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103 Cards in this Set

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1.The ANS works to do what?
1. maintain normal internal functions and work with the somatic nervous system.
2. The enteric nervous system is the ___ division of the ___. What is it and what does it innervate?
2. third; ANS; meshwork of nerve fibers that innervate the viscera (GI, pancreas, and gall bladder)
The ANS is working when?
All the time.
Name some parasympathetic functions in regards to pupils, saliva, heart, bronchi, GI, bile, and bladder.
Constricts pupils, stimulates flow of saliva, slows heartbeat, constricts bronchi, stimulates peristalsis and secretion, stimulates release of bile, contracts bladder.
The PNS arises from what structures?
Ganglion, medulla oblongata, vagus nerve, S2-S4, craniosacral.
Name some sympathetic functions in regards to pupils, saliva, heart, bronchi, GI, bile, and bladder.
Dilates pupils, inhibits flow of saliva, dilates bronchi, inhibits peristalsis and secretion, conversion of glycogen to glucose, secretion of adrenalin to noradrenalin, inhibits bladder contraction.
The SNS arises from what structures?
What does "cholinergic" refer to?
The effects of ACh.
Where do "cholinergic" effects take place?
PNS (PS ganglia and effector cells), parts of SNS (sympathetic ganglia, adrenal medulla, sweat glands), some CNS neurons, somatic nerves innervating skeletal muscle.
What does "adrenergic" refer to?
Effects of noradrenaline (norepinephrine).
Where do "adrenergic" effects take place?
Postganglionic sympathetic fibers at end-organ tissues.
What are the two types of cholinergic receptors?
Muscarinic and Nicotinic
Where are nicotinic receptors located?
Ganglia (ANS, SNS, PNS) and skeletal muscle.
Where are muscarinic receptors?
1. Glands (lacrimal, sweat, gastric)
2. Smooth muscle (bronchial, GI, bladder, blood vessels)
3. Heart (SA and AV node)
Alpha blockers bind ___ to alpha receptors.
Alpha blockers Interfere with the ability of ____ or other ____to provoke what?
Alpha blockers interfere with ability of catecholamines or other sympathomimetics to provoke alpha responses on the heart & peripheral vasculature.
How do alpha blockers affect the effects of epinephrine on insulin production?
The inhibitory effect of epinephrine on insulin production is prevented, thus insulin production is NOT reduced.
Name three major side effects of alpha blockers.
Orthostatic hypotension, baroreceptor-mediated reflex tachycardia, impotence.
The absence of beta blockade with alpha blockers allows for what?
Maximum expression of cardiac stimulation from norepinephrine.
What is competitive inhibition and which alpha antagonist drugs have this property?
1. reversible binding with receptors
2. phentolamine, prazosin, yohimbine
What is a covalent receptor bond and which alpha antagonists bind this way?
1. irreversible and insurmountable blockade
2. phenoxybenzamine
How can you reverse phenoxybenzamine effects?
You can't. Once the blockade is in effect, even massive doses of sympathomimetics are ineffective UNTIL METABOLISM OF phenoxybenzamine takes place.
What receptors do phentolamine and phenoxybenzamine antagonize?
Postsynaptic alpha 1, presynaptic alpha 2
Prazosin receptor?
Alpha 1
Yohimbine receptor?
Alpha 2
Phenoxybenzamine (Dibenzyline).

Type of bond, receptor, onset and elimination?
Selective A1 and 2 blocker, covalent bond (ethyleneimine), a1>a2, slow onset (>60 minutes to reach peak, IV or PO, d/t the long time needed for structural change to take place that renders drug active), Te1/2 24 hours (cumulative)
What are the cardiac effects of phenoxybenzamine (dibenzyline)?
*Orthostatic hypotension if hypotension or hypovolemia
*impairment of compensatory vasocx-> exaggerated drop in BP in response to blood loss or vasod. drugs
*CO, renal bloodflow unchanged (unless preexisting renal vasocx
Cerebral effects of phenoxybenzamine (dibenzyline)?
*crosses bbb
*N/V, sedation, depression, lethargy
Phenoxybenzamine (dibenzyline) effects on insulin, glycogenolysis, eyes, and other tissues?
*prevents inhibitory effects of epi on the secretion of insulin (more secreted)
*catecholamine induced glycogenolysis in skeletal muscle/fat not altered
*nasal stuffiness-d/t unapposed alpha blockade vasod. in mucus membranes
What is the main thing phenoxybenzamine (dibenzyline) is used for?
Preoperative treatment of HTN in pts with pheochromocytoma b/c with chronic alpha blockade, it relieves intense periph. vasocx, allowing expansion of IV volume as reflected by a drop in HCT.
What is the dose of phenoxybenzamine (dibenzyline)?
0.5-1mg/kg PO
What are other indications for phenoxybenzamine (dibenzyline)?
*Pt with excessive vasocx with assoc. tissue ischemia (hemorrhagic shock) but only after IV resuscitation.
*Reynauds, any dz with large component of vasocx.
What is the action of phentolamine?
*transient non-selective alpha blockade (10-15min)
What are the alpha1 and 2 effects of phentolamine?
*A1: peripheral vasod and decreased BP within 2 min; elicits baroreceptor-mediated cardiac stim. reflex
*A2: enhances neural release of N.E.; CO/HR, angina, dysrhythmias
What are some other effects of phentolamine?
Parasympathetic override: hyperperistalsis, abdominal pain, diarrhea.
What are the indications for phentolamine? Doses?
*Acute HTN emergencies, intraop mgmt of pheochr., ANS hyperreflexia (30-70mcg/kg IV (prompt/transient decrease in BP, may use drip)
*Accidental EV injection of sympathomimetic drug (2.5-5mg in 10ml for local infiltration)
What is the action of yohimbine?
Blocks presynaptic alpha 2 receptors -> enhanced release of N.E. from nerve endings
What does yohimbine treat?
*Idiopathic orthostatic hypotension
5 other signs of cyanide tox?
Methhemoglobinemia, increased MVO2 content, tachycardia, increased ICP, met acidosis.
What is the action of Prazosin?
*selective postsyn. A1 blocker
*leaves intact the inhibitory action of A2 receptor activity on N.E. release from nerve endings -> less likely than nonselective to cause reflex tachycardia
*dilates both arterioles and veins
Clinical use of prazosin? Dose?
*Preop tx of HTN in pt with pheochromocytoma (0.5-1mg/kg PO)
How do beta blockers work at the receptor level?
*Bind to beta adrenergic receptors and block effects of cate. and symptathom. on the heart and smooth muscles of the airways and blood vessels
Why should BB be continued during the perioperative period?
To avoid reflex SNS hyperactivity.
What type of inhibition do BB exert?
Competitive inhibition.
Can BB be reversed?
Yes. With beta agonist by displacement if large amt given.
What happens with chronic BB administration?
Beta blockes are derived from what?
Isoproterenol, a beta agonist
What determines if a a drug is a beta agonist or antagonist?
Substitutions on benzene ring.
Which forms are more potent: levorotatory or dextrorotatory?
Levorotatory; lefties rock! For example, propranolol has <1% the potency of the levorotatory form.
Which drugs are nonselective BB?
Propranolol, nadolol, timolol, pindolol.
Which drugs are cardioselective for B1?
Esmolol, atenolol, metoprolol, acebutolol, betaxolol.
Beta-receptor selectivity is ___-___.
When is beta receptor selectivity lost?
When large doses of the antagonist is given.
Which drugs are pure beta antagonists and what does this mean?
metoprolol, atenolol, propranolol, nadolol

These have absent intrinsic sympathomimetic activity.
Which drugs are partial beta antagonists and what does this mean?
timolol, pindolol, acebutolol, betaxolol

These have intrinsic sympathomimetic activity.
How are partial and pure beta antagonists different?
*Partial ant. cause less direct myocardial depression and less heart rate slowing than pure BB.
*Partial BB may be better tolerated in pts with poor left ventricular function.
What is unique about propranolol?
*First clinical BB.
*Standard to which all others are compared.
What receptors are blocked by propranolol?
B1 and B2 (equal antagonism) nonselectively

Pure antagonist
With propranolol, what heart rate indicates optimal plasma concentration?
What are the cardiac effects of propranolol?
*Decreased HR, MC, CO d/t B1
*Increased PVR, CVR d/t B2
*although prolongation of sys dilation and dilation of cardiac ventricles increase MO2 requirements, O2 sparing effects of decreased HR and MC predominated (compensate)
GI effects of propranolol?
*rapid GI absorption
*95% 1st pass absorption, limiting bioavailability
*Up to 20 fold variation in 1st pass availability in similarly doses pts.
Dose of propranolol?
PO 40-800mg/d
IV 0.05mg/kg in increments of 0.5-1mg q5min

(note the large disparity in PO vs IV dosing)
Describe clearance, t1/2 of propranolol.
*hepatic clearance
*t1/2: 2-3 hours
*elimination decreased when hepatic BF decreased. May decrease its own clearance rate by decreasing CO and hepatic BF.
*Renal failure does not alter but increased metabolites do accumulate.
Describe L.A. drug interactions with propranolol.
*Propranolol decreases clearance of amide L.A. by decreasing hepatic BF and inhibition of liver metab.
*Bupivicaine clearance decreased 35%.
*Higher chance of tox
Describe opioid drug interactions with propranolol.
*pulm 1st pass uptake of fentanyl highly decreased.
*2-4x injected fentanyl enters sys. circ (inc. OD risk)
*response reflects ability of one basic lipophilic amine to inhibit pulmonary uptake of another.
What type of antagonist is metoprolol?
Beta 1, selective. Prevents inotropic and chronotropic responses to beta stimulation.
Is it ok to use Metoprolol in pts with PVD/COPD? Why or why not?
Yes, because there are no beta2 blocking properties at normal dose of 2-15mg IV.
What happens if larger doses of metoprolol are given?
It becomes nonselective.
Describe PK of metoprolol.
*high hepatic first pass metabolism (only 40% reaches systemic circulation)
*poorly protein bound (10%)
*T1/2e - 3 hours
What is the MOST selective beta blocker?
Why is periop tx with atenolol beneficial?
Prevents post-MI in CAD pts.
What are the CNS effects?
Enters CNS in small amounts but still produces fatique/depression.
Can it be used in IDDM patients? Why/why not?
*It can in IDDM patients when HTN is not controlled by other antiHTNs.
*It does not potentiate insulin-induced hypoglycemia seen with other nonselective BB.
Describe atenolol PK.
*50% of PO dose absorbed by GI. *Little to no hepatic metab. *Renal excretion. *t1/2e: 6-8 hours
What are the dosage ranges for atenolol?
PO: 50-100mg/day

IV: 5mg over 5min followed by another 5mg 10min later (for acute MI).
How does renal failure affect elimination of atenolol?
Prolongs greater than 24 hours.
What is esmolol?
Short acting B1 blocker given only IV.
What is the dose of esmolol?
What are the indications for esmolol?
*Intraop HTN/tachycardia from noxious stim and intubation.
*Prior to ECT.
*Pheochromocytoma, thyrotoxicosis, PIH, epinephrine or cocaine induced CV toxicity
Why is esmolol used for intraop HTN/tachycardia?
Lidocaine and fentanyl used perioperatively to blunt stress response only blunts BP, not heart rate.
Why is esmolol used for ECT?
Attenuation of HR increase and decrease length of seizure.
What is the pH of esmolol?
Ph 4.5-5.5
Describe the t1/2e and metabolism of esmolol.
9 min. Metabolized by plasma esterases (different from plasma cholinesterase) completely independent of hepatic and renal function.
After dosing with esmolol, how long does it take to peak and how long until heart rate returns to pre-drug level?
Takes 5min to peak, 10-30min to return to pre-drug HR.
CNS effects of atenolol?
Poor lipid solubility prevents large amounts from crossing BBB but IT STILL CROSSES.
What does the magnitude of BB s/e depend on?
Selectivity and presence/absence of intrinsic sympathomimetic activity.
BB's have ___ side effects.
BB's may alter airway ___, ___/___ metabolism and distribution of ___ ___.
Resistance, carbohydrate/lipid, extracellular ions.
CNS commonalities of BB's? Placenta?
All cross the BBB and placenta to some extent.
GI effects of BB's?
Problems with chronic use?
Fever, rash, myopathy, alopecia, thrombocytopenia.
When should you absolutely NOT use BB's?
In pts with AV block or hx of heart failure caused by tachycardia.
What types of BB should not be used in COPD, PVD or Diabetes and why?
Nonselective BB's or high doses of selective BB's. In COPD may cause bronchocx. In PVD, causes peripheral vasocx. In diabetes, hypoglycemia may be masked d/t no increase in HR.
What type of BB is labetalol?
Selective A1, nonselective BB. Thought to also have selective B2 agonism.
With labetalol, ___ ___ receptors are spared, and released ___ continues to ___ further release of ___.
Presynaptic A1, NE, catacholamines.
Compare the potency of labetalol to phenatolamine and propranolol.
1/5-1/10 as potent as phenatolamine
1/3-1/4 as potent as propranolol
What is the beta to alpha potency ratio of labetalol?
7:1 (IV)

3:1 (PO)
Describe the metabolism, elimination and t1/2e of labetalol.
*Metabolized via conjugation of glucuronic acid.
*5% recovered unchanged in urine.
*t1/2e: 5-8 hours, prolonged in liver dz, unchanged in renal dz.
How does labetalol decrease BP and HR?
*BP:by decreasing SVR. Causes vasod. via alpha one blockade and partial beta2 agonist activity.
*HR: by attenuating reflex tachy via beta blockade
How is cardiac output affected by labetalol?
What is the dose of labetalol and how soon should BP be lowered?
*0.1-0.5mg/kg and BP is lowered within 5-10 minutes.
*20-80mg IV q10min for HTN emergencies
*10mg PRN for controlled hypotension
Clinical uses of labetalol?
*HTN emergencies (ex: epi overdose from local) *Pheo pts with rebound HTN after withdrawal of clonidine *Tx of angina pectoris *Purposeful controlled hypotension
Labetalol s/e?
*Most common-ortho hypo *bronchospasm in susceptible pts *CHF, bradycardia, heart block *incomplete alpha blockade in the presence of more complete beta blockade = exc alpha stimulation