All Mechanism of Action and Classification Drugs

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Adverse Drug Effects

Introduction-Classification-Categorization
Concept & Idea by- Solution Pharmacy
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Drug/ Medicine Adverse Effect
Drug is a chemical moiety (either natural or synthetic) Any effect produced by the drug which is not
which is used for the prevention, diagnosis and Disease expected or not desired and unintended is called
treatment of any disease or disorder. Disease is caused Disorder adverse drug effects. It is one of the broad definitions
by microorganism mainly and disorders And Disorders which cover many subtypes from simple to serious
are result of imbalance of various biochemicals within effects.
body itself.
Diagnosis
Treatment
Drug/Medicine

Desirable Effects Undesirable Effects

Desirable effect means all those effect produced by All those effect given by drug which is not good
drug which we are expecting and willing to get. for us and it may cause simple to dangerous
effect.
Example
Paracetamol, Nimesulide, Ibuprofen, Aspirin,
Indomethacin Aspirin
Different Categories
Predicted Unpredicted
NSAIDS Type A or Augmented Side Effects Type B or Bizarre
Rashes, Etching
Non Steroidal Anti-inflammatory Drugs
Secondary Effects
Suspension of bacterial flora
Analgesic Effect Toxic Effects- Poisoning
Reduce pain by inhibiting PG synthesis Intolerance

and increasing pain threshold potential.
Antipyretic Effect Drug Allergy- Humoral & Cell Mediated
Photosensitivity- Phototoxic and Photo allergic

Reduce fever by controlling thermoregulatory center in brain
Drug Dependence
Physiological-Physical-Drug Abuse-Drug Addiction-Drug Habituation
Anti-Inflammatory Effects
Drug Withdrawal reaction- Alcohol and LSD
Reduce inflammation by inhibiting COX-I and COX- Teratogenicity- Thalidomide

II
Mutagenisity or Carcinogenicity
Drug Induced Disease- Peptic Ulcer by NSAIDS
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Antianginal Drugs
Classification & Mechanism of Action
Based on KD Tripathi
Angina is a chest pain or we can say that it is a signal informing us that there is lack of oxygen supply to myocardium. This is generally occurring
at the left side of the chest. It has 02 main types- (1) Classical Angina (Common form) - Those type of angina which may arise due to over work
like- exercise, emotion etc. (2) Variant or prinzmetal’s Angina (uncommon form) - Attack occurs at rest or during sleep and doesn’t disappear
after rest.
Nitrates Beta Blocker Ca+ Channel K+ Channel Opener Others

Propranolol, Metoprolol, Blocker Nicorandil Dipyridamole, Trimetazidine,
Atenolol, and others Phenyl alkylamine- Ranolazine, Oxyphedrine
Verapamil,
Short Acting Benzothiazepine-
Glyceryl Trinitrate Diltiazem,
(GTN, Nitro Glycerin) Dihydropyridines-
Nifedipin, Felodipine,
Amlodipine, Nitrendipine,
Nimodipine, Lacidipine,
Long Acting Lercanidipine, Benidipine
Isosorbide dinitrate, Isosorbide
mononitrate, Erythrityl tetranitrate
Pentaerythritol tetranitrate
Other Clinical
Application of K+ Channel Opener
1. Angina Pectoris
2. Hypertension
3. Congestive heart failure
4. Myocardial salvage in MI
5. Alopecia
6. Bronchial asthma
7. Urinary urge incontinence
8. Premature labour (Ref- KD Tripathi)
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Antiarryhythmics Drugs
Classification and Mechanism of Action
Class- I Class- II Class- III Class- IV Other

+ + +
Na channel blocker B adrenoreceptor K channel blocker Ca channel blocker Antiarrythmic Drugs
Disopyramide, Flecainide Atenolol, Esmolol, Metoprolol Amiodarone, Dofetilide, Diltiazem, Verapamil Adenosine, Digoxin,
Lidocaine, Mexiletine Dronedarone, Ibutilide, Sotalol Magnesium sulfate
Procainamide, Propafenone,
Quinidine
Causes of Arrhythmia
1. Abnormal Automaticity- SA node shows the fastest rate of phase 4 depolarization and therefore, exhibits a
Nerve Impulse higher rate of discharge than that occurring in other pacemaker cells exhibiting automaticity
2. Abnormality in impulse conduction- Impulse from higher pacemaker centers are normally conducted down
pathways that bifurcate o activate the entire ventricular surface. A phenomenon is called reentry may occur if
Normal Conduction Unidirectional Block unidirectional block occurs. Reference- Lippincott (Pharmacology) 6th Edition
Ventricle Wall
Block

Anti Microbial Drugs
Classification According to Mechanism of Action
Classification Reference- KD Tripathi (Pharmacology)
Inhibit Cause Leakage Inhibit Cause misreading or Inhibit Interfere with Interfere with
Cell wall synthesis From cell membrane Protein Synthesis RNA and affect DNA gyrase DNA function DNA synthesis
permeability
Penicillin Polymyxines
Tetracycline Aminoglycosides Fluoroquinolones Rifampin Acyclovir
Cephalosporins Colistin Streptomycin Ciprofloxacin etc Metronidazole Zidovudine
Gentamycin
Nystatin Cloramphenicol
Cycloserine
Sulfonamides, PAS, Sulfones, Interfere with
Trimethoprim, Ethambutol,
Erythromycin Intermediary Metabolism
Bacitracin polymers
Bacitracin Amphotericin- B
Clindamycin
Vancomycin Hamycin Linezolid
Note- Mnemonics are based on my thoughts; it may or may

not useful to you. It’s always better to create your own so you
may memorize it.

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Anti Microbial Drugs
Classification According to Various Parameters
Classification Reference- KD Tripathi (Pharmacology)
Types of Organism
Against which primarily
Spectrum of Activity Type of Activity
Active
Antibacterial Bacteriostatic Bacteriosidal

Penicillins, Aminoglycosides
Erythromycin etc Narrow Broad
Spectrum Spectrum Sulfonamide Penicillin
Antifungal
Griseofulvin, Amphotericin B, Aminoglycosides
Penicillin G Tetracycline Tetracycline
Ketoconazole etc
Polypeptides
Chloramphenicol
Antiviral Streptomycin Chloramphenicol
Acyclovir, Amantadine,
Erythromycin Rifampin
Zidovudine etc Erythromycin
Isoniazide
Ethambutol
Antiprotozoal
Chloroquine, Pyrimethamine, Pyrazinamide
Metronidazole, Diloxanide etc Linezolid
Cephalosporin
Anthalmentic
Mebendazole, Pyrantel, Vancomycin
Niclosamide, Diethyl
carbamazine etc Nalidixic Acid
Ciprofloxacin
Metronidazole
Cotrimoxazole
Antihistamine Drug
H1 Blocker H2 Blocker H3 Blocker H4 Blocker
Conventional Antihistaminic
Highly Sedative Moderately Sedative Mild Sedative 2nd Generation

Chlorpheniramine, Dexchlorpheniramine,
Diphenhydramine, Dimenhydrinate, Pheniramine, Cyproheptadine, Meclizine,
Dimethindene, Triprolidine, Mebhydroline,
Promethazine, Hydroxyzine Buclizine, Cinnarizine
Cyclizine
Fexofenadine, Loratadine, Desloratadine, Cetirigine, Levocetrizine, Azelastine, Mizolastine, Ebastine, Rupatadine
Pharmacological Action
1 Antagonism of Histamine – Reverse Histamine induced bronchoconstriction, Intestinal and other smooth muscle
contraction
2 Antiallergic Action – Suppress type I Hypersensitivity reaction. Urticaria, itching and angioedema are well controlled.
3 CNS – Few of them depress CNS. Few are effective in preventing motion sickness. Few reduce tremor, Rigidity, antitussive
4 Local anesthetics – Some antihistaminic are strong and some are having weak membrane stabilizing property.
5 Blood Pressure- Most antihistaminic drug cause fall in BP on IV injection.
Diagrams and explainations are made by solution-pharmacy to make you better understand.
Classification and Mechanism of Action for Antihistamine Drug
Key Point to Understand- ‘Histamine’ is made up of two simple words- Histo (Tissue) + Amine. If we add
them together the meaningful sentence will be- Amine released from tissue. Histamine is stored and release
from mast cells. Other tissue like- Skin, gastric and intestinal mucosa, lungs, liver and placenta. Histamine
receptors are of basically 02 types- (1) H1 and H2. H3 is also available. Histamine initiate allergic reaction
thus antihistaminic drugs give relief from allergy by blocking any of the histamine receptor.
Antihistamine Drug
H1 Blocker H2 Blocker H3 Blocker H4 Blocker
H2 Antihistaminic
Cimetidine, Ranitidine, Famotidine, Roxatidine
H2 Receptor antagonist and regulation of gastric acid secretion

Gastric acid (Hcl) is secreted by the parietal cells from the mucosa of gastrointestinal tract, and
that is stimulated by acetylcholine, histamine, and gastrin. The receptor medicated binding of
acetylcholine, histamine, and gastrin result into activation of protein kinase which ultimately
stimulate the H+/K+ ATP. Thus it is very simple that if someone is willing to inhibit the release of
gastric acid he or she has to inhibit the binding of any of the above agent to their respective
receptor. So the H2 Receptor antagonist doesn’t allow the agent to bind to the receptor and inhibit
the release of gastric acid.
Histamine Blocker
Acetylcholine Histamine Gastrin
Gastric Acid secretion stimulation

Diagrams and explainations are made by solution-pharmacy to make you better understand.
Anti-Hypertensive Drugs
Prevention is always better than cure
Classification- KD Tripathi
1 2 3 4 5 6 7 8 9
ACE Angiotensin Calcium Channel Beta+Alfa Alfa Central

Diuretics Blocker Blocker Beta Blocker Blocker Blocker Sympatholytics Vasodilator
Inhibitor
Examples of above listed Class Thiazide Diuretics Channel is closed
Channel is Open
Thiazide- Hydrochlorothiazide, Chlorthiazide, Indapamide Increase Water & Sodium Excretion
High Ceiling- Furosemide
K+ Sparing- Spironelactone, Amiloride
Captopril, Enalapril, Linsopril, Perindopril, Short Term Effect Long Term Effect
Ramipril, Fosinopril etc.
Decrease Blood Volume Channel isDecrease

Open Sodium content in cell
Losartan, Candesartan, Irbesartan, Valsartan, Telmisartan 04
Verapamil, Diltiazem, Nifedipin, Felodipine,

Decrease cardiac output Decrease Calcium channel Blocker
Muscles sensitivity to vasopresser
Amlodipine, Lacidipine
Decrease Peripheral Resistance

Propranolol, Metoprolol, Atenolol Increase
01
Heart rate
Contractility
Labetalol, Carvedilol Conduction
Decrease Blood Pressure
Beta Receptor Blocker 05

Prazocin, Terazocin, Doxazosin, Angiotensinogen
Phentolamine, Phenoxybenzamine
Renin from Kidney Decrease output of Symp. Nervous system
Blood
Clonidine, Methyldopa Angiotensin I Increase vasodilatation of vascular muscle Pressure
(Inactive) Angiotensin II
Arteriolar- Hydralazine, Minoxidil, Diazoxide Decrease sod. And water retention

Arteriolar+ Venous- Sodium Nitropruside ACE Inhibitors Aldosterone Production
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ANTIVIRAL DRUG
Anti-Herpes Virus Anti-Hepatitis virus or

Idoxuridine, Trifluridine, Acyclovir, Anti-Influenza Virus Anti-Retrovirus
Amantadine, Rimantadine, Nonselective antiviral drugs
Valacyclovir, Famciclovir, Ganciclovir, Primarily for Hepatitis B
Oseltamivir, Zanamavir
Valganciclovir, Cidofovir, Foscarnet,, Lamivudine, Adefovir, Dipivoxil, Tenofovir
Fomivirsen Primarily for Hepatitis C, Ribavirin, Interferon Alpha
Nucleoside reverse transcriptase

Inhibitors (NRTIs)
Zidovudine (AZT), Didanosine, Stavudine,
Lamivudine, Abacavir, Emtricitabine,
Tenofovir, (Nt RTI)
Non Nucleoside
Reverse transcriptase Inhibitors
(NNRTIs)
Nevirapine, Efavirenz, Delavirdine
Protease Inhibitors
Ritonavir
Atazanavir, Indinavir, Nelfinavir,
Saquinavir, Amprenavir, Lopinavir
Entry (Fusion) Inhibitor

Enfuvirtide
CCR5 Receptor Inhibitor

Maraviroc
Integrase Inhibitor- Raltegravir

Viral Reach solution at- www.facebook.com/pharmavideo/ Mature Virus
1 fusion with host cell
Virus Budding (Viral release) 8 Neuraminidase
Fusion Inhibitor Inhibitor
Enfurvirtide (HIV) 2 Penetration Interferon-Alfa (HBV, HCV)
Packaging and
3 Un-Coating 7 Assembling Protease
Amantadine
Rimantadine (Influenza)
Inhibitors
Viral RNA Viral Protein
Translation
4 Reverse transcription Viral genomic mRNA

Viral mRNA
Reverse Transcriptase
Inhibitor Viral DNA Host DNA Transcription
6 Transcription
Integrase
Cytoplasm Nucleus
5
Integration of Host Integrase
DNA with Viral DNA
Inhibitors
7
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Penetration 6 Budding (Viral release)

1
Herpes Virus
Host cell Packaging and

Assembling of virion
5
2
Viral Protein
Uncoating Translation
Host DNA
Viral mRNA
Viral DNA Viral mRNA
3
4
Synthesis of viral
DNA
Acyclovir, Foscarnet,
Ganciclovir
Inhibition of
× New viral DNA
Nucleus Cytoplasm
Viral DNA polymerase
Anti- herpes drug’s mechanism of action

Classification, Mechanism of Action and Tricks for
Drugs for Cough

A B C D
Pharyngeal Demulcents Expectorants /Mucokinetics Antitussive

Lozenges, Cough Drops, Those which helps to Cough center suppressers Adjuvant Antitussive
Linctuses Syrup, Glycerin, Expel the cough. Drug which decrease Bronchodilators, Salbutamol,
Liquorice or which increase the kinetic sensitivity of cough center. terbutaline
movement of cough
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Mechanism of Action Example of the Class Mechanism of Action Example of the Class
Sodium citrate, Potassium citrate, Potassium Iodide, Opioids Codeine, Pholcodeine कफ को फे क दो
Bronchial secretion enhancer Guaiphenesin, Balsum of tolu, Vasaka, Ammonium Noscapine, Dextromethorphan, Chlophedianol
Chloride. सेक्रेशन पे प्रभाव पड़ेगा इससे गले से बेहतर Non Opioids
नहीं देना चोकलेट कफ में
वोइस आनी चालू होगी Chlorpheniramine, Diphenhydramine, Promethazine.
Mucolytics Bromhexine, Ambroxole ,Acetyl cysteine Antihistaminic
चलो डटट को प्रप्रवेंट करें ( Asthma is related with dust)
Carbocisteine, बैठा आवाज अब चालू हो जाएगा
Key points- Coughing is a protective phenomenon until it does not hurt or create uneasiness. Cough is a protective reflex which tries to expel or
eliminate the unwanted particles from our air passage along with mucus and other watery substances. The arising of cough is from stimulation of
mechano or chemoreceptor present in throat, respiratory passage or in any other associated part of lungs. The main objectives of using anti cough
drugs are to reduce the viscosity of cough so that they may be easy expelled. And this may achieve by breaking the bond between cough mucus which
are used to bind them together.
A
Mechanism Distance in bond
Demulcents (Less viscous)
Closely bond
(More Viscous)
Irritant Mucus
Expectorants B
Mechanism
Viscosity of mucus
Demulcents sooth Due to bond between them
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Expectorant or Mucokinetics are the drugs which produce their action
Demulcent sooth and cover the irritant and the stimulus released either by increasing mucus production or by decreasing the viscosity of
by irritant. This is not a treatment; this is just a temporary relief. fluid so they become thin and easily expelled out.
Opioids increase cough threshold Histamine Mast Cells

01
Cough Center Activate Cough Start

Ag
Binding sites
Low threshold Irritant
Reduce tussal impulse 02
Allergens
C
Antitussive Mechanism
Antitussive are the agent or drug which generally increase
the threshold of cough center, or reduce the tussal impulse or Mechanism of Action
act by both mechanism.
* All Diagrams (Except Brain) and explanations are made by solution pharmacy
Note- All mechanisms of action are converted into diagram by Solution-Pharmacy. These are not available elsewhere
Cough Activation
Many H1 antihistaminic drugs showed their role as
C
Antitussive agent. They produced antitussive action due to Mechanism
Their sedative and anticholinergic action, but lack selectivity for cough center.
* Diagrams Except brain) is made by solution to make you better understand

Drugs for Constipation

Classification based on KD Tripathi (Pharmacology)
Bulk Stool Stimulant Osmotic

Forming Agents Softener Purgative Purgative
Example Example Diphenylmethanes Magnesium Salt
Phenolphthalein, Bisacodyl Sulfate, Hydroxide
Bran Docusates (DOSS) Sodium picosulfate
Psyllium (Plantago)
Sodium Salt
Liquid Paraffin Antraquinones Sulfate, Phosphate, Sodium-
Senna, Cascara Sagrada Potassium tartrate, Lactose
Ispaghula
5HT4 Agonist
Tegaseroid
Mechanism of Action Water
Osmosis
Methyl Cellulose
Fixed Oil
Castor Oil
Intestine
Mechanism of Action Mechanism of Action
* Mechanism of Action- Representation by Solution Pharmacy
Key point- Constipation is not a single disease or disorder; it is a root cause for several GIT related problems. When
there is lack of water in large intestine and lack of fiber intake in diet, constipation take place. Constipation’s treatment
lies within the problem itself. Target for the treatment include-
1. Increase amount of water inside intestine

2. Increase fibers content in diet
3. Increase expel of stools by increasing peristaltic movement
4. Stimulating or irritating the colon to force the evacuation of stools
5. Increase retention of sufficient water inside intestine
*Based on our concept. Reference not available

Diabetes Mellitus (DM)
Introduction to basic Points
TYPE- I Diabetes Mellitus TYPE- II Diabetes Mellitus

Insulin Dependent Non Insulin Dependent
Juvenile onset D. Mellitus Maturity onset Juvenile DM
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As name indicate “Insulin Dependent” that means In case of Non Insulin dependent diabetes mellitus the
body is dependent on Insulin from outside source, situation is not same as “Insulin Dependent” because the
because body’s Insulin production center (beta cell Insulin production center is get weakened but not
in Pancreases) is destroyed due to any reason. And if destroyed, so if we try to make that center healthier our
there is no Functional beta cell available so how problem will be solved. There is one more reason that is-
Insulin will be made, that’s why we take Insulin to Insulin is in appropriate amount but there is some
manage deficiency. resistance to its binding to Insulin receptor.
* Diagrams are Made by solution to make you better understand
Profile Insulin Dependent Non Insulin Dependent

Body is not in condition to make sufficient
Insulin production Body can make sufficient Insulin
Insulin
Status of Beta cell Destruction of Beta cell No loss or Destruction of Beta cell
(1) Abnormality of gluco-receptor
(2) Reduced sensitivity of peripheral tissue
Cause Autoimmune disorder
for Insulin
(3) Excess of hyperglycemic hormones
Treatment Insulin from external sources Oral hypo glycaemic Drugs
Non Insulin Dependent

Diabetes Mellitus (DM)
Improve Insulin Availability Overcome Insulin Resistance

Exogenous Insulin Biguanides
Sulfonylureas Thiazolidinediones
Meglitinide/Phenylalanine analogus Alfa-Glucosidase Inhibitors
FOOD
Containing Glucose
Beta Cell Type I
Pancreases- Insulin Diabetes Mellitus
Destroy
Glucose
Type II
Diabetes Mellitus
Create resistance
In Insulin binding to receptor
Utilized by Cell for various

Activity
(1) In absence of Insulin unused glucose is stored in blood
and excreted in urine (2) Increase blood sugar increase
osmotic difference and demand more water (Trust)
(3) Excess sugar in tiny capillary may obstruct eye’s vessels
(4) Unavailability of glucose in cell cause weakness
Reference- Lippincott Pharmacology
Hypothalamus
Growth hormone Corticotropin Throtropin Gonadotropin Prolactin Prolactin

Releasing hormone Releasing hormone Releasing hormone Releasing hormone Inhibiting hormone Releasing hormone
Flow Chart by- Solution Pharmacy

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Growth hormone Adrenocorticotropic Throtropin Follicle Luteinizing Luteinizing Prolactin

Hormone Stimulating hormone Stimulating hormone Hormone (Female) Hormone (Male)
Lever Adrenal Cortex Thyroid Ovary Ovary Testis Brest
Insulin like Glucocorticoids,

growth factor Mineralocorticoids,
Thyroxin Estrogen Progesterone Testosterone
Androgens
Summarized Flow Chart- Hypothalamic and Anterior Pituitary Hormones
Immunity
Immunology
Immunology is made of Immune + logy = Immunology. That means the complete study of Immune (Our body’s bodyguard) system which majorly include antigen and
antibody and their interaction, resulting in desirable or undesirable biological action. Reference- NK Jain (Microbiology)
Natural Immunity Acquired Immunity
Species Racial Individual Active Passive
Natural/Clinical Artificial Natural Artificial

Species Subclinical Vaccine- Dead or Extract Congenital Antiserum
Man is susceptible for plague but not attenuated Toxoids
Colostrums Antitoxin
fowls. Mice are not affected by typhoid
fever but man suffers.
Race
Negroes possess high resistance to
Natural Natural Acquired Immunity
yellow fever than white man. Negroes Antibody formed in a mother in response to
It acquires when a person recover from- diphtheria, small pox and
and white Indian are more susceptible to disease may be transferred to fetus through the
poliomyelitis. A person become immune because it’s his antibody
TB than Caucasian race. placental blood.
producing cell has received an adequate stimulus.
Individuals Artificially Acquired Immunity

Children of age-2-5 are susceptible to Artificial This is acquired by injecting the preparation
diphtheria whereas most adult are This is acquired by the administration of antigen usually by known s antiserum. These are the Antibodies
immune to it. injection. Example- Vaccine either live or dead. produced in animal.

Principle & Mechanism of Drug Action (Pharmacodynamic)
Irritation Mechanism of Drug Action

Example- Counter Bulk Laxative
Irritant like- drugs for Physical
constipation
Other Mechanism Main Mechanism
Stimulation
Example- Adrenaline. Stimulates heart, Chemical
Principle of Drug Action

pilocarpine stimulates salivary glands.
Depression Antacid neutralize acid by its basic nature Enzyme Ion Chanel Transporter Receptor
Example- Barbiturate depresses CNS,
Quinidine depresses heart, and Omeprazole Ions
depress gastric acid secretion. Substrate Inhibitor
Open
Replacement
Example- Levodopa in Parkinson’s,
Insulin in diabetes and Iron in Anemia. Modulator Close
Cytotoxic Substrate
Selective Cytotoxic action on invading Inhibitor
NO Product
parasite or cancer cell without affecting host
cell. Example- Penicillin, Chloroquine, Product
Zidovudine, cyclophosphamide.
Agonist Competitive
Agonist
RECEPTOR
00 km
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Transducer Action
NSAID
Non steroidal anti-inflammatory Drugs
*Classification- KD
Tripathi
Non-Selective Preferential Selective Analgesic-Antipyretic

with poor
COX Inhibitor COX2 Inhibitor COX2 Inhibitor Anti-inflammatory
Nimesulide, Diclofenac, Celecoxib, Etoricoxib, Parecoxib Action
Aceclofenac, Meloxicam, Etodolac
Category Example
Salicylates Aspirin Example
Propionic acid derivative Ibuproprofen, Naproxen, Ketoprofen, Flurbiprofen Paracetamol (Acetaminophen)
Fenamate Mephenmic acid www.facebook.com/pharmavideo/ Metamizol, Propiphenazone
Enolic acid derivative Piroxicam, Tenoxicam Nefopam
Acetic acid derivative Ketorolac, Indomethacin, Nabumetone
*Constitutive = Constant Production
Pyrazolone derivative Phenylbutazone, Oxyphenbutazone
Key Point (Solution) - As name Indicate NSAIDs are those agents which are used to get relief from pain, inflammation and fever.
And as per the COX pathway we understand that COX-1 and COX-2 ultimately form prostaglandin which initiates perception of
pain and inflammation. So anyhow if we block or inhibit the synthesis of PG we may reduce pain and inflammation. Although
COX-1 is constitutive in nature thus it always get secreted without induction of injury and called as a house keeper so it’s better to
inhibit COX-2 rather than COX-1.
* Tissue Injury
(Applicable for COX-2)
Breakdown of Membrane Phospholipids
Arachidonic acid
Mechanism of Action
Cyclooxygenase Pathway
*Rough Idea- Lippincott
COX-2 gene transcription

COX-1 perform housekeeping function
COX-1 gene transcription Induced by-

Oxidative Stress, Injury, Ischemia, Seizures
Like neutralizing gastric acids
Glucocorticoids Inhibit
mRNA
mRNA
Inhibit
Selective
Non-Selective COX-2Inhibitor
Inhibit COX Inhibitor Celecoxib, Etoricoxib, Parecoxib
Non-Selective
Inhibit Inhibit
COX Inhibitor
COX- 1 Side Effect- Gastric Ulcer COX- 2
PROSTAGLANDIN
S
*Diagrams and explainations are made by solution-pharmacy
Antiparkinsonian Drugs
Drug affecting brain dopaminergic system Classification- KD Tripathi Drug affecting brain cholinergic system
Dopamine Precursor
Levodopa Central Anticholinergic
Trihexyphenidyl, Procyclidine, Biperiden
Peripheral “ACLBSEBRPT” Acetylcholine Level Badalne Se Brain

decarboxylase inhibitor Rog Parkinson Taklif deta hai.
Crbidopa, Benserazide Acetylcholine लेवल बदलने से ब्रेन ब्रेन रोग पार्किन्सन तिलीफ देता है Antihistaminic
Orphenadrine, Promethazine
Dopaminergic Agonist
Bromocriptine, Ropinirole,
Pramipexole Parkinsonism
MAO- B Inhibitor
Selegiline
Dopamine
COMT Inhibitor
Entacapone, Tolcapone Acetylcholine
Dopamine Facilitators Imbalance between Acetylcholine and Dopamine

Amantadine
Parkinsonism is an extra pyramidal motor disorder, symptoms includes- rigidity, tremors, with defective
gesture and posture. Parkinsonism is a result of imbalance between acetylcholine and dopamine. When
there is remarkably decrease in dopamine level or increase in acetylcholine level, Parkinsonism take place.
As cause is clear their treatment is also very clear. Treatment goal is to restore the balance between above
said neurotransmitters either by increasing dopamine by eternal source or by decreasing the level of
acetylcholine.

DRUG USED FOR PEPTIC ULCER

Based on KD Tripathi Classification
Reduction of Neutralization of Ulcer Protective Anti H Pylori

Gastric acid Secretion Gastric acid Drugs
H2 Antihistaminic Systemic Example Example

Cimetidine, Ranitidine, Famotidine, Sodium bicarbonate, Sodium citrate Sucralfate, Colloidal bismuth sub
Amoxicillin, Clarithromycin
Roxatidine citrate
Metronidazole, Tinidazole
Tetracycline
No systemic
MgOH, Magnesium trisilicate, Aluminum
Proton Pump Inhibitor hydroxide gel, Magaldrate, Calcium carbonate
Omeprazole, Esomeprazole,
Lansoprazole, Pantoprazole,
Rabeprazole, Dexrabeprazole
NaHCO3+HCL NaCl+H2O+CO2 Base
Anticholinergic Drugs Pylori

Pirenzepine, Propantheline, Antibiotics
Oxyphenonium
Acid + Base
Prostaglandin Analogue
Misoprostol
Anti Pylori
Ulcer
Coating
Neutralization
Diagram Idea- Lippincott Pharmacology
Key point- Peptic ulcer is result of imbalance between attacking gastric acid and protective bicarbonate system. Gastric
acid secretion is regulated by cholinergic system, Histaminic system, stress, Hyperacidity, Microorganism and somehow
smoking and spicy diet. The first attempt towards treatment is neutralization of hyper acidity by using antacids which
are chemically base and they give their action by neutralizing acid. Protective drug are not the treatment they can mask
the pain or irritation signal arising from the ulcer. Anti microbial drug may only be effective in case of infection.
* Diagram Idea and Designing concept by- Solution Pharmacy- www.facebook.com/pharmavideo/

PHARMACOLOGY
Study of Pharmacokinetics and Pharmacodynamic profile
Trick- In Pharmacodynamic & Pharmacokinetics ‘Pharmaco’ word

Pharmacodynamic is common. And now in Dynamic the 1st word is D and in Drug the Pharmacokinetics
What does drug do to the body? first word is also D so Dynamic is related to Drugs.
What does body do to the drug?
We take drugs because we are having-
A D M E
A
Diseases Disorder
Absorption of medicine from their
s Caused by site of administration to produce
Caused by External Substance
Imbalance of internal biochemical response.
What happens when we take those drugs/medicines?

Distribute throughout the Metabolism breakdown
body after absorption complex molecules to
small molecules that it may
Desired Effects Undesired Effects be used
Diagnosed Prevention Treatment Side Effect Adverse Effect Toxic Effect Unwanted and toxic
substance get excreted via-
Fatal Effect urine, stool, sperm, gas etc
Vaccine
Bismuth
Extension of ADR
Sulphate Paracetamol- Reduce fever (Temperature)
Antacids- Reduce Acidity (Neutralization) Side Effects- fatigue, nausea, vomiting, decreased blood
Penicillin- Prevention from Infections cell counts, hair loss, and mouth sores.
Adverse Effects- stomach irritation and bleeding often
occur in people who regularly use aspirin or other
Fluorescence X-Ray These are examples of what DRUGS are doing to the BODY
nonsteroidal anti-inflammatory drugs (NSAIDs)

Antirheumatoid Drugs
Disease Modifying AR Drugs Biological Response Modifier Adjuvant Drugs

Immunosuppressant- Etanercept
(Methotrexate, Azathioprine, Cyclosporine) Corticosteroids
Infliximab, Adalimumab,
Sulfasalazine, Chloroquine, Leflunomide, Gold Prednisolone and others
sod. Thiomalate, Auranofin, d-Penicillamine Anakinra
Key point- Antirheumatoid arthritis (RA) is an autoimmune disease In RA there is joint inflammation, synovial
proliferation and destruction of articular cartilage. These inflammatory cells secrete lysosomal enzyme which
damage cartilage and erode bone, while PG produced in the process cause vasodilatation and pain.
2 ATP + CO2 + Glutamine Carbamoyl Phosphate Dihydroorotate

NAD+
Dihydroorotate
2 ADP + Pi + Glutamate NADH + H+
Dehydrogenase
Orotate
Orotidine 5’
Mechanism of Action Monophosphate
Leflunomide is an immunomodulatory OMP
agent that preferentially cause fully arrest of the autoimmune
Uridine 5’
lymphocytes through its action on Dihydroorotate Dehydrogenase.
Monophosphate
Purine DNA-RNA
Anti- Gout Drugs Hypoxanthine

Allopurinol
Xanthine Oxidase
Febuxostat
Xanthine
Allopurinol
For Acute Gout For Chronic Gout Xanthine Oxidase
Febuxostat
Uric Acid
Uricosurics Synthesis Uric Acid

Colchicine, Corticosteroids
Inhibitor
Probenecid, Hydrolytic enzyme
Phagocytosis of uric Lysosome
Sulfinpyrazone,
acid crystal by
NSAID,
Allopurinol, Febuxostat
neutrophils
Neutrophil
Leukotriene Colchicine
Releases
Rupture of Lysosome,
followed by death of phagocyte & release of hydrolytic enzyme
Acute Inflammation
Diagrams and explainations are made by solution-pharmacy to make you better understand
SEDATIVE - HYPNOTICS
These drugs make exited patient calm and cool
with and without causing sleep. They are differ only in concentration
SEDATIVE D T F N A
HYPNOTICS
दिमाग ठं डा रखने से फटाफट नींि आती है
Sedative are those drugs which make Hypnotics are the drugs which make
L O D A C
patient calm and relax without person calm but also induce sleep.
लो डराने आ गया क्लाससदफके शन
causing sleep, although patient may This is extension of sedative dose of
C C D L
feel dizziness and may loss alertness any drugs. Sedative in large dose act
चलो चले िवाई लेने एंटी कनवलसन का
or responsiveness. as hypnotics
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𝐁𝐚𝐫𝐛𝐢𝐭𝐮𝐫𝐚𝐭𝐞 𝐁𝐞𝐧𝐳𝐨𝐝𝐢𝐚𝐳𝐞𝐩𝐢𝐧𝐞 𝐍𝐞𝐰𝐞𝐫 𝐍𝐨𝐧 𝐁𝐙𝐃 𝐇𝐲𝐩𝐧𝐨𝐭𝐢𝐜𝐬

Sedation − Sleep − Anaesthasia Zopiclone, Zolpidem, Zaleplon
− Coma
𝐋𝐨𝐧𝐠 𝐀𝐜𝐭𝐢𝐧𝐠 𝐒𝐡𝐨𝐫𝐭 𝐀𝐜𝐭𝐢𝐧𝐠 𝐔𝐥𝐭𝐫𝐚 𝐒𝐡𝐨𝐫𝐭 𝐀𝐜𝐭𝐢𝐧𝐠

Phenobarbitone 𝑺𝒕𝒂𝒈𝒆 − 𝟎
Butobarbitone Thiopentone
Phenobarbitone Methohexitone 𝑨𝒘𝒂𝒌𝒆
𝐶𝑜𝑛𝑠𝑡𝑖𝑡𝑢𝑡𝑒 1 − 2%
Hypnotic Antianxiety Anticonvulsant 𝑺𝒕𝒂𝒈𝒆 − 𝟎𝟏

Diazepam Lorazepam Clonazepam 𝑫𝒐𝒛𝒊𝒏𝒈
Temazepam Oxazepam Clobazam 𝐶𝑜𝑛𝑠𝑡𝑖𝑡𝑢𝑡𝑒 3 − 6%
Flurazepam Diazepam Diazepam
Nitrazepam Alprazolam Lorazepam
Alprazolam Chlordiazepoxide चलो चलें िवाई लेने एंटी 𝑺𝒕𝒂𝒈𝒆 − 𝟎𝟐
दिमाग ठं डा रखने से लो डराने आ गया CONVULSION का 𝑼𝒏𝒆𝒒𝒖𝒊𝒗𝒐𝒄𝒂𝒍 𝑺𝒍𝒆𝒆𝒑
Different stages of Sleep pattern

फटाफट नींि आती है क्लाससदफके शन 𝐶𝑜𝑛𝑠𝑡𝑖𝑡𝑢𝑡𝑒 40 − 50%
Cl-
𝑺𝒕𝒂𝒈𝒆 − 𝟎𝟑
GABA Site 𝑫𝒆𝒆𝒑 𝒔𝒍𝒆𝒆𝒑 𝒕𝒓𝒂𝒏𝒔𝒊𝒕𝒊𝒐𝒏
α β 𝐶𝑜𝑛𝑠𝑡𝑖𝑡𝑢𝑡𝑒 5 − 8%
α
Chloride Channel
𝑺𝒕𝒂𝒈𝒆 − 𝟎𝟒
Wide open
𝑪𝒆𝒓𝒆𝒃𝒓𝒂𝒍 𝑺𝒍𝒆𝒆𝒑
𝐶𝑜𝑛𝑠𝑡𝑖𝑡𝑢𝑡𝑒 10 − 20%
Cell
Membrane
𝑹𝑬𝑴 𝒔𝒍𝒆𝒆𝒑
GABA Site
𝑷𝒂𝒓𝒂𝒅𝒐𝒙𝒊𝒄𝒂𝒍 𝑺𝒍𝒆𝒆𝒑
BZD Site 𝐶𝑜𝑛𝑠𝑡𝑖𝑡𝑢𝑡𝑒 20 − 30%
β α γ
α α
Benzodiazepine Mechanism Schematic Diagram
Pharmacological Action
Mechanism of Action
Target of Benzodiazepine are on GABA receptor, because GABA
is major inhibitory neurotransmitter in CNS. GABA is consisting
Reduction of Anxiety
of five- alpha, beta, gamma subunits that span the postsynaptic
membrane. The influx of chloride Ions cause hyper polarization of
the neuron and decrease neurotransmitter by inhibiting the Sedative-Hypnotics
formation of action potentials.
Empty receptor is inactive and Binding of GABA open the

Anterograde Amnesia
coupled chloride channel is closed chloride channel cause hyper
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Muscle Relaxant
Mechanism of Action in various steps
Entries of chloride hyper polarize Binding of GABA is enhanced by
cells, make them difficult to benzodiazepine; result in more
depolarize and reduce neural entry of negative chloride ions.
By Targeting GABA receptor
excitability
Methods Available for Sterilization
PHYSICAL Mostly Preferred over Chemical CHEMICAL
Sunligh Heat Radiation Filtration

GAS Liquid
t Non-Ionizing & Ionizing Radiations
Electromagnetic- Particulate s
Below 1000C
Dry Heat Moist Heat At 1000C

Ethylene
Above 1000C Alcohol
Oxide
Formaldehyde Aldehydes
Autoclave Phenolics
Halogens
Heavy Metals
Hot Air Oven, Red Heat, Infrared, Flaming, Incineration Surfactants
Dyes
Earthen ware, Asbestos, Sintered glass, Membrane
Good for Large Surface Area
Pressure Vent
Pressure Meter Steam Circulation
1. Liquid media
Object to be sterilized
2. Nonflammable liquids
3. Glassware: empty and inverted
4. Dry hard items, either unwrapped
or in porous wrap
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Outer Jacket
Heating Coil Autoclave Stands
PRINCIPLE (Autoclave)
Water inside autoclave converts into vapor
and create pressure and when object
containing M.O. is placed inside the
autoclave this moist heat + Vapor coagulate
the protein of Microorganism and finally
killed them. It is more powerful than dry heat.
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PUSHPENDRA KUMAR PATEL*
Short Description on
Organ Bath Assemblies
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Figure- solution/SOB*- Labelled diagram of student organ bath
Introduction- Student organ bath or simply organ bath is an apparatus widely used in
pharmacology laboratory and various educational Institutes, research and development sector.
Organ bath is not a single apparatus but it is a combination of many small units which
include-
1. Bath chamber
2. Organ tube
3. Glass coil
4. PSS reservoir
5. Heater
6. Thermostat
7. Stirrer or mixer
8. Oxygen tube
9. Aerator
10. Leaver
11. Load
12. Sherrington rotating drum (Kymograph Drum)
13. Kymograph Paper
Use- When we have to perform the invitro studies of any given drug, we need to isolate
the organ from suitable experimental animal. Once organ is isolated it should be
immediately transferred into physiological salt solution (PSS). Organ bath is having
several important component and assembly as mentioned above; all are equally important
and have individualized functions. Once organ is placed into PSS other arrangement are
made. These include-
Page | 1
*This notes and diagram is made by solution pharmacy, exclusively for pharmacy students
1. Cleaning the organ bath assembly
2. Attaching or arranging all small hooks, clamp and water pipes.
3. Fixing the lever and stick the kymograph paper on rotating drum.
4. Kymograph paper should be either smoked or have to use colour ink at the end of
lever.
5. Fill the water into 2/3 portion of organ bath or up to suitable length depending
upon the unit of organ bath.
6. Switch on the mains and heater
7. Wash the organ tube with PSS once
8. Fill the PSS into organ bath and hold it.
9. Start providing oxygen by aerator machine
10. Attach the aeration tube into the organ bath
11. Now tie the tissue of isolated organ which you have to study (This process may be
modified)
12. Tie the other end of thread into writing lever
13. Attach the lever with rotating drum and wait till resting or constant line appears
14. Inject the drug into organ bath and carefully examine the changes in muscle
strength by observing kymograph paper.
15. Release the clamp of organ bath to let the PSS flow outside the organ tube if you
want to reduce the strength of dose, if you want to increase the dose, no need to
change the PSS. (It is for same drug)
16. For every new drug injection the old PSS must be change.
17. Ensure the temperature of water bath; it should not increase than optimum
temperature.
Description of various parts
1. Bath chamber- Bath chamber is made of good quality plastic (PVC) it is of two types-
Single unit and double unit. In single unit there is only one place for organ
tube, thus you can perform one study at one time, or you need to wash the
tissue with PSS before changing drug. Double unit organ bath is having
two holding place for organ tube, that’s why we can perform two studies at
same time. It depend on you weather you want to check the effect of
various dose of same drug or you can check two separate drug’s effect on
muscle. At the bottom of bath chamber there is two outlets, one is for
drainage of water and second is for the PSS.
2. Organ Tube- Organ tube is the soul of organ bath because the king of experiment lies or
rest in this chamber. Organ tube is a glass tube having two sides opening.
Out of which one is for expelling used PSS and second is for inlet of PSS.
PSS is not filled directly from the top of organ tube, but it is filled from
this side inlet unit.
Page | 2
3. Glass coil- Glass coil is coil like structure (As name indicate) its function is very simple. If
we supply PSS directly to the organ tube from straight pipe, its
temperature may not be equal to outer temperature that is about 370C, so
the PSS is supplied through this pipe, by doing so the PSS take a longer
time to reach organ tube and contact time of PSS increase with water
available in the bath chamber and this the temperature of PSS slightly
increase and matched with outer temperature.
4. PSS reservoir- PSS reservoir is a simple vessel which holds PSS to be supplied to organ in
organ tube. PSS is essential solution containing all electrolytes which are
necessary for the intact tissue. These include maintenance of is tonicity,
conductivity and contractility etc. Example of PSS includes- (1) Frog
ringer solution (2) Ringer or Ringer Locke solution (3) De Jalon solution
(4) Tyroid solution (5) Kerbs-Henslet solution.
5. Heater- Heater is heating devices which maintain the desired (370C) temperature of
water inside the organ bath. Optimum temperature is important for the
tissue attached in a organ bath, because this help to maintain its live
condition. And the contraction or relaxation of muscle may affected by
variation in temperature.
6. Thermostat- Thermostat is very basic devise available in every home. The objective of
Thermostat is to maintain the temperature we have set. Thermostat is
based on auto cut principle. When the temperature exceed from set
temperature, it automatically stop the heater, and once when temperature
start falling it again start the heater so that water start heating.
7. Stirrer or Mixer- Stirrer is a device or part of devise which is used to homogenize the
temperature of water inside the organ bath. If we don’t use stirrer the
temperature of water may vary part to part and this is not suitable for
tissue. So the basic work of mixer is to mix the heat throughout the water
bath.
8. Oxygen Tube- Oxygen tube is one of the most important parts of student organ bath.
Oxygen tube carries oxygen directly to the tissue tied. Tissue is tied at the
end of oxygen tube and it gets oxygen form this tube which is fitted to
aerator at the other end. One end of aerator tube is consisting of thin metal
wire and in this metal wire we tied the tissue and the other end of tissue
will be tied with the lever. Any changes in the tissue will be recorded in
the kymograph paper by the lever.
9. Aerator- This is a common device used to supply the vital air that is oxygen. It
generates oxygen and pump to the aeration tube where our tissue is
located. Aerator is also used in the aquarium and the purpose is same, to
generate and supply oxygen to the tissue.
Page | 3
10. Lever- This is the main part of any organ bath. Lever is a simple writing device
which records every movement or changes in the strength of muscle by
drug we applied. One end of the lever is attached to the tissue and when
we inject the drug into the organ tube, its effect can be easily seen in
muscle, either in form of contraction or relaxation. When muscle get
contracted it pull the thread and thread pulls the lever and it may seen by
upward graph and the opposite is applicable for muscle relaxation. There
are various types of lever available- (1) Simple lever (2) Frontal lever (3)
Starling’s heart lever (4) Brodie’s Universal lever
(1) Diagram of Frontal Lever
(2) Frontal Lever
(3) Diagram of Starling’s heart lever
11. Load- Load is nothing but an object which provide optimum load and tension to
the lever so that proper recording will be achieved.
12. Sherrington rotating drum (Kymograph Drum) - It is another main parts or assembly
of student organ bath. It is a rotating devise, which keep rotating and recording the changes in
tension of lever. It has several basic units’ like- gear and clutch which allow us to set the
desired RPM (rotation per minutes) at the back of this there is a lock which lock and unlock
the machine. In front of the devise there is counter which count the RPM by touching the
other hand. Kymograph is attached with kymograph paper, this is used either by coating with
smoke or by using colour pen.
References- All materials and notes are made by solution pharmacy
Page | 4

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Adverse Drug Effects

Concept & Idea by- Solution Pharmacy

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Desirable Effects Undesirable Effects

Analgesic Effect Toxic Effects- Poisoning

Reduce pain by inhibiting PG synthesis Intolerance

Antipyretic Effect Drug Allergy- Humoral & Cell Mediated

Photosensitivity- Phototoxic and Photo allergic

Reduce inflammation by inhibiting COX-I and COX- Teratogenicity- Thalidomide

Drug Induced Disease- Peptic Ulcer by NSAIDS

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Nitrates Beta Blocker Ca+ Channel K+ Channel Opener Others

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Class- I Class- II Class- III Class- IV Other

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Vancomycin Hamycin Linezolid

Note- Mnemonics are based on my thoughts; it may or may

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Antibacterial Bacteriostatic Bacteriosidal

H1 Blocker H2 Blocker H3 Blocker H4 Blocker

Highly Sedative Moderately Sedative Mild Sedative 2nd Generation

Fexofenadine, Loratadine, Desloratadine, Cetirigine, Levocetrizine, Azelastine, Mizolastine, Ebastine, Rupatadine

5 Blood Pressure- Most antihistaminic drug cause fall in BP on IV injection.

Classification and Mechanism of Action for Antihistamine Drug

H1 Blocker H2 Blocker H3 Blocker H4 Blocker

Cimetidine, Ranitidine, Famotidine, Roxatidine

H2 Receptor antagonist and regulation of gastric acid secretion

Acetylcholine Histamine Gastrin

Gastric Acid secretion stimulation

ACE Angiotensin Calcium Channel Beta+Alfa Alfa Central

Examples of above listed Class Thiazide Diuretics Channel is closed

Decrease Blood Volume Channel isDecrease

Verapamil, Diltiazem, Nifedipin, Felodipine,

Decrease Peripheral Resistance

Beta Receptor Blocker 05

Arteriolar- Hydralazine, Minoxidil, Diazoxide Decrease sod. And water retention

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Anti-Herpes Virus Anti-Hepatitis virus or

Nucleoside reverse transcriptase

Entry (Fusion) Inhibitor

CCR5 Receptor Inhibitor

Integrase Inhibitor- Raltegravir

4 Reverse transcription Viral genomic mRNA

Penetration 6 Budding (Viral release)

Host cell Packaging and

Anti- herpes drug’s mechanism of action

Drugs for Cough

Pharyngeal Demulcents Expectorants /Mucokinetics Antitussive

Opioids increase cough threshold Histamine Mast Cells

Cough Center Activate Cough Start

Low threshold Irritant

Reduce tussal impulse 02

* Diagrams Except brain) is made by solution to make you better understand

Drugs for Constipation

Bulk Stool Stimulant Osmotic

* Mechanism of Action- Representation by Solution Pharmacy

1. Increase amount of water inside intestine

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TYPE- I Diabetes Mellitus TYPE- II Diabetes Mellitus

* Diagrams are Made by solution to make you better understand

Profile Insulin Dependent Non Insulin Dependent