - 2ry Addison. See actions.
- Antagoists are used. - Withdrawal therapy.
- Test cortex.
Adrenostatic Estrogen Progestogens Anti-progestogens

Cushing. 1. Contracption & -- 1. Contraception, Mifepristone:
lactation. prevents abortion &
Anti-rape.
2. Replacement in 1ry amenorrhea.
& 2ry hypogonadism. 2. Uterine bleeding, Danazol (anti
3. Osteoporosis. dysmenorrhea & gonadotrophin):
4. Vaginitis. endometriosis. 1. Gynecomastia &
5. Atherosclerosis. 3. Premenstrual tension. fibrocystic disease. 2.
6. Hirsutism. Endometriosis.
7. Acne. 3. Amenorrhea.
8. Endometriosis,
Asoprisnil:
dysmenorrhea &
uterine bleeding. 1. Fibroid.
9. Cancer prostate. 2. Endometriosis.
3. Uterine bleeding.
CHAPTER FIVE
Chemotherapy
Give an account
1- Write A Short Note On β Lactamase Inhibitors?

Examples: Clavulanic Acid, Sulbactam & Tazobactam
They Bind with The Enzyme →Irreversible Inhibition → Suicide Substrate.
They have very weak or no Antibacterial Activity.
They protect Penicillin from Inactivation by β Lactamase secreted by some Bacteria
e.g. Proteus, E-Coli, Pseudomonas, Staph Aureus & H. Influenza. (P.E.P.S.I).
Preparations:
1- Clavulonic Acid +Amoxicillin = Co-Amoxiclav & Augmentin Orally.
2- Clavulonic Acid + Tivarcillin = Timentine IV.
3- Sulbactam +Ampicillin = Unasyn Oral, IV & IM.
4- Tazobactam +Piperacillin = Tazocin & Zocyn IV.
2- Give an account for The Mechanism of Action & Classification of Penicillin

&Mention One Member in Each Group & Discuss its Therapeutic Uses.
Give an Account On Penicillin Antibacterial Activity & Mention Adverse Effects of

Penicillin.
I. Bactericidal Antibiotics.
II. Bind to Specific PBP causing:
1- ↓Transpeptidase Enzyme Responsible for Cross Linking of Peptidoglycans, a final
Step in Cell Wall Synthesis.
2- Activation of Autolytic Enzymes (Autolysins) → Lysis of Cell Wall.
3- Bacteria imbibe Water due to its Interior High Osmotic Pressure →Rupture &
Death of The Microbe.
4- They affect mainly Growing Bacteria rather than resting Ones.

Classification-: They are 8 Groups:
1- Benzyl Penicillin (Penicillin G)
2- Long Acting Penicillin →Procaine Penicillin G.
3- Acid-resistant Penicillin →Phynoxymethyl Penicillin (Penicillin V)
4- β Lactamase -resistant Penicillin →Methicillin.
5- Acid & β Lactamase -resistant Penicillin →Oxacillin.
6-Broad Spectrum Penicillin →Ampicillin.
7-Extended Spectrum (Antipseudomonal) Penicillin →Azlocillin.
8-Reversed Spectrum Penicillin (Amidino-penicillins) →Mecillinam .
Therapeutic Indications:
I. TTT of:
1- Gram +ve Cocci:
• Streptococcal Infections E.g. Pharyngitis.
• Streptococcus Mutans →Carcinogenic.
• Streptococcal Infections E.g. Boils →Add β Lactamase Inhibitor / Use

βLactamase Penicillins (Ampiclox).
• Pneumococcal Infections →Lobar Pneumonia.
2- Gram –ve Cocci:

• Meningococcal Meningitis →Benzyl Penicillin (6).
• Gonorrhoea.
3- Gram +ve Bacilli: Anthrax, Diphtheria, Tetanus & Gas Gangrene.

4- Spirochetes: Treponema Pallidum (Syphilis).
• Acute Ulcerative Gingivitis (Vencent`s Gingivitis) caused by Spirochetes &
Fusiform •Bacteria → treat by Penicillin + Metronidazole.
5- Actinomycosis.
6- Pseudomonas → Antipseudomonal + Aminoglycosides e.g. Gentamicin.
7- Gram –ve Bacilli → Use Broad Spectrum Penicillin E.g. Ampicillin &
Amoxicillin.
• Urinary Tract Infections.
• Typhoid Fever.
•H. Influenza → Broad Spectrum Penicillin + β Lactamase Inhibitor.

• H. Pylori → Peptic Ulcer: Amoxicillin for Weeks.
II. Prophylaxis of:

•Streptococcal Infections in Rheumatic Fever.
Benzathine Penicillin for 5 Years or up to the age of 20.

•Bacterial Endocarditis: in patients with Rheumatic Fever or Prosthetic Cardiac
Valves.
Procaine Penicillin IM 2-3 hours before Dental Procedures.
•Gonorrhoeal Neonatal Ophthalmic: Benzyl Penicillin Eye Drops.
Bacterial Activity:
I- Bactericidal Antibiotics.
II- Mechanism of Action Mentioned Above.
III- Selectivity: Human Cells don`t contain Peptidoglycan Cell Wall.

IV- Resistance:
1-Natural Absence of Cell Wall e.g. Mycoplasma.
2- Plasmid Mediated (Acquired):
• Production of + β Lactamase Enzyme.
• Alteration of PBP.
• Decreased Permeability to Antibiotics.
V- Spectrum:
I. Narrow Spectrum Penicillins:
1- Gram +ve Cocci: Strept, Staph & Pneumococci.
2- Gram –ve Cocci: N.gonorrhea & N.meningitidis .
3- Gram+ve Bacilli: C.tetani , C.perfringens , C.diphtheriae & B. anthracis .
4- Anaerobes except β Lactamase secreting Bacteroides Fragilis .
5- Spirochetes: Treponema Pllidum (Syphilis) & Acute Ulcerative Gingivitis
6- Actinomyocytes: Actinomyces Israeli.
II. Broad Spectrum Penicillins:
The Above +
Gram-ve Bacilli: Salmonella typhi, Paratyphi, Shigella, H.Influenza, H.Pylori &
E.Coli.
Not Effective Against Proteus, Pseudomonas & Klebseilla.
III. Extended Spectrum:
The 2 Above + Klebseilla, Proteus & Pseudomonas.

Adverse Effects:
1- Allergy: Urticaria, Angioedema & Anaphylactic Shock.
• Avoided by Ask for History & Dermal Sensitivity Test.
• TTT of Anaphylactic Shock: Adrenaline, Cortisone & Antihistaminic.

• Never Reuse.
•Cross Allergy with Cephalosporin (10%).
2. Jarisch Herxheimer Reaction:

• Only 1st Injection in Spirochetal Infections e.g Syphilis.
•TTT by Cortisol.
•Continue Penicillin Therapy.
3. Diarrhea
due to Superinfections especially after oral Ampicillin.
• Candida Albicans → Monilial Thrush & Diarrhea, ttt by Nystatin.
• Antibiotic associated (Pseudomembranous Colitis) caused by Enterotoxins

produced by Staph or Clostridium Difficile), ttt by oral Vancomycin or
Metronidazole.
4. CNS Irritation
(Seizures) occurs if LD or Intrathecal Injection.
5. Usually we use Na / K Salts of Penicillins
LD→ Na or K Overdose → danger in Renal & Cardiac Patients.
6.Benzathine Penicillin → Pain, Enduration & Tenderness.
7.Ampicillin → Skin Rash (10%) & in all Patients with Infective Mononucleosis,
Leukemia & taking Allopurinol.
8.Methicillin → Nephritis.
9.Carboxy-penicillins e.g Carbenicillin → Platelet Dysfunction → Bleeding.
3- Give an Account On Mode of Action, Antibacterial Activity & Toxicity of

Aminoglycosides.
Mode of Action:
1. They bind to 30S Ribosomal Subunit.
2. ↓Ptn Synthesis & May interfere with the Cytoplasmic Membrane Function.
3. Concentrate inside Bacteria by O2- requiring Active Transport Mechanism.
4. Blocked by Chloramphenicol.
5. Not Effective Against Anaerobes.
6. More Active in Alkaline Media.
7. Reducing Agents e.g. Vit .C decreases their Activity.
Antibacterial Activity:
I. Bactericidal Antibiotics.
II. Mechanism of Action → Above.
III. Narrow Spectrum:
1. Mainly Against Gram –ve Bacilli including Pseudomonas, Proteus &
Klebsiella.
2. Some Gram +ve Cocci e.g β Lactamase producing Staph. Aureus &
Enterococci
3. Mycobacterium TB is Sensitive to Streptomycin, Kanamicin, Amikacin &
gentamicin.
4. Not Active against Anaerobes.
5. Usually combined with Penicillin (Synergism).
IV. Resistance;
1. Deletion / Alteration in 30S Receptors (Chromosomal Mutation).
2. Decreased Active Uptake into Bacteria (Plasmid / Chromosomal).
3. Plasmid- induced increased Metabolizing Enzymes
Amikacin & Netilmicin are Resistant to these Enzymes.
Toxicity:
I. Ototoxicity:
1. Irreversible Damage to Vestibulo-auditory 8th cranial nerve → Vertigo & Deafness.
2.Toxicity increases with increased Dose, Duration & Age, Impaired Renal Function
& Concurrent Use of Loop Diuretics, Salicylates & Chloroquine.
3.Do Frequent Audiograms.
II. Nephrotoxicity
1. Usually reversible.
2.Increases in patients with poor kidney functions or concurrent use of Frusemide.
III. Skeletal Muscle Relaxation;

1. ↓Prejunctional release of A. Ch. & ↓sensitivity of post synaptic sites (Curare Like
action).
2. May cause respiratory muscle paralysis if injected into pleural or peritoneal
Cavity especially in myasthenic Patients.
Reversed by IV Ca Gluconate & Anti-Ch.E.
e.g Neostigmine / Edrophonium + Artificial Respiration.
IV. Allergic Manifestations e.g. Contact Dermatitis.
V. Drug Interactions:
1. Amphotericin-B, Polymixins, Cephalosporins & Frusemide increase their
Nephrotoxicity.
2.Loop Diuretics, Chloroquine & Aspirin increase their Ototoxicity.
3. They Potentiate Competitive N.M Blockers e.g Curare.
4. Aminoglycosides + Penicillins → Synergism but never mixed in the same Container
5. Chloramphenicol →↓ Bacterial Uptake of Aminoglycosides.
4- Discuss Antibacterial Activity, Therapeutic Uses & Side Effects of Co-trimoxazole?

Antibacterial Activity:
DHPS DHPR
PABA Folic Acid THFA
# Sulfonamides # Trimethoprim
1. They produce Sequential Block in The Synthesis of Folinic Acid & DNA →
Synergism.
2. More Potent, wider Spectrum & Less Bacterial Resistant than each Drug alone.
Therapeutic Uses:
1. Respiratory Tract Infection.
2. Urinary Tract Infection.
3. Gonococcal Infection (Urethral & Oropharyngeal).
4. Shigella & Salmonella Enteritis.
5. Systemic Salmonella (Typhoid Fever & Carrier).
6.Prostatitis
7. Prevention & TTT of Toxoplasmosis.
8. Prevention & TTT of Nocardia (Drug of Choice).
9.Prevention & TTT of Pneumocystis carnii in AIDS. used by IV Infusion.
Adverse Effects:
ABCDDDD+ Megaloplastic Anemia
1.Allergy:
• Manifestations: Fever, Photosensitivity & Stevens-Jhonson Syndrome.
• Cross Allergy with other Sulphonamides.
2. Blood dyscrasias.
• Hemolysis in Patients with G6PD Deficiency.
•Bone Marrow Inhibition.
3. Crystaluria: avoided by plenty of fluid intake & Alkalinization of Urine.

4. Diarrhea → GIT Disturbances & Superinfection.
5. Damage → Nephrotoxicity & Hepatotoxicity.
6. Displace Bilirubin → Kernictrus. Avoid During Pregnancy & Lactation.
7. Drug Interaction:
• Displace Warfarin & Tolbutamine → Initial Increase in their Activity.
• Methenamine → release Formaldehyde → inactivates Sulfa.
8. Megaloblastic Anemia.
5- Discuss Clinical Uses of Fluoroquinolone & What Are Adverse Effects of

Fluroquinolone, Generations & Spectrum?
Generations: (4)
I. The 1st Generation Quinolones:
Nalidixic Acid → Prevention & TTT of UTI, Not Pseudomonal or Systemic.
II. 2nd Generation Fluoroquinolones:
More Powerful 60Times > Quinolones.
Useful in: Systemic Infections:
Norfloxacin, Ofloxacin & Ciprofloxacin.
Uses:
1. RTI: Not Effective in Pneumonia & Sinusitis by Pneumococci.
-Effective in Mycobacterial Infections e.g Multidrug Resistant TB.
2. GIT:
• Diarrhea e.g. Traveller`s Diarrhea caused by Salmonella, Shigella, E.Coli &
Helicobacter.
• Typhoid Fever.
• Intraabdominal Infections.
3. UTI.
4. Prostatitis.
5. STD eg Gonorrhea, Chlamydia but NOT Syphilis.
6. Soft Tissues, Bone & Joint Infections.
7. Septicemia.
8. Not against MRSA, Pneumococci, Enterococci, Spirochetes & Anaerobes.
III. 3rd Generation of Fluroquinolones:
• Retain Gram –ve Organism + Gram +ve.
• Levofloxacin, Moxifluxacin & Sprafloxacin.

IV. 4th Generation of Fluoroquinolones:
Gram –ve Organism + Gram +ve + Anaerobes.
Trovafloxacin but Hepatotoxic.
Spectrum
Fluoroquinolones > 60 Times Quinolones.
1. Active Mainly against Gram -ve Organisms (Pseudomonas, H.Influenza &
Gonorrhea ) .
2. Less Active Against Gram +ve Organisms (Not Pneumococci or Enterococci).
3. Active Against Mycobacterium Including TB Not M.Avium.
4. Mycoplasma.
5. Chlamydia.
6. Not Active Against Spirochetes & Anaerobes.
Adverse Effects:
1- Allergy (Hypersensitivity).
2- Photosensitivity, Use Sun Screens & Sun-blocks.
3- CNS: headache, dizziness & Confusion → Avoid Driving.
Seizures especially if used with NSAID → Avoid in Epileptics.
4- GIT Upsets.
5- Chondrolytic → Reversible Arthropathy → Avoid in Pregnancy, Lactation &
Children Up to 18 Years.
6- Rupture of Tendons (Achilles endon) specially in elderly taking Glucocorticoids.
7- Nephrotoxic & Crystaluria.
8- Drug Interactions:
I- Ciprofloxacin & Ofloxacin →Enzyme Inhibitors →↓ Metabolism of Theophylline,
Warfarin & Sulfonamides.
II- Cimetidine → ↓ Metabolism of Fluoroquinolones.
II- Sucralfate, Antacids (Mg & Al) & Food Supplements (Fe & Zn) →↓ Absorption of
Fluoroquinolones.
IV- Fluoroquinolones + NSAID → Seizures.
6- Compare Between Ciprofloxacin & Rifampicin (Mechanism of Action,

Antibacterial Activity, Therapeutic Uses & Toxicity).
Rifampicin Ciprofloxacin
↓ DNA Dependent RNA • ↓ DNA gyrase enzyme (Bacterial
Mech. of Polymerase Enzyme →↓ RNA Only) (Topoisomerase II, IV)

action Synthesis. →↓Rejoining Step→↓DNA
Replication.
1- Bactericidal Antibiotic. 1- Bactericidal
Antibiotic.
2- Mech. Of Action as Above.
2- As Above.
3- Spectrum:
Antibacterial 3- Mentioned in The Previous
•Mycobacterium TB & Leprosy.
Activity Question(Q5)
•Some Gram +ve & -ve Bacteria.
•Chlamydia & Pox Virus.
1. 1st Line Drug in TB + Isoniazid.

2. Leprosy.
Therapeutic 3. Drug of choice in Prophylaxis of Mentioned Above.Q5

Uses Meningococcal Meningitis.
4. Resistant Bacterial Infections
E.g. Staph.
1. Orange Red Discoloration of
Secretions E.g. Tears, Saliva,
Sweat, Sputum & Urine. Mentioned Above.
Toxicity 2. Allergy: Flu Like Syndrome.
3. GIT Upsets.
4. CNS: Headache, Confusion &
Ataxia.
5. Hepatic Microsomal Enzyme
Inducer →↑Metabolism of Oral
Anticoagulants, Hypoglycemic,
Contraceptives, Corticosteroids,
Digitalis & Methadone →
Withdrawal Manifestations.
7- Explain Why Chloramphenicol, Tetracycline & Quinolones are Contraindicated in

Infants & Neonates?
Chloramphenicol: As It causes:
1. Bone Marrow Depression.
2. Gray Baby Syndrome in Premature Neonates.
Chloramohenicol Is Not Properly Metabolized→ Cumulation →Toxicity →Vomiting,
Hypotension, Hypothermia, Hypotonia, Shock, Collapse & Gray Discoloration of
Skin.
Tetracycline: As It causes:
Teeth & Bone Abnormality If taken during Pregnancy & Early Childhood → Chelated
by Ca & deposited in Early Formed Teeth & Bone:
1. Teeth: Permanent Yellow-Brown Discoloration & Enamel dysplasia.
2. Bone: Deformity & Inhibition of Growth.
3. Tetracycline should be avoided in Pregnancy, Lactation & Children Up to The
Age of 8 Years.
It is contraindicated After Expiry Date as it is Nephrotoxic Specially After Expiry
Date.
Quinolones:
As it is Chondrolytic & causes Reversible Arthropathy.
8- Compare Between Mechanism of Action, Spectrum & Side Effects of Rifampicin &
Isoniazid?
Isoniazid Rifampicin
1. Tuberculostatic &_cidal. As Mentioned
Mechanism
of Action 2. ↓Synthesis of Mycolic Acid →↓ Cell Wall Synthesis. above. Q6
Extracellular & Intracellular M.Tuberculosis . As Mentioned

Spectrum above.
I. Idiosyncracy.
1. Slow Acetylators →↑ INH →Peripheral Neuritis
TTT→ Vit B6 (Pyridoxine).
2. Rapid Acetylators → Acetyl Isoniazid →
Hepatotoxicity.
As Mentioned
Side Effects 3. Hemolysis in Patients with Favism. above.
II. Drug Interactions:
1. Isoniazid → Enzyme Inhibitor →↓ Metabolism of
Phenytoin →↑ It`s Plasma Level.
2. Rifampicin → Enzyme Inducer →↑ Acetylation of
INH → Hepatotoxicity.
9- Some Antibiotics Are Hepatic Microsomal Enzyme Inducers,

Give 3 Examples, Discuss Their Mechanism of Action & Side Effects.
Chloramphenicol Erythromycin Ciprofloxacin

Bind with 50S Ribosomal Binds Irreversibly ↓ Bacterial
Subunit →↓ Transpeptidation →↓ with 50S DNA gyrase
ptn Synthesis. Ribosomal Subunit (Topoisomerase
→↓Translocation II, IV) →↓
→↓ ptn Synthesis. Rejoining Step
Mechanism →↓ DNA
of Replication →
Action Bactericidal.
I. Bone marrow inhibition I. Most Common Is

Epigastric Pain.
Blood dyscrasias
1- Reversible dose dependent II. Cholestatic
inhibition of erythropoiesis Jaundice, Most
due to inhibition of probably due to
mitochondrial protein Esteolate Ester.
synthesis. III. LD of
2. Fetal aplastic anemia which Erythromycin →
is irreversible, dose Reversible
independent and may be Ototoxicity.
idiosyncrasy. LESS likely to IV. Drug
occur with Thiamphenicol Interactions:
II. Gray Baby Syndrome 1. Erythromycin Noticed Above
Side
In premature neonates, →↓Cytochrome P450 in Q5.
Effects
chloramphenicol is NOT →↓Metabolism of
properly metabolized → Theophylline,
cumulation → Toxicity→ vomiting, Carbamazepines &
hypotension, hypothermia, Warfarin → Toxic
hypotonia, shock, collapse, Gray Conc.
discoloration of skin.
2.↓ Intestinal Flora
III. GIT upset, superinfection. →↓ Metabolism of
IV. Hepatic mitochondria Digoxin → ↑ Its
enzyme inhibition Potentiate Absorption.
Phenytoin, Theophylline,
Warfarin(anticoagulant),
Tolbutamide&
Chlorpropamide(hypoglycemic).
10- Discuss Action of Clavulanic Acid Amoxicillin.:

Is a broad Spectrum Penicillin which is Active Against gram +ve & -ve Organisms
including gram –ve Bacilli e.g. Salmonella, Shigella, H.influenza , H.pylori & E.coli
But Not Effective against Klebseilla , Proteus & Pseudomonas Aerogenosa .
Clavulonic Acid:
Is a β Lactamase Enzyme Inhibitor. They have No or Weak Antibacterial Activity,
They Protect Penicillin From Inactivation By β Lactamase Enzymes secreted from
Proteus, E. coli, Pseudomonas, Staph Aureus & H.influenza . (PEPSI)
11- Discuss The Action of Sulphamethoxazole & Trimethoprim.

Sulphamethoxazole
Action:
I. Bacteriolstatic
DHPS DHPR
PABA Folic Acid THFA
# Trimethoprim
# Sulfonamides
II. Compaete with PABA →↓ Dihydropteroate synthetase(DHFR) →↓ Folic acid

synthesis
Folic acid is essential for synthesis of bacterial purines& DNA.
Mammalian cells can utilize preformed folic acid.
III. Synergists: inhibitors of DHFR e.g. Trimethoprim → Sequential block.
IV. Antagonists: Except Mefendine.
1. PABA 2. Pus 3. Procaine
V. Spectrum
1. Gram +ve & -ve bacteria (NOT Pseudomonas or Protus)
now many strains (Staph, Strept, Pneumo, Meningio, Gonococci) → Resistant.
2. Chlamydia trachomatis
3. Nocardia (Actinomycete)
4.Some protozoa (Pneumocystis carnii)
5.Not active against → Rikettsia, Spirochetes or viruses.
Trimethoprim
Action: SEE Q 4
12- Metronidazole, Mechanism of Action, Uses & Adverse Effects.

Produced by Anaerobic Bacteria & Protozoa → Active Metabolite → Binds to DNA →↓
Nucleic Acid Formation.
Uses:
I. Antiamebic → Direct Amebicidal.
1. Tissue Amibicidal
(Gut wall, Hepatic & Extraintestinal).
Drug of Choice in Amebiasis (Intra& Extraintestinal & Hepatic).
Dose: Adult 750mg tds Orally for 5-10 Days.

Children 35-50mg/kg/day for 7 Days.
2. Less Effective as Luminal Amibicide. It is Rapidly absorbed → Low Intra-
intestinal Luminal Concentration.
II. Antitrichomoniasis: D.O.C.
Adult Dose 2mg Single Dose P.O. or 250mg tds P.O. for 7days + Topical Gel / Vaginal
Suppository.
III. Antigiardiasis: D.O.C. The Same Dose as Amebiasis.
IV. Powerful Bactericidal Against:
1. Peptic Ulcer with H.Pylori .
2. Pseudomembranous Colitis (C.difficile ) .
3. Sepsis caused by Anaerobic Bacteroids.
• Post-Surgical. •Septicemia •Osteomyelitis.
• Abscess of Brain & Lung.

• Intraabdominal & Pelvic Infections.
4. Acute Ulcerative Gingivitis & Dental Infections (Fusobacterium).
5. Anaerobic Vaginitis (Gardnerella Vaginalis).
V. Disulfiram-like Action.
VI. Sensitize Hypoxic Tumor Cells to Ionizing Radiation.
Adverse Effects:
1. Allergy.
2. CNS: Headache, Dizziness & Vertigo.
3. GIT: Nausea, Vomiting, Diarrhea, Furry Tongue & Metallic Taste in Mouth.
4. Intensification of Moniliasis.
5. Leukopenia.
6. Suppression of Cellular Immunity.
7. Mutagenic → Carcinogenic and / or Teratogenic.
13- Describe The Antibacterial Spectrum, Kinetics, Uses & Adverse Effects of β
Lactam Carbapenems.
Spectrum:
Gram +ve & -ve Aerobes & Anaerobes Growing or not.
Kinetics:
•½ -1 gm/6hours IV.
• Metabolized &
Inactivated by Renal Tubular Dihydropeptidase Enzyme (Imipenem),
but Meropenem isn’t metabolized by Dihydropeptidase Enzyme.
Uses:
• Acts by Binding to PBP-2 →↓ Cell Wall Synthesis → Bactericidal.
• Acts On Wide Variety Spectrum of Bacteria Mentioned Above.
Adverse Effects:
1. Allergy & Partial Cross Allergy with Penicillins.
2. GIT Disturbances.
3. Seizures which are less in Meropenem.
4. Imipenem → Toxic Metabolite → Nephrotoxicity
5. Cilastatin (Dihydropeptidase Enzyme Inhibitor).
14- Compare The Antibacterial activity, Mechanism of Action & Toxic Effects of the
Following: Amoxicillin, Isoniazid & Ofloxacin.
Amoxicillin Isoniazid Ofloxacin

• Bind to PBP Enzyme:
↓ Transpeptidase Enzyme
Responsible Foe Crpss-
linking of Peptidoglycans, A
Mechanism of Action.
Final Step in Cell Wall Enter bacteria by Passive

Synthesis →↓ Synthesis. ↓Mycolic Acid Diffusion Through porins
•Activate Autolysins → Lysis Synthesis →↓Cell →↓ Bacterial DNA Gyrase
of Cell Wall. Wall Synthesis. (Topoisomerase II, IV)
Enzyme →↓Rejoining Step
•Bacteria Imbibe Water due
→↓ DNA Replication.
to Interior High Osmotic
Pressure →Rupture & Death of
The Microbe.
•They Affect Mainly Growing
Than Resting ones.
I. Bactericidal.
Tuberculostatic & Spectrum:
Antibacterial II. Selectivity Cidal. Fluoroquinolones >60
Activity times Quinolones.
(No peptidoglycan in human
1. Mainly Gram –ve
cells.) organisms.
III. Resistance. 2. Less Active Against
Gram +ve.
1. Absence of cell wall
naturally (Mycoplasma). 3. Mycobacteria
Including TB, Not
2. Plasmid Mediated
M.Avium .
Acquired Resistance.Β-
Lactamase Production. 4. Mycoplasma.
Alteration of PBP. 5. Chlamydia.
Decreased Permeability. 6. Not Against
IV Spectrum: Spirochetes &
Anaerobes.
1. Gram +ve Cocci.
Resistance:
2. Gram –ve Cocci.
1- Chromosomal
3. Gram +ve Bacilli.
Mutation in Gyrase
4. Anaerobes Except β Enzyme (MRSA).
Lactamase Secreting
2- No Cross Resistance
Fragilis.
with Other Drugs.
5. Spirochetes.
6. Actinomyocetes.
7.Gram –ve Bacilli.
Not Effective Against
Klebsiella, Proteus &
Pseudomonas, Aeruginosa,
βAbse
1. Allergic Reactions & Cross 1.Allergy.
I. Idiosyncracy:
Allergy with Cephalosporins
1. Slow Acetylators 2.Photosensitivity.
(10%).
→↑ INH →Peripheral 3. CNS: headache,
2. Jarisch –Herxhiemer Neuritis. dizziness & confusion.
Reactions.
2. Rapid Acetylators Seizures Especially When
Adverse 3. Diarrhea. → Acetyl Isoniazid → used with NSAID.
Effects 4. CNS Irritation (Seizures). hepatotoxicity. 4. GIT Upsets.
5. Na / K Overload in Case of 3. Hemolysis in 5. Chondrolytic →
Using Salts of Penicillins. Patients with Reversible Arthropathy.
Favism.
6. Rupture of Tendons.
II. Drug
7. Nephrotoxic &
Interactions:
1. Isoniazid → Crystaluria.
Enzyme Inhibitor 8. Drug Interactions:
→↓ Metabolism of
Phenytoin →↑ It`s I↓ Metabolism of
plasma level. Theophylline, Warfarin
& Sulfonamides.
2. Rifampicin →
Enzyme Inducer →↑ II. Cimetidine →↓
Acetylation of INH Metabolism of
→ Hepatotoxicity. Ofloxacin.
III. Fluroquinolones +
NSAID → Seizures.
IV. Sucralfate &
Antacids (Al, Mg) &
Food Supplements (Fe,
Zn) →↓Absorption.
15. Mention Drugs Used in TTT of TB, Then Mention One Main Side Effect of 3 Of
them.
I. 1st Line Drugs:
• Rifampicin → See Before.
• Isoniazid → See Before.
• Pyrazinamide → Allergy & Hepatotoxic.

• Ethambutol → Allergy & Optic Neuritis.
• Streptomycin → Ototoxic & Nephrotoxic.
II. 2nd Line Drugs:

• Para-amino-salycilic Acid → GIT, Hepatotoxic.
•Ethionamide → Allergy, GIT & Hepatotoxic.

•Cycloserine → Allergy, GIT & CNS (Psychosis).
• Amikacin & Kanamycin → Ototoxic, Nephrotoxic & N-M Blocker.
•Viomycin & Capreomycin → Ototoxic, Nephrotoxic.
16. Write A Short Note On Antimicrobial Used in Typhoid.

Describe Mechanism of Action Used in Selected Drugs.
I. Acute Attack:
1. 1st Choice Drugs:
1- Cotimoxasole: They cause Sequential Block in Synthesis of Folinic Acid &DNA.

2- Ceftriaxone or Cefoperazone → Bactericidal & decrease Cell Wall Synthesis as
Penicillins (See Q No.2).
3- Ciprofloxacin → enter Cell by Passive Diffusion Through Porins → ↓Bacterial
DNA Gyrase →↓ Rejoining Step →↓ DNA Replication → Bactericidal.
2. 2nd Choice Drugs:
Ampicillin or Amoxicillin → see Q No. 14.
3. 3rd Choice Drugs:
Chloramphenicol → It binds with 50S Ribosomal Subunit →↓ Transpeptidation →↓
Ptn Synthesis.
II. Carrier Stage:
1- Ampicillin or Amoxicillin + Probenecid.
2- Cotrimoxazole + Rifampicin (Act by ↓ DNA Dependent RNA Polymerase
Enzyme).
3- Cholectstectomy may be required.
17. Cephalosporins Are Commonly Used in Clinical Practice. Classify Them & Mention
Their Mechanism of Action.
β Lactam Antibiotics having The Same Mechanism of Penicillins but less Susceptible to
β Lactamases, they bind to PBP:
1. ↓ Transpeptidase Enzyme Responsible for Cross Linking of Peptidoglycans, a final
step in cell wall synthesis.
2. Activate Autolysins → Lysis of Cell Wall.
3. Bacteria Imbiba Water causing its Death & Rupture due to High Osmotic Pressure.
4. They Mainly Affect Growing Bacteria rather than Restiong Ones.
Classification:
4 Generations each has Oral & Parentral Except The 4th Only Parenteral.
I. 1st Generation: Cef ‫ ﻣﺶ‬Ceph ‫اﻟﻮﺣﻴﺪ اﻟﲆ ﺑﺘﺘﻜﺘﺐ‬
Oral Parentral
Cephlexin Cephapirin
Cephadroxil
Cephradin Cephradin
Cephazolin Cephazolin .
•Broad Spectrum Active Mainly Against Gram +ve > Gram –ve , but not
H.influenza , Proteus & P.aerogenosa.
•βLactamase Resistant.
• No Cross Meninges, So Not Effective in Meningitis.
II. 2nd Generation: Spectrum

‫زﻳﻨﺎت ﻓﻰ ﻣﴪﺣﻴﺔ اﻟﺰﻋﻴﻢ ﻛﺒﲑة ﺑﻘﻰ وأوﺳﻊ‬
Oral Parenteral ↑
Cefuroxime (Zinnat) Cefuroxime (Zinnat).
Cefaclor Cefamandole
Cefprozil Cefoxitin (Anaerobes).
Broader Spectrum: Similar to 1st Generation but more Active against Gram-ve & less
Active against Gram +ve.
Active against H.influenza & Anaerobes , but not Pseudomonas.
More Resistance to β Lactamase Enzymes.
Don`t Pass BBB except Zinnat.
III. 3rd Generation:
3rd → CefTriaxone.
Oral Parentral
Cefixime Cefotaxime
Cefpodoxime Ceftriaxone
Cefoperazone
Ceftazidime.
Broader Spectrum Against Gram +ve, -ve, Aerobes & Anaerobes.
Similar to 2nd Generation, but less on gram +ve 7 more on gram –ve.
More Resistant to β Lactamase.
Excellent pass BBB.
IV. 4Th Generation:
Cefepime
Cefpirome
،anaerobes‫واﻟـ‬gram -ve ‫ ﺿﺪ اﻟـ‬activity ‫ﺑﺘﺰﻳﺪ اﻟـ‬generation ‫ ﻛﻞ ﻣﺎ ﺑﻴﺰﻳﺪ اﻟـ‬-
gram +ve ..‫وﺑﺘﻘﻞ ﺿﺪ اﻟـ‬
powerful against anaerobes‫ ﻣﻦ اﻟﺠﻴﻞ اﻟﺘﺎﱏ‬Cefoxitin ‫ﺑﺲ‬
‫ﺑﺘﺰﻳﺪ ﺑﺰﻳﺎدة‬resistance ‫ﺑﺲ اﻟـ‬B lactamases ‫ ﻟﻠـ‬resistant ‫ﺑﺘﺒﻘﻲ‬generations ‫ و ﻛﻞ اﻟـ‬-

generation.‫اﻟـ‬
،‫ ﻣﻦ اﻟﺠﻴﻞ اﻟﺘﺎﱏ ﺑﻴﻌﺪى‬Cefuroxime ‫ﻣﺎ ﻋﺪا‬BBB ‫ ﻣﺶ ﺑﻴﻌﺪوا اﻟـ‬generations 2 ‫ و أول‬-
‫ﻟﻜﻦ اﻟﺘﺎﻟﺖ واﻟﺮاﺑﻊ ﺑﻴﻌﺪوا‬
renal impairment‫ ﻓﻴﻨﻔﻌﻮا ﰲ اﻟـ‬excreted in bile ‫ دول‬Ceftriaxone ‫و‬Cefoperazone ‫و اﻟـ‬
18. Compare The Following Drugs Regarding Mechanism of Action, Adverse Effects &
Mention One Example of Each Quinolones & Aminoglycosides.
Quinolones Aminoglycosides
↓Bacterial DNA Gyrase Enzyme Binds to 30S Ribosomal Subunits →↓
(Topoisomerase II, IV) Ptn Synthesis → May Interfere with
→↓Rejoining Step →↓ DNA Cytoplasmic Membrane Function.
Mech. Of
Replication →↓ Bactericidal.
Action They Concentrate Inside Bacteria by
O2 Requiring Active Transport
Mechanism.
1- Allergy (Hypersensitivity). I. Ototoxicity:
2- Photosensitivity, Use Sun 1. Irreversible Damage to
Screens & Sun-blocks. Vestibulo-auditory 8th cranial
nerve → Vertigo & Deafness.
3- CNS: headache, dizziness &
Confusion → Avoid Driving. 2. Toxicity increases with
increased Dose, Duration & Age,
Seizures especially if used with
Impaired Renal Function &
NSAID → Avoid in Epileptics.
Concurrent Use of Loop Diuretics,
4- GIT Upsets. Salicylates & Chloroquine.
5- Chondrolytics →Reversible c- Do Frequent Audiograms.
Arthropathy → Avoid in
Adverse II. Nephrotoxicity:
Pregnancy, Lactation & Children
Effects
Up to 18 Years. 1. Usually Reversible.
6- Rupture of Tendons (Achilles 2. Increases in Patients with Poor
Tendon) specially in elderly taking Kidney Functions or Concurrent
Glucocorticoids. Use of Frusemide.
7- Nephrotoxic & Crystaluria III. Skeletal Muscle Relaxation;
8- Drug Interactions: 1. ↓Prejunctional Release Of A.Ch
& ↓Sensitvity Of Post Synaptic
I. Ciprofloxacin & Ofloxacin
Sites ( Curare Like Action ).
→Enzyme Inhibitors →↓
Metabolism of Theophylline, 2. May cause Respiratory Muscle
Paralysis if injected into Pleural or
Warfarin & Sulfonamides. Peritoneal Cavity especially in

Myasthenic Patients.
II. Cimetidine → ↓ Metabolism
of Fluoroquinolones. Reversed by IV Ca Gluconate &
Anti-Ch.E.
III. Sucralfate, Antacids (Mg &
Al) & Food Supplements (Fe & e.g Neostigmine / Edrophonium +
Zn) →↓ Absorption of Artificial Respiration.
Fluoroquinolones. IV. Allergic Manifstations e.g Contact
IV. Fluoroquinolones + NSAID Dermatitis.
→ Seizures. V. Drug Interactions:
1. Amphotericin-B, Polymixins,
Cephalosporins & Frusemide
increase their Nephrotoxicity.
2. Loop Diuretics, Chloroquine &
Aspirin increase their Ototoxicity.
3. They Potentiate Competitive
N.M Blockers e.g Curare.
4. Aminoglycosides + Penicillins →
Synergism but never mixed in the
same Container.
5. Chloramphenicol →↓ Bacterial
Uptake of Aminoglycosides.
Ciprofloxacin. Gentamicin.
Examples
Ofloxacin. Neomycin.
19. Comment On the Following Statement as True or False & Explain Your Answer?
Prescribing Erythromycin necessities, The Readjustment of the Dose of
Theophylline.
The Statement Is True.
Explanation: Erythromycin Is a Hepatic Microsomal Enzyme Inhibitor inhibiting
Cytochrome P450 →↓ Metabolism of Theophylline Causing Toxic Concentration of the
Drug.
20. Explain The Pharmacological Basis Of TTT Of H.influenza Infection Using A

Combination Of Amoxicillin & Clavulonic Acid .
H.influenza is a gram –ve β Lactamase Secreting Bacteria , So we use :
1- Amoxicillin as its Broad Spectrum Antibiotic that is Active against it exerting its
Action by affecting the cell wall by binding to PBP causing:
• ↓ Transpeptidase Enzyme.
• Activate Autolysins.
• Bacteria imbibe water due to high osmotic pressure → Rupture & Death.
•Affect Growing > Resting.
But If we used Amoxicilln alone it will be deactivated by β Lactamase, so we use

Clavulonic Acid (β Lactamase Inhibitor).
Amoxicillin + Clavulonic Acid = Augmentin.
21. Comment True or False & Explain.

Sulbactam Protects Ampicillin from Inactivation by Some Bacteria.
True.
Sulbactam is a β Lactamase Inhibitor so when added to Ampicillin → (unasyn) it
protects it from inactivation by β Lactamase secreted from Some Bacteria.
‫ﺗﺠﻤﻴﻌــﺎت‬
I- Doesn’t need readjustment in real impairment:
1.Nafcillin 2. Deoxycyclin 3. Ceftriaxone 4. Cefoperazone
II- Bactericidal:
1.B-lactam 2. Quinolones 3.Aminoglycosides 4. Rifampicin
III. bacteriostatic:
1.Sulphonamides 2. Chloramphenicol 3. Retracycline
IV. Acne vulgaris:
1.Tetracycline 2.Erythromycin 3. Clindamycin
V. carrriers:
1. Staph.: Fusidic acid
2. Meningococcal: Minocycline
3. Typhoid: Co-trimoxazole
VI. Side effects of Tetracycline:
• 2T: Teeth, Teratogenic
• 2GIT: Upset, Super infection
• 2 Specific organs: Hepatotoxic, Nephrotoxic
• 2 Sensitivity: Hyper, Photo
• 2 Specific drugs: Minocycline, Democlocycline
VII. Enzymes:
• Penicillin: 1. Amidase 2.B-lactamase
• Imipenem: Dihydropeptidase
• Chloramphenicol: Acetyltransfers
VIII. Ototoxic:
• Vancomycin
• Aminoglycosides
• Loop diuretics
• Chloroquine
• Salicylates
IX. prostate:
1.Erythromycin (Fluid) 2. Fluoroquinolones (Tissue) 3. Sulfa
Types of Organisms :
1. Bacteria
COCCI BACILLI SPIROCHETES
+Ve -Ve +Ve -Ve

1. Staph 1. Neisseria 1. Anthraces (SHESH) 1. Vincent
2. Strept gonorrhoea 2. Diphtheria 2. Palladium
1. Salmonella
3. Pneumococci 2. Neisseria 3. C. Tetani 2. H. influenza
4. MRSA meningitis 4. C. 3. E. Coli
5. Enterococci perfringes 4. Shigella
5. C. 5. H. Pylori
Botalinum
6. C. Dificcile (KPP)
6. Klebsiella
7.
Pseudomonas
8. Proteus
. Other
Mycobacterium
Mycoplasma
Chlamydia
Actinomycosis
Amoeba
Toxoplasma
Pneumocystis cornii
chemotherapy
Cell wall ptn synthesis DNA
late 30s
early mycolic mRNA PABA
steps steps gyrase
acid tetrac 50s +DHFR PABa
ylin refampc quoenlo
isonzide amphenc co- sulfonamid
in nes es
amino oles trimexo
glycos azole cotrimoxaz
1)B- macrolide ole
cyclo lactam ides s PASA
serin - penicillin
clindamyc sulfone
e - in
cephalosp
orins linozlide-
-maono
streptgra
bactams min
carbapen fusidic
ems acid
2)
vancomyc
in-
tiecoplani
n
S=static
D=depends on concentration
N.B : drugs are classified into minor (small) drugs as Monobactams and major
drugs as Penicillin.
Short drugs
Cell Wall Protein DNA
Cycloserine Fusidic acid PASA

Monbactams Linezolide Dapson
Carpapenems Streptogramin
Vancomycin Paromomycin
Isonazid Clindomycin
Drugs with small effects and specific uses :
Drug USES Adverse effects

1. Aerobic / Gram +ve
Monobactams (Aztreonam)
organisms _
2. In Allergic to penicillin
1. (Aerobic & Nonaerobic) / 1. Nephrotoxic
Carbapenems (Imiperems)
(Gram +ve & -ve organisms)
2. Nosocomial infections
1. Gram +ve organisms 1. Nephrotoxic
Vancomycim / Teicoplanin
2. MRSA , Enterococci , 2. Ototoxic
C.difficile , multidrug resistant
3. Red Man syndrome &
organisms & dental prophylaxis
shock
1. Staphylococcal infection 1. Mild GIT upsets
Fusidic acid
and carrier
2. Osteomyelitis
3. Skin and Nasal infection
1. Vancomycin resistant 1. Thrombocytopenia
Linezolid / Streptomycin
Enterococci 2. Neutropenia
1. Gonorrhea -
Spectiromycin
1. Amoeba -
Paromomycin
1. TB and Leprosy 1. Allergy
Ethionamide
2. GIT
3. Hepatotoxic
1. TB 1. Allergy
Cycloserine
2. GIT
3. Psychosis
1. Leprosy 1. Fever
Dapsore
2. Hepatitis
3. Exfoliate dermatitis
4. Met-HB
5. Hemolytic anaemia
6. Lymphadenopathy
1. bone and teeth 1. GIT disturbance
clindamycin
2. intra-abdominal infection 2. pseudomembranous
3. acne vulgaris 3. colitis impaired liver
pervent TB relapce 1. allergy
pyrazinamide
2. hepatotoxic
3. GIT
4. Hyperuricemia
TB 1. Alllergy
PASA
2. GIT
3. inhbit ####
4. nephrotoxic
TB 1. Allergy
Ethambutol
2. GIT
3. optic neuritis
TB
Isoniazide
Major drugs:
1. Penicillin
2. Cephalosporin
3. Tetracycline
4. Amphenol
5. Aminoglycosides
6. Macrolides
7. Quinolones
8. Co-trimoxazole
9. Rifampicin
Drugs (pharmacokinetics)
1. Benzyl Penicillin
P.K.
Absorption → Orally → acid resistant (1h before / 2h after food)
Distribution → - bound to plasma protein
- cross placenta barrier and BBB (if inflamed)
- concentration → all over the body
Metabolism → penicillinase (B-lactamase) & Amidase → 6-amino penicillanic acid
Excretion → urine except Nafcillin in Bile
Disadvantages
Short duration → procaine / Benzathine
sensitive (acid) → phenoxymethyl
Sensitive (B-lactamase) → Methicillin
Spectrum (narrow) →Ampicillin & Amoxicillin or carobxy-penicillin & Ureido-
penicillin
2. Broad Spectrum
Absorption
1. Orally (acid resistant)
Distribution
1. Bound to plasma protein
2. Pass BBB in meningitis and placenta barrier (not teratogenic)
Metabolism
1. Penicillinase (B lactamase) → Penicillioic acid
2. Amidase → 6-amino-penicillanic acid
Excretion
1. all renal
2. Nafcillin (in bile)
3. Aminoglycosides
Members :
1. streptomycin
2. Gentamicin
3. Neomycin
4. Paromomycin
5. Spectromycin
P.K
Absorption → poorly oral
Distribution → extra-cellular , limited passage of across BBB but pass placental barrier ,
concentrated in renal cortex and endolymph ,perilymph of inner ear .
Excretion → Urine by passive glomerular filteration
4. Macrolides (Erythromycin , Claeithromycin , Azithromycin)

P.K.
Absorption → Orally
Distribution → accumulate in macrophages & PMNL
Metabolism → liver
Excretion → Bile
5. Cephalosporins
Members :
1st generation
Oral → Cephalexin , Cephadroxil , cephradin & Cephazolin
Parenteral → Cephapirin , Cephazoline & Cephradin
2nd generation
Oral → Cefactor , Cefprozil & Cefuroxime
Parenteral → Cefuroxime , Cefamandole , Cefoxitin
3rd generation
Oral → Cefotaxime & Cefpodxime
Parenteral → Cefotaxime , Ceftriaxone , Cefoperzaone , Ceftazidime & Moxalactam
4th generation
Parenteral → Cefepine
P.K.
Absorption → Oral & parenteral
Distribution → all over the body & 3rd generation pass BBB
Metabolism → partially acetylated
Excretion → Urine as Cefotaxime & Bile as Ceftriaxone and Cefoperazone
6. Tetracyclines
Tetracyclines
Low lipid solubility High lipid solubility
Members : Members :
1. Tetracycline 1. Doxycycline
2. Oxytetracycline 2. Minocycline
3. Chlortetracyclin
4. Demeclocycline
P.K. P.K.
Absorption → incomplete orally ( ↓ by Milk , Absorption → complete orally ( ↓ by Milk ,

Ca+2 , Mg+2 , Fe+2 , Al+3 ) Ca+2 , Mg+2 , Fe+2 , Al+3 )
Distribution → moderately bound to Plasma Distribution → all over the body ,

protein , pass BBB and placental barrier , concentrated at bone and teath
concentrated at bone and teath
Metabolism → conjugated in liver
Metabolism → glucuronide conjugation
Excretion → Minocycline in ( tears , saliva ,
Excretion → Urine , Bile and Milk milk , bile , stool , urine ) and Doxycycline in
(stool)
7. Amphenicols
Members :
Chloramphenicol & Thiamphenicol
P.K.
Absorption → Orally and Rectally
Distribution → all over the body & concentration in CSF , Aqueous humor, milk & bile.
Metabolism → conjugated with glucuronic acid.
Excreted → urine & milk
8. Rifampicin
P.K.
Absorption→ well absorbed orally
Distribution → all over the body
Metabolism → partially deacetylated
Excretion → Bile , Urine , tears , saliva , sweats and sputum.
9. Quinolones
Members :
1st generation → Nalidixic acid
2nd generation → Norfloxacin , Ofloxacin , Ciprofloxacin
3rd generation → Levofloxacin , Moxifloxacin , Sprafloxacin
4th generation → Trovafloxacin
P.K.
Absorption → orally & injection ( ↓ by Sucralfate & Antacids containing Mg+2 , Al+3 &
food supplements containing Fe+2 , Zn+2 )
Distribution → intracellular , low CSF levels , concentrated in prostate
Metabolism → liver
Excretion → Urine & Bile
Drugs (used for)
1. Penicillin:
I. All cocci except (MRSA & Enterococci)
II. Spirochetes
III. Bacilli (+ve , SHESH , KPP )
IV. Actiremycin
2. Cephalosporin:
I. Infections resistant to Penicillin
II. Gram –ve cocci
III. Gram –ve bacilli
IV. Anerobic infections
V. Respiratory & Urinary infections
3. Monobactams :
I. Aerobic gram –ve
4. Cabanems :
I. Nosocomial infections
5. Vancomycin :
1- 3 resistant (MRSA , Enterococci , C.difficile )
6. Tetracyclin
Used for
1. Mycoplasma , Rickettsia , Chlamydia& Amoeba

2. ENT and RT infections
3. Enteritis & bacillary infections
4. urinary & sexually diseases
5. eye & skin infections
6. Meningococcai carriers
7. Amphenicols
Used for
1. Rickettsia
2. Eye , ENT , RT , GIT & Urinary infections
3. Bacterial meningitis specially Gram-ve H.influenza
4. In eye and ear infection (topically)
8. Aminoglycosides
Used for
Gram –ve bacilli (SHESH & KPP) , Staph , Enterococci , TB
9. Gentamicin , Amikacin , Neomycin , Tobramycin

Used for
1. Enterococci
2. Staphylococci
3. KPPES ( Klebsiella , Proteus , Pseudomonas , Enterobacter , Serratia )
10. Neomycin
Used for
1. orally as intestinal antiseptic
2. Orally in hyperlipidaemia
3. Topically on skin and mucus membrane
4. Inhalation in chest infection
11. Erythromycin
Used for
Mycoplasma and Chlamydia
12. Clindamycin
Used for
1. Acne vulgaris
2. Bone and teath
13. Quinolones
Used for
1. Mycobacterium
2. Mycoplasma
3. Chlamydia
14. Co-trimoxazole
Used for
1. Pneumocystis carnii in AIDS
2. Toxoplasmosis
3. Nocardiosis
15. Spectinomycin
Used for
Gonorrhoea
16. Paromomycin
Used for
Oral direct Amebicide
17. Fusidic acid

Used for
Staphylococcus infection
18. Spectrum
penicillin cephalosporins Monobactam vancomycin tetracyclin amphencol

Narrow 1st: Narrow Those not treated Broad Broad
all except by cephalosporins
+> - Aerobes gram +/- +/-
SHESH
Excpt HPP -ve MRCA Mycoplasma Aerobes /
Enterococci
nd : ->+ except 2 Spirochetes anerobes
p Cl.dificel Chlamidia Typhoid
+<<- rd3 Gram +ve Rickettsia Menisol##
Aerobes /non ###
anerobes
th4
+<<-
Quonelones carbapenems aminoglycosides Macrolides linezolie

Gram –ve Vere wide Narrow + KPP Similar to VR
spectrum narrow enterococli
No aginst +myco###
penicillin +
spirochetes +/- Not anerobes HHBL
anerobes Aerobic/ non
Mycoplasma
chlamydia
spirochetes
Adverse effect
1. Co-Trimoxazole
I. ABCDDDD
II. Megaloplastic anemia
2. Others
Adverse Effects
Tetracycline Penicillin Cephalosporins Amphenicol Macrolides Quinolones
1. Irritation 1. Candida-albicans 1. Irritation 1. Irritation Epigastric pain GIT upset
GIT 2. ↓ Vit. B/K 2. Pseudo collitis 2. Superinfection 2. Superinfection
3. Pseudo collitis
1. 1. Hypersensitivity 1. 1. Hypersensitivity
Hypersensitivity 2. Jarisch-herxheimer Hypersensitivity 2. Photosensitivity
B - -
2. Photosensitivity reactions 2. Disulfiram like
action
1. Fanconi 1. Nephritis 1. IM irritant Bone marrow 1. Ototoxic 1. Chondrolytic
syndrome 2. CNS 2. IV irritant (reversible & 2. Cholestatic 2. Rupture of
Cytotoxic 2. CNS 3. Platelet dysfunction 3. Nephrotoxic irreversible) jaundice tendons
3. Hepatotoxic 4. Rash & pain 4. Biliary Sludge 3. Nephrotoxic
4. Teeth & Bone 4. CNS
Anti ADH ↑ Na+/K+ Hypoprothrom- HME inhibitor Inhibit metabolism of
binemia ( theophylline ,
carbamazepine , -
warfarin & Digoxin )
Teratogenic Gray baby

Teratogenicity - - - -
syndrome

Lymph Notes - Pharmacology (2nd Term)

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Lymph Notes - Pharmacology (2nd Term)

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LY M P H N O T E S

1. Ten Examples of systemic anti-Coagulants & Mechanism Of Action of One Of

2. Three Drugs used As Sclerosing Agents.

1. Between Hypolipidemic Drugs.

P.O.C Statins Niacin

Absorbed Orally, taken at Orally.

1. Hepatotoxic → ↑ Serum 1. Cutaneous Flush & Peruritis.

Potentiate Action Of Potentiate actions Of

P.O.C (Fibric Acid Derivatives) bile acid binding resins.

1. GIT Upsets. 1. GIT upsets especially

4. Contraindications 1. Pregnancy, Lactation. ______

______ ↓ Absorption Of Other Drugs As :

Inhibitors Of Intestinal Sterol Absorption CETP Inhibitors

1. Give 4 Examples of Fibrinolytic Drugs & Mention The Mechanism Of Action Of

2. What Are The Therapeutic Uses & Drug Interactions Of Warfarin?

Therapeutic Uses: See comparison between Heparin & Warfarin.

Enhance The Action Of Warfarin Inhibit the action of warfarin

Ph. kinetics Ph. Dynamics. Ph. kinetics Ph. Dynamics.

Displacement Potentiate Inhibition Of Decrease

Increase Increase Clotting

Aspirin “ COX Inhibitor “ and (Thromboxane Synthase inhibitor)

ADP Receptor Antagonist Glycoprotein IIb/IIIa Antagonist

5. Write A Short Account On Phosphodiesterase Inhibitors.

Dipyridamole acts through :

- Dipyridamole is used in Combination with Aspirin, Ineffective If used alone.

6. Compare Between Warfarin & Heparin.

C.O.P Heparin Warfarin

- Potentiates Anti-thrombin - Prevents Reductive

Explain The Pharmacological Basis Of:

1. Low Molecular Weight Heparin (LMWH) as Enoxaparin have replaced

2. Oral Anticoagulant Drugs should be Stopped 3-4Days Before Operations.

3. Protamine Sulphate is used as Antidote For Heparin Toxicity.

4. Clopidogrel Is Better Than Ticlopidine.

1. Mixed agonist- antagonist narcotic opioids. Mention their mechanism of action on

3. Uses & adverse eﬀects of Indomethacin.

1. Methadone is used in treating Morphine addicts.

2. Loperamide and Diphenoxylate are better than Morphine in treating diarrhoea.

1. Morphine & Meperidine (Pethidine).

Distributed all over the

Therapeutic uses: 4Ps: 1. Alone in biliary and renal

4. Pre anaesthetic morphine).

2. Morphine & Codeine (Methyl morphine).

Morphine Codeine (methyl-

Saliva , stomach , bile , milk

Mechanism of action: Stimulates specific opioid Similar to morphine But:

V.M.C & excitation epilepsy

3. Paracetamol and Diclofenac.

Give an account on:

Adverse eﬀects of Aspirin.

1. Advantages of Fosphenytoin over Phenytoin.

2. Drugs used in: Grand mal Epilepsy-Petit mal Epilepsy.

Grand mal Epilepsy:

4. Drugs contraindicated in gout (hyperuricemia).

5. Adverse eﬀects of Probenecid.

1. Mechanism of action, uses and adverse eﬀects of Ethosuximide.

3. Adverse eﬀects of Phenobarbitone.

5. Tolerance & Dependence (Addiction).

1. Colchicine and Allopurinol: adverse eﬀects, uses & actions.

Inhibit cell division.

2. Phenytoin and Carbamazepine (Mechanism of action, Uses and Adverse Eﬀects).

21. The Mechanism of action of L-Dopa and adverse eﬀects

22. Drug interactions of L-DOPA

23. Action, uses, adverse eﬀects and drug interactions of chlorpromazine