Pharmacology Final Flashcards
(3) Natural catecholamines
Epinephrine, Norepinephrine, and Dopamine
(2) synthetic catecholamines
Isoproterenol and Dobutamine
(2) Synthetic Non-Catecholamines
Ephedrine and Phenylephrine
Which catecholamines do not stimulate Alpha?
Isoproterenol and Dobutamine
Which catecholamine has no affect on Beta-1?
Phenylephrine
Which catecholamines have a negative effect CO and HR?
Norepinephrine and Phenylephrine
Which catecholamines cause the greatest increase in peripheral vascular resistance?
Norepinephrine and Phenylephrine
Which (3) catecholamines cause the greatest decrease in airway resistance?
Epinephrine, Isoproterenol, and Ephedrine
Which catecholamine has a direct and indirect mechanism of action?
ephedrine
Which catecholamines cause the greatest increase in MAP?
Norepinephrine and Phenylephrine
Example of Prototype Sympathomimetic
Epinephrine
Where is Epineprhine synthesized and stored?
adrenal medulla
Why shouldn’t Epi be given orally?
rapidly metabolized by the GI and liver
What explains Epi’s lack of cerebral effects?
poor lipid solubility
Primary locations of Alpha-1 receptors
cutaneous, splanchnic, and renal vascular beds
Which catecholamines have the greatest risk of dysrhythmia?
Epinephrine and Isoproterenol
How does epinephrine affect the cardiac cycle?
accelerates rate of spontaneous depolarization (phase 4)
- increases HR
- increases likelihood of dysrhythmia
Avoidance of Epi in Beta Blockades
Epi induces bronchoconstriction from stimulation of alpha-receptors in the presence of a beta-blockade
Which catecholamine has the greatest effect on metabolism?
Epinephrine
Ocular effects of Epinephrine
mydriasis
(dilation of the pupil)
(3) Coagulation effects of Epinephrine
- accelerates coagulation due to hypercoagulable state
- increases total leukocyte, but causes eosinopenia
- increases factor V activity
Synthesis and storage of Norepinephrine
postganglionic sympathetic nerve endings
Norepinephrine produces arterial and venous vasoconstriction in all vascular beds except in _____
coronary arteries
- Norepinephrine dilates coronary arteries
Why should Norepinephrine be used cautiously in patients with right ventricular failure?
increases venous return and pulmonary artery pressure
Pathway of Catecholamine Systhesis
Phenylalanine
Tyrosine
Dopa
Dopamine
Norepinephrine
Epinephrine
Unique features of Dopamine
able to increase contractility, renal blood flow, GFR, sodium excretion, and urine output simultaneously
Renal dose of Dopamine
1 - 3 ug/kg/min
increass splanchnic and renal blood flow
Negative side effects of Dopamine
tachycardia and increase PVR
- not good for right heart failure
Most potent sympathomimetic with Beta activity
Isoproterenol
Clinical uses for Isoproterenol
heart block and RV failure
Clinical uses for Dobutamine
CHF, weaning from CPB, and pulmonary hypertension
Effects of Ephedrine
increases:
HR, CO, BP, and coronary blood flow
In which two disease states is Phenylephrine particularly useful?
aortic stenosis and CAD
- increases coronary perfusion without chronotropic side effects
Phenylephrine Overdose
activates SNS
(hypertension, tachycardia, and baroreceptor-mediated bradycardia)
- Phentolamine
- alpha-1 antagonist
- may use NTG and nitroprusside
- beta blockers are contraindicated
(3) most common Beta-2 Agonists
Albuterol, Metaproterenol, and Terbutaline
In addition to bronchospasm, what else can Beta-2 Agonists treat?
premature uterine contractions
(tocolytics)
Clinical uses for Digoxin
supraventricular tachydysrhythmias
(paroxysmal atrial tachycardia, A-fib, A-flutter)
Digoxin Features
cardiac glycoside that decreases conduction through the AV node
- IV onset 10-30 minutes
- inhibits Na+/K+ ATPase
- increases CO, SV, renal perfusion
- decreases LVEDP
- can co-administer with beta blockers
(5) Causes of Digoxin Toxicity
- renal dysfunction
- hypoxemia
- hypokalemia
- hypercalcemia
- hypermagnesemia
EKG changes in Digoxin
scaphoid effect
Diagnosis of Digoxin Toxicity
anorexia, nausea, and plasma concentration
- will also see EKG changes
- arrhythmias
- long PR and heart block
Treatment of Digoxin Toxicity
- correct the causes
- treat cardiac dysrhythmias
- phenytoin, lidocaine, or atropine
- temporary pacemaker
- if complete heart block
Contraindications for Digoxin
HOCM and WPW
Hypertrophic Obstructive Cardiomyopathies (HOCM)
idiopathic LVH and subaortic stenosis
- leading cause of death in young athletes
- Digoxin contraindicated
Wolff-Parkinson-White Syndrome (WPW)
pre-excitation syndrome due to secondary accessory AV pathway (bundle of Kent)
- EKG shows delta wave and short PR interval
- “circus rhythm”
(5) Adverse Drug Interactions with Digoxin
- Quinidine
- Succinylcholine
- Sympathomimetics with B-agonist effects
- IV calcium
- some diuretics
Effects of Phosphodiesterase Inhibitors
positive inotropic effects with vasodilation
- act independently of B-receptors; therefore, effective in B-blocked patients
- enhance actions of catecholamines
- improves location of Starling curve
(2) Types of Phosphodiesterase Inhibitors
Amrinone and Milrinone
Total serum calcium includes:
Ca2+ bound to albumin, complexed with citrate and phosphate, and free (ionized) Ca2+
- free calcium is the active ion that can be measured
Events needing Calcium
- massive transfusion
- calcium binds to the citrate in PRBCs
- CP bypass
- due to multiple units of blood
- parathyroidectomy
- if hyperparathyroidism
How is Calcium Chloride administered?
through a central line
- has a very low pH
- always aspirate line first
Another term for the Sympathetic system
thoraco-lumbar
Another name for the Parasympathetic System
Cranio-Sacral
Major tissues affected by Alpha-1
Smooth muscle and sphincters
Major tissues affected by Alpha-2
nerve endings
Major tissues effected by Beta-1
Cardiac and Kidney muscle
Major tissues effected by Beta-2
smooth muscle, bronchi, liver, and skeletal muscle
Major tissue effected by Beta-3
Adipose
Major tissue effected by DA-1
Smooth muscle, renal, mesenteric, and cardiac
Major functions of Alpha-1
contraction and constriction
Major function of Alpha-2
decrease transmitter release
Major function of Beta-1
increase HR, contractility, and renal secretion
Major function of Beta-2
relax smooth muscle
increases gluconeogenesis, glycogenolysis, and potassium uptake
Major function of Beta-3
increase lipolysis
Major function of DA-1
relax renal vascular smooth muscle
(higher doses activates Beta-1 and alpha-1)
What two enzymes inactivate catecholamines?
MAO and COMT
Dose of Epinephrine for Cardiac Arrest
0.1 mL/kg of 1:1000 via ETT
or
0.1 mL/kg of 1:10,000 via IV/IO
Epinephrine dose for Status Asthmaticus
0.01 mg/kg of 1:1000 sq
(2) Non-Selective Alpha Antagonists
Phentolamine and Phenoxybenzamine
(4) Alpha-1 Antagonist
Prazosin, Doxazosin, Terazosin, and Tamulosin
-osin
(2) Alpha-2 Agonists
Clonidine and Dexmedetomidine
(2) Combined Alpha and Beta Antagonists
Lavetolol and Carvedilol
Which part of the nervous system uses Norepinephrine (rather than acetylcholine)?
sympathetic post-ganglionic
Alpha-2 (CNS) agonist acts like an ______ antagonist
Alpha-1
Phentolamine
(regitine)
non-selective alpha antagonist
- peripheral vasodilation and decrease BP
Phentolamine Clinical Uses
treatment for acute hypertensive emergencies
- pheochromocytoma
- autonomic hyperreflexia
Phenoxybenzamine
(dibenzyline)
non-reversible and non-selective Alpha Antagonist
- used preoperatively for Pheochromocytoma
- Raynauds
- preferentially dilates cutaneous arteries
Pheochromocytoma
tumor of the adrenal medulla
- secretes excessive amounts of Epi and NE
- Malignant hypertension
Pheochromocytoma
(preoperative preparation)
- alpha blockade
- phenoxybenzamine
- add CCB if needed
- Beta blocker for tachycardia
- fluid replacement
In a patient treated with propranolol and phenoxybenzamine prior to resection of a solitary pheochromocytoma, would you expect postoperative hypotension or hypertension?
Hypotension
- hypovolemia
- residual BB and alpha blockade
- adrenal insufficiency
Doxazosin
(cardura)
Alpha-1 Antagonist
- treatment for hypertension and BPH
- relaxes prostatic and vascular smooth muscle
Prazosin
(minipres)
alpha-1 Antagonist
- used for HTN and CHF
- dilates arterioles and veins
Terazosin
(hytrin)
Alpha-1 Antagonist
- used for BPH
- relaxes prostatic smooth muscle
Tamulosin
(flomax)
Alpha-1 Antagonist
- used for BPH
- may cause orthostatic hypotension and syncope
Alpha-2 Receptor Agonists
bind pre-synaptically and reduce NE release
- mostly in CNS
- uses a negative feedback mechanism
Clonidine
centrally-acting Alpha Agonist
- decreases HR and BP
- added to regional anesthetics
Dexmedetomidine
Alpha-2 Agonist
- sedative and analgesic
- central sympatholytic effects
- avoid in liver failure
(3) Non-selective Beta Antagonists
Propranolol, Labetalol, and Sotalol
Blockade of Beta-1 in the kidney
decreases renin
- vasodilation and decreased BP
- decreased aldosterone
- salt and water retention
- decreased NE release
Best drug for controlling Torsades de Pointess in patients with prolonged QTc
Propranolol
Best drugs to give patients with CHF
Metoprolol and Carvedilol
Labetalol
(normodyne and trandate)
Alpha-1 and non-selective Beta Antagonist
- used for hypertension and controlled hypotension
- 1 - 5 min onset
Treatment for Beta Blocker Toxicity
- Atropine
- Isoproterenol
- Dobutamine
- Glucagon
- Calcium Chloride
Blockade of Beta-2 receptors in the bronchi will cause _____
bronchoconstriction
Why should Beta-1 blockers be used with caution in diabetic patients?
can impair receovery from hypogylcemia and mask symptoms of hyperglycemia
Which beta blocker does not cross the placenta?
esmolol
Contraindications to Beta Blockers
- heart blocks and sinus arrest
- hypovolemic patients with compensatory tachycardia
- COPD (relative)
- conditions that would result in unopposed alpha stimulation
- cocaine and pheochromocytoma
Propranolol decreases the clearance of _____ local anesthetics
amide
- increased LA toxicity
- especially bupivicaine
Esmolol
(brevibloc)
short-acting Beta-1 Antagonist
- fast onset and half-life
- hydrolysis by plasma esterases
Metoprolol
(lopressor)
Beta-1 Antagonist
- large doses become non-selective
Atenolol
(tenormin)
most selective Beta-1 Antagonist
- used in CAD patients at high risk of MI
Timolol
Beta Antagonist
- eyedrops used for Glaucoma
- systemic absorption can cause bradycardia and increase airway resistance
Carvedilol
(coreg)
Alpha-1 and non-selective Beta Antagonist
- weak vasodilator
- treats mild CHF and hypertension
Which types of CCB are selective for the AV node?
Benzothiazepines and Phenylalkylamines
Which type of CCB is selective for arteriolar beds?
Dihydropyridines
Calcium Channel Blockers
decrease HR by decreasing the speed of conduction through the SA and AV node
- reduce contractility and relax vascular smooth muscle
- treats coronary spasms, angina, and SVT
(1) Benzothiazepine example
Diltiazem
(1) Phenylalkylamine example
Verapamil
Verapamil
CCB
(phenylalkylamine)
- slows conduction through AV node
- negative chronotropic effect on SA node
- avoid in WPW
Nifedipie
CCB
(dihydropyridines)
- coronary and peripheral arterial vasodilation
- no AV or SA node depression
Which CCB has the greatest vasodilating effects?
Nicardipine
Nimodipine
CCB
(dihydropyridine)
- CNS vasodilation of large cerebral arteries
- good for cerebral vasospasm following sub-arachnoid hemorrhage
What causes cerebral vasospasms?
influx of Ca2+ ions causing contraction of smooth muscle cells in large cerebral arteries
Diltiazem
(cardizem)
CCB
- selective for AV node
- used for SVT and angina
(benzothiazepine)
Which (2) CCB increase risk of LA toxicity
Verapamil and Diltiazem
(4) ACE inhibitor examples
Captopril, Enalopril, Lisinopril, and Ramipril
-pril
ACE Inhibitors
treat hypertension secondary to increases renin production
- may delay onset of renal disease in DM
- no bronchospasm or bradycardia