B R I C K S N O T E S |1

MODULE 4: PHARMACOLOGY Gs: stimulate

adenylyl
Nerve
Growth
Thyroid
hormones
Lecture by Christopher Dacanay, RPh, MD; Roma Mikaela cyclase Factor
Ambrocio, RPh; Trishia Gwyneth Dabon, RPh; Mona Lisa Gi: inhibit Insulin-like
Lomarda, RPh; and Faima Nain, RPh
adenylyl growth
INTRODUCTION TO PHARMACOLOGY
cyclase factor
DEFINITION OF TERMS
NON-TARGET PROTEIN MEDIATED
• Pharmacology: study of drugs
• Colligative/Mass Effect
• Drugs: any article/agent used in the mitigation, diagnosis,
o Example/s: Mannitol
prevention, treatment, and cure of diseases in humans
o Indication/s: decrease intracranial pressure,
and animals
decrease intraocular pressure
• Pharmacokinetics: body to drug (refer to
• Chemical Antagonism
Biopharmaceutics notes)
o Example/s: Neutralization, Complexation
• Pharmacodynamics: drug to body
• Counterfeit Mechanism
CLASSIFICATION OF DRUGS
o Example/s: Antimetabolite
FUNCTIONAL MODIFIER
BASED ON DRUG-RECEPTOR INTERACTION
• Alter the biochemical and physiologic activity of the cell FEATURES
• Examples: Analgesics, Monoclonal antibodies
• Affinity: ability to bind to receptors
REPLENISHERS
• Intrinsic Activity: ability to generate an effect

m
• Supplement deficient substances in the body TYPES OF LIGANDS
• Examples: Insulin, Vit B12
• Agonist: favors ACTIVE form of receptors

.co
DIAGNOSTIC AGENTS
o Full Agonist: IA = 1
• Diagnosis of a disease o Partial Agonist: 0 < IA < 1
• Examples: Edrophonium, Dobutamine • Antagonist: favors an EQUILIBRIUM of the ACTIVE and

ail
CHEMOTHERAPEUTIC AGENTS INACTIVE form of receptor
• For management of a disease Antagonist – Based on MOA
m
• Examples: Cancer chemotherapy, Antimicrobials Chemical Antagonism React with one another
PHARMACODYNAMICS Physiologic Antagonism Same effect, Diff receptor
@g
Pharmacologic Antagonism Diff effect, Same receptor
BASED ON MECHANISM OF ACTION
TARGET PROTEIN MEDIATED Antagonist – Based on Reversibility
os

• Structural Protein: develop cellular framework Reversible Non-covalent (<24 hours)

o Example/s: Colchicine, Taxanes Irreversible Covalent (> 24 hours)
• Regulatory Protein: regulate biochemical and physiologic
ll

activity of the cell Antagonist – Based on Surmountability

ba

o Channels: act as passageway Surmountable Competitive

Channels Same active site
Voltage-Gated Ion Ligand-Gated Ion Channels
lle

Non-surmountable Non-competitive
Channels Active site and Allosteric
Depends on membrane Any substance that binds to site
e

potential receptors • Inverse Agonist: favors INACTIVE form of receptor

ab

Na-channel – depolarization Na-channel associated with DRUG-RECEPTOR INTEACTION THEORIES

K-channel – prolong Nicotinic Receptor CLARK
refractory period Cl-channel associated with • All receptors are occupied to produce maximal effect
an

Ca-channel GABA Receptor PATON

o Carriers: facilitate active transport across
• Rate theory
membranes
aly

• Proper stimulus to elicit effect

§ Example/s: Na-K ATPase pump
ARIENS AND STEPHENSON
o Enzymes: hasten chemical reaction
§ Example/s: COX, ACE, MAO, COMT • As long as receptors are occupied there is an effect
o Receptors: cell components where the ligand DOSE-RESPONSE CURVES
could bind GRADED DOSE RESPONSE CURVE
Receptors
Type I Type II Type III Type IV
Ionotropic Metabotropic Enzyme- Nuclear
linked
7-trans- Gene-
membrane transcription
spanning linked
G-protein
coupled
Receptor • Parameters:
Milliseconds Seconds Minutes Hours o Efficacy: maximum achievable response
Nicotinic Gq: stimulate Tyrosinase Steroids § AKA: Ceiling Effect
receptors phospholipase kinase Fat-soluble o Ceiling dose: smallest dose required to achieve
GABA C à IP3 and Insulin vitamins the maximum achievable response
receptors DAG
 B R I C K S N O T E S |2
oED50: dose required to achieve 50% of § Meissner: submucosal
maximum achievable response § Auerbach: Myenteric
§ Inversely proportional to POTENCY SYMPATHETIC VS PARASYMPATHETIC NERVOUS SYSTEM
o Potency: dose needed to achieve 50% of SYMPATHETIC PARASYMPATHETIC
maximum response Pre-ganglion Short Long
o Slope: degree of changes in response to a Ganglion close to spinal near to target organ
change of dose cord
QUANTAL DOSE RESPONSE CURVE Post-ganglion Long Short
Main NT NE Ach
Ganglion NT Ach
Ganglion Nicotinic
receptor
Neuroeffector NE Ach
NT
Neuroeffector Adrenergic Cholinergic
receptor Muscarinic
Anatomical Thoracolumbar Craniosacral
• Parameters: origin
o ED50: beneficial effect in 50% of the population Ligand Catecholamines Ach

m
o TD50: median toxic dose Receptors Alpha, beta, Muscarinic. Nicotinic
o Therapeutic Index: measure of relative safety dopamine

.co
!"#$
§ 𝑇ℎ𝑒𝑟𝑎𝑝𝑒𝑢𝑡𝑖𝑐 𝐼𝑛𝑑𝑒𝑥 = %"#$ Effects Fight, fright, flight Rest, Digest
o Margin of Safety SUMMARY OF EFFECTS
Eyes Mydriasis Miosis

ail
AUTONOMIC NERVOUS SYSTEM Heart Tachycardia Bradycardia
OVERVIEW OF THE NERVOUS SYSTEM m Lungs Bronchodilation Bronchoconstriction
GIT Dec peristalsis Inc peristalsis
Urinary Urinary retention Urination
Nervous System
@g
bladder
Detrusor Relax Contract
Central Nervous Peripheral bladder
System Nervous System
Urethra Close Open
os

Autonomic
sphincter
Somatic Nervous
Brain Spinal Cord
System (voluntary)
Nervous System Males Shoot Point (erection)
ll

(involuntary)
(ejaculation)
ba

Parasympathetic Sweat glands Apocrine Eccrine

Nervous System
(rest or digest)
SYMPATHETIC NERVOUS SYSTEM
lle

Sympathetic
Nervous System
BIOSYNTHESIS
(fight or flight)
• Site: brain (locus ceruleus), adrenal medulla,
e

postganglionic sympathetic fibers

Enteric Nervous
• Steps:
ab

System

AUTONOMIC VS SOMATIC NERVOUS SYSTEM Tyrosine

AUTONOMIC SOMATIC
an

Tyrosine hydroxylase
Two neuron system One neuron system (no
(preganglionic, ganglion, ganglia) Levodopa
aly

and postganglionic neuron)

DOPA-decarboxylase
Supply every part of the ONLY skeletal muscles
body EXCEPT skeletal Dopamine
muscles
Ganglionic NO Ganglionic Dopamine hydroxylase

Neurotransmitter (NT): Neurotransmitter Norepinephrine

Acetylcholine (Ach) NO Ganglionic receptor
Ganglionic receptor: Phenylethanolamine-N-methyltransferase (PENMT)
Nicotinic
Epinephrine
Involuntary Voluntary
Effector organ: Everything Neuroeffector NT: Ach • Rate-Limiting Enzyme: Tyrosine Hydroxylase
EXCEPT skeletal muscles Neuroeffector organ: • Rate-Limiting Step: Hydroxylation
Effector NT: Depends Skeletal muscle • Important drugs to note:
(Parasympa: Ach; Sympa: Neuroeffector receptor: o Metyrosine: inhibits Tyrosine hydroxylase
Epi) Nicotinic o Reserpine: inhibits vesicular uptake of
AUTONOMIC NERVOUS SYSTEM Dopamine
• ENTERIC NERVOUS SYSTEM Decrease NE levels Increase NE levels
o Exclusive: GIT (supply or innervates motor Catechol-O-methyl COMT-inhibitors
activity of pancreas, liver and intestines) transferase (COMT) (Tolcapone, Entacapone)
o GIT motility and secretion (plexuses) Monoamine Oxidase (MAO) MAO-inhibitors (Selegiline)
NE reuptake Inhibit NE reuptake
 B R I C K S N O T E S |3
Inhibits NE NE reuptake inhibitors: • Selective
Guanethidine Reboxetine, Cocaine, SELECTIVE SYMPATHETIC AGONIST
Guanadrel Tricyclic Antidepressants, Alpha-1 Phenylephrine Nasal
Bretylium Methylphenidate, Methoxamine decongestants
Modafinil Midodrine
Increase release of NE: Naphazoline ADR: rebound
Amphetamine, Ephedrine, Metazoline congestion, urinary
Tyramine, Angiotensin II, Oxymetazoline retention, Raynaud
Phentermine, syndrome, increase
Phenmetrazine, blood pressure
Phenylpropanolamine Alpha-2 Clonidine Inhibit NE release
RECEPTORS AND EFFECTS Apraclonidine
RECEPTOR EFFECT Brimonidine ADR: rebound
Alpha-1 Gq Vasoconstriction Methyldopa hypertension
Mydriasis Guanabenz (Clonidine),
Urinary retention Guanfacine hepatotoxicity,
Piloerection Tizanidine sedation,
Alpha-2 Gi Regulate NE release Rilmenidine depression, false
Promote platelet aggregation Moxanidine (+) Coomb’s test

m
Inhibit lipolysis Dexmedetomidine (Methyldopa)
Beta-1 Gs Heart: Increase rate, Beta-1 and Isoproterenol 1st drug used as

.co
conduction, and contraction Beta-2 Isoprenaline MDI for bronchial
Kidney: renin formation asthma
(Juxtaglomerular cells)

ail
Beta-2 Gs Lungs: Bronchodilation ADR: Tachyphylaxis
Uterus: Uterine relaxation Beta-1 Dobutamine 1st line for
Inc Glucose levels cardiogenic shock
m
(Gluconeogenesis, Pharmacologic
Glycogenolysis) stress test (with
@g

Tremors Dipyridamole)
Beta-3 Stimulate lipolysis
Dopamine D1, D5: Kidney (renal ADR:
os

vasodilation) Tachyarrhythmia
D1, D2, D3, D4, D5: CNS Beta-2 Short-Acting Bronchodilation for
ll

SYMPATHETIC AGONIST Salbutamol/Albuterol asthma

Terbutaline
ba

• AKA: Sympathomimetic Agents

Metaproterenol Tocolytics: mgt of
DIRECT-ACTING
Long Acting pre-term labor
• MOA: directly bind to sympathetic receptors
lle

Bambuterol Terbutaline,
NON-SELECTIVE SELECTIVE
Indacaterol Isoxsuprene,
Natural Catecholamines Specific receptors Formoterol Ritodrine
e

Epinephrine (EPI): B1, B2, Alpha-1 Salmeterol

a1 Alpha-2
ab

ADR: Hypokalemia,
Norepinephrine (NE): B1, a1 Beta-1 Tremors,
Dopamine (DA): D1, B1, a1 Beta-2 Tachycardia
an

Beta-3 Beta-3 Mirabegron Increase lipolysis

Metabolism: MAO and Dopamine- Fenoldopam For severe
COMT
aly

1 hypertension
EPI and NE: D2 and D4 Bromocriptine For
Vanillylmandelic acid hyperprolactinemia
DA: Homovanillic acid
INDIRECT-ACTING
• Non-Selective
• MOA: increase release of NE, inhibit NE reuptake
o Epinephrine/Adrenaline: 1st line cardiac
INDIRECT ACTING SYMPATHETIC AGONIST
stimulant in cardiac arrest; 1st line for
Methamphetamine Increase CNS stimulation
anaphylactic shock, local vasoconstrictor
Modafinil (memory enhancers)
§ Prodrug: Dipivefrin – for glaucoma (inc
Amphetamine Cause too much dryness
drainage of aqueous humor)
Phenmetrazine For narcolepsy (EXCEPT
o Norepinephrine/Noradrenaline: 1st line
Phentermine Methamphetamine)
inotrope in septic shock
Methamphetamine Decrease appetite for
o Dopamine: alternative for septic shock and
Sibutramine weight loss
cardiogenic shock
Amphetamine
§ Low dose (<5 mcg/kg/min): renal
Methylphenidate For ADHD
vasodilation (D1)
Amphetamine
§ Intermediate dose (5-10 mcg/kg/min):
Tricyclic Antidepressants Inhibit NE reuptake
(+) inotrope, chromotrope, dromotrope
(B1) Reboxetine
§ High dose (>10 mcg/kg/min): Cocaine
vasoconstriction (a1) Tyramine Increase exocytosis of NE
Ephedrine
 B R I C K S N O T E S |4
Amphetamine Active uptake of choline
Methamphetamine
Phenmetrazine Anorexiants Choline + Acetyl CoA via Choline
Phentermine Acyltransferase
Phenylpropanolamine
• ADR: Inc addiction, risk of stroke, and pulmonary Acetylcholine
hypertension
SYMPATHETIC ANTAGONIST
Vesicular uptake of Acetylcholine
• AKA: Sympatholytic Agents
ALPHA-BLOCKERS
NON-SELECTIVE SELECTIVE Release of Acetylcholine
Phenoxybenzamine: Alpha-1 Alpha-2
irreversible, non- Prazosin Yohimbine Binding of Acetylcholine
competitive Terazosin Rauwolfscine
Phentolamine: Doxazosin • Important drugs to note:
reversible, Tamsulosin NO clinical use o Hemicholinium: inhibits active uptake of choline
competitive anymore o Vesamicol: inhibits vesicular uptake of
Use: Anti-HTN Yohimbine: for Acetylcholine
Use: HTN in patients and Benign erectile o Botulinum toxin: inhibits release of

m
with Prostatic dysfunction acetylcholine
pheochromocytoma Hyperplasia (OLD) o Acetylcholinesterase: metabolized

.co
• Effects: vasodilation, prostatic relaxation Acetylcholine
• ADR: reflex tachycardia, orthostatic hypertension RECEPTORS AND EFFECTS
BETA-BLOCKERS RECEPTOR EFFECT

ail
• Effects: decrease blood pressure, anti-arrhythmic, anti- M1 Gq Stomach (Increase acid secretion)
angina CNS
• Note: Non-selective Beta-blockers are contraindicated
m
M2 Gi Heart: Vagotonic, (-) chromotrope,
to asthmatic patients dromotrope
BASED ON SELECTIVITY
@g
M3 Gq Majority of Parasympathetic effect
NON-SELECTIVE CARDIOSELECTIVE (B1) Miosis
Nadolol Celiprolol Bronchoconstriction/Bronchospasm
Sotalol Nebivolol: most Inc Peristalsis
os

Timolol cardioselective Urination

Pindolol Bisoprolol Erection
ll

Propranolol: for Betaxolol Sweating

ba

performance anxiety, Esmolol: ultra-short acting (DUMBELS)

hyperthyroidism, migraine Acebutolol Nm Muscle contraction
prophylaxis Atenolol Nn/Ng Preganglionic fibers (nonspecific
lle

Metoprolol effect)
PARASYMPATHETIC AGONIST
Use: anti-HTN for post MI
e

• AKA: Parasympathomimetic Agents

INTRINSIC SYMPATHOMIMETIC ACTIVITY DIRECT-ACTING
ab

Carteolol With partial agonist • MOA: directly bind to parasympathetic receptors

Labetalol Less likely to cause rebound DIRECT ACTING PARASYMPATHETIC AGONIST
an

Acebutolol tachycardia Choline Esters Alkaloids

Pindolol Mixed Mixed
MEMBRANE STABILIZING ACTIVITY Carbachol Arecoline: from Areca
aly

Pindolol Local anesthetic effect Acetylcholine catechu (betel nut, nga

Propranolol CANNOT be used in eye Methacholine: provocative nga); euphoriant and aids
Acebutolol preparation challenge test in asthma digestion
Labetalol diagnosis
Metoprolol M-selective M-selective
MIXED ALPHA AND BETA BLOCKING EFFECT Bethanechol: relieve Muscarine
Carvedilol With vasodilation urinary retention Pilocarpine: from
Labetalol Pilocarpus microphyllus; for
• ADR: Bradycardia, Masking of hypoglycemic symptoms xerostomia and glaucoma
PARASYMPATHETIC NERVOUS SYSTEM N-selective
BIOSYNTHESIS Lobeline
• Site: brain, postganglionic parasympathetic fibers, Varenicline
preganglionic sympathetic and parasympathetic fibers Nicotine
• Steps: Use: for smoking cessation
• Rate-Limiting Enzyme: Choline acyltransferase INDIRECT ACTING
• Origin of Acetylcholine: Choline and acetyl CoA • MOA: Acetylcholinesterase (Ache) inhibitors
INDIRECT ACTING PARASYMPATHETIC AGONIST
Short-Acting (<30 mins) Edrophonium (Tensilon):
for Myasthenia Gravis
diagnosis
 B R I C K S N O T E S |5
Intermediate to Long Acting Carbamates (-stigmines): Steroid Suxamethonium
(2-24 hrs) reversible inhibitor of Ache; Rocuronium Succinylcholine
for management of Pancuronium
Myasthenia Gravis, arrow Isoquinoline
poison toxicity, curare Atracurium
toxicity, atropine toxicity Mivacurium
Very Long Acting (>24 hrs) Parathion, Malathion: MOA: compete with Ach MOA: Succinylcholine looks
insecticides (farmers) therefore Na channel will like Ach (no competition) à
Ecothiopate, Isothiopate: NOT open à NO desensitization à no
galucoma depolarization muscle contraction
Sarin, Tabun, Soman: mass ADR: anaphylactoid ADR: diaphragmatic
killing reaction, seizures paralysis, malignant
• EFFECT: Diarrhea, Urination, Miosis, Bradycardia, hyperthermia (Treatment:
Bronchoconstriction, Emesis, Lacrimation, Sweating, Dantrolene),
Salivation (DUMBBELSS) rhabdomyolysis
INDIRECT ACTING AGONISTS AFFECTING THE CNS
• MOA: reversible inhibitor of Ache • Anti-Nn or Ganglionic Blockers
• Donepezil, Rivastigmine, Galantamine, Tacrine: for o Hexamethonium, Mecamylamine,
Alzheimer’s disease Trimethaphan

m
PARASYMPATHETIC ANTAGONIST o Last resort drug (Anti-HTN)
• AKA: Parasympatholytic Agents

.co
ANTIMUSCARINIC AUTACOIDS
• MOA: blocks muscarinic receptors DEFINITION OF TERMS
ANTIMUSCARINICS • Autacoids - substances that are secreted near their site

ail
Atropine Prototype of action
Anti-M1: decrease acid secretion SIGNALING MECHANISMS
Anti-M2: vagolytic effect
m
AUTOCRINE
Anti-M3: Alice in wonderland effect • Act on the same cell that produced it
• Blind as a bat (Mydriasis)
@g
PARACRINE
• Dry as a bone (anhidrosis)
• Act on nearby cells
• Hot as a hare (hyperthermia)
ENDOCRINE
• Red as a beet (Flushing)
os

• Mad as a hatter (Agitation) • Act on distant cell; pass via bloodstream

• Treatment: -stigmines TYPES OF AUTACOIDS
BRADYKININ
ll

Use in combination with

Diphenoxylate to decrease addiction • Reason for dry cough and angioedema
ba

Scopolamine From Hyoscyamus niger • Bradykinin is originally converted to inactive products but
For motion sickness due to ACE, ACE inhibits the bradykinin conversion to its
lle

Biperiden Anti-EPS inactive product which leads to an increase in bradykinin.

Benztropine For parkinson’s disease EICOSANOIDS
Trihexyphenidyl EFFECT EICOSANOID
e

Orphenadrine Norgesic ® Vasodilation PGE, PGI2

ab

Cyclopentolate Mydriatic for open angle glaucoma Anti-PLT Aggregation

Homatropine Vasoconstriction TXA2
Tropicamide
an

PLT Aggregation
Ipratropium Short-Acting Muscarinic Antagonist Bronchodilation PGE, PGI2
As reliever for bronchial asthma Bronchoconstriction LTC4, LTD4
aly

Aclidinium Long-Acting Muscarinic Antagonist Cytoprotection PGE

Umeclidinium Controllers for COPD Uterine Contraction PGE, PGF
Glycopyronium Decrease in IOP PGE, PGF-2a
Oxytropium
Tiotropium DRUGS: EICOSANOIDS
Pirenzepine Decrease acid secretion
Epoprostenol Use: primary pulmonary HTN
Telenzepine
(PGI2) (vasoconstriction of pulmonary
Hyoscine-N-butyl Antispasmodic vasculature)
bromide Cervical dilation
Alprostadil (PGE1) Use: erectile dysfunction
ANTINICOTINICS Keep patency of ductus arteriosus
• Anti-Nm prior to life
o MOA: blocks nicotinic receptors
Dinoprostone MOA: increase collagenase activity
ANTINICOTINICS (Anti-Nm)
(PGE2) → cervical ripening
Non-Depolarizing Depolarizing Uterine contraction
Competitive Noncompetitive Use: abortion (2nd term)
Reversible Irreversible Augmentation of labor
Gestational trophoblastic disease
(implantation of placenta only)
 B R I C K S N O T E S |6
Latanoprost, Use: mgt of glaucoma (promoting § Anticholinergic properties (HAM
Bimatoprost (PDF- drainage of aqueous humor) blockade – 1st gen antihistamines)
2a) WOF: eyelashes increase in length § A1 blocking effect = orthostatic
and thickness (cosmetic use) hypotension
Misoprostol Use: prophylaxis for NSAID-induced o Use: dystonia and extrapyramidal symptoms
(Cytotec) (PGE1) ulcer H1 ANTAGONIST
Abortion (1st term) at 1-4 weeks • General uses:
SEROTONIN o Hypersensitivity reactions
• Location: platelets, brain, intestines o Atopic conditions (allergic rhinitis – nasal
SEROTONIN RECEPTORS pruritus, sneezing, rhinorrhea, nasal
5-HT1A Partial agonist: Buspirone obstruction)
Use: anxiety (generalized anxiety o Atopic dermatitis (eczema – +chronic, +family
disorder) hx, + pruritus)
5-HT1B/1D Agonist: -triptans (Sumatriptan, 1ST GENERATION AKA CLASSICAL ANTIHISTAMINES
Zolmitriptan) ETHANOLAMINE ETHYLENE- PIPERAZINE
MOA: vasoconstriction DIAMINE
Use: migraines (acute attacks) Most sedating and Pyrilamine Cyclizine
WOF: exacerbation of HTN highest Tripelennamine Hydroxyzine
C/I: coronary artery disease anticholinergic (Iterax®) →

m
5-HT2A Agonist: ergot derivatives (ergotamine, effects prodrug of
ergonovine) Diphenhydramine Cetirizine

.co
Use: migraine attacks Dimenhydrinate Meclizine
Uterine muscle contraction Carbinoxamine (Bonamine®) –
(abortifacient); controlling post Doxylamine motion sickness

ail
partum hemorrhage Use: sedation, (30 mins–1 hr
5-HT3 Antagonist: -setron sleep aid, before travel)
hypersensitivity Buclizine –
Ondansetron, Granisetron,
m
Palomosetron, Alosetron reaction, appetite
extrapyramidal stimulant
@g
MOA: target thee vomiting center in the
area postrema (medulla oblongata) symptoms
Use: chemotherapy-assoc. n/v (torticollis – stiff
Post-operative n/v neck) –
os

Alosetron – IBS-D Diphenhydramine

5-HT4 Agonist: Tegaserod ALKYLAMINE PHENOTHIAZINE PIPERIDINE
ll

MOA: increase peristalsis OTC preparation Promethazine - Cyproheptadine

for common colds adjunct for - 5-HT
ba

Use: IBS-C
HISTAMINE Chlorpheniramine anesthesia, antagonist;
RECEPTORS LOCATION FUNCTION Brompheniramine prevent delayed used for
lle

hypersensitivity serotonin
H1 Blood Vessels Vasodilation
reaction syndrome
Endothelial Cells Contraction (Edema)
e

Itch and Pain Pruritus and Pain 2ND GENERATION ANTIHISTAMINES

ab

Receptors LESS SEDATING TRUE NON-SEDATING

Triple Response Cetirizine Loratadine
Lewis:
an

Levocetirizine Desloratadine
1. Flare Acrivastine Fexofenadine – withdrawn
2. Red Line Bilastine
aly

3. Wheal
H2 Parietal Cells Gastric HCl Secretion Very polar drugs = does
(stomach) (highest at night) not cross BBB
H3 Brain Lowers histamine H2 ANTAGONIST
Mesenteric Plexus release (modulation) • Use: acid-peptic disease
• HISTAMINE AGONIST • Drugs:
o Histamine o Cimetidine
§ Use: provocative challenge test § Side effects: gynecomastia, impotence,
§ Current: patch testing decreased libido
o Betahistine (Serc®) o Ranitidine, Nizatidine
§ MOA: H1 agonist and H3 antagonist o Famotidine – most potent
§ Use: Mgt of Vertigo (Rotatory NOTE:
Dizziness), Mgt of Meniere’s Disease, Gastroesophageal Reflux Peptic Ulcer Disease
Vertigo, Tinnitus, Hearing loss, Excess Disease (GERD)
fluid in ears Regurgitation of acid (HCl) Ulcerative lesion on the FIT
• HISTAMINE ANTAGONIST from the stomach to the exposed to acid-peptic
o Effects: esophagus (transforms juices
§ Sedative effects (histamine = esophageal cells) Causes: H. pylori and
wakefulness) Can lead to cancer NSAIDS
§ Anti-emetic and anti-nausea properties,
 B R I C K S N O T E S |7
RHEUMATOLOGY ASPIRIN/ACETYLSALICYLIC ACID
Five Hallmarks/Pillars of Inflammation • Pharmacokinetic profile
Rubor Redness o Absorption: stomach (partial), small intestines
Calor Heat o Metabolism: hydrolysis
Dolor Pain o Excretion
Tumor Edema/Swelling § 1st order: <600 mg/day
Functio Laesa Loss of function § Zero order: >600 mg/day
COMMON DISORDERS • Pharmacodynamic profile
RHEUMATOID ARTHRITIS (RA) o Antiplatelet: <325 mg/day
• Autoimmune disease o Analgesic: <600 mg/day
• Features: Symmetric polyarthritis; Most common: Young o Antipyretic: 0.3 to 1.2 g/day
women; Hand deformities; Morning stiffness for >30 o Anti-inflammatory: 3.2 to 4.0 g/day
mins • Side effects:
• Diagnosis: Rheumatoid Factor (DF) o GIT: Peptic Ulcer Disease
• Treatment: Immunosuppressant, DMARDs o Kidneys: NSAID-induced acute kidney injury
(Methotrexate as 1st line) (based on uric acid level)
OSTEOARTHRITIS (OA) § <2g/day: Hyperuricemia
• Wear and tear (Degenerative) § >2g/day: Uricosuric effect
o Lungs: Aspirin-Exacerbated Respiratory Disease
• NOT an inflammation

m
(AERD) – Samter’s Triad
• Causes/Risk factors:
§ Aspirin allergy, Bronchial asthma, Nasal
o Age-related (elderly), Recreational, Obesity

.co
polyps
• Features: Affect weight bearing joints (hip, knee);
§ Treatment: LT antagonists
Morning stiffness for <30 mins
(Montelukast)
• Treatment: Paracetamol (1st line), weight loss

ail
• Salicylate Toxicity
SYSTEMATIC LUPUS ERYTHEMATOSUS (SLE)
Dose Effects
• Autoimmune
50 mg/dL Salicylism (headache, tinnitus, vertigo)
m
• Features
80 mg/dL Hyperthermia, Metabolic acidosis
o Cutaneous: malar rash (acute), discoid rash
110 mg/dL Hypoprothrombinemia
@g
(chronic)
150 mg/dL Renal and Respiratory Failure
o Kidneys: Proteinuria, Hematuria
Pediatric Reye’s syndrome
o Hematologic: ↓WBC, ↓ Hemoglobin, ↓platelet
o Treatment: NaHCO3 (urinary alkalinifier),
os

o Neurologic: agitation, seizures

Supportive treatment (dialysis, intubation)
• Diagnosis: Anti-nuclear antibody (ANA), Anti-dsDNA
PYRAZOLONE DERIVATIVE
(measure disease activity)
ll

• Treatment: Steroids (Glucocorticoids), Steroid-sparing • Drugs: Sulfinpyrazone (uricosuric), Oxyphenbutazone,

ba

agent (Hydroxychloroquine) Phenylbutazone

ANKYLOSING SPONDYLITIS • Side effects: Acute kidney injury (AKI), aplastic anemia,
• Autoimmune agranulocytosis, albuminuria (anascara)
lle

• Affects males more than females INDOLE DERIVATIVES

• Feature: fusion of vertebra (bamboo-spine deformity) • Drugs: Indomethacin
e

• Treatment: Steroids, Analgesics • MOA: inhibits COX-2 > COX-1

• Indication/s: Analgesic for gouty arthritis, Closes Patent
ab

ANALGESICS
• To relieve pain Ductus Arteriosus (PDA)
• Analgesics: Para-aminophenol derivatives, NSAIDs, PYRROLE-ALKANOIC ACID DERIVATIVES
an

Glucocorticoids, DMARDs • Drug: Tolmentin

PARA-AMINOPHENOL DERIVATIVES • Contraindicated: Gout
• Drugs: Phenacetin, Paracetamol OXICAM DERIVATIVES
aly

• Phenacetin: withdrawn due to nephrotoxicity and cases • Drug: Piroxicam

of methemoglobinemia o Highest risk of Peptic Ulcer Disease (PUD)
• Paracetamol/Acetaminophen (APAP) PHENYLACETIC DERIVATIVES
o MOA: inhibits COX • Drugs and their Indications
o Indication/s: Analgesic, Antipyretic o Ketorolac: analgesic, opioid replacement after
o NO anti-inflammatory effect surgery
o Dosage o Diclofenac Na/K: analgesic for post-operation
§ Child: 10-15 mg/kg/dose inflammation after eye surgery
§ Adult: 500 mg q4h, 3 g/day o Sulindac: active sulfide, reduce risk of colonic
§ Toxic dose: 4g/day polyps
§ Lethal dose: 15 g/day
• Side effects:
NON-STEROIDAL ANTI-INFLAMMATORY DRUGS o Stevens-Johnson Syndrome (SJS): <10% BSA
• AKA: NSAIDS
o SJS-TEN: 10-30% BSA
• Weak Acids (EXCEPT Nabumetone)
o Toxic Epidermal Necrolysis (TEN): >30% BSA
• MOA: inhibit Cyclooxygenase (COX)
FENAMATES
o COX-1: housekeeping, constitutive enzyme
o COX-2: inducible enzyme (produced in the • Drug: Mefenamic Acid
presence of an inflammation) • Indication/s: analgesic, antipyretic
NON-SELECTIVE NSAIDS PROPIONIC ACID DERIVATIVES
• MOA: inhibit COX-1 and COX-2 • Drugs and their Indications
 B R I C K S N O T E S |8
o Ibuprofen: closes patent ductus arteriosus (PDA) • MOA: D2 Receptor Agonist
o Ketoprofen: dual MOA – inhibits COX and LOX • Indication/s: adjunct for Parkinson’s disease, emetic (SQ)
o Naproxen: only NSAID marketed as a single HYDROMORPHONE, OXYMORPHONE
enantiomer, for tumor fever • 8-10X more potent than morphine
COX-2 SELECTIVE NSAIDS • Indication/s: analgesic
• MOA: inhibits COX-2 HYDROCODONE, OXYCODONE
COX-2 SELECTIVE NSAIDS • 8-10x more potent than codeine
Preferentially Selective Highly Selective • 1.5-2x more potent than morphine
Meloxicam Celecoxib SYNTHETIC OPIOIDS
Etoricoxib METHADONE
Rofecoxib
• 5x more potent than morphine
• Meloxicam: less GI side effects and less risk of PUD
• Advantages over morphine: Inc BA (dec extensive FPE);
• Etoricoxib: analgesic for gout
Longer duration; No active metabolites; Less tolerance;
• Rofecoxib: WITHDRAWN as it induces stroke
No typical “high” effect
• Valdecoxib: WITHDRAWN as it induces MI
• Indication/s: Good analgesic (alternative to morphine),
NARCOTIC ANALGESICS
for neuropathic pain, treatment of addiction to opioids
• AKA: Opiates/Opioids
MEPERIDINE
• MOA: mimic the effects of endogenous opioid peptides
(enkephalin, endorphin, dynorphin) • NO cardiovascular or biliary effect
• Side effect: Seizures

m
• Effects
CENTRAL EFFECTS PERIPHERAL EFFECTS o To avoid: Normeperidine
LOPERAMIDE AND DIPHENOXYLATE

.co
Miosis Hypotension
Euphoria Anti-diuretic effect (urinary • Indication/s: for diarrhea
retention in post-op) • Loperamide: less to no dependence effect

ail
Respiratory Depression Bradycardia • Diphenoxylate: with addictive properties
EXCEPT: Meperidine o Administer with Atropine to avoid unwanted
Analgesia Dec Peristalsis (ileus) effects (Diphenoxylate + Atropine: Lomotil®)
m
Sedation Biliary spasm FENTANYL
EXCEPT: Meperidine • 100x more potent than morphine
@g

Inc duration of labor • Indication/s: for severe, debilitating pain

• Side Effects TRAMADOL
OPIOID TOXICITY TOLERANCE DEPENDENCE • Weak opioid
os

Comatose Miosis Diarrhea • Indication/s: for mild pain

Pinpoint pupils Convulsion Yawning Classification of Narcotic Analgesics According to
ll

Respiratory Constipation Agitation Receptor Affinity

ba

depression Full Partial Full Mixed

Treatment: Treatment: Treatment: Agonists Agonists Antagonist Agonist/
Naloxone Opioid rotation, Detoxification, Antagonist
lle

Ketamine Methadone, Morphine Codeine Naloxone Pentazocine

Buprenorphine, Heroin Derivatives Naltrexone Nalbuphine
Clonidine Fentanyl Levallorphan Butorphanol
e

AVOID: Naloxone Methadone

ab

SPECIFIC OPIOIDS Meperidine

• Mu receptors: euphoria, central analgesia Levorphanol
an

• Kappa receptors: dysphoria, peripheral analgesia GLUCOCORTICOIDS

• Delta receptors: antidepressant, peripheral analgesia • MOA: Inhibit Phospholipase A2 (PLA2)
OPIATES/NATURAL OPIOIDS • Pulse therapy: intermittent dosing (3-4 days)
aly

MORPHINE • Drugs:
• Standard of comparison ORAL IV Intraarticular
• Extensive first pass effect Prednisone Hydrocortisone Methylpred
• Metabolism: glucuronidation Methyl- Triamcinolone
o Morphine-3-glucuronide: seizures (Morphine prednisolone Betamethasone
and Meperidine) Dexamethasone
o Morphine-6-glucuronide: inc analgesic effect • Side effects
CODEINE o Cushing’s Syndrome: easily bruised, moon face,
• AKA: 3-methylmorphine alopecia, central obesity, buffalo hump
• 0.1x potency of morphine (analgesic) o Immunosuppression
• Indication: Antitussive o Addison’s disease: adrenal crisis
THEBAINE o Osteoporosis
DISEASE MODIFYING ANTI-RHEUMATIC DRUGS
• Not used commercially
• AKA: DMARDS, SLOW-ACTING ANTI-RHEUMATIC DRUGS
• Source of Naloxone from Papaver bactreatum
(SAARDS)
SEMI-SYNTHETIC OPIOIDS
METHOTREXATE
HEROIN
• MOA: Inhibits dihydrofolate reductase, thymidylate
• AKA: diacetylmorphine
synthase, and 5-aminoimidazole-4-carboxamide
• Drug of abuse
ribonucleotide (AICAR) or 5-formamidoimidazole
APOMORPHINE
transformylase
• Only opioid with NO opioid activity
 B R I C K S N O T E S |9
• Indication/s: o No renal adjustments, CAN BE GIVEN to patients
o 1st line for Rheumatoid Arthritis, Psoriasis, with CKD, Less hypersensitivity
Ectopic Pregnancy PEGLOTICASE
• Side effects: Hepatotoxicity • MOA: Uricase Analogue
ANTIMALARIALS o Converts uric acid à Allantoin
• Drugs: Chloroquine, Hydroxychloroquine • PEGylated recombinant uricase (parenteral)
• MOA: Increase intracytoplasmic pH, Decrease antigen • Indication/s: chronic gout refractory to standard therapy
presentation
• Side effects: Cinchonism COAGULATION
o Visual disturbance, Hearing loss (reversible), • Antiplatelets, Anticoagulants, Fibrinolytics, Hypolipidemic
Tinnitus, Confusion, Diarrhea drugs
GOLD COMPOUNDS ANTIPLATELETS
• Drugs: Auranofin, Aurothioglucose, Aurothiomalate • Interfere with platelet activation, platelet adhesion,
• Side effects: Hypersensitivity, Nephrotic syndrome platelet aggregation
(proteinuria, hypoalbuminuria, edema) FACTORS THAT CONTRIBUTE TO PLATELET AGGREGATION
SULFASALAZINE • Thromboxane: from Arachidonic Acid
• Prodrug: converted to • ADP: P2Y12 receptor activation causes platelet
o Sulfapyridine: for RA aggregation
o 5-aminosalicylate: for inflammatory bowel • Glycoprotein IIb/IIIa: receptors found on the platelet

m
disease (Chron’s disease, ulcerative colitis) surface which facilitates binding of fibrinogen which
• Side effects: SJS connects two platelets

.co
ANTI-TUMOR NECROSIS FACTOR-a (ANTI-TNF-a) • cAMP: from ATP acted upon by adenylyl cyclase to form
cAMP and degraded by PDE
• Drugs: Adalimumab, Infliximab, Etanercept
o DECREASE in cAMP will cause CLOTTING
• Side effects: Hepatotoxicity, Increased risk for infection

ail
o INCREASE in cAMP will NOT cause clotting
LEFLUNOMIDE
ANTIPLATELET DRUGS
• Prodrug
m
• Aspirin: irreversibly inhibits COX enzyme (no conversion
• MOA: Inhibits pyrimidine synthesis
of arachidonic acid to thromboxane)
• Indication/s: alternative for RA, psoriatic arthritis
@g

• Side effects: Increased risk for infection o Adverse effects: hypersensitivity reaction,
hepatic encephalopathy (Reye’s syndrome),
GOUTY ARTHRITIS severe bleeding, GIT irritation or peptic ulcer
disease
os

• Deposition of Monosodium Urate (MSU) crystals in the

joints causing inflammation and joint destruction • Abciximab, Tirofiban, Eptifibatide: inhibits Glycoprotein
• Hyperuricemia: >7 mmol/L uric acid level IIb/IIIa
ll

• Clopidogrel, Ticlopidine: ADP inhibitors

• Progression: Asymptomatic hyperuricemia à Acute Gout
ba

• Cilostazol, Dipyridamole: inhibit PDE to increase cAMP

à Intercritical Gout à Chronic Gout
ANTICOAGULANTS
• Triggers: beer, innards, thiazide and loop diuretics
• Interfere with the coagulation cascade
ACUTE GOUT
lle

• New diagnosis or recent attack in a patient

• Features: painful joints, podagra
e

• Treatment: Colchicine, NSAIDs (Ibuprofen,

ab

Indomethacin), Glucocorticoids (Prednisone (PO),

Methylprednisolone (IV))
CHRONIC GOUT
an

• AKA: Chronic Tophaceous gout

• Treatment: Colchicine, Hypouricemic Agents, Uricosuric
aly

Agents
DRUGS FOR GOUTY ARTHRITIS
COLCHICINE ANTICOAGULANTS
• DOC for ACUTE Gouty attack • Natural anticoagulants:
• MOA: anti-mitotic o Anti-thrombin: inhibits factor IIa and Xa
• Side effects: Watery diarrhea o Protein C and S: inhibits factor Va and VIIIa
o If bloody diarrhea: DISCONTINUE COLCHICINE • Warfarin: inhibits Vitamin K-dependent clotting factors
HYPOURICEMIC AGENTS (factor IX, X, VII, II)
• Heparin: indirect thrombin inhibitors as it amplifies anti-
• Drugs: Allopurinol, Febuxostat
thrombin III
• Allopurinol
• Dabigatran: direct thrombin inhibitor
o MOA: Inhibits Xanthine Oxidase
• Apixaban, Rivaroxaban: direct Xa inhibitors AKA novel
o Indication/s: 1st line for Chronic hyperuricemia,
oral anticoagulants (NOACs)
§ Chemotherapy-induced hyperuricemia
SUMMARY: ANTICOAGULANTS
§ Tumor lysis syndrome
o Contraindicated: Patients with CKD Direct Indirect Vitamin K Direct Xa
FEBUXOSTAT Thrombin Thrombin Epoxide Inhibitor
Inhibitors Inhibitors Reductase
• MOA: Inhibits Xanthine Oxidase Inhibitor
• More selective to Xanthine Oxidase than Allopurinol Dabigatran Heparin Warfarin Rivaroxaban
• Advantages vs Allopurinol Argatroban (Enoxaparin, Apixaban
Lepirudin UFH, LMWH)
 B R I C K S N O T E S | 10
Fondaparinux o Adverse effects: gallstone formation
FIBRINOLYTICS (Cholelithiasis), electrolyte imbalance, rashes
• Used to lyse the thrombi/clot to recanalize the occluded SUMMARY OF HYPOLIPIDEMIC DRUGS
blood vessel (mainly coronary artery) DRUG CLASS MECHANISM LIPID EFFECT
• Work by activating the fibrinolytic system Statins Inhibit HMG-CoA Decrease LDL,
• Breakdown of Fibrin Triglycerides
• The process of dissolution of clot is called fibrinolysis Niacin Decrease adipose Decrease LDL,
lipase activity triglycerides
Increase HDL
Fibric Acid Activate hepatic Decrease
PPAR-alpha triglycerides, LDL
Increase HDL
Bile Resins Prevent bile acid Decrease LDL
absorption
Ezetimibe Inhibit intestinal Decrease LDL
cholesterol
FIBRINOLYTICS absorption
• Drugs:
o Streptokinase CARDIOVASCULAR PHARMACOLOGY

m
o Urokinase HYPERTENSION
o Reteplase (analogue of alteplase) HYPERTENSIVE CRISIS HYPERTENSIVE EMERGENCY

.co
o Alteplase (t-PA) (-) end-organ damage (+) end-organ damage to
o Tenecteplase brain, heart, kidneys, eyes
• Mechanism of Action: act as tissue plasminogen MGT: reduce BP gradually

ail
activators Captopril (PO) Esmolol, CCBs (Nicardipine)
• Indication: acute myocardial infarction, acute stroke & admit to ICU
(thrombotic type) HTN IN PREGNANCY
m
HYPOLIPIDEMIC AGENTS
• MGT: MHLN
• Normal values
@g
• Methyldopa - 1st line
o Total cholesterol: <200
• Labetalol
o Triglyceride: <150
• Hydralazine
o LDL: <130
• Nifedipine
os

o HDL: >40
o (+) Pre-eclampsia: Methyldopa +
HYPOLIPIDEMIC DRUGS
Magnesium Sulfate
ll

• HMG-CoA Reductase Inhibitors (statins): inhibit rate- o (+) Eclampsia: Delivery

limiting enzyme in cholesterol synthesis (HMG-CoA
ba

HTN MANAGEMENT
reductase); inhibits synthesis of cholesterol
• General Management
o Drugs:
PRE-HTN STAGE 1 OR 2 HTN
lle

§ Lovastatin
No drugs yet, lifestyle Lifestyle modifications + 1 or
§ Simvastatin
modifications combi drugs (CAT):
§ Pravastatin
e

Adopt DASH diet CCBs

§ Atorvastatin
ab

Low salt intake ARBs / ACEi

§ Rosuvastatin
Low smoking/alcohol Thiazides
o Works at night; except for Atorvastatin and
intake
Rosuvastatin as both have long half-life
an

Aerobic exercise CAT is the first line for HTN.

o Adverse effects: rhabdomyolysis and
Weight loss
hepatotoxicity
DIURETICS
aly

• Bile acid sequestrants/Bile acid binding resins: bind to

bile acids à excreted through feces à decrease bile acid • MOA: increase urine production
pool à raw material: cholesterol TYPES WHERE IT WORKS
o Drugs Carbonic Proximal Convoluted Tubule
§ Cholestyramine Anhydrase MOA: inhibit carbonic anhydrase in
§ Colestipol Inhibitors the PCT
• Ezetimibe: inhibits absorption of cholesterol Osmotic Thin Descending Limb of the LOH
• Cholesteryl Ester Transport Protein (CETP) Inhibitor: Diuretics MOA: osmosis in the TDL of LOH
inhibit cholesterol transport Loop Diuretics Thick Ascending Limb of the LOH
o Drugs MOA: inhibit Na/K/2Cl cotransporter
§ Torcetrapib in the TAL of LOH
§ Anacetrapib Thiazide Distal Convoluted Tubule
• Niacin (Vitamin B3): inhibits lipoprotein lipase (no Diuretics MOA: inhibit Na/Cl cotransporter in
synthesis of free fatty acids: the DCT
o Adverse effects: flushing or cutaneous K-Sparing Collecting Duct
vasodilation Diuretics Aldosterone Antagonist MOA:
• Fenofibrates: act as ligand to PPAR-alpha; activate PPAR- competitively blocks mineralocorticoid
alpha in the liver to decrease cholesterol synthesis receptor
o Drugs ENaC Inhibitors MOA:
§ Clofibrate blocks epithelial Na channel
§ Gemfibrozil
 B R I C K S N O T E S | 11
EXAMPLES OF DIURETICS Hydralazine
Carbonic Anhydrase Acetazolamide Mixed Vasodilators Na Nitroprusside
Inhibitors Brinzolamide CALCIUM CHANNEL BLOCKERS
Dorzolamide ACCORDING TO STRUCTURE
Osmotic Diuretics Mannitol Dihydropyridines Amlodipine
Urea Felodipine
Loop Diuretics Sulfonamide-like: Nifedipine
• Furosemide Nicardipine
• Bumetanide Non-DHPs Verapamil
Sulfonylurea-like: Torsemide Diltiazem
Phenoxyacetic Acid Derivative: ACCORDING TO ONSET
Ethacrynic Acid Intrinsically Long-acting Amlodipine
Thiazide Diuretics Benzothiazines Intrinsically Short-acting All the rest
• Hydrochlorothiazide Modified Long-acting Plendil ER
• Chlorothiazide Adalat GITS
Thiazide-like Versant XR
• Chlorthalidone RAAS INHIBITORS
• Metolazone
RAAS INHIBITORS
• Indapamide
ACE Inhibitors

m
K-Sparing Diuretics Aldosterone Antagonist: Active:
• Spironolactone • Captopril
• Lisinopril

.co
• Eplerenone
ENaC Inhibitors: • Enalaprilat
• Amiloride Prodrug:
• Enalapril

ail
• Triamterene
SYMPATHOLYTICS Angiotensin II Receptor (-sartan)
Blockers
• AKA Sympathoplegics
m
Renin Inhibitor Aliskiren
CENTRALLY- ACTING
HEART FAILURE
@g
Alpha-2 Agonist Clonidine
FOUR PILLARS OF HF MANAGEMENT
Release Inhibitors Guanadrel
Guanethidine • Aldosterone Antagonist
Reuptake Inhibitors Reserpine o Spironolactone
os

o Eplerenone
PERIPHERALLY-ACTING
• ACEi /ARBs w/ Neprilysin Inhibitor
Ganglionic Blockers Hexamethonium
• B-Blockers
ll

Mecamylamine
o Carvedilol
ba

Trimethaphan
o Bisoprolol
Alpha-1 Blocker Non-selective:
• SGLT2 Inhibitors
• Prazosin
lle

o Canagliflozin
• Alfuzosin
o Dapagliflozin
• Doxazosin
DRUGS FOR HEART FAILURE
e

• Terazosin
Selective: (a1A & a1D → prostate) Cardiac Glycosides Digoxin
ab

• Tamsulosin B1 Agonist Dobutamine

Beta Blockers Non-selective: Bipyridines Milrinone
Cilostazol
an

• Nadolol
• Sotalol ARRHYTHMIA
• Timolol • Electrical problem (irregular rhythm)
aly

• Propranolol CLASSIFICATION OF DRUGS FOR ARRHYTHMIA

• Pindolol • Vaughan-Williams Classification
• Penbutolol o Class I - Na Channel Blocker
• Carteolol o Class II - Beta Blocker
Mixed: o Class III - K Channel Blocker
• Labetalol o Class IV - Ca Channel Blocker
• Carvedilol CLASS I - Na Channel Blockers
Selective: IA prolong action potential Disopyramide
• Betaxolol Quinidine
• Atenolol Procainamide
• Acebutolol IB shorten action potential Phenytoin
• Bisoprolol Mexiletine
• Esmolol Tocainide
• Celiprolol Lidocaine
• Metoprolol IC no effect on action Moricizine
• Nebivolol potential Flecainide
VASODILATORS Propafenone
VASODILATORS CLASS II – Beta Blockers Propranolol
Arterial Vasodilators Minoxidil Esmolol
Diazoxide Acebutolol
 B R I C K S N O T E S | 12
CLASS III – K Channel Blockers Amiodarone • tx of hormone excess states
Dronedarone (endometriosis, endometrial CA,
Sotalol breast CA, prostate CA)
Dofetilide • t/e: male - feminizing effects; female
CLASS IV – Ca Channel Blockers Verapamil - masculinizing effects
Diltiazem PITUITARY HORMONES
Others Adenosine Anterior Prolactin (PRL)
Magnesium Sulfate Pituitary Effects:
Hormones • breast development and lactation
ENDOCRINE PHARMACOLOGY • stops ovulation and stops
DEFINITION OF TERMS spermatogenesis
• Endocrine System - ductless system Conditions:
CENTRAL PERIPHERAL 1. Hyperprolactinemia: inc. PRL
Hypothalamus Thyroid Gland a. Prolactinomas
Pituitary Gland Adrenal Gland b. Drug-induced
Pancreas 2. Hypoprolactinemia: dec. PRL
Ovaries a. Inhibit lactation
Testes
Growth Hormone

m
ENDOCRINE HORMONES Effects:
FEEDBACKS • Liver: linear body growth, organ size,

.co
lean body mass
POSITIVE FEEDBACK NEGATIVE FEEDBACK
• Muscles: protein synthesis, muscle
Major feedback Rare Feedback
growth
Ex. Thyroid Gland To Support

ail
• Adipocytes: (+) lipolysis = weight loss
Ex. Ovulation during
• Other cells: inhibit glucose uptake
menstrual cycle
Conditions:
m
1. Deficiency of Growth Hormone
SUMMARY OF AXIS
Pre-puberty: pituitary dwarfism
@g
H: Corticotropin- H: Thyrotropin-releasing Post-puberty: inc. risk of CV
releasing hormone (CRH) hormone (TRH) deaths due to dec. organ size
APG: Corticotropin / APG: TSH / Thyrotropin Tx: Depends on defective gland
os

ACTH PEG: Thyroid G Hypothalamus: GHRH, GH

PEG: Adrenal Cortex PH: T3, T4 Pituitary Effect: Somatotropin,
PH: Cortisol Mecasermin
ll

H: Gonadotropin- H: Growth hormone-releasing 2. Excess Growth Hormone

ba

releasing hormone hormone (GHRH) Pre-puberty: Pituitary Gigantism

(GnRH) APG: Somatotropin Post-puberty: Acromegaly (+
APG: FSH PEG: Liver cardiomegaly)
lle

PEG: Ovaries PH: Somatomedin Tx: Somatostatin GHIH

PH: Estrogen analogues (octreotide,
e

H: Somatostatin / Growth lanreotide)

H: Gonadotropin- hormone inhibiting hormone
ab

Pegvisomant
releasing hormone (GHIH) Posterior Do not follow an axis
(GnRH) Inhibit release of GH, TSH Pituitary
an

APG: LH Hormones Oxytocin

PEG: Ovaries • stimulates milk let down
PH: Progesterone • uterine contraction
aly

Legend: Drugs:
H - Hypothalamus • Oxytocin nasal spray - stimulates
APG - Anterior Pituitary Gland milk let down
PEG - Posterior Endocrine Gland • Oxytocin IV - oxytocic agent for labor
PH - Peripheral Hormone induction
• Atosiban - oxytocin antagonist;
HYPOTHALAMUS tocolytics
Drugs Gonadorelin
(analogues) – Goserelin Vasopressin/ADH
relin Buserelin • V1 receptor: vasoconstriction = inc.
Triptorelin BP
Nafarelin • V2 receptor: water reabsorption
Histrelin Conditions:
Effects: Intermittent/Pulsatile 1. Deficiency of Vasopressin:
• positive feedback Diabetes Insipidus
• tx of hypothalamic hypogonadism Tx:
Central: Vasopressin (non-sel),
Continuous/Sustained Desmopressin (selective)
• negative feedback Nephrogenic: Thiazide Diuretics
2. Excessive Vasopressin: SIADH
 B R I C K S N O T E S | 13
Tx: Meprednisone
Non-sel: Conivaptan, • Uses:
Demeclocycline o Adrenal:
Lithium § Dx: Cushing Syndrome
V2-sel: Tolvaptan, Lixivaptan § Tx: Glucocorticoid Deficiency & Excess
THYROID AND ANTITHYROID AGENTS o Non-adrenal
BIOSYNTHESIS OF THYROID HORMONE RELEASE § Allergy
• Site: Thyroid-Follicular Cells § collagen-vascular disorder
• Raw Material: Iodide (I-) § eye disorders
STEPS § respiratory disorder
1. ACTIVE UPTAKE OF IODIDE § GI disorder
2. PEROXIDASE-CATALYZED REACTIONS § hematologic disorder
3. PROTEOLYSIS § infections
4. RELEASE TO SYSTEMIC CIRCULATION § systemic inflammation
5. PERIPHERAL CONVERSION o Fetus
§ stimulation of lung maturation in fetus
DRUGS
• T/e: GC excess (Cushing’s Syndrome)
• Tx for T3 & T4 Deficiency (Hypothyroidism) o moon face
o Thyronine (T4) o buffalo hump
§ Isomers:

m
o truncal obesity
§ Levo - prep of choice (Levothyroxine) o thinning of skin
§ Dextro - 4% of the activity of

.co
o easy bruising
Levothyroxine o osteoporosis
o Liothyronine (T3) - 3-4x more potent than o hypokalemia
Levothyroxine

ail
o hyperglycemia
• Tx for T3 & T4 Excess (Hyperthyroidism) o edema
o Thioamides o hypertension
m
§ Propylthiouracil - inhibits Peroxidase PANCREATIC HORMONES
§ Methimazole aka Thiamazole CRITERION INSULIN GLUCAGON
@g
§ Carbimazole - prodrug of Methimazole
ORIGIN B cell A cell
o Anion Inhibitor
STIMULUS FOR RELEASE fed fasted
§ Inhibit Na-I symporter
RESPONSE hypoglycemia hyperglycemia
§ Perchlorate, Pertechnetate, Thiocyanate
os

METABOLISM:
o Iodides + -
Glycogenesis
§ Wolf-Chaikoff effect
- +
ll

Glycogenolysis
§ SSKI - Saturated Soln of KI
Lipogenesis + -
ba

§ Lugol's Soln
Lipolysis - +
o Radioactive Iodine (RAI)
INCRETINS
§ I131 - preferred tx for hyperthyroidism but
lle

not for pregnant px • GI hormones that are enhanced in response to high CHO
o B-blockers load
o inc. secretion of insulin
e

§ Inhibits sympathetic symptoms

§ Inhibit peripheral conversion of T4 to T3 o slow down gastric emptying
ab

§ Propranolol, Carvedilol o anorexiant

o Dexamethasone • Ex. glucagon-like peptide, gastrin insulinotropic peptide
AMYLIN
an

§ Inhibit peripheral conversion of T4 to T3

ADRENOCORTICAL HORMONES • Slows down gastric emptying
ADRENAL GLAND • Anorexiant
aly

• Zona Glomerulosa: Mineralocorticoids DRUGS FOR DIABETES MELLITUS

• Zona Fasciculata: Glucocorticoids DIABETES MELLITUS
• Zona Reticularis: Androgen • Metabolic Disorder: Chronic hyperglycemia
MINERALOCORTICOIDS TYPE 1 DM TYPE 2 DM
• Major: Aldosterone Insulin-dependent Non-insulin dependent
• Conditions: B cell destruction = Insulin is normal, receptors are
o Excess: Hyperaldosteronism absolute lack of insulin resistant = relative lack of insulin
§ Tx: Spironolactone, Eplerenone Tx: Insulin, Pramlintide Tx: Antidiabetic Agents (PO)
o Deficiency: Hypoaldosteronism INSULIN
§ Tx: Fludrocortisone • Used for T1DM, T2DM
GLUCOCORTICOIDS • MOA: Check pancreatic hormones table
• Major: Cortisol • DOA: *all SC except regular insulin (IV)
• Drugs according to Duration of Action: ACCORDING TO DURATION OF ACTION
ACCORDING TO DURATION OF ACTION RAPID- SHORT- INTERMEDIATE- LONG-
SHORT-ACTING INTERMEDIATE- LONG-ACTING ACTING ACTING ACTING ACTING
ACTING Lispro Regular Isophane Glargine
Hydrocortisone Triamcinolone Betamethasone Aspart (IV) Insulin (NPH) (Peakless)
Cortisone Fluocinolone Dexamethasone Glulisine Detemir
Prednisone Paramethasone
Prednisolone
 B R I C K S N O T E S | 14
ORAL HYPOGLYCEMIC AGENTS CENTRAL NERVOUS SYSTEM
INSULIN SECRETAGOGUES ION DIFFUSION
Sulfonylureas First Gen: • Movement of ions from the extracellular compartment to
• Chlorpropamide the intracellular compartment and vice versa
• Tolbutamide • Dependent upon:
• Tolazamide o Concentration gradient: difference in
• Acetohexamide concentration
Second Gen: o Electrical gradient: difference in electric charge
• Sulfonylureas: • Modified by: ‘Gated ion channels’
Glibenclamide / Glyburide, ACTION POTENTIAL
Gliclazide, Glipizide,
Glimepiride
Biguanides Metformin
Phenformin - withdrawn due to
lactic acidosis
Thiazolidinediones -glitazone
(Insulin Sensitizers) Pioglitazone
Rosiglitazone - withdrawn
(cardiotoxic)

m
a-glucosidase Acarbose
Inhibitors Voglibose

.co
• -70: Resting membrane potential (negatively charged)
Miglitol
• Na+ influx à reaches threshold potential à firing of
Incretin-based Drugs Incretin-mimetics (SQ):
neuron (All or None Principle) à Depolarization
• Exenatide

ail
• K+ efflux à charge will go back to the negative charge à
• Liraglutide,
Repolarization
• Lixisenatide
• Cl- influx à more negative à Hyperpolarization à
DPP-4 Inhibitors (PO):
m
Frequency of action potential will decrease
• Sitagliptin
• Clinical Correlation: It is the rate of action potential
• Vildagliptin
@g

propagation that determines neurologic function

• Linagliptin
(determined by frequency of action potentials)
• Saxagliptin
SEIZURE
• Teneligliptin
os

• Abnormal firing of neurons

SGLT2 Inhibitors Dapagliflozin
• What would be the effect on the membrane of increasing
Empagliflozin
Cl- influx during a seizure? Hyperpolarization to decrease
ll

Luseogliflozin
seizure activity
Canagliflozin
ba

SEIZURE CLASSIFICATIONS
Amylin Analogue Pramlintide (SQ)
• Generalized Onset (there is always impairment of
GONADAL HORMONES
lle

awareness)
PROGESTERONE AND ESTROGEN DRUGS o Motor (Tonic-clonic; other): AKA Grand-mal
• Mifepristone seizure
e

o progesterone antagonist o Non motor: Absence seizure (blank stare): AKA

ab

o contraceptive Petit Mal seizure

o abortifacient • Focal Onset AKA Partial Seizure
• Anastrozole, Letrozole o Simple: patient is conscious or aware
an

o aromatase inhibitors o Complex: patient is NOT aware

• SERMs (Selective Estrogen Receptor Modulators) ANTI-SEIZURE MEDICATIONS
aly

o partial agonist at estrogen receptors • AKA: anticonvulsants or anti-epileptic drugs

o alone: agonist • All have same approach: decrease propagation of action
o w/ full agonist: antagonists potentials
o ex. Tamoxifen - tx for estrogen (+) breast CA o Decrease Na+, Ca++ influx: delay
o Raloxifene - tx for osteoporosis depolarization/prolong repolarization
ANDROGEN DRUGS o Increase Cl- influx: hyperpolarize membrane
Androgens: ANTI-SEIZURE DRUGS
• Testosterone For Tonic-Clonic or Partial For Absence Seizures
• Androstenedione Seizures
• 5-Dihydrotestosterone - 10x more active than Carbamazepine Clonazepam
testosterone Lamotrigine Ethosuximide (Drug of
Drugs: Phenytoin Choice)
• 5-a reductase inhibitor Valproic Acid Valproic Acid
o ex. Finasteride, Dutasteride For Myoclonic Seizures Back-up and Adjunctive
o no stronger hormone Drugs
o MGT of BPH Clonazepam Felbamate
• Androgen Antagonist Lamotrigine Gabapentin
o Bicalutamide, Flutamide - tx of prostate CA Valproic Acid Lamotrigine
o Cyproterone Acetate - tx of excessive sexual drive Levetiracetam (Drug of
in men Choice for all seizures)
Phenobarbital
 B R I C K S N O T E S | 15
Tiagabine Trifluoperazine Ziprasidone
Topiramate Others
Vigabatrin Side effects: Side effects:
Zonisamide Worsening of negative Weight gain
Mechanism of Action: symptoms Hyperlipidemia
• Carbamazepine and Phenytoin: Na-channel blockers Extrapyramidal symptoms Hyperglycemia
• Lamotrigine: Ca and Na channel blocker Hyperprolactinemia
• Valproic Acid: Block Na channel; Enhance K channel ANTIDEPRESSANTS
• Ethosuximide: Blocks Ca at the thalamus MAO INHIBITORS AMINE ALPHA 2
• Levetiracetam: Selectively bind to SV2A to decrease REUPTAKE BLOCKERS
epileptiform bursts BLOCKERS
• Gabapentin and Pregabalin: Block Ca MAO-A NONSELECTIVE
BENZODIAZEPINES AND BARBITURATES SELECTIVE TRICYCLICS
• Enhance Cl- influx by acting on GABA-mediated Cl- Moclobemide Amipramine
channel à hyperpolarization Imipramine
• Anticonvulsants AKA Sedative-Hypnotics MAO-A degrades Clomipramine
• Mechanism of Action: NE, 5-HT, HETEROCYCLICS
o Benzodiazepine: increase FREQUENCY of Dopamine Bupropion
opening Mirtazapine

m
o Barbiturates: increase DURATION of opening NON-SELECTIVE 5-HT SELECTIVE
BENZODIAZEPINES BARBITURATES Phenelzine SEROTONIN-

.co
Diazepam (Valium®) Ultra-Short Acting Isocarboxazid NOREPINEPHRINE
Midazolam (Versed®) Thiopental (Pentothal®) Tranylcypromine REUPTAKE
Alprazolam (Xanax®) Indication: Anesthesia INHIBITOR (SNRI)

ail
Lorazepam (Ativan®) MAO-B Duloxetine
Triazolam (Halcion®) SELECTIVE Venlafaxine
“Non-benzo benzo” Short Acting Selegiline Desvenlafaxine
m
Zolpidem (Ambien®): Amobarbital SELECTIVE
hypnotic only Pentobarbital MAO-B degrades SEROTONINE
@g

Buspirone (BusPar®): Secobarbital (Seconal®) Dopamine only REUPTAKE

anxiolytic only Indication: Insomnia INHIBITOR (SSRI)
Long Acting Sertraline
os

Phenobarbital (Luminal®) Fluoxetine

Indication: Seizures Fluvoxamine
ll

• Diazepam: Drug of choice for Status Epilepticus Escitalopram

• Side effect: Sedation Note:
ba

MOOD AND PSYCHOTIC DISORDERS • SNRI cause more complicated side effects (orthostatic
Mood Disorder Psychotic Disorder hypotension, arrhythmia, sedation)
lle

Anxiety Disorder Schizophrenia • SSRI more tolerant; drug of choice for depression (side
Major Depression effects: insomnia, weight gain)
DOPAMINERGIC PATHWAYS OF THE BRAIN BIPOLAR DRUGS
e

• Mesolimbic Dopamine Pathway: pleasure and reward CLASSIC DRUG NEWER AGENTS
ab

• Mesocortical Dopamine Pathway: emotions, behavior, Lithium (Drug of Choice) Carbamazepine

memory, and decision making MOA: Inhibits NE release, Clonazepam
an

• Nigrostriatal Dopamine Pathway: movement increases NE metabolism, Olanzapine

• Tuberoinfundibular Dopamine Pathway: endocrine increases NE reuptake Valproic Acid
pathway (dopamine as prolactin inhibitory hormone) Others
aly

SCHIZOPHRENIA PARKINSON’S DISEASE

POSITIVE SYMPTOMS NEGATIVE SYMPTOMS • Loss of dopaminergic neurons in the substantia nigra
Hallucination Anorexia (lack of dopamine nigrostriatal pathway)
Illusion Depression • Signs and symptoms: Tremor, bradykinesia, rigid
Delusion Loss of ability to work muscles, impaired posture and balance, loss of automatic
Loss of drive movements, speech changes, writing changes.
Excessive dopamine in the Lack of dopamine in the • Goal: Increase dopamine
mesolimbic pathway mesocortical pathway DRUGS FOR PARKINSON’S DISEASE
ANTIPSYCHOTICS • Carbidopa/Levodopa
• AKA: anticonvulsants or anti-epileptic drugs o Carbidopa: inhibits DOPA decarboxylase in the
• All have same approach: decrease propagation of action periphery
potentials • Entacapone, Tolcapone: inhibit COMT
TYPICAL ANTIPSYCHOTICS ATYPICAL ANTIPSYCHOTICS • Bromocriptine, Pergolide, Pramipexole, Ropinirole:
Dopamine agonist
Classic Drugs Newer Agents
• Selegiline, Rasagiline: MAO-B inhibitor
Blocks D2 receptors Block both D2 and 5-HT2A
• Amantadine (Symmetrel®): increase release of
receptors
dopamine from unaffected neurons (anti-viral agent for
Chlorpromazine Clozapine
Parkinson’s)
Fluphenazine Olanzapine
• Benztropine (Cogentin®): Centrally acting anticholinergic
Haloperidol (most potent) Quetiapine
Thioridazine Risperidone
 B R I C K S N O T E S | 16
ANESTHESIA Bromhexine Carbocisteine
STAGES OF ANESTHESIA DRY COUGH
STAGE DESCRIPTION • Without mucus
1 - ANALGESIA • Patient still awake • Goal: cough suppression
• Causes amnesia • Treatment: Antitussives
2 - EXCITATION AND • Hyperactivity Drugs for Dry Cough
DELIRIUM • Irregular vital signs Centrally Acting Peripherally Acting
3 - SURGICAL • Back to regular vital signs Activate mu receptors in Block peripheral cough
ANESTHESIA • Target stage in operation the brain receptors
4 - RESPIRATORY • Possible flat lining (coma Codeine Butamirate citrate
DEPRESSION and death) Noscapine Levodropropizine
GENERAL ANESTHETICS Dextromethorphan
• SITE OF ACTION: CNS BRONCHOSPASTIC DISORDERS
• CONCENTRATION: Measured using partial pressure • Bronchospastic disorders: Bronchial asthma, chronic
• POTENCY: measured through Minimum Alveolar obstructive pulmonary disease (COPD)
Concentration • Involves: Bronchial tone
• Potency and MAC: Inversely proportional o Induces constriction: Acetylcholine, Adenosine
• ONSET OF ACTION: Depends on Blood Gas Coefficient o Induces dilation: cAMP
and Respiratory Rate DEFINITION OF TERMS

m
↓MAC = ↑ Potency
• Reliever: treat acute exacerbations of bronchial asthma
↓BGC = Faster onset
and COPD

.co
↑Respiratory rate = Faster onset
• Controller: prevent exacerbations
INHALATIONAL INTRAVENOUS
DRUGS FOR BRONCHOSPASTIC DISORDERS
• Nitrous oxide • USA Barbiturates
• Goal: ↑ cAMP, ↓ Acetylcholine and Adenosine

ail
• Desflurane • SA Benzodiazepines
• Bronchodilators: B2 Agonists, Antimuscarinics,
• Sevoflurane • Neuromuscular Blockers
Methylxanthines
• Isoflurane • Opioid Analgesics
m
Beta-2 Agonists
• Enflurane • Combined Therapies
• Halothane • Propofol MOA: increase cAMP (bronchodilation)
@g

• Methoxyflurane • Ketamine Short-Acting B2 Agonists Long-Acting B2 Agonists

• Etomidate (SABA) (LABA)
LOCAL ANESTHETICS Relievers for Asthma Controllers for COPD (w/
os

ESTER AMIDE inhaled glucocorticoids)

Salbutamol/Albuterol Salmeterol
Degraded by plasma Degraded by amidases
Terbutaline (SQ) Formoterol
ll

esterases
Metaproterenol Bambuterol
ba

Short DOA Long DOA

Pirbuterol Indacaterol
Procaine Lidocaine
Toxic Effects: Tremors, Hypokalemia, Ventricular
Tetracaine Mepivacaine
Tachycardia (overdose)
lle

Cocaine Bupivacaine
Benzocaine Prilocaine
Antimuscarinics
Articaine
e

MOA: inhibit Acetylcholine

ab

RESPIRATORY DRUGS Short-Acting Muscarinic Long-Acting Muscarinic

• Colds, Cough, Bronchospastic disorders Antagonist (SAMA) Antagonist (LAMA)
COLDS Relievers for COPD Controllers
an

• AKA: “acute coryza” Ipratropium Tiotropium

COMMON COLDS Oxytropium
aly

Toxic Effects: Dry mouth, Urine retention

• Cause: viral (corona-, adeno-, rhino-)
• Self-limiting (not more than 7 days)
Methylxanthines
• Treat only if symptomatic
o Headache: Aspirin, Paracetamol MOA: inhibit adenosine and PDE-4
o Nasal congestion: Alpha-1 agonists • Theophylline (NTI)
(Phenylephrine, Oxymetazoline, • Aminophylline (ethylenediamine salt of
Phenylpropanolamine) theophylline; 80% theophylline)
ALLERGIC COLDS Toxic Effects: Insomnia, Arrhythmia, Hypotension
• Cause: allergy • Mast Cell Stabilizers
• Treatment: H1 antagonist (Antihistamines) o Drugs: Cromolyn Na, Nedocromil
COUGH o MOA: Inhibit degranulation of histamine and
PRODUCTIVE COUGH promote K+ and Cl- opening
• Anti-inflammatory Agents: Leukotriene modifiers,
• With mucus Glucocorticoids
• Goal: Decrease viscosity of mucus Leukotriene Modifiers
• Treatment:
LOX Inhibitor LT Receptor Inhibitors
Drugs for Productive Cough
Zileuton Montelukast
Mucoregulators Mucolytic Expectorant
Zafirlukast
Increases water Breaks down Stimulates
Use: Treatment of NSAID-induced bronchial asthma
portion of mucus sulfide bonds bronchial glands
Ambroxol N-acetylcysteine Guaifenesin
 B R I C K S N O T E S | 17
Glucocorticoids Bismuth salts
Inhaled Oral IV M1 Blockers Pirenzepine
Budesonide Prednisone Hydrocortisone Telenzepine
Fluticasone (+ Dexamethasone Methyl- Triple Therapy Omeprazole,
Salmeterol) Methyl- prednisolone Metronidazole, Amoxicillin
Toxic Effects: prednisolone (IV) or Clarithromycin
Oral Thrush (PO) Quadruple Therapy Tetracycline, Omeprazole,
Remedy: Metronidazole, Bismuth
Gargle after GASTROPARESIS AND DYSPEPSIA
each use • Paralysis of the muscles of the stomach and possibly
other parts of the gastrointestinal tract due to damage to
GASTROINTESTINAL SYSTEM gastrointestinal nerves or muscle
DEFINITION OF TERMS DRUGS FOR GASTROPARESIS AND DYSPEPSIA
• Acid-peptic disease - A group of disorders involving Prokinetics / Cholinergic Pilocarpine
erosion or ulceration of the mucosal lining of the agonists Bethanechol
gastrointestinal tract Neostigmine
• Antiemetic- A drug that reduces nausea and vomiting
• Gastroesophageal Reflux Disease (GERD)- Esophageal ADR: DUMBBELLS
irritation or inflammation due to reflux of stomach acid Dopamine Antagonists Metoclopramide

m
• Gastroparesis- Paralysis of the muscles of the stomach Domperidone
and possibly other parts of the gastrointestinal tract due CONSTIPATION

.co
to damage to gastrointestinal nerves or muscles • Passing of stools for less than 3 times a week due to the
• Prokinetic - drug that promotes gastrointestinal motility lack of fiber, fluids, or exercise.
• Proton Pump - the parietal cell that uses energy to TYPES OF LAXATIVE

ail
secrete protons into the stomach Bulk-forming Psyllium
GERD Methylcellulose
• AKA: Heartburn Polycarbophil
m
SYMPTOMS Stool softener / Emollient Docusate sodium
Glycerin
@g
1. Burning or paining in the chest
2. Acid Taste Mineral oil
3. Abdominal Pain Osmotic MgO, Sorbitol, Lactulose,
CONTRIBUTING FACTORS Magnesium citrate, Sodium
os

1. Pregnancy Phosphate, PEG

2. Overeating Stimulant/ irritant Anthraquinone Glycosides,
ll

3. Eating on the run Castor oil, Bisacodyl,

Phenolphthalein
ba

4. Eating late at night

5. Drinking alcohol Saline Fleet enema, Na
6. Cigarette smoking biphosphate
lle

7. High fat content foods, Spicy foods, Citrus DIARRHEA

Hyperacidity and Peptic Ulcer Disease • Stools are loose and watery which can be caused by
poisoning, microorganisms, food intolerance
e

CONTRIBUTING FACTORS
medications, and more.
ab

1. H. pylori → proven cause

DRUGS FOR DIARRHEA
2. NSAIDs → proven cause
3. Acidic Agents DOC Oral Rehydration Salts
an

4. Pepsin Probiotics Erceflora , Colostrum

5. Smoking Anticholinergics Atropine
FACTORS DECREASING Opioids Loperamide,
aly

1. Mucus production Diphenoxylate

2. Buffers ANTIEMETICS
3. Perfusion • Control vomiting
4. Prostaglandins ANTIEMETIC DRUGS
DRUGS FOR PUD Cholinergic agonists Neostigmine, Bethanechol
Antacids Sodium bicarbonate D2 antagonists Metoclopramide, Domperidone
Calcium carbonate H1 Antagonists Diphenhydramine,
Aluminum hydroxide Phenothiazine, Orphenadrine
Magnesium hydroxide Anticholinergics Scopolamine
H2 Receptor Antagonists Cimetidine 5-HT3 antagonists -setrons
Famotidine IBS AND IBD
Ranitidine
Nizatidine
Proton Pump Inhibitors Omeprazole
Esomeprazole
Lansoprazole
Dexlansoprazole
Pantoprazole
Mucosal Protectants Misoprostol
Sucralfate
 B R I C K S N O T E S | 18
IBS Treatment • Primary Chemotherapy - administered as the main
1. Avoid certain foods that could trigger your treatment for advanced cancer with no alternative
symptoms treatment
2. Eat high-fiber foods • Neoadjuvant Chemotherapy - administered for localized
3. Drink plenty of fluids disease when surgery or radiation are inadequate
4. Get enough sleep • Adjuvant Chemotherapy - administered as adjunct to
→ Fiber Supplements (Psyllium) local methods of treatment including surgery and
→ Anticholinergics (Dicyclomine, Hyoscyamines) radiation therapy
→ 5-HT3 Blockers for diarrhea (-setrons) CELL CYCLE
→ 5-HT4 Agonists for constipation (Cisapride, Tegeserod, G0
Prucalopride) • Resting period
IBD Treatment Interphase
• G1 - cell increases in size and produce enzymes needed
for DNA synthesis
• S - DNA synthesis
• G2 - cell grows more and produce new proteins & RNA
Mitosis
• Cell divides and forms two new cells
• Consists of Prophase, Metaphase, Anaphase, and

m
Telophase
Cell Cycle and Chemotherapy

.co
• Cell Cycle-Specific Agents (CCS) selectively targets
ONCOLOGY tumor cells when they are in the cell cycle only
Oncology • Cell Cycle-Nonspecific Agents (CCNS) targets tumor

ail
A sub-specialty of medicine dedicated to the investigation, cells when they are in the cell cycle and when they are in
diagnosis, and treatment of people with cancer the resting phase
m
DEFINITION OF RELATED TERMS DIRECT DNA-INTERACTING AGENTS
Cancer Alkylators
@g

A disease characterized by a defect in the normal control Transfers their alkyl groups to various cellular components,
mechanisms that govern cell survival, proliferation, and eventually leading to miscoding, and inhibition of DNA
differentiation synthesis and function.
os

Neoplasm Nitrosureas Cyclophosphamide, Ifosfamide

Aka Tumor. An abnormal mass of tissues formed by cells that Platinum Analogs Cisplatin, Carboplatin, Oxaliplatin
Others Mechlorethamine, Carmustine,
ll

behave abnormally. It can either be:

• Benign - Tumors that grow large but do not spread, or Lamustine, Procarbazine,
ba

invade, nearby tissues or other parts of the body Dacarbazine, Temozolomide,

• Malignant - Tumors that can spread into, or invade, Busulfan
lle

nearby tissues. They can also spread to other parts of the Antitumor Antibiotics
body through blood and lymph systems Binds to DNA through intercalation between specific bases
Metastasis and block the synthesis of RNA, DNA, or both; cause DNA
e

The ability to undergo repeated cycles of proliferation and strand scission; and interfere with cell replication.
ab

migrate to distant sites in the body Anthracyclines From Streptomyces peucetius

GENERAL PRINCIPLES OF CANCER
Characteristics Daunorubicin, Doxorubicin,
an

• Uncontrolled proliferation Idarubicin, Mitoxanthrone

• Loss of function Mitomycin From Streptomyces caespitosus
aly

• Invasiveness Bleomycin From Streptomyces verticillus

• Ability to metastasize Topoisomerase Inhibitors
Causes Inhibits the enzymes responsible for preventing DNA from
• Exposures (e.g., environmental exposure, chemical getting tangled and for relieving pressure in supercoiled DNA
carcinogens) during replication.
• Viruses (e.g., HPV 16 & 18 - Cervical cancer) Topoisomerase I Inhibitors Topoisomerase II Inhibitors
• Genetics Breaks only one strand of Breaks both strands of DNA
o Inactivation of tumor suppressor genes DNA
General Chemotherapy Classification From Camptotheca From Podophyllum
acuminata peltatum
• Conventional agents - target DNA structure or cell cycle
“Camptothecins” “Podophyllotoxins”
• Targeted agents - target specific factors important in
Topotecan, Irinotecan Etoposide
maintaining a malignant state
• Hormonal Therapies - therapy based on effect of INDIRECT DNA-INTERACTING AGENTS
biochemical pathways Antimetabolites
• Biologic Therapies - use of macromolecules with the Interferes with enzymes or their reaction by mimicking the
capacity to regulate host immune response molecules necessary for DNA synthesis. They can be
Cancer Treatment Combinations structural analogues, or folate cofactors.
Treatments are usually composed of combined Antifolates Methotrexate, Permetexed,
chemotherapy for better efficiency and to avoid drug Pralatrexate
resistance Fluoropyrimidines 5-Fluorouracil, Capecitabine
 B R I C K S N O T E S | 19
Deoxycytidine Cytarabine, Gemcitabine • Concentration-dependent type of killing
Analogs o Quinolones
Purine Antagonists 6-Mercaptopurine, 6-Thioguanine, o Aminoglycosides
Fludarabine, Cladribine o Azithromycin – only macrolide that follows
Antimitotic concentration-dependent type of killing
Inhibits synthesis of or function of microtubules/tubulin, o Metronidazole
causing arrest of cells in the M phase. o Polymyxins
Taxanes Paclitaxel, Docetaxel, Cabazitaxel o Daptomycin
Vinca Alkaloids Vinblastine, Vincristine, Vinorelbine o Note: the higher the Cmax the better is the
MOLECULARLY TARGETED AGENTS killing property; given LESS frequently
Targets • Time-dependent type of killing: more common
o All other antibacterial agents (majority)
• Biochemical pathways
o Note: the longer the time the blood contains the
• Signals
antibiotic, the better is the killing property;
• Regulation
given MORE frequently
Tyrosine-Kinase Imatinib, Dasatinib, Nilotinib
SUMMARY: MECHANISM OF ACTION
Inhibitors
Growth Factor Cetuximab, Panitumumab, • Inhibition of cell wall synthesis
Receptor Inhibitors Trastuzumab • Injury to plasma membrane
Vascular Bevacizumab • Inhibition of protein synthesis

m
Endothelial Growth • Inhibition of synthesis of essential metabolites
Factor Inhibitors • Inhibition of nucleic acid replication and transcription

.co
CELL WALL INHIBITORS
TOXICITIES
• NOTE: NOT all cell wall synthesis inhibitors are beta-
Chemoman
lactam antibiotics
Represents the toxicities of common anti-CA drugs

ail
BETA-LACTAM ANTIBIOTICS
• Cisplatin and Carboplatin – ototoxicity and
nephrotoxicity
m
• Vincristine – peripheral neuropathy
• Bleomycin and Busulfan – Pulmonary fibrosis
@g
• Trastuzumab and Doxorubicin – cardiotoxicity
• Cyclophosphamide – hemorrhagic cystitis
• Methotrexate, 5-Fluorouracil, 6-Mercaptopurine –
os

myelosuppression
ll
ba

• MOA: Binds with one or more PCPs causing selective

inhibition of transpeptidase, carboxypeptidase, and
endopeptidase reactions
lle

o Activate endogenous autolytic enzymes in the

cell wall
• Penicillin
e

o 1929: Alexander Fleming (Penicillium notatum)

ab

Rescue Drugs o Structure: Beta-lactam attached to thiazolidine

ring
Drugs administered as chemo protectants
o Nucleus: 6-aminopenicillanic acid (6-APA)
an

Anti-Cancer Drug Chemoprotectant

PENICILLINS
Anthracyclines Dexrazoxane
Natural Beta- Penicillin G (Benzyl Penicillin) – given
Cisplatin Amifostine
aly

Lactam Antibiotics parenterally

Ifosfamide, Cyclophosphamide MESNA
• Crystalline/Aqueous Pen G – IV
Methotrexate Leucovorin
• Benzathine Pen G/Procaine Pen
G – IM (depot effect)
ANTIBACTERIALS
Penicillin V (Phenoxy methyl
ANTI-BACTERIAL AGENTS
Penicillin) – given orally; acid-stable
• Substance produced by microorganism which has the
capacity to inhibit growth and cause the destruction of Coverage: Gram (+) organisms; NO
other microorganisms coverage for gram (-) EXCEPT N.
• -static: inhibit growth meningitidis, T. pallidum, Leptospira
• -cidal: kill or cause the destruction spp; Anaerobes EXCEPT Bacteroides
GENERAL PRINCIPLES fragilis
Penicillinase- Methicillin – withdrawn due to
resistant Penicillin interstitial nephritis and due to
AKA resistance (MRSA)
Antistaphylococcal • DOC for Community-Acquired
Penicillin MRSA: Clindamycin
• DOC for Hospital-Acquired
MRSA: Vancomycin
 B R I C K S N O T E S | 20
Nafcillin – safe to patients with renal
problems; (S/E: agranulocytosis) Coverage: 3rd gen + Pseudomonas
Isoxazolyl Penicillin – best absorbed th
5 Generation Ceftaroline, Ceftobiprole (ROL)
Cloxacillin
Oxacillin Coverage: 4th gen + MRSA
Dicloxacillin • Carbapenems
Aminopenicillin Ampicillin – given IV o Differ with penicillin in that the sulfur atom has
AKA Broad Amoxicillin – given PO been replaced by a carbon atom
spectrum Penicillin o Ertapenem, Meropenem, Imipenem,
Coverage: Gram (+) organism; Doripenem
limited Gram (-); Anaerobes EXCEPT § Imipenem + Cilastatin
B. fragilis § Doripenem: most effective for
Anti-pseudomonal Carboxypenicillins P.aeruginosa
Penicillin Carbenicillin o Coverage: Gram (+) organism, Gram (-),
Ticarcillin Anaerobes, and Pseudomonas aeruginosa
Ureidopenicillin (EXCEPT Ertapenem)
Piperacillin – most potent o DOC for ESBL infections
Azlocillin o ADR: Most epileptogenic class of beta-lactam
Mezlocillin antibiotics (trigger seizure attacks) – Imipenem

m
Beta-lactamase Do NOT have significant antibacterial (most epileptogenic)
Inhibitors activity, instead they bind to and • Monobactam

.co
inactivate beta-lactamases o Aztreonam
Clavulanic Acid, Sulbactam, o Only available in IV form; widely distributed
Tazobactam o Excreted in urine

ail
• Augmentin: Amoxicillin + o Coverage: Gram (-), Pseudomonas aeruginosa
Clavulanic Acid o ADR: Transaminitis (elevation of SGPT and
• Timentin: Ticarcillin + Clavulanic SGOT)
m
Acid POLYPEPTIDES
• Unasyn: Ampicillin + Sulbactam • MOA: inhibits cell wall synthesis by binding to the D-Ala-
@g

• Piptaz/Tazocin/Zosyn: D-Ala terminus

Piperacillin + Tazobactam o Inhibits transglycosylase (prevents elongation
Exhibit Potentiation (1+0=2) and cross-linking)
os

• Vancomycin
Coverage: Gram (+) organisms, o DOC for MRSA (IV), pseudomembranous colitis
Limited Gram (-); Anaerobes
ll

(PO)
INCLUDING B. fragilis o ADR: flushing (Red Man/Red Neck syndrome),
ba

o ADRs: Cross hypersensitivity (alternative: Nephrotoxicity

Macrolides); Maculopapular rash, Gi § Treatment: Antihistamines,
lle

disturbances; Bleeding (Ticarcillin); Diphenhydramine

Pseudomembranous colitis (Ampicillin) PLASMA MEMBRANE INHIBITORS
• Cephalosporins POLYMYXINS
e

o Structure: Beta-lactam attached to • Polymyxin B (topical) and Polymyxin E or Colistin

ab

dihydrothiazine ring (parenteral)

o Nucleus: 7-aminocephalosporanic acid (7-ACA) • Act as cationic detergents
o Cross-sensitivity with penicillin • Last line for Multidrug-resistant organisms – NEVER DOC
an

o Classified into 5 generations • NOT recommended as monotherapy

CEPHALOSPORINS PROTEIN SYNTHESIS INHIBITORS
aly

1st Generation CEPH including Cefalexin, Cefadroxil, • Target bacterial translation process
Cefazolin • 30S – Aminoglycosides, Tetracyclines
• 50S – Macrolides, Chloramphenicol, Clindamycin
Coverage: PEcK (Proteus, E.coli, (Lincosamides)
Klebsiella) • All protein synthesis inhibitors are BACTERIOSTATIC
2nd Generation CEF + vowel including PRO EXCEPT AMINOGLYCOSIDES as they are BACTERICIDAL
(CefPROzil) and META 30S INHIBITORS
(CefMETAzole) and Loracarbef • Aminoglycosides
o Neomycin, Tobramycin, Gentamicin,
Coverage: HENPEcK (H. influenzae,
Streptomycin, Kanamycin, Amikacin
Enterobacter, Neisseria) + Anaerobes
o “mycin” – from Streptomyces
3rd Generation CEF + consonant including MONEY o “micin” – from Micromonospora
(cefoPERAzone), TAXES o Synergistic with beta-lactam antibiotics
(cefoTAXime), FIXERS (cefixime),
o Antagonism with bacteriostatic antibiotics
Moxalactam o All must be given PARENTERALLY EXCEPT
NEOMYCIN (topical and oral only)
Coverage: HENPEcKSSS (Serratia,
o Coverage: Gram (+) EXCEPT Strep. Pneumoniae;
Salmonella, Shigella)
Gram (-); Pseudomonas; NO COVERAGE for
NOTE: Ceftazidime, Cefoperazone
atypical and anaerobes
(coverage for Pseudomonas)
4th Generation Cefepime, Cefpirome (PI-PI)
 B R I C K S N O T E S | 21
o ADR: Nephrotoxicity (Neomycin, Tobramycin, dose to <50 mg/kg/d; due to lack of
Gentamicin); Vestibulotoxicity (Streptomycin, glucuronidation reaction in infants)
Gentamicin); Ototoxicity (Neomycin, Amikacin, ANTIMETABOLITES
Kanamycin) CO-TRIMOXAZOLE (TMP-SMX)
o The MOST toxic aminoglycoside: Tobramycin • MOA: inhibit dihydropteroate synthase (Sulfonamide)
• Tetracyclines and dihydrofolate reductase (Trimethoprim)
o Structure: Naphthacene ring • Coverage: Gram (+); Gram (-); Atypical organisms
ACCORDING TO DURATION OF ACTION • DOC: Strenotrophomonas maltophilia, Burkholderia
Short-Acting Intermediate- Long Acting cepacian, Pneumocystis jiroveci, Toxoplasma gondii
Acting • Use: prostatitis
Tetracycline Demeclocycline Doxycycline • ADR: Crystalluria, Hemolytic anemia, Rashes,
Chlortetracycline Metacycline Minocycline Agranulocytosis or Thrombocytopenia, N/V, Kernicterus,
Oxytetracycline Steven’s Johnson Syndrome (SJS)
o Impaired by food (EXCEPT Doxycycline, NUCLEIC ACID SYNTHESIS INHIBITORS
Minocycline), antacids, dairy products, divalent QUINOLONES
cations à can cause COMPLEX formation or • Nalidixic Acid and Fluoroquinolones
CHELATION • MOA: Interfere with DNA gyrase and DNA topoisomerase
o Excreted in bile and urine (EXCEPT Doxycycline IV
excreted through bile) • BACTERICIDAL

m
o Tigecycline: covers almost all organisms EXCEPT QUINOLONES
3PM (Pseudomonas, Proteus, Providencia, Generation Fluoroquinolone Antimicrobial Spectrum

.co
Morganella) 1st Nalidixic Acid Moderate gram (-)
o Coverage: Gram (+); Gram (-); atypical activity
organisms; Anaerobes; NO COVERAGE for 2nd Ciprofloxacin Expanded gram (-)

ail
Pseudomonas aeruginosa activity
o BROADEST SPECTRUM ANTIBIOTIC
Some activity against
o DOC: atypical organisms
m Gram (+) and atypical
o ADR: GI disturbances, permanent teeth organisms
discoloration and enamel hypoplasia, bone
@g
Synergistic with beta-
deformity/growth retardation lactams
50S INHIBITORS rd
3 Levofloxacin Expanded gram (-)
• Macrolides Improved activity against
os

o Structure: a large lactone ring gram (+) and atypical

o Clarithromycin, Azithromycin, Roxithromycin, organisms
ll

Erythromycin Excellent activity against

§ Erythromycin: stimulates motilin
ba

S. pneumoniae
release (diarrhea) 4th Moxifloxacin Improved gram (+)
• From Streptomyces erytheus Gemifloxacin activity and anaerobic
lle

• Formerly: Ilotycin activity

§ Clarithromycin: more potent than • Coverage: Gram (+), Gram (-); Atypical; Anaerobes
Erythromycin (additional methyl group) (Moxifloxacin ONLY); P. aeruginosa (Ciprofloxacin and
e

§ Azithromycin: once a day dosing Levofloxacin ONLY)

ab

o Coverage: Gram (+), Gram (-), atypical organism; • Respiratory Fluoroquinolones: Moxifloxacin,
NO COVERAGE for Pseudomonas and anaerobes Gemifloxacin, Levofloxacin
o Use: Community-acquired pneumonia;
an

• Use: 2nd line for TB

alternative for penicillin allergy • ADR: Hyperglycemia (EXCEPT Gatifloxacin which can
• Lincosamides cause HYPOglycemia); Arthropathy (cartilage damage);
aly

o Lincomycin: sulfur-containing antibiotics QT Prolongation

isolated from Steptomyces lincolnensis METRONIDAZOLE
§ Can cause Steven’s Johnson Syndrome • MOA: Prodrug, converted inside the anaerobic
(SJS) microorganism by the redox enzyme pyruvate-ferredoxin
o Clindamycin: against non-spore forming oxidoreductase
anaerobic bacteria (Bacteroides fragilis) • Coverage: anaerobic microorganisms below the
§ Coverage: Gram (+); MRSA; Anaerobes diaphragm and the brain; Protozoans (Giardia,
§ ADR: pseudomembranous enterocolitis Entamoeba, Trichomonas)
§ Anaerobic infection above respiratory • ADR: GI disturbance, dry mouth, furry tongue, metallic
diaphragm except the brain: taste
Clindamycin
§ Anaerobic infection below respiratory
diaphragm including the brain:
Metronidazole
• Chloramphenicol
o Previous DOC for Typhoid fever (New DOC:
Ceftriaxone)
o ADR: bone marrow suppression
(myelosuppression) or aplastic anemia
(reversible); Gray baby syndrome (cyanotic; limit