Comprehensive Table of Drugs: Cholinergic Agonists (Parasympathomimetics)

COMPREHENSIVE TABLE OF DRUGS
1 st Shifting Period
NOTE: Should there be any discrepancies between this table and what’s written in the transes, please consult KATZUNG for confirmation and go instead with what’s indicated in the textbook . Thank you!
CHOLINERGIC AGONISTS (PARASYMPATHOMIMETICS)

A. CHOLINORECEPTOR-ACTIVATING
Mechanism of Action Organ System Effects Adverse Effects Indications Contraindications Other Notes
 Eyes very rapidly hydrolyzes, therefore needing a
Acetylcholine  Miosis large amount given in IV to take effect (but only
Binds to and activates muscarinic or  Accommodation for near vision lasts 5-20 seconds)
nicotinic receptors.
 Contraction of both the smooth
muscles of the iris and the ciliary
2 Major mechanisms:
muscles facilitate aqueous humor
outflow into the canal of Schlemm,
draining the anterior chamber and
1) Ach release activates
thus helping in the treatment of
muscarinic receptors on
glaucoma.
effector cells & alters
Methacoline  Cardiovascular System more resistant to hydrolysis
organ function directly.
 (-) inotropic, chronotropic,
2) Ach Release interacts with dromotropic effects
the muscarinic receptors  Reduction in peripheral vascular
on nerve terminals to resistance
inhibit release of  Vasodilation  Decreased BP 
neurotransmitter. reflex increase in heart rate
 Direct cardiac actions of
Carbachol muscarinic stimulants are
Monique · Wine · Jamie · Juria · Lenard Section 2D – Batch 2014 PHARMACOLOGY: COMPREHENSIVE TABLE OF DRUGS (1st Shifting Period) | Page 1 of 29
post-op ileus, reflux
esopahagitis, urinary more resistant to hydrolysis and has longer
Bethanecol
mediated by M 2 receptors while retention duration of action
vasodilation arises from activation
of M 3 receptors.
 Respiratory System
 Bronchoconstriction
 Stimulation of bronchial gland
secretions
 Gastrointestinal System
 Increased motility
 Relaxation of sphincters
 Stimulation of gastric secretions,
but less stimulation in pancreatic
and intestinal secretions
 The M3 receptor is required for
direct activation of smooth muscle
contraction while the M2 receptor
reduces cAMP formation and
relaxation caused by adrenergic
agonists.
 Genitourinary System
 Stimulation of detrusor muscle and
B. CHOLINESTERASE INHIBITORS
SIMPLE ALCOHOL  Hydrolyzes acetylcholine to Same as cholinoreceptor activating  Short acting (2-10 minutes)
Myasthenia Gravis, Ileus,
Edrophonium choline and acetic acid.
 Increases the endogenous
Arrhythmias  Heavily bound by H-bond to AChE
CARBAMATES acetylcholine concentration in Myasthenia Gravis, Ileus Poorly absorbed in the conjunctiva, skin, and
Neostigmine lungs because their permanent charge renders
them lipid-insoluble. This warrants larger doses
Pyridostigmine Myasthenia Gravis in oral administration than when they are given
through parenteral means.
Myasthenia Gravis
Glaucoma &
Accommodative eotopia Well-absorbed from all sites and distributed well
in the CNS, but more toxic than other
Physostigmine
Anti muscarinic drug carbamates.
intoxication (atropine, TCA,
anti depressants)
synaptic clefts & neuroeffector
junctions (amplifiers).
 Some can also inhibit are well-absorbed in the skin, lung, GIT, and
butyrylcholinesterase conjunctiva, thus making them dangerous.
ORGANOPHOSPHATES:
Echothiophate (pseudocholinesterase), but
has little significance because highly polar and more stable than other
this enzyme is not important in organophosphates.
the physiologic termination of
Parathion synaptic acetylcholine action. are lipid soluble and readily absorbed in all
CNS toxicity
Malathion routes, even in the CNS
Pilocarpine Glaucoma
Dry mouth with Sjogren’s
Cevimeline syndrome, radiation
damage of salivary gland
Donepezil, Galantamine,
Alzheimer’s disease
Rivastigmine
CHOLINERGIC ANTAGONISTS (PARASYMPATHOLYTICS)

A. ANTI – MUSACRINIC DRUGS
 Reversible blockade of actions  Central Nervous System anti-diarrheal, anti-
of cholinomimetics at  Atropine has minimal stimulant sialogogic, antidote to
muscarinic receptors effects on the CNS (especially the muscarinic poisoning
(competitive binding and parasympathetic medullary
inhibition). centers) and a slow, long-lasting
 How do acetylcholine and sedative effect on the brain. for bradycardia in acute
anti-muscarinic drugs bind  Scopolamine has more marked myocardial infarction
Atropine to muscarinic receptors? central effects: drowsiness and
Aspartate in the third amnesia; can also cause for routine pre-operative
transmembrane segment of the excitement, agitation, medications to counter the
muscarinic receptors forms a hallucinations, and coma in toxic increase in airway
nitrogen bond with the nitrogen doses. secretions and
ion of acetylcholine and the  Reduction of tremors in laryngospasms induced by
anti-muscarinic drugs, which Parkinson’s disease. Parkinsonian anesthetics
explains their competitive tremors are caused by a relative
binding. excess of cholinergic activity  Mydriasis anti-spasmodic, anti-motion
 When atropine binds to the because of a deficiency of  Cycloplegia sickness
 Angle-closure glaucoma
muscarinic receptor, it prevents dopaminergic activity in the basal  Atropine poisoning: dry
for reduced amnesia  Benign Prostatic
two mechanisms: the release of ganglia-striatum system. mouth, mydriasis, hot
associated with surgical or Hyperplasia
IP3 and the inhibition of  Motion sickness appears to and flushed skin,
obstetric delivery  Gastric ulcer (because of
adenylyl cyclase. involve muscarinic cholinergic agitation, delirium for as
slowing of gastric emptying rapidly and widely distributed in the CNS, where
transmission. Best alleviated by long as one week.
Scopolamine for routine pre-operative time, causing increased it has a greater effect there than other anti-
 Since the blockade produced scopolamine. Remember: “Dry as a
medications to counter the gastric secretions and muscarinic drugs.
by these drugs is reversible,  Eyes bone, blind as a bat,
increase in airway possible aggravation of
their effects can be overcome  The pupillary constrictor muscle red as a beet, mad
secretions and gastric ulcer)
by increased concentrations of depends on muscarinic cholinergic as a hatter.”
acetylcholine or other activation. This activation is  Hyperthermia, laryngospasms induced by
muscarinic agonists. blocked by anti-muscarinic drugs especially in children anesthetics
 Because they do not block and results in mydriasis (pupillary
nicotinic receptors, these drugs dilation).
Dicyclomine have little to no action at  Cyclopegia – weakening the anti-spasmodic
Benzropine skeletal neuromuscular contraction of the ciliary muscle, Anti - parkinsonism
junctions or autonomic ganglia. resulting in the loss of the ability to mydriatic, cycloplegic
 Muscarinic receptors are accommodate and thus cannot
constitutively active, and drugs focus on near vision. for synechia (adhesion in
that block the actions of  Decreased lacrimal secretion uveitis and iritis)
acetylcholine are inverse  Cardiovascular System
Homatropine agonists that shift the Also used for complete
 Tachycardia due to sensitivity of
equilibrium of the receptor to its ophthalmologic
the sinoatrial node to muscarinic
inactive state. examination through
receptor blockade (particularly the
 Most sensitive in salivary, induction of temporary
prejunctional M1 receptors) that
bronchial, and sweat glands. ciliary paralysis
results in vagal slowing. Lower
doses sometimes produce initial
Ipratropium
Tiotropium
 Least sensitive in gastric bradycardia before tachycardia
parietal cells. manifests.
 Atropine more effectively blocks  Reduced PR interval in the
exogenously-administered ECG – due to blocking of
cholinoceptor agonists than muscarinic receptors in AV node
endogenously-released  Constriction of coronary
acetylcholine. arteries and skeletal muscle
vessels; can also cause
cutaneous vasodilation in upper
parts of the body in toxic doses.
 Has little effect on blood pressure.
 Respiratory System
 Bronchodilation
 Reduced tracehobronchial
secretions
 The effectiveness of non-selective
anti-muscarinic drugs are not as
useful in treating COPD because
the blockade of M2 receptors on
postganglionic parasympathetic
for bladder spasm after
urologic surgery and
reducing urinary
incontinence with
Oxybutynin
neurologic diseases; this
drug is selective for M3
receptors.
is also used to reduce

Propiverine incontinence and has
lesser CNS toxicity.
B. ANTI –NICOTINIC DRUGS/ GANGLION BLOCKERS
Tetraethylammonium (TEA)  Central Nervous System hypertension very short duration of action
(Mecamylamine) introduced clinically as the first drug effective for
Hexamethonium (C6) hypertension
 Readily crosses the blood-brain management of hypertension
barrier to enter the CNS a secondary amine developed to improve the
 Sedation Possible adjunct with degree and extent of absorption in the GI tract
 Tremor transdermal nicotine since quaternary amine ganglion-blocking
 Choreiform movements patches to reduce nicotinic compounds are poorly and erratically absorbed
Mecamylamine
 Mental aberrations cravings in patients after oral administration.
 Reversibly blocks acetylcholine
 Eyes attempting to quit smoking
action at nicotinic receptors of
 Cycloplegia Blocks central nicotinic receptors
both parasympathetic and
Malignant hypertension
sympathetic ganglia. Some can  Loss of accommodation (ciliary
also block the ion channel muscle loses innervations from
gated by nicotinic PNS)
cholinoceptor.  Moderate dilation of pupil
 Subject to both depolarizing  Cardiovascular System
and non-depolarizing blockade,  Vasodilation
but most ganglion blockers now  Hypotension (especially orthostatic
are classified as non- hypotension) d/t decreased
depolarizing competitive peripheral resistance and venous
antagonists. return and blocked postural Treatment of hypertensive
 Hexamethonium – produces reflexes that prevent venous emergencies
blockade by occupying sites in pooling
or on the nicotinic ion channel ,  Marked decrease in arteriolar and Dissecting aortic aneurysm
not the nicotinic receptor itself. venomotor tone
 Trimethaphan – blocks the  Diminished cardiac contractility Producing hypotension to
short-acting; inactive orally, therefore given
receptor, not the ion channel. (negative inotropic effect) reduce bleeding in
Trimethaphan through IV.
 Since their blockades are  Moderate tachycardia neurosurgeries
reversible, their effects can be  Gastrointestinal System
counteracted by increasing the  Reduced secretion, but not Treatment of patients
concentration of acetylcholine enough to effectively treat peptic undergoing
or other agonists. ulcer disease electroconvulsive therapy
 Profound inhibition of motility
 constipation Malignant hypertension
 Genitourinary System
 Hesitancy in urination
 Urinary retention in men with BPH
 Erection and ejaculation may be
prevented by moderate doses
 Reduced thermoregulatory
sweating
ADRENERGIC AGONISTS
Mechanism of Action Organ System Effect Adverse Effects Indications Contraindications Other notes
Phenylephrine Direct Agonist – directly bind and activate Eyes – mydriasis, cyclopegia, decrease Nasal congestion Alpha agonist
receptors aqueous humor production Chronic orthostatic hypotension
Milodrine Hypotension Alpha 1 agonist
Alpha 2 agonist
Also found effective in treatment of
Clonidine Hypertension
diarrhea in diabetics with autonomic
neuropathy
Methyldopa Hypertension Alpha 2 agonist
Cardiovascular System –
Norepinephrine Indirect Agonists – displace stored NE Acute hypotension
vasoconstriction, (+) inotropy and
Phenylephrine from nerve endings (eg. Tyramine) or Acute hypotension
chronotropy
Methoxamine inhibit reuptake of release NE (ex. Acute hypotension
Cocaine and tricyclic antidepressants) Cardiac arrest and complete heart
Epinephrine Respiratory System – bronchodilation
block
α1 – increases DAG, IP3 thus activates Cardiac arrest and complete heart
Isoproterenol Gastrointestinal Tract – decrease
protein kinases block
motility and secretion
Albuterol Bronchial asthma Beta 2 selective
Metaproterenol α2 – inhibits adenylcyclase thus Bronchial asthma Beta 2 selective
GUT – slow voiding and urinary
Terbutaline decreases CAMP Bronchial asthma Beta 2 selective
retention
Isoproterenol Bronchial asthma Beta selective
β1,2,3 – stimulates adenylyl cyclase,
Epinephrine Glands – decrease sweat, lacrimal, Anaphylactic
increases ATP to CAMP conversion,
Phenylephrine nasopharyngeal constriction Mydriatic
increases Ca influx inside myocardial
Apraclonidine cells, promotes relaxation of smooth Glaucoma
Brimonidine CNS - stimulant Glaucoma
muscle
Ritodrine Suppressing premature labor
Terbutaline Endocrine - Suppressing premature labor
D1 – stimulates adenylcyclase,
Ephedrine vasodilation Stress incontinence
Psuedoephrine Beta - increase lipolysis, Stress incontinence
Amphetamine glycogenolysis, insulin Euphoriant
D2 – inhibits adenylyl cyclase, opens K
Methylphenidate channels, decreases Cainfux ADHD
Alpha - inhibit or opposite alpha
For sedation under intensive care
Dexmedetomidine
situations and during anaesthesia
Modafinil narcolepsy
Mitodrine Chronic orthostatic hypotension
Ephedrine Chronic orthostatic hypotension
ADRENERGIC ANTAGONISTS
Alpha receptor Antagonists Blockade of peripheral dopamine Eyes - contraction of iris sphincter, α antagonist drugs as stated in
receptors – minor clinical importance at ciliary muscle mechanism of action may cause Pheochromocytoma, erectile
Phentolamine present orthostatic hypertension, vasodilation Reversible antagonist
dysfunction
Cardiovascular System – vasodilation, leading to tachycardia Chronic hypertension, peripheral Reversible antagonist
Prazosin Blockade of CNS dopamine receptors – (-) inotropy and chronotrophy vascular disease, urinary obstruction
Labetalol clinically significant Eyes – blockade of receptors in other Hypertensive emergencies Reversible antagonist
Respiratory System – tissues leading to miosis
Pheochromocytoma, peripheral
Phenoxybenzamine α1 receptor antagonist drugs  bronchoconstriction, increase T-B Irreversible antagonist
vascular disease
vasodilation and tachycardia secretion Gut – blockade of α1 receptors in
Chronic hypertension, urinary
Terazosin base of bladder and prostate leading
obstruction
α1 receptor antagonist drugs  acts on Gastrointestinal Tract – increase motility to resistance to urine flow and urinary
receptors on vascular smooth muscle  and secretion retention Chronic hypertension, urinary
Doxazosin
decreased arteriolar and venous tone  obstruction
Indoramin decreased peripheral vascular resistance GUT – increase voiding Chronic hypertension
and blood pressure  vasodilation  Chronic hypertension, urinary
Urapidil
increased venous pooling in the periphery obstruction
Chlorpromazine Chronic hypertension
Haloperidol Chronic hypertension
Tamsulosin Urinary obstruction
Alfuzosin Urinary obstruction
Urapidil Urinary obstruction
Beta Receptor Antagonists

Propranolol Hypertension Non-selective
Metoprolol Hypertension Selective, non partial agonist
Atenolol Hypertension Selective, non partial agonist
Bisoprolol Hypertension Selective, non partial agonist
Pindolol Hypertension Selective, partial agonist
Metoprolol CHF
Bisoprolol CHF
Carvediol CHF
Timolol Glaucoma
Betaxolol Glaucoma
 cannot maintain BP in the upright Glands – increase sweat, lacrimal and
Labetalolol position  orthostatic hypotension nasopharyngeal secretion Hypertension
Ischemic heart disease, glaucoma,
Timolol
α1 receptor antagonist drugs  CNS – decrease migraine and tremors neurologic disorders
prevent pressor effects of usual doses of Ischemic heart disease,
Propranolol
α agonists Endocrine – inhibit lipolysis hyperthyroidism, neurologic disorders
glycogenolysis, T4-T3 and increase Ischemic heart disease, heart failure,
Metoprolol
VLDL neurologic disorders
Sotalol α1 selective antagonist drugs – convert a Cardiac arrythmia
Bisoprolol pressor to a depressor, response of Heart failure
Carvediol agonists with both α and β effects (eg. Heart failure
Betaxolol epinephrine) Glaucoma
Carteolol Glaucoma
Levobunolol B receptor antagonist drugs – HPN, Glaucoma
Metipranolol ischemic heart disease, arrhythmias, Glaucoma
Atenolol endocrinologic and neurologic disorders, Neurologic disorders
Nadol glaucoma Neurologic disorders
INOTROPIC CARDIOTONICS
A. SS ADRENOCEPTOR & DOPAMINE RECEPTOR AGONISTS
 Stimulation of cardiac β1
adrenoceptor→↑inotrophy>↑chronotr
ophy
CVS: hypotension due to β receptor
Dobutamine  Peripheral vasodilation Tachycardia, Arrhythmia, Angina Acute Heart failure Synthetic analog of Dopamine
stimulation
 ↑ myocardial oxygen demand
 ↑ CO
 ↓ ventricular filling
 Stimulation of peripheral
postjunctional D1 and prejunctional Tachycardia, arrhythmia, peripheral
Dopamine Acute heart failure
D2 receptors vasoconstriction
 Splanchnic and renal vasodilation
B. α-ß NON-SELECTIVE
 Sympathetic agonist
 Physiologic antagonist of Histamine-1 Drug of choice in anaphylactic shock
Epinephrine
receptors
Does not act on β2 receptors (cannot
Norephinephrine Stimulates heart and blood vessels
be used in asthma)
C. BYPIRIDINES (PHOSPHODIESTERASE INHIBITORS)
MILRINONE (drug of choice)
Less toxic than Inamrinone
Levosimendan Inhibits phosphodiesterase III
(PDEIII)→↑cAMP→ vasodilation→ Ventricular Arrhythmia Half-life: 3-6 hours
inotropic effect Excretion: 10-40% urine
Inamrinone Toxic for bone marrow and liver
D. CARDIAC GLYCOSIDES (DIGITALIS)

 Inhibits Na-K ATPase (channel Less mortality than digitoxin
receptor antagonist) Former primary drug
 Works in tandem with the Na-Ca Very narrow PI
Digoxin Acute Congestive Heart Failure
exchange channel: inhibition of Na-K FAB ANTIBODY- Antidote to adv
ATPase  increase in intracellular effect
Na (sodium retention)  increase in Half-life:36-40 hours
intracellular Ca (calcium retention) Digitalis-induced arrhythmia (V
 ↑ binding of Ca (sequestered Arrhythmia)
from SR) with troponin C  ↑
excitation-contraction coupling
Digitoxin
through the sliding mechanism of
Longer-acting
actin and myosin filaments  ↑
myocardial contractility
NON-INOTROPIC CARDIOTONICS
A. VASODILATORS
 Venodilation → reduction in preload
Isosorbide Dinitrate (ISDN)
 Releases nitric oxide Severe headache due to vasodilation Venodilator
Isosorbide Mononitrate (ISMN)
 Activates guanylylcyclase (Monday Disease)
 Arteriolar dilatation→ reduction in
afterload SLE (sue to acetylating property in
Hydralazine Arteriodilator
 Reduces blood pressure and afterload Phase II metabolism either fast or
 Results in increased cardiac output slow)
 Releases NO spontaneously
Sodium Nitroprusside Cyanide Poisoning
 Activates guanylylcyclase
B. ANGIOTENSIN-CONVERTING ENZYMES INHIBITORS (ACE INHIBITORS)
CAPTOPRIL  Reduce aldosterone secretion  Dry Cough Heart Failure (with diuretics) Pregnant women (fetal
ENALAPRIL reducing salt and water retention  Angioedema nephrotoxicity)
LISINOPRIL reducing preload
PERINDOPRIL  Reduce peripheral resitance
reducing afterload
 Reduction in tissue angiotensin levels
 reduce sympathetic activity
QUINAPRIL (diminution of angiotensin’s
RAMIPRIL presynaptic effects)
 Reduces long term remodeling of the
heart and vessels  reduction in
mortality and morbidity
C. ANGIOTENSIN II BLOCKERS
LOSARTAN
VALSARTAN EPROSARTAN – long-acting; given
EPROSARTAN once a day
Same CI as that of ACE inhibitors
OLMESARTAN
CANDESARTAN
D. DIURETICS (See page 15 for more comprehensive information on diuretics)
LOOP DIURETICS
 Reduction of facilitation of sympathetic
nervous system
 Preload reduction: reduction of excess
Furosemide
plasma volume and edema fluid
 Afterload reduction: lowered blood
pressure
POTASSIUM-SPARING DIURETICS
Spironolactone
Genitourinary: antiandrogenic
Act on the collecting tubule→ blocks the
Eplerenone No antiandrogenic effect
release of aldosterone
Lowering of electrolyte
Ethacrynic acid Hyperuricemia
Autotoxicity leading to deafness
E. β ADRENOCEPTOR BLOCKERS
 Reduction in damaging the
Bisoprolol sympathetic influences in the heart
Carvedilol (Tachycardia, arrhythmias) Bradycardia, precipitate
Metropolol  Inhibition of renin release Chronic Heart Failure
decompensation of cardiac function
Propanolol (PO/IM)
Esmolol (IO)  Carvedilol: Peripheral vasodilation
via α-adrenoceptor blockade
ANTI-ARRHYTHMICS
A. CLASS 1 – Sodium-Channel Blocking
Subgroup 1A
 Slows down upstroke of action Torsade de pointes arrhythmia, Atrial and Ventricular Arrhythmias
Procainamide
potential and conduction syncope, SLE-like syndrome
Quinidine  Prolongs QRS duration and action Torsade de pointes, Syncope, Rarely used because of cardiac and
potential Cinchonism (headache, dizziness and extracardiac adverse effects
tinnitus), Nausea, Vomiting
Same as quinidine, may precipitate
Cardiac antimuscarininc effects even
Disopyramide heart failure, atropine-like activity, Supraventricular Arrhythmias Heart failure, glaucoma
 Ganglion Blocker: ↓ peripheral more marked than those of quinidine
worsening of pre-existing glaucoma
vascular resistance
Subgroup 1B
Blocks activated and inactivated sodium Hypotension, Asystole, malignant HPN Ventricular tachycardia
Lidocaine channels with rapid kinetics (rare), CNS manifestations Ventricular fibrillation Local anesthetic
Alters Na, K, Ca conductance, membrane
Nystagmus, ataxia, drowsiness,
potentials and the concentration of amino
Gingival hyperplasia, Peripheral Digitalis Induced Arrhythmias Antiseizure
acids and nuerotransmitters: (NE, Ach,
Phenytoin neuropathy Ventricular Arrhythmia Orally administered
GABA)
Increased metabolism: phenytoin,
Mexiletine Similar to lidocaine Hypotension and CNS symptoms Ventricular Arrhythmias phenobarbital, rifampin
Decreased: cimetidine
Subgroup 1C
 Potent blocker of Na and K channels Supraventricular Arrhythmia, SV
May cause severe exacerbation of Increased metabolism: propranolol,
with slow unblocking kinetics Tachycardia, VT, Wolff-Parkinsons-
arrhythmia, Brugada Syndrome quinidine. amiodarone
Flecainide  (-) chronotrophic effect White Arrhythmias
 Similar to quinidine but does not
Metallic taste, constipation,arrhythmia Increased metabolism: Warfarin,
prolong AP
Propafenone exacerbation digoxin, metropolol
 (-) chronotrophic effect
Potent sodium channel blocker that does Withdrawn from market
Moricizine Ventricular Arrhythmia
not prolong AP Phenothiazine derivative
B. CLASS 2 – ß-ADRENOCEPTOR-BLOCKING DRUGS
Propranolol (non-selective)
Timolol  Inhibit catecholamine binding at beta- Hypotension, bradycardia, CHF,
Metropolol receptors Wheezes, Raynaud’s, Depression,
Esmolol (Intraoperative Arrhythmia,  Direct membrane stabilizing property Hypoglycemia, Insomnia, Decreased
IV)  (-) inotropic, chronotrophic effects libido
Acetabulol (oral)
C. CLASS 3 – K-Channel Blockers
Bradycardia, Hypo/Hyperthyroidism,
asymptomatic corneal deposits, dose-
Amiodarone Bioavailability: 35-65%
Multiple actions: related pulmonary toxicity (pulmonary
fibrosis) Ventricular Arrhythmia
 Class IV- ↑AV nodal conduction
Supraventricular Arrhythmia (low Structural analog of amiodarone
 Class I- depresses Vmax
doses) Lacks iodine atoms
 Class II- noncompetitively blocks α Ventricular Tachycardia 1st antiarrhythmic drug to
Dronedarone and β Similar with amiodarone without the demonstrate a reduction in
thyroid and pulmonary toxicity mortality/hospitalization in patients
with AF
 Multi-channel blocker
 Prolongs atrial effective refractory Dysgeusia (disturbance of taste),
Vernakalant period sneezing, paresthesia, cough, Atrial Fibrillation New Class III drug
 Slows conduction over AV node hypotension
 Does not change QT interval
 Non-specific β-adrenergic receptor-
blocker (class 2) Dose-related incidence of Torsade de 100% bioavailability
Sotalol Ventricular Arrhythmias
 Action potential (repolarization) pointes excretion: kidneys
prolonging (class 3)
Ibutilide Ibutilide: activate slow inward sodium IV for Ibutilide
Dofetilide current QT Prolongation SVT Dofetilide: PO, 100% bioavailability
D. CLASS 4 – Calcium Channel Blocking Drugs
 Reduces the plateau height of the
action potential, slightly shortens
Dose-related cardiotoxic effects, can Prototype
action potential, and slightly prolongs SVT
induce AV block in large dosages, Bioavailability: 20%
Verapamil total Purkinje fiber AP Reduction of ventricular rate in AF and
constipation, lassitude, nervousness, PO dosage>IV dosage because of 1st
 Peripheral vasodilation→transient flutter
peripheral edema pass effect
hypotension
 (-) inotropic effects
Inhibits the AV node by acting with α1
receptors that opens the adenosine Contraindicated in the presence of
Drug of choice for prompt conversion Naturally occurs in the body
Adenosine sensitive K channel to hyperpolarize and Flushing, dyspnea, chest pressure Methylxanthines due to inhibition of
of paroxysmal SVT to sinus rhythm T ½: 1 to 6 secs
inhibit AV node and indirectly inhibit action
calcium channel opening
Slowing sinus node discharge rate,
Digoxin shortening atrial refractoriness, prolonging See cardiotonics
AV nodal refractoriness
ANTIHYPERLIPIDEMICS
A. COMPETITIVE INHIBITORS OF HMG-COA REDUCTASE (REDUCTASE INHIBITORS) – “STATINS”
 Most effective in reducing LDL
together
 Inhibits HMG-CoA  Decrease oxidative stress
Pravastatin Reductasepreventing the formation  Decrease vascular inflammation
of mevalonate (rate limiting step of  Increases stability of
sterol synthesis) atherosclerotic lesion
 Induces an increase in high affinity  Has an open active lactone ring
LDL receptors on hepatocytes  Inactive lactone prodrug
Lovastatin  Increases both fractional catabolic  Hydrolyzed in the GIT→ β
rate of LDL and liver’s extraction of hydroxyl derivatives
LDL precursors (VLDL remnants)
Myopathy – cessation upon removal  Same as Lovastatin
Simvastatin from the blood→↓ LDL
of therapy  More potent than lovastatin
 Interfere with the synthesis of lipid Hepatic toxicity  Most effective in reducing LDL
intermediates with important Cataract Pregnant and lactating women and together
biological effects Pancreatitis those likely to become pregnant,  Decrease oxidative stress
 May ↑ HDL cholesterol by preventing Headache hepatic and renal impairment,
the geranylation of Rho A and Drugs used to lower lipid levels in the  Decrease vascular inflammation
Fluvastatin Dizziness porphyria, untreated
phosphorylation of peroxisome body (e.g. cholesterol, LDL)  Increases stability of
Insomnia hypothyroidism atherosclerotic lesion
proliferator-activated receptor Blurred vision
(PPARa)- factor that regulates APO  Fluorine containing
Dysgeusia
A1 transcription  Almost completely absorbed
Skin rashes
 Fluorine containing
Rosuvastatin
 19 hours (long lasting)
Same as rosuvastatin but only lasts
Atorvastatin
for 14 hours
B. FIBRIC ACID DERIVATIVES (FIBRATES) – LIPOPROTEIN LIPASE STIMULANTS

General:
 Absorption: >90% with meal
Cholesterol gallstones- reflecting ↑ in  Plasma protein binding: >95%
cholesterol content of bile  Excretion: Predominantly as
glucoronide conjugates
Effects on plasma levels of Hepatotoxicity – ↑ aminotransferases
Hypertriglyceridemia with ↑ VLDL or  Conjugates:
Lipoprotein: or alkaline phosphatases
chylomicrons  80-90% in urine; smaller amounts
 ↓VLDL and chylomicron
in feces;
 ↓or↑ LDL Myositis, myopathy, rhabdomyolysis, (Katzung) 60% in urine as
Hypertriglyceridemia- Type I, IV, V
 Mosly only modest ↓ in myoglobinuria, renal failure
 Increases peripheral clearance of glucoronide conjugates; 25% in
Fenofibrate LDL
lipoproteins Familial combined hyperlipidemi feces
Gemfibrozil  Others, especially with GIT – anorexia, nausea, GI discomfort
(Type IIb), VLDL is ↑
Bezafibrate  Peroxisome proliferator-activated combined hyperlipidemia, LDL
Ciprofibrate receptor α agonist often ↑ Skin rashes, urticarial, hair loss
Familial dysbetalipoproteinemia (Type Monitor:
 Moderate ↑ in HDL III)
Fatigue, headache, impotence  Serum levels of creatine kinase,
Effects on plasma levels of lipids: aminotransferases, and plasma
Hypertriglyceridemia d/t treatment with proteins
 ↓TG Anemia, leucopenia
viral protease inhibitors
 ↓Cholesterol  Renal function tests
Hypokalemia, arrhythmias  Thyroid status
↓ WBC or Hct T ½: Fenofibrate- 20 hrs

Gemfibrozil- 1.5 hrs
Clofibrate- 15 hrs.
C. STEROL ABSORPTION INHIBITOR
 Blocks sterol transporter NPC1L1 in
intestine brush border→ inhibits  Readily absorbed
reabsorption of cholesterol excreted  Conjugated in intestine to an
in bile: ↓ LDL and phytosterols active glucoronide
 Selective inhibitor of intestinal  Familial combined hyperlipidemia  Enterohepatic circulation
absorption of cholesterol & when LDL is increased  T ½ of active metabolite: 22 hrs
Ezetimibe
phytosterols  Familial hypercholesterolemia  80% excreted in the feces
 Inhibit absorption of cholesterol both (heterozygous, homozygous)
in diet and in bile Drug interactions:
 Actions: ↓ LDL, minimal ↑ in HDL - ↑ with fibrates
cholesterol - ↓ with cholestyramine
 Synergistic with statin
 NIACIN – VLDL SECRETION INHIBITORS
 Skin and mucous membrane:
Effect on plasma levels of o Harmless cutaneous
lipoproteins: vasodilator (flush),
 ↓VLDL, IDL, LDL, Lp(a), ↑ HDL uncomfortable sensation of
 Most effective agent for wamth and pruritus Monitor serum levels of: glucose,
increasing levels of HDL o Rashes, dry skin, dry mucous aminotransferase, uric acid, albumin,
 Only antihyperlipidemic membranes CK
o Acanthosisnigricans Acanthosisnigricans
drug that decreases Lp(a)
Peptic ulcer/severe pepric disease
significantly Pharmacokinetics:
Decreases catabolism of apoA1; reduces Hepatic disease
Nicotinic Acid (Vit. B3) and  Estrogen and Neomycin  GIT Absorption – almost complete
VLDL secretion from liver→↑ HDL, ↓ LDL Diabetes mellitus
derivatives also decreases Lp(a) significantly o Hepatotoxicity Metabolism – extensive
and TG Gout
o Myopathy Excretion – urine mostly as
Pregnancy
Effect on plasma levels of lipids: o Metabolic: Hyperglycemia, metabolites;
Patients on hypertensive therapy
 ↓ TG Hyperuricemia Doses – daily vitamin requirement as
 ↓ Cholesterol antihyperlipideic
 CVS: Arrhythmia, hypotension T ½ - 60 mins.
Other effects:  Ocular toxicity: Amblyopia
 ↓ Fibrinogen (reversible)- reduced vision in an
 ↑ Tissue plasminogen activator eye not correctable by a manifest
refraction; Maculopathy
 BILE ACID BINDING RESINS
↓ absorption of
- Folic acid
- Drugs
 Binds bile acids in gut preventing - Fat soluble vitamins
reabsorption, increases cholesterol Hypertriglyceridemia
Colestipol
catabolism, up regulates receptors GI: constipation, sensation of fullness, Hypoprothrombonemia Diverticulitis Large polymeric cationic exchange
Cholestyramine
→↓ LDL discomfort Hemorrhoids resins and insoluble in water
Colesevelan
 Enhanced conversion of cholesterol to Increase bleeding tendency Biliary obstruction
bile acid
Increase effects of anticoagulants
Hypertriglyceridemia
ANTI-HYPERTENSIVES
DRUGS THAT ALTER SNS FUNCTION
A. Centrally acting Sympathoplegic drugs
rarely used - Methyldopa - Clonidine -Reduce sympathetic outflow from vasomotor center in brain -increase sensitivity -only used for HPN in pregnancy -Dry mouth -sedation -depression -Lactation > prolactin secretion (Methyldopa) -HPN
to baroreceptor center Central α adrenoceptor stimulation -Decrease TPR, HR, crisis > inc SNS activity (Clonidine withdrawal)
CO -Decrease renal vascular resistance
B. Ganglion- Blocking drugs
Trimetaphan - Block nicotinic receptors on postganglionic neurons of SNS and PNS - Not used Severe hypotension Sexual dysfunction Constipation Urinary retention Glaucoma
C. Adrenergic Neuron Blocking Drugs

- Guanethidine - Guanadrel >do not enter CNS - Reserpine -Inhibit release of NE from sympathetic nerves transported by NET -interferes Postural hypotension Sedation Depression Extrapyramidal s/sx GI sx
with VMAT >depletes NE, dopamine, 5HT in central and peripheral nerve endings
D. Adrenoceptor Antagonists
1. Beta Blockers - Decrease CO, TPR, HR
- Propranolol Cardioselective: - Metoprolol - Atenolol - Nadolol - - depress RAAS by blocking the intrarenal & extrarenal B-receptors involved in - most widely used - long half lives > OD Bradycardia DM Peripheral vascular insufficiency
Betaxolol - Bisoprolol Partial Agonists: - Pindolol - Acebutolol With α renin secretion - same as propranolol in B1 blockade but less potent B2 - less administration - useful in pt with
blocker: - Labetalol - Carvedilol CO & HR depression than other B blockers bradycardia & Peripheral Vasc Disease -
tx of HPN in pt with pheochromocytoma
and HPN crisis - tx ofpt with HF & HPN
2. α1 Blockers
Selective: - Prazosin - Terazosin - Doxazosin Non-selective: - -Blocks α1 receptors in arterioles, venules -Vasodilation - tx of BPH & HPN - dx & tx of 1st dose effect > occurs in salt & H2O depleted pt > reduce 1st dose & administer at h.s.
Phentolamine Phenoxybenzamine pheochromocytoma Dizziness Headache Lassitude
II. DIRECT VASODILATORS

A. Arteriolar - HPN emergencies Tachycardia flushing Hypertrichosis HA
- Hydralazine - Minoxidil - Diazoxide - Fenoldopam
B. Arteriovenous
Sodium Nitroprusside Activates guanylyl cyclase > inc intracellular cGMP > relaxed smooth muscle Cyanide Accumulation
Calcium Channel Blockers
Dihydropyridine: - Nifedipine - Amlodipine - Nicardipine - Nisoldipine > -bind to L-type Ca++ channel (heart smooth muscle) -decrease trans-membrane -Decrease myocardial contractile force - Cardiac depression peripheral edema flushing dizziness
More selective vasodilator > Less cardiac depressant than - Verapamil Ca++ current -smooth muscle relaxation decrease myocardial O2 requirement -
& - Diltiazem - Nimodipine: cerebral blood vessels decrease HR (Verapamil, Diltiazem)
-relief vasospasm in coronary artery RX:
Angina pectoris -Decrease AV node
conduction RX: - Supraventricular
tachycardia
- AF
Peripheral vasodilator RX: - HPN

- Raynaud’s phenomenon
Nicardipine RX: Severe HPN – thru IV

III. ANGIOTENSIN INHIBITORS
1. ACE inhibitors
Excreted in kidneys except Fosinopril - Enalapril - Lisinopril - - Inhibits peptidyl transferase and inactivates bradykinin - ---- Reduced SNS - Tx in pt with chronic kidney disease and Acute renal failure Hyperkalemia Dry cough Angioedema CI for pregnant pt
Benazepril - Perindopril - Quinapril - Ramipril - Trandolapril stimulation - Low Na+ delivery - Low Na+ distal renal tubule - Low renal arterial DM - Tx of HF - reduced incidence of DM
Pressure in pt with MI
2. Angiotensin Receptor Blocker

- Valsartan - Candesartan - Eprosartan - Irbesartan - Telmisartan - - No effect on bradykinin Metabolism > more selective blocker of angiotensin - pt with HF and chronic kidney disease - Same with ACE inh except for the cough and angioedema
Olmesartan effects than ACE inh can be given to DM nephropathy
3. Renin blockers
Clonidine (central SNS) β blockers (renal, extrarenal) Aliskiren Reduces plasma renin activity, angiotensin I, II, aldosterone Greater anti HPN
effect
ANTI-HYPERTENSIVES: DIURETICS
A. CARBONIC ANHYDRASE INHIBITORS
 Acts on the proximal convoluted  Glaucoma (Dorsolamide,
tubules where reabsorption of Brinzolamide – topical or
sodium bicarbonate occurs eyedrop forms for organ
 Sodium bicarbonate will be selectivity)  decreased  Prototype drug
absorbed through the sodium- formation of aqueous humor  Well-absorbed after oral
hydrogen exchanger  Na ions  Hyperchloremic metabolic acidosis  Metabolic alkalosis  administration
will be reabsorbed into the decreased bicarbonate  Excretion of the drug is by secretion
 Renal stones: decreased citrate
interstitium of the kidneys while H reabsorption in the proximal tubule S2 segment
Inhibition of bicarbonate reabsorption in excretion, Ca++ salt precipitation d/t
will be secreted to the tubular presence of alkaline pH  Acute mountain sickness  Hepatic encephalopathy/hepatic  Onset of action: 30 minutes to 2
the proximal convoluted tubule 
lumen decreased production of CSF coma/impaired liver function – hours
depletion of bicarbonate  increased  Renal potassium wasting
Acetazolamide  H ions will combine with  Urinary alkalinization: alkaline pH decreases urinary NH4  Duration: 12 hours
NaCl reabsorption in the rest of the renal  Drowsiness
bicarbonate to form carbonic acid decreased bicarbonate excretion  85% of the bicarbonate reabsorptive
tubules  Paresthesias
 Carbonic acid will dissociate to reabsorption  increased capacity of the proximal convoluted
 Nervous system toxicity (seen in
H2O and CO2 by the enzyme urinary pH  enhanced tubule is inhibited.
patients with renal failure)
carbonic anhydrase excretion of weak acids  Diuretic efficacy of acetazolamide
 Allergic reactions
 Acetazolamide inhibits this  Adjuvants in treatment of decreases significantly with use over
enzyme  No sodium ion will be epilepsy, hypokalemic periodic several days.
reabsorbed due to the decreased paralysis, and in increasing
ability to exchange Na with H urinary phosphate excretion
ions  Blocks sodium during severe
bicarbonate rabsorption hypophosphatemia.
B. LOOP DIURETICS
 Acts on the Loop of Henle,  Most effective type of diuretics
particularly in the thick ascending because of the large sodium
limb chloride absorptive capacity of the
 Hypokalemia/Hypokalemic
 Inhibits Na-K-2Cl transporter in thick ascending limb  effect is not
Metabolic Acidosis
the thick ascending limb   Pulmonary edema diminuted by acidosis, unlike other
 Hypomagnesemia
decreased NaCl, Mg, Ca  Acute hypercalcemia (inhibits types of diuretics
Furosemide 20/40 mg tab; 20mg amp –  Ototoxicity (reversible)
reabsorption Ca++ reabsorption)  Onset: 2-3 hours (furosemide); 1
prototype drug  Hyperuricemia, gout (d/t increased  Allergic reaction
 Increases renal blood flow   Hyperkalemia (inhibits K+ hour (torsemide)
Butenamide (Lasix) 1mg tab; 0.5mg amp reabsorption of uric acid in renal  Liver cirrhosis
useful for patients with decreased reabsorption)  Duration: 2-3 hours (furosemide);
Torsemide (not available locally) tubules secondary to  Borderline renal failure
urine output  Acute renal failure (increase rate 4-6 hours (torsemide)
Ethacrynic Acid (not available locally) hypervolemia)
 Also shown to induce expression of urine flow by increasing renal  Rapidly absorbed
 Allergic reaction (loop diuretics are
of COX-2  increased synthesis blood flow; increased K+  Eliminated by the kidney by
of prostaglandins (PGE2) from sulfonamides)
excretion) glomerular filtration and tubular
arachidonic acid  inhibits salt  Severe dehydration (d/t excessive secretion
transport in the thick ascending urine output)
 Diuretic activity of loop diuretics
limb (this can be blocked by correlates with their secretion by the
NSAIDs) proximal tubule.
C. THIAZIDES
Chlorothiazide  Blocks NaCl transporter in the  Metabolic alkalosis  Hypertension
Hydrochlorothiazide (12.5/25 mg tab) distal convoluted tubule   Hyperuricemia  Congestive Heart Failure  Hydrocholorthiazide: prototype
Indapamide (1.5mg tab) inhibits NaCl reabsorption, but  Hyperglycemia (d/t impaired  Hypercalciuria drug
increases Ca reabsorption  All thiazides can be administered
 Increase in calcium reabsorption
insulin release and decreased  Nephrogenic diabetes insipidus orally but there are differences in
glucose utilization)
is postulated to result from effects their metabolism: Chlorothiazide is
in both the proximal and distal not very lipid soluble and must be
convoluted tubules: given in large doses; this is the only
 PCT: thiazide-induced thiazide available for parenteral
volume depletion  administration.
enhanced Na+ and passive  All thiazides are secreted by the
Ca++ reabsorption organic acid secretory system in the
 DCT: thiazide-induced proximal convoluted tubule and
blockade of Na entry  compete with the secretion of uric
decreased intracellular Na  Hyperlipidemia acid by that system  thiazides
 enhances Na-Ca  Dilutional hyponatremia (d/t ADH may blunt uric acid secretion and
exchange in the basolateral production secondary to elevate serum uric acid level.
membrane  increased Ca hypovolemia)  Usually combined with other drugs,
reabsorption  Allergy such as beta blockers, ARBs, and
ACE inhibitors to potentiate the
effects of controlling blood pressure.
There are drugs available that
already have combined beta
blocker/ARB/ACE inhibitor and
diuretic effects.
 However, if diuretics are to be given
with calcium channel-blockers, they
should be given separately.
D. POTASSIUM-SPARING DIURETICS
Spironolactone  K-sparing diuretics prevent K+  Hyperkalemia  Hyperaldosteronism  Acute Renal Failure  Direct Antagonists of Aldosterone
Eplerenone secretion by antagonizing the  Metabolic acidosis  Primary – Conn’s  Hyperkalemia Receptors
Amiloride effects of aldosterone at the late  Gynecomastia, impotence – syndrome  Liver disease  Spironolactone
Triamterene distal and cortical collecting Spirinolactone  Secondary – CHF, liver  Synthetic steroid that
tubules.  ARF – Triamterene + Indomethacin cirrhosis, nephrotic acts as a competitive
 Inhibition may occur by direct  Renal stones – Triamterene syndrome antagonist to
pharmacologic antagonism of aldosterone
mineralocorticoid receptors  Substantial inactivation
(spironolactone, eplerenone) or by of spironolactone occurs
inhibition of Na+ influx through ion in the liver
channels in the luminal membrane  Rather slow onset of
(amiloride, triamterene) action, requiring several
 Spironolactone and eplerenone days before full
bind to mineralocorticoid receptors therapeutic effect is
and blunt aldosterone activity. achieved
Amiloride and triamterene do not  Eplerenone
block aldosterone, but instead  More selective: less
directly interfere with Na+ entry active on androgen,
through the epithelial Na+ channels progesterone receptors
(ENaC) in the apical membrane of  Spironolactone analog
the collecting tubule. Since K+ with much greater
secretion is coupled with Na+ entry selectivity for the
in this segment, these agents are mineralocorticoid
also effective potassium-sparing receptor
diuretics  Several hundred-fold
less active on androgen
and progesterone
receptors than
spironolactone
 Fewer adverse effects
 Inhibitors of Na+ influx through
ion channels in luminal
membrane
 Amiloride
 Triamterene
 Metabolized in the liver,
but renal excretion is a
major route of
elimination for the active
form and the
metabolites
 Because triamterene is
extensively metabolized,
it has a shorter half-life
and must be given more
frequently than
amiloride (which is not
metabolized)
 Amiloride and triamterene are direct
inhibitors of Na+ influx in the CCT
(cortical collecting tubule).
E. OSMOTIC DIURETICS
 Osmotic diuretics have their major
effect in the proximal tubule and
the descending limb of Henle's
loop. Through osmotic effects, they
also oppose the action of ADH in
 Mannitol – prototypic drug; the only
the collecting tubule.
 Congestive heart failure osmotic diuretic available
 Prevents the normal absorption of
 Decreases intracranial pressure  Mannitol is poorly absorbed by the
water by interposing a  Increased ECF volume
Mannitol  Decreases intraocular pressure GI tract, and when administered
countervailing osmotic force  Hyponatremia
orally it causes osmotic diarrhea. For
resulting to increased urine  Dehydration
systemic effect, mannitol must be
volume.
given parenterally.
 Increase in urine flow rate
decreases the contact time
between fluid and the tubular
epithelium, thus reducing Na+ as
well as water reabsorption.
F. ADH AGONISTS
Renal action appears to be mediated
Vasopresin
primarily via V2 receptors although V1a Central Diabetes Insipidus
Desmopresin
receptors may also be involved.
G. ADH RECEPTOR ANTAGONISTS
 ADH antagonists inhibit the effects
of ADH in the collecting tubule Syndrome of Inappropriate
Conivaptan (only drug approved for use)
 Both lithium and demeclocycline Diuretic Hormone (SIADH)
Lixivaptan Nephrogenic Diabetes Insipidus
appear to reduce the formation of
Tolvaptan
cyclic adenosine monophosphate Congestive Heart Failure
(cAMP) in response to ADH
ANTI-ANGINA
A. NITRATES
 Nitroglycerin
 considered as the
prototype of the group
 not sensitive to sunlight
but may lose its potency
due to volatilization and
adsorption to plastic
surfaces, therefore it
should be kept in a tightly
closed glass containers
 Isosorbide dinitrate/mononitrate
 sublingual administration
to prevent first pass effect
in the liver
 can also be given
transdermally by placing a
Nitrates will be removed of its nitrate
 Hypotension because it is not only patch on any part of the
group by Gluthatione S-Transferase  dilation of veins – decreased chest or even in the
the coronary vessels that are
which will release the free nitrate. The preload (venous return) abdomen; will be
dilated but also the other blood
Nitroglycerin free nitrate will then be converted to  dilation of arteries – decreased LV vessels (peripheral blood vessels) absorbed in the skin 
Isosorbide Dinitrate (ISDN) nitric oxide. The nitric oxide causes Angina Increased intracranial pressure mucous membrane and
volume and wall tension (decrease  Tachycardia
Isosorbide Mononitrate (ISMN) activation of guanylylcyclase and an will produce the
afterload)  Severe headache (due to
increase in cGMP which, in turn, would therapeutic effect
cause smooth muscle relaxation as vasodilation of cerebral vessels)
 Onset: 1-3 minutes
stated in the previous mode of action.
 Duration: 15-30 minutes
 Types of Administration: SL,
Transdermal, SR
 1-3 minutes of administration would
provide immediate relief of the
chest pain. If the chest pain is not
relieved, wait for another 15
minutes then administer again
(duration of action: 15-30 minutes).
If the chest pain is not yet relieved
by this, the patient must have a
probable MI and should be
admitted immediately to an ICU.
 Slow Release tablets:
 used as maintenance
 given once a day
B. SILDENAFIL, TADANAFIL, VARDENAFIL
Sildenafil Sildenafil is a drug used for the Sexual impotence Patients taking nitrates
Tadanafil treatment of impotence or erectile Erectile dysfunction
dysfunction which blocks the action of
phosphodiesterase. By blocking PDE,
there will be an increase in cGMP
Vardenafil
which will result to relaxation. This
mode of action can also aggravate the
hypotensive effects of the nitrates.
C. NEW DRUGS FOR ANGINA
 Activate cardiac potassium
channels thereby hyperpolarizing  Better than the nitrates
the smooth muscle membrane  Available in 5, 10, 20 mg doses
therefore decreasing heart rate Decreased HR and is given twice a day every 12
Nicorandil
(myocardial protection) Dilation of coronary vessels hours
 Can also release nitric oxide in  A nicotinamide nitrate ester
the endothelium thereby dilating
the coronary vessels
Inhibit oxidation of fatty acids in the
20 mg (given 3x a day) 35 mg (every
Trimetazidine myocardium thereby improving the
12 hrs)
metabolic status of ischemic tissues
Blocks the late Na current also
Ranolizine blocking the calcium causing decrease Decreased myocardial contractility
myocardial contractility
Inhibits hyperpolarization by the Decreased HR
Ivabradine activated Na channels in the SA node Other effects similar to calcium channel
thereby decreasing heart rate blockers
MUCOKINETICS (EXPECTORANTS)
A. DIRECTLY-ACTING
Decrease sputum viscosity and
increase sputum volume thereby Nausea, gastric disturbances, Productive cough Hypersensitivity
Guaiphenesin/Guaifenesin decreasing difficulty in expectoration drowsiness and rash
 Increase bronchial secretion by salt

Na+, K+ citrate/acetate action Productive cough
 ↑ Na content→↑ H2O content
B. REFLEXLY-ACTING
 Cause irritative action on bronchial
mucosa resulting to production of Productive cough Irritant to gastric mucosa
Ammonium chloride excess respiratory tract fluid w/c is Nausea and vomiting
easier to cough
Potassium Iodide Productive cough

C. MUCOLYTIC
Depolymerizes polysaccharide directly
as well as by liberating lysosomal Rhinorrhea, lacrimation, gastric Hypersensitivity
Bromhexine
enzymes w/c breaks down the fiber irritation Productive cough
network in the tenacious sputum
Ambroxol Makes the phlegm in the airway
thinner and less sticky by increasing Mild GI effects and allergic reaction Hypersensitivity, epileptic patients Metabolite of Bromhexine
the body’s natural production of Productive cough
surfactant (anti-glue)
Splits disulphide bonds linking proteins
Acetylcysteine in the mucus thereby reducing mucus Productive cough Hypersensitivity Also used in management of
viscosity paracetamol poisoning
Nausea, gastric discomfort, GI Hypersensitivity, Active peptic ulcer,
Carbocisteine Liquefies viscid sputum Productive cough
bleeding, skin rash children under 2 years old
ANTITUSSIVES
A. NARCOTIC ANTITUSSIVE
Pholcodeine- has similar efficacy
(TD)Sedations, nausea, constipation
Directly suppresses cough center by Asthmatic px, px with diminished as codeine with longer duration
Codeine Higher dose: respiratory depression, Dry cough
binding to distinct receptors in medulla respiratory reserves (12hrs) with no analgesic or
drowsiness
addictive property
B. NON-NARCOTIC ANTITUSSIVES
Depress cough center in medulla and Stupor, ataxia, respiratory depression, children below 6 yrs., px taking
Dextromethorpan Spasmodic cough A synthetic compound
increasing the threshold for cough convulsion in children MOA inhibitors
Equally antitussive as codeine
Headache and Nausea Spasmodic cough *Asthmatic patients No narcotic, analgesic or
Noscapine Depress cough dependance properties
C. ANTI-HISTAMINICS
Drowsiness
Chlorpheniramine Nausea
Urinary retention Lack selectivity for cough centers
Diphenhydramine Sedative and anti-cholinergic action Vomiting
Blurred vision No efficacy in asthma
Promethazine Constipation
Headache
ANTI-ASTHMA
(BRONCHODILATOR RELIEVERS AND CONTROLLERS)
A. ß 2 AGONISTS
Terbutaline
Albuterol R isomer activate beta receptor
Salbutamol S isomer causes inflammation
Promotes bronchodilation
Fenoterol Throbbing headache, Tremors,
Activate G protein→↑ cAMP→↓ Asthma
tachycardia, palpitation
intracellular Ca
Formoterol Long acting
Salmeterol No anti-inflammatory property
B. SYMPATHOMIMETIC
Tachycardia, arryhtmia, worsening of Onset- 15 mins.
Epinephrine Bronchodilation CV: vasoconstriction Status asthmaticus
angina pectoris Duration- 60-90 mins.
C. MUSCARINIC ANTAGONISTS
Atropine Prototype drug
Only have partial reversible property
Ipratropium Treatment of asthma for COPD
Inhibit the effect of acetylcholine at
Inhibits M3 receptors
muscarinic receptors
Dizziness, ↑ intraocular pressure, Approved as treatment for COPD
Tiotropium
tachycardia
D. METHYLXANTHINES
Uncertain: phosphodiesterase Res: bronchodilation Anorexia, nausea, vomiting, abdominal
inhibition, adenosine receptor CV: cardiac stimulation discomfort, anxiety, headache,
Theophylline
antagonist (Katzung) Musculoskeletal: increased skeletal seizures, arrhythmias, insomnia Asthma, COPD Narrow therapeutic window
muscle strength (diaphragm)
Competitive nonselective PDE inhibitor
Aminophylline IV Non selective adenosine receptor Res: bronchodilation Bronchial asthma Less potent and shorter acting than
antagonist theophylline
ANTI-ASTHMA
(ANTI-INFLAMMATORY CONTROLLERS)
A. CORTICOSTEROIDS
 Oropharyngeal
candidiasis – inhaled
 effective in improving all indices
 Reduce airway reactivity give spacer devices
of asthma control—severity of
 Increase airway diameter  Hoarseness – advise
symptoms, tests of airway
 Inhibit lymphocytic, to drink H20 or
ORAL: caliber and bronchial reactivity,
eosinophilic airway mucosal gurgle after inhaler
frequency of exacerbations, and
inflammation  Adrenal insufficiency
Prednisone , Methyprednisolone (dose depend on severity) quality of life
 Reduce frequency of asthma – best time 8am to
INHALED:  Corticosteroid + LABA (Long
attacks mimic diurnal
Budesonide, Fluticasone (Long Acting q 12 hrs) Acting β2 Agonist) ( inhaled)
variation
 Potentiate effects of β2  Slow growth rate –
 Budesonide + Formeterol
agonists  Fluticasone + Salmeterol
children
(Seretide)
 Osteoperosis -
cataract
B. ANTI-LEUKOTRIENES
 prevent Leukotriene synthesis
5 – lipoxygenase inhibitor ( not available )
 Prevent LT action
Zileuton
liver toxicity  Bronchoconstriction, bronchial reactivity,
LTD4 – receptor Antagonist
Montelukast, Zafirlukast (available in market) mucosal edema, mucus hypersecretion
C. MAST CELL STABILIZERS

– inhibits degranulation of mast
INHALED: Aspirin-induced asthma
cell (inhibits histamine &
Na Cromoglycate
serotonin)
 are minor and are
localized to the sites
Inhibit antigen, exercise- induced of deposition.
asthma, slightly bronchial  throat irritation
reactivity  cough
Inhibit mast cell degranulation
 mouth dryness
Produces an alteration in the
 rarely, chest
function of delayed chloride
tightness, and allergic Cromolyn - poorly absorbed from the
channels in the cell membrane,
wheezing rhinoconjunctivitis gastrointestinal tract and must be inhaled as
inhibiting cell activation. This
 can be prevented by Applying the solution by a microfine powder or aerosolized solution.
Cromolyn, Nedocromil action on airway nerves is
inhaling a 2- nasal spray or eye Nedocromil also has a very low
thought to be responsible for
adrenoceptor drops several times a bioavailability and is available only in
nedocromil's inhibition of cough;
agonist before day is effective in about metered-dose aerosol form.
on mast cells, for inhibition of the
cromolyn or 75% of patient
early response to antigen
challenge; and on eosinophils, nedocromil
for inhibition of the inflammatory treatment
response to inhalation of  Serious adverse
allergens effects are rare
 Reversible
dermatitis, myositis,
or gastroenteritis
D. METHYLXANTHINES
Theophylline, theobromine, caffeine Inhibit phosphodiesterase, CNS: nervousness, tremors, Pentoxyfylline – decrease blood viscosity
increase CAMP ( relax smooth arousal ( for Reynaud or stroke due to thrombosis)
muscle, cardiac stimulation, CVS: + chronotropy, inotropy Their major source is beverages (tea, cocoa,
bronchodilation) in some tissues GIT: stimulate acid, enzyme and coffee, respectively)
including CGMP secretion ( give after meals) The importance of theophylline as a
PDE4 appears to be the most Kidneys: Increase GFR, Reduce therapeutic agent in the treatment of asthma
directly involved in actions of tubular Na reabsorption ( weak has waned as the greater effectiveness of
methylxanthines on airway diuretics) inhaled adrenoceptor agents for acute
smooth muscle and on Respiratory: relax muscles asthma and of inhaled anti-inflammatory
inflammatory cells. The inhibition Skeletal muscles: improve agents for chronic asthma has been
of PDE4 in inflammatory cells contraction of diaphragm established, but theophylline's very low cost
reduces their release of is an important advantage for economically
cytokines and chemokines, disadvantaged patients in societies in which
which in turn results in a health care resources are limited.
decrease in immune cell
migration and activation
Another proposed mechanism is
inhibition of cell-surface
receptors for adenosine. These
receptors modulate adenylyl
cyclase activity, and adenosine
has been shown to provoke
contraction of isolated airway
smooth muscle and histamine
release from airway mast cells. It
has been shown, however, that
xanthine derivatives devoid of
adenosine antagonism (eg,
enprofylline) may be potent in
inhibiting bronchoconstriction in
asthmatic subjects.
-research suggests that the
efficacy of theophyllines may be
due to a third mechanism of
action: enhancement of histone
deacetylation. Acetylation of core
histones is necessary for
activation of inflammatory gene
transcription. Corticosteroids act,
at least in part, by recruiting
histone deacetylases to the site
of inflammatory gene
transcription, an action enhanced
by low-dose theophylline.
E. ANTI – IgE MONOCLONAL ANTIBODIES

 decreases frequency & severity
inhibits binding of IgE to mast For chronic severe of asthma exacerbations
Omalizumab
cells asthma  inadequate control by high
dose inhaled steroid + LABA
 with IgE mediated sensitivity
AUTACOIDS
Role MOA Organ System Effects Antagonists
1. HISTAMINE
 Found in skin, GI Binds with membrane receptors: CNS I. Physiologic Antagonist
mucosa, lungs, liver, H1 *stimulate sensory nerve endings (pain, itch) Epinephrine
placenta, brain *smooth muscle *endothelium II. Inhibitors of Histamine Release
 Mediator of CVS Cromolyn, Nedocromil, β2 agonists inhibits degranulation of mast cells
immediate allergic & H2 *vasodilatation III. Histamine Receptor Antagonist
*gastric mucosa *cardiac muscle *brain * (+) inotropy A. H1 Receptor Antagonists (1st Generation)  for hypersensitivity reactions
inflammatory *immune cells * (-) chronotropy *fluid transudation 1. Sedation (1st generation, side effect) Highly sedative
reactions Diphenhydramineq6-8
 Gastric acid H3 RS * bronchoconstriction (H1) Dimhenhydrinateq8
secretion *pre-synaptic brain Promethazine (parenteral)
*myenteric plexus GIT Hydroxyzine (itarax) LA
*increased intestinal motility
H4 * increased gastric acid Moderately Sedative
*eosinophils *neutrophils *CD4T cells * increased pepsin Buclizine (appetite stimulant)
*Intrinsic Factor secretion Cinnarizine (vertigo/motion sickness)
Meclizine
Pheniramine
Cyproheptadine
Mild Sedative
Chlorpheniramine
Clemastine LA
Dimethidine
Methdilazine NA
Mepyramine NA
Triprolidine NA
Cyclizine NA
2.Anti-emetic, anti-nausea (Meniere’s syndrome) Rx:
Scopolamine (not available)
Promethazine (IM) Dimenhydrinate
Cyclizine
Meclizine (Bonamine)
Betahistine
Cenarizine
3.Anti-Parkinsonism  suppress extra-pyramidal Rx: Diphenhydramine
symptoms
4.Anti-cholinergic  urinary retention, blurred vision High anti-cholinergic action

(side effects) Promethazine
Diphenhydramine (Benadryl)
Dimenhydrinate
Pheniramine
Cyproheptadine
Low anti-cholinergic action

Chlorpheniramine
Hydroxyzine
Cyclizine
Meclizine
Minimal/ absent anti-cholinergic action

Clemastine
Terfenadine (arrhythmia effect)
Astemizole
Loratidine ( Alerta )
Ebastine
Cetirizine
5.Adrenoceptor-blocking (α)  orthostatic Rx: Promethazine (should be in supine postion)
hypotension
6. Serotonin blocking Cyproheptadine (appetite stimulant)
7.Allergy  Urticaria, Allergic rhinitis

Side Effects/Toxicity
Sedation, decreased alertness & concentration, motor incoordination, light-headedness, dryness of mouth, urinary hesitancy, blurring of vision
Cyclizine, Meclizine  teratogenic
B. H1 Blockers (2nd generation)
 Higher H1 selectivity Loratadine
 No anti-cholinergic side effects Desloratadine
 no CNS depressant property (Do not potentiate Cetirizine  inhibits H release & cytotoxic mediators from platelets & eosinophil chemotaxis
alcohol, benzodiazepine) Azelastine
 Inhibit late phase allergic reaction by acting on Ebastine
LT, anti-platelet activating effect Terfenadine  blocks cardiac K+ channels (overdose); Torsades de pointes
 Poor anti-pruritic, anti-emetic, anti-tussive Fexofenadine  no arrhthymogenic potential
properties
 Used for: Allergic rhinitis, conjunctivitis, hay
fever, urticaria, atopic eczema, acute allergic
reactions
C. H1 Blockers (3rd generation)
Levocetirizine
D. H2 Blockers
 Anti-ulcer Cimetidine  Cytochrome P450 inhibitor, anti-androgen effects
Ranitidine
Famotidine
Nizatidine
SEROTONIN
 Major source in CNS I. Serotonin (5-HT) Agonists
intestines (90%) *Vomiting A. 5HT1A Receptor
 Platelets *Pain Buspirone (anxiolytic)
 Brainstem (mood, *Itch B. 5HT1D Receptor
sleep, appetite, pain *Bezold-Jarisch reflex (5HT3) *chemoreceptor Amlotriptan NA
perception, reflex – marked outflow of vagal stimulation to Sumatriptan
temperature & BP the heart  bradycardia Zolmitriptan (constrict cerebral vessel)(migraine headache)
regulation, vomiting) C. 5HT4-Cisapride(toxic)
 Synthesized from CVS *vasoconstriction (5HT2) except skeletal Tegaserod (partial agonist) irritable bowel syndrome
tryptophan muscle, heart II. Serotonin (5-HT) Antagonists
 Degraded by MAO *platelet aggregation 1. 5HT1-5HT2 Methysergide
 5HT1,2,3,4,5,6,7 Ketanserin  blocks platelet aggregation for stroke Ritanserindecreases thromboxane formation
RS *bronchoconstriction (5HT2) 2. 5HT2
receptors for stroke
3. 5HT2, H1 Cyproheptadin  for cold-induced urticaria for carcinoid syndrome
GIT 4. 5HT3 Ondansetron  chemotherapy-induced nausea & vomiting
*increases motility thru ACh (5HT4)
Therapeutic Uses
1. controls S/S carcinoid,
Skeletal muscles *serotonin syndrome (5HT2) Cyproheptadine  sedative, stimulates appetite, good anti-pruritic
post-gastrectomy dumping syndrome
– *hyperthermia
Ketanserin  blocks platelet aggregation for stroke Ritanserindecreases thromboxane formation
2. Raynaud’s disease
for stroke
3. Anti-emetic Ondansetron
(anti-cancer, radiotherapy)
4. Migraine prophylaxis,
Methysergide
Carcinoid,
post-gastrectomy dumping syndrome
Sumatriptan
5. Migraine (better tolerated)
Zolmitriptan
Risperidine
6. Schizophrenia
Clozapine
ERGOT ALKALOIDS
Amine Alkaloids  Ergotamine, Ergonovine,
 Ergometrine Methysergide – migraine
 CNS – powerful hallucinogen headache (partial agonist α &
 Ergonomine (Lysergic Acid Diethylamide or LSD)  Nausea, vomiting (high dose) 5HT2)
Amino Acid/Peptide Alkaloids agonist, partial agonist, antagonist at α
 Ergotamine receptors, serotonin receptors, CNS  Bromocriptine inhibits prolactin  Prolonged vasospasm   Uterus – postpartum
 CVS – vasoconstriction d/t partial gangrene, bowel infarction hemorrhage, induces labor
 Regotoxine dopamine receptors
agonist effects at α adrenoceptors  Drowsiness, hallucinations  Ergonovine, Oxytocin
Semi-Synthetic Alkaloids
(parenteral),
 Ergometrine
Methylergometrine
 Ergonomine (Methergine) parenteral or oral
EICOSANOIDS
Mechanism of Action Organ System Effect Adverse Indications Contraindications Other notes
Effects
Arachidonic Acid Arachidonic Acid  CVS  Lipid-derived autacoids
Prostaglandins  Oxygenated by 4 routes:  TXA2, PGF2α – vasoconstriction,  Oxygenation products of polyunsaturated long chain fatty acids
 Lipoxygenase: bronchoconstriction, contraction of  Plant & fish oil precursors
HETEs, leukotrienes, lipoxins uterus  Arachidonic Acid – most important precursor
 Cytochrome P450  PGI2/prostacyclin, PGE1 –
(epoxygenase) – EETs, vasodilatation, bronchodila, relaxes Eicosanoid Inhibitors
vasodilator uterus  Corticosteroids: inhibits all pathways by stimulating synthesis of
 Icoeicosanoid:  Epoprostenol (PGI2) – pulmonary inhibitory protein, inhibit phospholipase A  prevent arachidonic acid
Isoprostane, vasoconstrictor HPN release
 Cyclooxygenase:  Alprostadil (PGE1) – patency of  Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): blocks
PG, prostacyclin, DA prostaglandin & thromboxane formation by inhibiting cyclooxygenase
thromboxane  COX inhibitor (Indomethacin) – activity
 PGH synthase-1 (COX-1): gastric closes ductus arteriosus  Aspirin (Acetylsalicylic Acid) – irreversible acetylation of platelet
epithelial protection  GIT cyclooxygenase (other drugs not irreversible); inhibits TXA2
 PGH synthase-2 (COX-2): source  Misoprostol/cytotec (PGE1) – for synthesis
in inflammation peptic ulcer (NSAID- induced), for  Mechanism of action: irreversibly inhibits platelet COX1
abortion (8-10 days)
Prostaglandin  Enprostil NA (PGE) – inhibit HCl  Indications: transient ischemic attack (TIA), CAD
Bind to receptors on cell surface secretion (coronary artery disease)
 Respiratory System  Adverse Effects:
 PGE2, PGI2 – bronchodilatation  Gastric/duodenal ulcer
 PGD2, TXA2 – bronchoconstriction  Hepatotoxic
 PGF2α, LT – bronchoconstriction  Allergy (most common)
 Platelet aggregation  Non-selective COX inhibitors – blocks prostaglandin, TXA2
 PGD2, PGE2, PGI2 – inhibit synthesis
 TXA2 – stimulate  Pyrazone – Phenylbutazone, Oxybutazone
 Aspirin – inhibits platelet COX1  Indole – Indomethacin, Sulindac
 Kidney  Propionic acid – Ibuprofen, Naproxen, ketoprofen
 PGE2, PGI2 – vasodilatation  Anthranilic acid – Mefenamic acid
 TXA2 – vasoconstriction  Aryl-acetic acid – Diclofenac
 Reproductive system  Oxicam – Piroxicam, Tenoxicam
 PGF2α, PGE2- uterine contraction,  Pyrolopyrole – Ketorolac
soften cervix  COX-2 Selective Inhibitors
 Dinoprostone, Misoprostol,  Mechanism of action: bind to and block active site of
Carboprost COX2 enzyme (reversible)
 PGE2, PGF2α – SE dysmenorrhea  Less GI effects, no platelet effect
(take NSAIDs)  Adverse Effects:
 Alprostadil (PGE1) – relax smooth  Fluid retention
muscle of corpora cavernosa for  Hypertension
erectile dysfunction  Hepatotoxic
 Nephrotoxic
Effects of lipooxygenase, cytochrome  Rashes
P450 metabolites:
 CVS
 12Hydroxyeicosatetraenoic
(HETE) – chemoattractant for
smooth muscles
 LTC4, LTD4 – myocardial
depressant, constriction of coronary
arteries
 GIT
 LTB4 – chemoattractant for PMNs
 Respiratory
 LTC4, LTD4 – bronchoconstriction,
mucus secretion, plasma exudation
 Blood
 LTB4 – chemoattractant for T cell,
eosinophils, monocytes, mast cells
 Renal System
 20 HETE – vasoconstriction
 EET – vasodilatation, natriuresis
VASOACTIVE PEPTIDES
ANGIOTENSIN RECEPTOR ANTAGONISTS
Arteriolar dilation
Selective competitive antagonist of decreased aldosterone secretion Hypertension Eprosartan, irbesartan, candesartan, olmesartan,
Valsartan angiotensin AT1 receptors increased sodium and water excretion telmisarta - similar to valsartan
CONVERTING ENZYME INHIBITORS

Arteriolar dilation
Inhibits conversion of angiotensin I to
decreased aldosterone secretion Hypertension heart failure
Enalapril angiotensin II
increased sodium and water excretion
Captopril and many others -similar to enalapril
RENIN INHIBITORS
Arteriolar dilation
Inhibits catalytic activity of renin decreased aldosterone secretion Hypertension
Aliskiren increased sodium and water excretion
KININ ANTAGONISTS
Potential use for
Selective antagonist of kinin B2 Blocks effects of kinins on pain, hyperalgesia,
inflammatory pain and
Icatibant receptors and inflammation
inflammation
VASOPRESSIN AGONISTS
Agonist of vasopressin V1 (and V2)
Vasoconstriction Vasodilatory shock
Arginine vasopressin receptors Terlipressin - more selective for V1 receptor
VASOPRESSIN ANTAGONISTS
Potential use in
Antagonist of vasopressin V1 (and V2) Vasodilation hypertension and heart Relcovaptan – increased selectivity for V 1
Conivaptan receptors failure hyponatremia receptor
NATRIURETIC PEPTIDES
Increased sodium and water excretion
Agonist of natriuretic peptide receptors
Nesiritide vasodilation Heart failure
VASOPEPTIDASE INHIBITORS
Decreases metabolism of natriuretic
Vasodilation
Omapatrilat peptides and formation of angiotensin II
increased sodium and water excretion
Hypertension heart failure
ENDOTHELIN ANTAGONISTS
Nonselective antagonist of endothelin Pulmonary arterial
Vasodilation Sitaxsentan, Ambrisentan - selective for ETA
Bosentan ETA and ETB receptors hypertension
receptors
VASOACTIVE INTESTINAL PEPTIDE AGONISTS

Vasodilation
Selective and nonselective agonists of Type 2 diabetes chronic
Multiple metabolic, endocrine, and other
Under development VPAC1 and VPAC2 receptors
effects
obstructive pulmonary
disease
SUBSTANCE P ANTAGONISTS
Prevention of
Selective antagonist of tachykinin NK1 Blocks several central nervous system effects
chemotherapy-induced
receptors of substance P
Aprepitant nausea and vomiting
NEUROTENSIN AGONISTS
Potential for treatment of
Agonist of central neurotensin
PD149163 Interacts with central dopamine systems schizophrenia and
receptors
Parkinson's disease
NEUROTENSIN ANTAGONISTS
Antagonist of central and peripheral Blocks some central and peripheral
None identified
Meclinertant neurotensin receptors (vasodilator) actions of neurotensin
CALCITONIN GENE-RELATED PEPTIDE ANTAGONISTS

Antagonist of calcitonin gene-related Blocks some central and peripheral
BIBN4096BS peptide (CGRP) (vasodilator) actions of CGRP
Migraine
NEUROPEPTIDE Y ANTAGONISTS
Selective antagonist of neuropeptide Y1 Blocks vasoconstrictor response to None identified
BIBP3226 receptors neurotensin
Urotensin Antagonists
Peptide antagonist of urotensin Blocks potent vasoconstrictor action of
Palosuran receptors endothelin Diabetic renal failure
NITRIC OXIDE
1. blood vessels
 vasodilator
 inhibits PMN adhesion to endothelium
2. respiratory system
NO activates soluble guanylyl cyclase  relax smooth muscles Hypoxic respiratory failure
to elevate cGMP levels in vascular  for pulmonary hypertension and ARDS and pulmonary
Nitric Oxide Methemoglobinemia Inhaled gas
smooth muscle 3. platelets hypertension
 inhibits platelet adhesion, aggregation,
enhance fibrinolysis
4. CNS
 modifies NT release, learning & brain
development

Comprehensive Table of Drugs: Cholinergic Agonists (Parasympathomimetics)

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Comprehensive Table of Drugs: Cholinergic Agonists (Parasympathomimetics)

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COMPREHENSIVE TABLE OF DRUGS

CHOLINERGIC AGONISTS (PARASYMPATHOMIMETICS)

CHOLINERGIC ANTAGONISTS (PARASYMPATHOLYTICS)

is also used to reduce

Beta Receptor Antagonists

D. CARDIAC GLYCOSIDES (DIGITALIS)

B. FIBRIC ACID DERIVATIVES (FIBRATES) – LIPOPROTEIN LIPASE STIMULANTS

↓ WBC or Hct T ½: Fenofibrate- 20 hrs

C. Adrenergic Neuron Blocking Drugs

II. DIRECT VASODILATORS

- Hydralazine - Minoxidil - Diazoxide - Fenoldopam

Peripheral vasodilator RX: - HPN

Nicardipine RX: Severe HPN – thru IV

2. Angiotensin Receptor Blocker

 Increase bronchial secretion by salt

Potassium Iodide Productive cough

C. MAST CELL STABILIZERS

E. ANTI – IgE MONOCLONAL ANTIBODIES

4.Anti-cholinergic  urinary retention, blurred vision High anti-cholinergic action

Low anti-cholinergic action

Minimal/ absent anti-cholinergic action

6. Serotonin blocking Cyproheptadine (appetite stimulant)

7.Allergy  Urticaria, Allergic rhinitis

CONVERTING ENZYME INHIBITORS

VASOACTIVE INTESTINAL PEPTIDE AGONISTS

CALCITONIN GENE-RELATED PEPTIDE ANTAGONISTS

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