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
NICOTI NI C RECEPTORS
Found in autonomic ganglia of the PNS and the SNS
Ligand-gated Na+/K+ channels
Activated by nicotine and ACh

MUSCARI NI C 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 INHIBI TORS are i ndi rect agoni sts
End in -stignine

BOTULINUM TOXIN prevents rel ease of neurotransmi tter at al l
chol i nergi c termi nal s

ACETYLCHOLINE RECEPTORS
ATROPINE (from Atropa bel l adonna)
Increased heart rate
Increased conduction velocity through the AV node
Bronchodilation
Increased body temperature (decreased sweating)

Bl ockage i s reversible i . e. can be overcome by a l arger
concentration of acetylcholine or muscari nic agoni st

MUSCARINIC RECEPTOR BLOCKERS




ALPHA RECEPTORS
ALPHA RECEPTORS
1 (heart and ki dney)
Increase intracellular cAMP
Increased heart rate and contractility
Increased renin release
Increased lipolysis

2 (respiratory and vascular smooth muscl e)
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 sodi um retention and bl ood vol ume

1. VASODILATORS: rel ax vascular smooth muscl e i n resi stance
vessels

1. ACE INHIBITORS: reduce peri pheral vascular resi stance and
bl ood vol ume

2. SYMPATHOLYTICS: reduce peripheral vascular resi stance and
cardi ac output


ANTIHYPERTENSIVES
DIURETICS



ACE i nhi bitors i nhi bit the production of angi otensin II from
angi otensi n I

Counteract the ef fects of reni n- angiotensin system wi thout
refl ex sympathetic acti vation

Lower bl ood pressure pri nci pally by decreasi ng peri pheral
vascular resi stance

Tx l ong- term treatment of congestive heart fai l ure, post -
myocardial i nfarcti on, and hypertension



ACE INHIBITORS (-PRILS)
RENIN-ANGTIOTENSIN SYSTEM
Vasodilator of both
arterioles and vei ns
Can cause decreased cardiac
output

Administered i ntravenously
to treat hypertensi ve
emergencies

NO causes vasodilation
through acti vation of
guanylate cycl ase i n
vascular smooth muscl e

Of ten admi nistered wi th a
- bl ocker


NITROPRUSSIDE
GOAL = SNS
PHOSPHODIESTERASE-3 INHIBITORS
Milrinone
Mechani sms of arrhythmia
Increased automaticity of pacemaker or nonpacemaker cells
Reentrant pathways
Triggered activity

Goal of anti arrhythmia drugs:
ANTIARRHYTHMIA DRUGS
CLASS IA: moderate bl ock
phase 0 upstroke rate; prolonged AP duration
Quinidine

CLASS IB: mi l d bl ock
phase 0 upstroke rate; shortened AP duration
Lidocaine

CLASS IC: marked bl ock
phase 0 upstroke rate; no change in AP duration
Flecainide

CLASS I : BLOCK FAST NA+ CHANNELS
CLASS II: -BLOCKERS (-OLOLS)

CLASS III: BLOCK K+ CHANNELS
(TILIDES)
CLASS IV: BLOCK L-TYPE CALCIUM
CHANNELS
Verapamil
Diltiazem
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