Pharm Review
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Transcript of Pharm Review
HIGH YIELD PHARMACOLOGY
ANS PHARMACOLOGY
PARASYMPATHETIC DIVISION = “rest and digest” Decreased heart rate Bronchioles constrict Increased motility and secretion in the digestive tract Increased secretion from the salivary glands, pancreas Sweating Release of urine
AUTONOMIC NERVOUS SYSTEM
SYMPATHETIC DIVISION = “fight or flight” Increased heart rate Blood vessels to the heart and the extremities dilate Liver produces glucose to provide energy for muscle
contraction Bronchioles dilate Pupils dilate Urinary retention
AUTONOMIC NERVOUS SYSTEM
NICOTINIC RECEPTORS Found in autonomic ganglia of the PNS and the SNS Ligand-gated Na+/K+ channels Activated by nicotine and ACh
MUSCARINIC RECEPTORS Found in neuromuscular junctions G protein-coupled receptors that act through 2 nd messengers 5 subtypes: M1, M2, M3, M4, M5 Activated by muscarine and ACh
CHOLINESTERASE INHIBITORS are indirect agonists End in -stignine
BOTULINUM TOXIN prevents release of neurotransmitter at all cholinergic terminals
ACETYLCHOLINE RECEPTORS
ATROPINE (from Atropa belladonna) Increased heart rate Increased conduction velocity through the AV node Bronchodilation Increased body temperature (decreased sweating)
Blockage is reversible i.e. can be overcome by a larger concentration of acetylcholine or muscarinic agonist
MUSCARINIC RECEPTOR BLOCKERS
ALPHA RECEPTORS
ALPHA RECEPTORS
β1 (heart and kidney) Increase intracellular cAMP Increased heart rate and contractility Increased renin release Increased lipolysis
β2 (respiratory and vascular smooth muscle) Increase intracellular cAMP Vasodilation Bronchodilation (hormonal epinephrine) Increased heart rate and contractility Increased lipolysis Increased insulin release
ADRENERGIC RECEPTORS
ADRENERGIC AGONISTS
EFFECTS OF ADRENERGIC AGONISTS
DIRECT SYMPATHOMIMETICS
Increase the release of stored catecholamines Amphetamine
Block reuptake of catecholamines Duloxetine, cocaine
Block the enzymatic breakdown of norepinephrine MAO and COMT inhibitors
INDIRECT SYMPATHOMIMETICS
CARDIAC PHARMACOLOGY
CARDIAC FAILURE Cardiac glycosides Sympathomimetics Phosphodiesterase-3
inhibitors Vasoconstrictors
HYPERTENSION Diuretics Vasoconstrictors Sympatholytics
ARRHYTHMIAS Class I: Fast Na+
channel blockers Class II: Beta
blockers Class III: K+
channel blockers Class IV: L-type
Ca2+ channel blockers
Adenosine
OVERVIEW
At a given left ventricular end-diastolic pressure, cardiac output is lower than in a normal heart
Diuretics reduce LVEDP
Inotropic drugs shift the curve upward, toward normal
HEART FAILURE
Inhibits sodium-potassium ATPase, which increases intracellular Ca2+ and force of contraction
Increases vagal tone Decreases heart rate Decreases conduction
velocity at the AV node Increases refractory period
Toxic effects = sinus bradycardia and SA block
CARDIAC GLYCOSIDES (DIGITALIS)
ELECTRICAL EFFECTS OF DIGITALIS
Delayed afterdepolarizations may develop resulting in triggered tachyarrhythmias
1. DIURETICS: decrease sodium retention and blood volume
2. VASODILATORS: relax vascular smooth muscle in resistance vessels
3. ACE INHIBITORS: reduce peripheral vascular resistance and blood volume
4. SYMPATHOLYTICS: reduce peripheral vascular resistance and cardiac output
ANTIHYPERTENSIVES
DIURETICS
ACE inhibitors inhibit the production of angiotensin II from angiotensin I
Counteract the effects of renin-angiotensin system without reflex sympathetic activation
Lower blood pressure principally by decreasing peripheral vascular resistance
Tx long-term treatment of congestive heart failure, post-myocardial infarction, and hypertension
ACE INHIBITORS (-PRILS)
RENIN-ANGTIOTENSIN SYSTEM
Vasodilator of both arterioles and veins Can cause decreased cardiac
output
Administered intravenously to treat hypertensive emergencies
NO causes vasodilation through activation of guanylate cyclase in vascular smooth muscle
Often administered with a β-blocker
NITROPRUSSIDE
GOAL = SNS
PHOSPHODIESTERASE-3 INHIBITORS
Milrinone
Mechanisms of arrhythmia Increased automaticity of pacemaker or nonpacemaker cells Reentrant pathways Triggered activity
Goal of antiarrhythmia drugs:
ANTIARRHYTHMIA DRUGS
CLASS IA: moderate block ↓↓ phase 0 upstroke rate; prolonged AP duration Quinidine
CLASS IB: mild block ↓phase 0 upstroke rate; shortened AP duration Lidocaine
CLASS IC: marked block ↓↓↓ phase 0 upstroke rate; no change in AP duration Flecainide
CLASS I: BLOCK FAST NA+ CHANNELS
CLASS II: β-BLOCKERS (-OLOLS)
CLASS III: BLOCK K+ CHANNELS (–TILIDES)
CLASS IV: BLOCK L-TYPE CALCIUM CHANNELS
VerapamilDiltiazem
ADENOSINE
Administered intravenously, adenosine is the most effective drug for the rapid termination of reentrant SVT,
such as AV nodal reentrant tachycardia.
RESPIRATORY PHARMACOLOGY
ASTHMA Characterized by acute episodes of bronchoconstriction
caused by underlying air-way inflammation Leukotrienes and histamine induce smooth muscle
contraction, mucus secretion, and recruitment of inflammatory cells
CHRONIC BRONCHITIS Pulmonary obstruction caused by excessive production of
mucus due to hyperactivity of mucus-secreting goblet cells
RHINITIS Decrease in nasal airways due to thickening of the mucosa
and increased mucus secretion
GLUCOCORTICOIDS
LEUKOTRIENE INHIBITORS
MAST CELL STABILIZERS
ANTI-INFLAMMATORY DRUGS