ANS

Question 1

nicotinic

Answer 1

•acetylcholine •ionotropic (ion channel) •location: -parasympathetic and sympathetic ganglia -chromaffin cells of adrenal medulla -neuromuscular junction of somatic nerves and skeletal muscle •direct agonists: -nicotine “depolarization shock” loss of activity of the post ganglionic neuron, increased parasympathetic and sympathetic •antagonists: -ganglionic blockers -neuromuscular blocking agents

Question 2

muscarinic

Answer 2

•acetylcholine •metabotopic: Gq -M1 - neurons -M3 - sweat, salivary, lacrimal, GI, eye, bronchial, smooth muscle -M5 Gi -M2 - heart and smooth muscle -M4 location: -parasympathetic -sympathetic - sweat glands ***decrease heart rate - chronotropic ***decrease heart force of contractility •••artery and vein dilation via EDRF (NO) absence of cholinergic innervation •direct agonists “SLUDGE” -acetylcholine -bethanecol -methacholine -pilocarpine •anragonists -atropine -scopolamine -ipratropium

Question 3

agonists for both nicotinic and muscarinic receptors - reversible

Answer 3

•physostigmine •neostigmine •pyridostigmine •edrophonium •donezepil •tacrine

Question 4

agonists for both nicotinic and muscarinic receptors - irreversible

Answer 4

•malthion •sarin and other nerve gases

Question 5

alpha 1

Answer 5

•norepinephrine •epinephrine •metabotropic Gq location: -sympathetic ***artery vasoconstriction + ***vein vasoconstriction •direct agonist -norepinephrine -epinephrine -phenylephrine -dopamine - high doses •antagonist -phentolamine -phenoxybenzamine -prazosin -terazoin -doxazosin

Question 6

beta 1

Answer 6

•norepinephrine •epinephrine •metabotropic Gs location: -sympathetic •••increase rate of contractility chronotropic ***increase force of contractility ionotropic renin release lipolysis •direct agonist -norepinephrine -epinephrine -dobutamine -isoproteronol -dopamine - moderate dose •indirect agonist -pseudoephedrine -meth and aphetamine -cocaine *antagonist -propranolol -tmolol -metoprolol

Question 7

beta 2

Answer 7

*epinephrine •metabotropic - Gs location: -sympathetic ***skeletal muscle vasodilation •direct agonist -epinephrine -metaproterenol -isoproterenol •antagonist -propanolol -timolol

Question 8

rapid reflex control of high BP

Answer 8

•decrease in sympathetic and increase in parasympathetic •dilation of vessels –> decrease CO -arteries - decrease in total peripheral arterial resistance -veins- decrease in venous return –> decrease in preload,blood pools in veins •decrease in HR and contractility –> decrease CO •contractility is still increased (parasympathetic does not affect contractility) so the mean pulse pressure goes up mean pulse pressure = SBP (nothing is affecting this) - DBP (goes up a little, not much)

Question 9

rapid reflex control of low BP

Answer 9

•increase in sympathetic and decrease in parasympathetic •constriction of vessels –> increase CO -arteries - increase in total peripheral arterial resistance -veins- increase in venous return –> increase in preload,blood does not pool in veins •increase in HR and contractility –> increase CO

Question 10

pathway of baroreceptor nerves

Answer 10

•nerves –> medulla oblongata (NST) —> cardiovascular centers (pons + medulla oblongata) 1. vasomotor control center -diameter of blood vessels -sympathetic 2. cardiac control center -cardiac accelerator (HR) - sympathetic -cardiac decelerator (HR) - parasympathetic -cardiac contractility - sympathetic ONLY

Question 11

aortic arch

Answer 11

•baroreceptors and chemoreceptors •vagus nerve - CN X

Question 12

carotid sinus

Answer 12

•baroreceptors and chemoreceptors •glossopharyngeal nerve - CN IX

Question 13

rapid reflex control of blood volume increase

Answer 13

•increased HR –> increased CO –> increased blood to kidneys –> water and sodium excretion which decreases blood volume •stimulate secretion of atrial natriuretic peptide from atrial muscle cells –> renal artery dilation –> increased blood filtering and decreased reabsorption of sodium and water •vagus –> hypothalamus too! -decrease in vasopressin (ADH) –> decrease in water reabsorption

Question 14

rapid reflex control of blood volume decrease

Answer 14

•decreased HR –> decreased CO –> decreased blood to kidneys –> restricts water and sodium excretion which increases blood volume •no stimulation of secretion of atrial natriuretic peptide •vagus –> hypothalamus too! -increase in vasopressin (ADH) –> increase in water reabsorption

Question 15

chemoreceptors

Answer 15

•aortic and carotid sinuses •monitor the pO2, pCO2, pH •glossopharyngeal and vagus nerves –> respiratory centers in medulla oblongata and pons —> cardiovascular centers •hypoxemia, hypercapnia, acidemia all: * increase sympathetic on vessels –> vasoconstriction –> increased TPR -blood flow limited to periphery (saved for the brain and heart) -decreases metabolic rate and Co2 production -increased venous constriction –> no blood pooling and an increased preload and CO *decreased sympathetic on heart –> decreased HR and decreased contractility *increased parasympathetic on heart –> decreased HR

Question 16

Gs

Answer 16

•increases cAMP, PKA •indirectly alter ion channel function •change gene transcription

Question 17

Gi

Answer 17

•decrease cAMP, PKA •indirectly alter ion channel •change gene transcription

Question 18

Gq

Answer 18

•phospholipase C –> PIP2 –> IP3 –> Ca++ •phospholipase CC –> PIP2 —> DAG –> protein kinase C

Question 19

G

Answer 19

•PLA2 –> arachidonic acid –> 12 lipoxygense –> 12 HPETE • PLA2 –> arachidonic acid –> cyclooxygenase (COX 1 constitutive, COX 2 inducible) –> prostaglandins, thromboxane •PLA2 –> arachidonic acid –> 5 lipoxygenase –> leukotrienes

Question 20

norepinephrine

Answer 20

•adrenergic agonist •produces marked pressor effects that can be used to raise blood pressure and increase contractility of the heart in cases of severe hypotensive shock. •This pressor property is problematic, however, because it causes profound constriction of renal blood vessels and can reduce renal blood flow to a dangerous level. •As norepinephrine is a catecholamine, it is not effective when given orally because of extensive metabolism in the stomach, small bowel and liver. Thus, it has to be given intravenously. • However, if the drug solution extravasates into tissues around the vein and arterioles, potentially harmful intense vasoconstriction can occur. •Local administration of an alpha-l receptor antagonist can reverse the vasoconstrictor effect. •Norepinephrine does not cross the blood-brain barrier (BBB).

Question 21

epinephrine

Answer 21

•adrenergic agonist •(Adrenalin) is used as a cardiac stimulant in emergencies and as a bronchial dilator. Its bronchial dilator effect occurs via beta-2 receptors but is complicated by cardiac stimulation (beta-l) and elevations in blood pressure (alpha-l). •Epinephrine can be life-saving in the emergency management of anaphylactic shock, which is characterized by severe bronchial constriction and cardiovascular collapse. •Epinephrine and other beta-l agonists can produce cardiac arrhythmias when used in high doses. •Epinephrine can also be included as a vasoconstrictor agent in some local anesthetic preparations (1:100,000 dilution) to limit diffusion of the local anesthetic away from the injection site thereby prolonging its duration of action. •It does not cross the BBB. •At relatively high concentrations epinephrine acts on vascular alpha-l receptors to induce contraction. •At higher doses the beta-2 agonist action is overwhelmed by the alpha-1 effect. •Local anesthetic preparations containing epinephrine must be used with care in areas with terminal end arteries, such as fingers, to avoid gangrene caused by intense vasoconstriction. •Epinephrine is a catecholamine and is essentially inactive when administered orally. It is generally given intravenously for systemic action, and by inhalation for bronchial dilation.

Question 22

increase in vasoconstriction …

Answer 22

…increases diastolic BP because it measures peripheral circulation

Question 23

increase in contractility…

Answer 23

…increases systolic BP because the pressure on the heart increases

Question 24

nicotine

Answer 24

•cholinergic nicotinic receptor agonists •is a natural plant alkaloid obtained from tobacco leaves. Nicotine’s therapeutic use is that of an aid to smoking cessation. Its greater relevance to medicine results from tobacco use. Nicotine has both central and peripheral effects. It is a mild CNS stimulant which can stimulate respiration and induce vomiting. Tolerance to the respiratory stimulant and emetic effects occur readily with continued use. In the periphery, low doses of nicotine, associated with use of tobacco, stimulate ganglionic nicotinic cholinergic receptors in both sympathetic and parasympathetic divisions.

Question 25

varencline

Answer 25

•cholinergic nicotinic receptor agonists •)[Chantix] is a partial agonist at the alpha4-beta2 subunit of the nicotinic cholinergic receptor in the CNS and is used to treat nicotine addiction. It occupies nicotinic cholinergic receptors on dopamine neurons thereby preventing nicotine from stimulating those receptors. Partial agonist.

Question 26

ganglionic blockers

Answer 26

•nicotinic receptor antagonist

Question 27

neuromuscular blocking agents

Answer 27

•nicotinic receptor antagonist

Question 28

bethanecol

Answer 28

•cholinergic muscarinic agonist •has a structure conferring negligible metabolism by cholinesterase and thus a long duration of action and selectivity for muscarinic cholinergic receptors. When given orally or subcutaneously in therapeutic doses, it exerts only mild cardiovascular effects (some hypotension, slowing of heart rate) while acting mainly in the gastrointestinal tract and urinary bladder. Its principal use is to increase tone and contractions of the intestine and bladder in patients with postpartum or postsurgical ileus and urinary retention. However, in high doses it can precipitate a cholinergic crisis. •Certain adverse responses to muscarinic cholinergic agonists can be life threatening: cardiac slowing or arrest, severe hypotension, and bronchial constriction are special hazards. These adverse effects can be blocked or reversed by a muscarinic receptor antagonist. Therefore atropine should always be readily available whenever muscarinic agonists are administered parenterally.

Question 29

pilocarpine

Answer 29

•cholinergic muscarinic agonist •is a natural plant alkaloid that exhibits primarily muscarinic receptor agonist actions. It does not have an ester linkage and therefore it is not degraded by cholinesterases. Pilocarpine can be used topically in the eye for management of glaucoma or to treat patients with dry mouth (xerostomia). •Certain adverse responses to muscarinic cholinergic agonists can be life threatening: cardiac slowing or arrest, severe hypotension, and bronchial constriction are special hazards. These adverse effects can be blocked or reversed by a muscarinic receptor antagonist. Therefore atropine should always be readily available whenever muscarinic agonists are administered parenterally.

Question 30

physostigmine

Answer 30

•indirect acting cholinesterase inhibitor - reversible •Inhibition of acetylcholinesterase leads to an increase in synaptic levels of acetylcholine. These agents are not selective since they enhance the levels of acetylcholine which can activate both nicotinic and muscarinic receptors. •Physostime can be used as an antidote to atropine poisoning, but is only occasionally used for this purpose

Question 31

pilocarpine

Answer 31

•cholinergic muscarinic agonist •is a natural plant alkaloid that exhibits primarily muscarinic receptor agonist actions. It does not have an ester linkage and therefore it is not degraded by cholinesterases. Pilocarpine can be used topically in the eye for management of glaucoma or to treat patients with dry mouth (xerostomia). •Certain adverse responses to muscarinic cholinergic agonists can be life threatening: cardiac slowing or arrest, severe hypotension, and bronchial constriction are special hazards. These adverse effects can be blocked or reversed by a muscarinic receptor antagonist. Therefore atropine should always be readily available whenever muscarinic agonists are administered parenterally.

Question 32

atropine

Answer 32

•muscarinic receptor antagonist the prototype muscarinic receptor antagonist. It is a natural plant alkaloid obtained from the belladonna plant (deadly nightshade) or from Jimson weed (a ubiquitous plant in the Southwest). Atropine is a tertiary amine and can penetrate into the CNS. It blocks all subtypes of muscarinic receptors. •Atropine produces the pharmacological effects expected of blocking muscarinic receptors in the parasympathetic nervous system. In the eye, it blocks contractions of constrictor pupillae muscles to produce mydriasis and blocks contraction of ciliary muscles to produce cycloplegia (loss of accommodation). In the gastrointestinal tract, atropine reduces motility and the secretion of saliva, gastric acid and pancreatic juice. Atropine inhibits contractions of the stomach, small bowel and large bowel, thus delaying transit through the digestive system. Atropine will also inhibit contractions of the bladder, thus interfering with the ability to urinate. •Atropine decreases thermoregulatory sweating by blocking receptor actions of acetylcholine released from the sympathetic cholinergic fibers that innervate most sweat glands. Although atropine is remarkably selective as a muscarinic receptor antagonist, it produces at least one effect that appears not to be related to muscarinic blockade: it can dilate blood vessels in the facial blush area to induce a transient “atropine flush.” •Atropine can induce mild tachycardia by blocking muscarinic receptors in the heart. However, its effects on blood pressure are usually negligible. Atropine can readily antagonize the vasodilatation and hypotension produced by cholinergic drugs acting on vascular muscarinic receptors. •Therapeutic uses -Muscarinic receptor antagonists are classic examples of selective drugs (in terms of receptor actions) that exert nonspecific effects because muscarinic receptors are located in many different organs throughout the body. Also they can produce undesired side effects even when used in doses adequate to achieve a therapeutic goal. Nevertheless, the muscarinic receptor antagonists are useful in a number of circumstances where the side effects can be minimized by route of administration or where the benefits outweigh the disadvantages. Such uses include scopolamine for motion sickness. Muscarinic antagonists are also used in the management of tremors caused by Parkinson’s disease.

Question 33

scopoloamine

Answer 33

•muscarinic receptor antagonist •is also a natural belladonna alkaloid. It is pharmacologically and structurally similar to atropine, but it has more CNS effects than atropine (especially drowsiness and amnesia). Scopolamine (in a patch formulation) has been used prophylactically to prevent vertigo (motion sickness). The cholinergic side effects of scopolamine are very similar to those of atropine. •Therapeutic uses -Muscarinic receptor antagonists are classic examples of selective drugs (in terms of receptor actions) that exert nonspecific effects because muscarinic receptors are located in many different organs throughout the body. Also they can produce undesired side effects even when used in doses adequate to achieve a therapeutic goal. Nevertheless, the muscarinic receptor antagonists are useful in a number of circumstances where the side effects can be minimized by route of administration or where the benefits outweigh the disadvantages. Such uses include scopolamine for motion sickness. Muscarinic antagonists are also used in the management of tremors caused by Parkinson’s disease.

Question 34

ipratropium

Answer 34

•muscarinic receptor antagonist •s a charged quaternary amine compound that when inhaled dilates the bronchioles without significantly affecting respiratory secretions. It is used particularly for treating chronic obstructive pulmonary disease (COPD). •Because of its positive charge it does not cross the blood-brain-barrier. •Therapeutic uses -Muscarinic receptor antagonists are classic examples of selective drugs (in terms of receptor actions) that exert nonspecific effects because muscarinic receptors are located in many different organs throughout the body. Also they can produce undesired side effects even when used in doses adequate to achieve a therapeutic goal. Nevertheless, the muscarinic receptor antagonists are useful in a number of circumstances where the side effects can be minimized by route of administration or where the benefits outweigh the disadvantages. Such uses include scopolamine for motion sickness. Muscarinic antagonists are also used in the management of tremors caused by Parkinson’s disease.

Question 35

malathion

Answer 35

•indirect acting cholinesterase inhibitor - irrevesible •The irreversible cholinesterase inhibitors are mostly organic phosphate esters and are commonly called “organophosphate” cholinesterase inhibitors. After interacting with the active site of acetylcholinesterase, the organophosphate inhibitors are hydrolyzed, but the phosphorylated esteratic site is extremely stable and resistant to hydrolysis. These agents have a long duration of action. •the prototype organophosphate insecticide. It can be used to treat pediculosis (lice). It is much less toxic to mammals than to insects. However, humans exposed to large amounts, can suffer intoxication as with any other organophosphate cholinesterase inhibitor. •Overdose with a centrally-acting cholinesterase inhibitor can be life-threatening. Central actions can result in confusion, ataxia, convulsions, coma and respiratory paralysis. Hazardous peripheral effects include excessive bronchial secretions, hypotension, and involuntary twitching of skeletal muscle that can progress to paralysis. The cause of death is usually respiratory failure. The treatment of first choice in severe intoxications with centrally acting cholinesterase inhibitors is a muscarinic cholinergic receptor antagonist (eg. atropine), given in large doses to combat the central manifestations as well as the peripheral signs mediated by overstimulation of muscarinic receptors (i.e. cholinergic crisis). •In addition to atropine, the neuromuscular component of organophosphate intoxication can be treated with PRALIDOXIME [pra li dox eem] (Protopam), a cholinesterase reactivator. Pralidoxime and related oxime compounds compete for the alkyl phosphate group attached to the esteratic site of acetylcholinesterase if treatment is initiated quickly enough after exposure. If the exposure has been prolonged, the phosphorylated enzyme becomes fully “aged,” making pralidoxime essentially useless. •Pralidoxime is a quaternary ammonium derivative and does not penetrate into the brain. It cannot reactivate acetylcholinesterase in the central nervous system. Atropine is the best treatment for central signs of intoxication with organophosphates.

Question 36

sarin and other nerve gases

Answer 36

•indirect acting cholinesterase inhibitor - irrevesible •The irreversible cholinesterase inhibitors are mostly organic phosphate esters and are commonly called “organophosphate” cholinesterase inhibitors. After interacting with the active site of acetylcholinesterase, the organophosphate inhibitors are hydrolyzed, but the phosphorylated esteratic site is extremely stable and resistant to hydrolysis. These agents have a long duration of action. •Overdose with a centrally-acting cholinesterase inhibitor can be life-threatening. Central actions can result in confusion, ataxia, convulsions, coma and respiratory paralysis. Hazardous peripheral effects include excessive bronchial secretions, hypotension, and involuntary twitching of skeletal muscle that can progress to paralysis. The cause of death is usually respiratory failure. The treatment of first choice in severe intoxications with centrally acting cholinesterase inhibitors is a muscarinic cholinergic receptor antagonist (eg. atropine), given in large doses to combat the central manifestations as well as the peripheral signs mediated by overstimulation of muscarinic receptors (i.e. cholinergic crisis). •In addition to atropine, the neuromuscular component of organophosphate intoxication can be treated with PRALIDOXIME [pra li dox eem] (Protopam), a cholinesterase reactivator. Pralidoxime and related oxime compounds compete for the alkyl phosphate group attached to the esteratic site of acetylcholinesterase if treatment is initiated quickly enough after exposure. If the exposure has been prolonged, the phosphorylated enzyme becomes fully “aged,” making pralidoxime essentially useless. •Pralidoxime is a quaternary ammonium derivative and does not penetrate into the brain. It cannot reactivate acetylcholinesterase in the central nervous system. Atropine is the best treatment for central signs of intoxication with organophosphates.

Question 37

Wild mushrooms of the Amanita genus (eg. inocybe and clitocybe)

Answer 37

Wild mushrooms of the Amanita genus (eg. inocybe and clitocybe) contain muscarine in concentrations that can within 30-60 minutes of ingestion produce salivation, lacrimation, nausea, vomiting, headache, visual disturbances, abdominal cramps, diarrhea, bronchospasm, bradycardia, hypotension, and shock. As noted above, these symptoms of a cholinergic excess can be treated with the muscarinic receptor antagonist, atropine.

Question 38

neostigmine

Answer 38

•indirect acting cholinesterase inhibitor •Inhibition of acetylcholinesterase leads to an increase in synaptic levels of acetylcholine. These agents are not selective since they enhance the levels of acetylcholine which can activate both nicotinic and muscarinic receptors. •myasthenia gravis

Question 39

atropine poisoning

Answer 39

•Atropine poisoning produces symptoms of parasympathetic blockade (dilated pupils, decreased bowel sounds, tachycardia, dry mouth), dry skin, flushing, fever (due to inhibition of sweating), delirium, hallucinations, and restlessness that may convert to coma. Treatment is symptomatic, but may include administration of physostigmine. •children: coma and death (red, hot delirious) •adults: memory loss and confusion Therapeutic uses of antimuscarinics: Reverse bradycardia Produce mydriasis and cycloplegia Parkinson’s disease Bladder & G.I. as an antispasmotic Antimuscarinic side effects: dry mouth, dry skin tachycardia dilated pupils (photophobia decreased gut and bladder activity sedation, excitation, confusion

Question 40

phenylephrine

Answer 40

•adrenergic agonist • (Neo-Synephrine), the prototype alpha-l agonist, is used primarily as a vasoconstrictor. •When it is applied topically to the nasal mucosa, it induces vasoconstriction which shrinks the nasal mucosa and reduces mucus secretion, thus increasing the flow of air. •Phenylephrine can be administered systemically to raise blood pressure in a hypotensive condition (eg. shock) •Phenylephrine and its relative, methoxamine, can also be administered systemically in paroxysmal supraventricular tachycardia to induce vagally mediated reflex slowing of the heart

Question 41

dopamine

Answer 41

•adrenergic agonist •is used almost exclusively as an i.v. drip in the management of shock. •In low doses, its preferential action is to stimulate dopamine receptors producing relaxation of vascular smooth muscle in renal blood vessels, thereby improving renal blood flow which is compromised in shock. •Moderate doses stimulate beta-1’s in the heart to increase cardiac output. •Higher doses of dopamine will also recruit actions at alpha-l adrenergic receptors to produce vasoconstriction, and raise blood pressure, but because of the offsetting effects of dopamine receptor-mediated dilatation in renal vessels, the net vasoconstriction is less in the renal vasculature than in other vascular beds. •Dopamine has a brief duration of action due to rapid inactivation by monoamine oxidase enzymes in the liver.

Question 42

clonidine

Answer 42

•adrenergic agonist •(Catapres) is a selective alpha-2 receptor agonist used primarily as an antihypertensive drug. •By virtue of its alpha-2 receptor agonist activity, it acts at presynaptic receptors to inhibit release of norepinephrine. •If given intravenously, it can act at postjunctional alpha-2 receptors to induce some vasoconstriction. •However, when used as an antihypertensive drug, its antihypertensive effects resulted from actions at alpha-2 receptors in the CNS resulting in decreased sympathetic outflow to the heart and blood vessels.

Question 43

dobutamine

Answer 43

•adrenergic agonist •is a beta-l agonist used as a short term treatment in adults with cardiac decompensation due to depressed myocardial contractility or to stimulate the heart in cases of cardiogenic shock. •Cardiogenic shock occurs typically after myocardial infarction when the pumping action of the heart is not sufficient to maintain adequate blood pressure

Question 44

phentolamine

Answer 44

•alpha adrenergic antagonist •(Regitine) is a competitive antagonist at both alpha-1 and alpha-2 receptors. •Because of its antagonist activity at presynaptic alpha2 receptors, phentolamine can cause excess norepinephrine secretion from cardiac adrenergic neurons resulting in tachycardia mediated by beta-1 receptor activation. •It can be used to treat the vasospasm of Raynaud’s disease, and the hypertension caused by pheochromocytoma. •It can be added to a solution of papaverine and prostaglandin (alprostadil) for corpus cavernosum injections to treat erectile dysfunction

Question 45

phenoxybenzamine

Answer 45

•alpha adrenergic antagonist • (Dibenzyline) is little used in medicine, because it is a noncompetitive antagonist at alpha-1 and alpha-2 receptors. • It interacts with the receptors to form covalent bonds, thus leaving the receptors permanently blocked until new receptors are synthesized (about 24 hrs). •The blockade induced by phenoxybenzamine cannot be overcome by even large amounts of norepinephrine. •Like phentolamine, blockade of presynaptic alpha-2 receptors in adrenergic neurons innervating the heart results in dramatic tachycardia because of excess release of neural norepinephrine, which acts on beta-1 receptors in the heart. •If used it would be for the same conditions phentolamine is prescribed.

Question 46

prazosin

Answer 46

•alpha adrenergic antagonist • (Minipress) is the prototype selective alpha-l receptor antagonist. •Prazosin lowers blood pressure by blocking vascular alpha-l receptors, thus interfering with the vasoconstrictor effects of norepinephrine. •However, its use in the management of hypertension has declined. •Prazosin does not block alpha-2 receptors, and thus does not increase neural release of norepinephrine by presynaptic actions. •Often a first full dose can produce syncope. Thus, initial treatment should be initiated using lower doses.

Question 47

terazosin

Answer 47

•alpha adrenergic antagonist •and doxazosin (Hytrin) have similar effects and are also now drugs of choice for the treatment of benign prostatic hypertrophy (BPH).

Question 48

doxazosin

Answer 48

•alpha adrenergic antagonist •and terazosin have similar effects and are also now drugs of choice for the treatment of benign prostatic hypertrophy (BPH).

Question 49

propanolol

Answer 49

•beta adrenergic antagonist •(Inderal) acts as a competitive antagonist at both beta-l and beta-2 receptors. •It blocks the cardio stimulatory effects of neuronally secreted norepinephrine and circulating epinephrine. By blocking cardiac beta-l receptors, propranolol decreases cardiac work and cardiac output. These actions are important in the management of hypertension, angina, and cardiac arrhythmias. •Propranolol also blocks the renal beta-1 receptors responsible for the elaboration of renin, which catalyzes the formation of angiotensin. •Because of powerful vasoconstrictor and volume expanding effects of angiotensin, inhibition of renin release is important in the management of hypertension. •Propranolol has also been used for treating migraine headaches and anxiety. •Propranolol depresses cardiac contractility and should be avoided in patients with very severe heart failure. • It also blocks bronchial beta-2 receptors and can seriously exacerbate asthma. •Propranolol and other beta blockers should be avoided in patients with a known history of asthma.

Question 50

timolol

Answer 50

•beta adrenergic antagonist • is both a beta-l and beta-2 blocker used topically in the eye for management of glaucoma. •Timolol also has antihypertensive and antiarrhythmic effects. •Timolol and related beta antagonists may reduce the incidence of fatal arrhythmias following myocardial infarction. •It should also be avoided in patients with asthma.

Question 51

metoprolol

Answer 51

•beta adrenergic antagonist •is the prototype selective beta-l antagonist. •The beta-l antagonists are sometimes termed “cardioselective” beta blockers because beta-l receptors are of importance mainly in the heart. •The beta-l antagonists are used mainly for management of hypertension as they decrease cardiac output and inhibit release of renin from the kidneys. •Like the beta-1/beta-2 antagonists, metoprolol and other selective beta-l antagonists may produce cardiac decompensation in patients with borderline heart failure. •Metoprolol and other beta-l antagonists are less prone than the combined beta-1/beta-2 blockers to induce bronchial constriction in patients with asthma. •However, the drugs are not perfectly selective and great care must be exercised in the use of any beta antagonist in asthma patients. •Other therapeutically used beta-1 antagonists include: acebutolol, atenolol and esmolol.

Question 52

Answer 52

Question 53

norepinephrine acts on…

Answer 53

• alpha 1
• alpha 2
• beta 1

Question 54

epinephrine acts on …

Answer 54

• alpha 1
• alpha 2
• beta 1
• beta 2

Question 55

phenyephrine acts on …

Answer 55

•alpha 1

Question 56

ephedrine acts on…

Answer 56

• alpha 1
• alpha 2
• beta 1
• beta 2

Question 57

clonidine acts on…

Answer 57

•alpha 2

Question 58

isoproterenol acts on…

Answer 58

• beta 1
• beta 2

Question 59

dobutamine acts on…

Answer 59

•beta 1

Question 60

metaproterenol acts on…

Answer 60

•beta 2