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Pharm #2-SIUE
SIUE Don's #2 Pharm Test
| Question | Answer |
|---|---|
| Neurotransmitters (Name some) | Acetylcholine, Epiephrine, Norepinephrine, Dopamine, Serotonin, Gamma-aminobutyric acid, glycine, & aspartic acid |
| What breaks down ACh? | Cholinesterase |
| What breaks down Epi, Norepi, Dopamine, & serotonin the nonoamines? | Monoamine axidase |
| Acetylcholine is a neurotransmitter for the PNS or CNS? | Neurotransmitter for both the peripheral nervous system and central nervous system. One of the many neurotrnansmitters in the autonomic NS, and the only in the somatic NS. |
| Cholinesterase does what? | It is an enzyme that breaks down ACh into acetic acid and choline. |
| The autonomic nervous system | consists of the PSNS and CNS. Consist of preganglionic fibers, ganglia, and postganglionic fibers. |
| In the PNS what is the the NT that is released by all pre and post ganglionic neurons? What fiber does it act on? | ACh and acts on cholinergic fibers. |
| Craniosacral division | PNS |
| Thoracolumbar division | SNS |
| In the SNS what NT is released by the preganglionic neurons and post ganglionic neurons? What fibers does the SNS act on? | ACh from the preganglionic neurons, norepi is the NT that is released by practically all postganglionic neurons except for sweat glands which releases ACH. The SNS acts on adrenergic fibers |
| Besides in the PSN what else releases ACh as a NT? | Postganglionic neurons in the SNS in which go to sweat glands, all motor neurons in the skeletal muscles, and all preganglionic neurons in the SNS. |
| Two primary receptor sites in the peripheral nervous system. | Cholinergic and adrenergic receptors. Cholinergic mediate responses to ACh, where as adrenergic mediate responses to mostly epi and norepi. |
| Muscarininc receptors are effector cells of which systems? | SNS and PSNS |
| Where are nicotinic receptors located? | Between pre and post ganglionic neurons in both types. Also an effector cell (muscle fiber) of somatic neuron. |
| PSN action pathway | ACh released from preganglionic neuron. Binds with a nicotinic receptor. ACh is released from the nicotinic postganglionic neuron where it binds to muscarinic receptors on various organs. |
| SNS action pathway w norepi | ACh released from preganglionic neuron, binds w nicotinic receptor. Nicotinic postganglionic receptor releases Norepi which binds with a or B receptors on various organs. |
| SNS action pathway w ACh | ACh released from preganglionic neuron, binds w nicotinic receptor. Nicotinic postganglionic receptor releases ACh which binds to muscarinic receptor for sweat glands. |
| SNS action pathway w Epi | ACh released from preganglionic neuron, binds w nicotinic receptor on the adrenal medulla. Nicotinic postganglionic receptor releases epi which binds w a or B receptors on various organs. |
| Somatic Motor system action pathway | ACh is released from a motor neuron, it binds directly to a nicotinic receptor on skeletal muscle. |
| What happens when there is a direct action (from a drug) on a cholinergic receptor? | The drug will act on the receptor and compete w the NT ACh. |
| What happens when there is an indirect action (from a drug) on a cholinergic receptor? | The drug could change the amount of circulating ACh, or act on acetylcholinesterase, or act on the uptake of ACh. |
| What are the two classes of direct muscarinic agonist? Give examples of each. | Choline esters-succinylcholine, and alkaloids-naturally occuring chemical compound that contains N,C,H Cocaine, caffeine, nicotine, morphine. |
| If a drug (chemical) has a direct muscarinic action, does is effect the nicotinic receptor to achieve its effect? | No. If it is selective, it has NO nicotinic action, only muscarinic. It is not selective to muscarinic subtypes though. M1-M5. |
| If a muscarinic receptor gets stimulated what organs and system are affected? | All PSNS organs. Eye-contraction of iris;heart-decreased rate;Lung-constriction of bronchi & increased secretions;bladder-relaxation;GI-salivation inc gastric secretions & motility;sweat glands-sweating;sex organs-erection;blood vessels-vasodilation. |
| If a nicotinic receptor gets stimulated what organs and system are affected? | All autonomic nervous system ganglia and the adrenal medulla-stimulation of PSNS & SNS postganglionic nerves & release of epi from adrenal medulla.Neuromuscular junction-contraction of skeletal muscle. |
| M3 muscarinic receptor on endothelial cells does what to the cardiovascular system? | Causes production of nitric oxide which then promotes vasodilation of the vessels. Nitric oxide is the most potent vasodilator. |
| M4 is a presynaptic receptor on adrenergic terminals that does what to the cardiovascular system? | Causes a decrease release of norepi, and therefore decreased vasoconstriction. |
| M2 receptor has what effect on the cardiovascular system? | Inhibits adenylate cyclase activity and enhanced K current that causes bradycardia. Hyperpolarizes cell so that it is not as easy to fire and causes bradycardia. |
| M3 receptor has what proposed GI effects? | Stimulates phosphatase C=increased intracellular Ca=contractions and secretions. Peristalsis is increased. Relaxes GI sphincters. |
| Neostigmine is a muscarinic antagonist that increases motility, but what is a big concern with using this medication? | It causes bradycardia. |
| M3 receptor proposed effects on the GU system? | Increases ureteral peristalsis. Contracts detrusor myo, decreases capacity of bladder and aids in urination, and relaxes sphincters. |
| M3 receptor effects on vision? | Contraction produces miosis. Contraction of ciliary muscle-accommodates near vision, decreases intraocular pressure=tx for wide angle glaucoma. |
| Muscarinic receptors may have what effects in CNS? | Play a role in learning & memory. Alzheimer's (indirect cholinergic agonists are being used for Tx. |
| Muscarinic receptors could cause what effects with the pulmonary system? | Could cause bronchoconstriction, and stimulates most glands. |
| Fast acting, short lasting choline esters | Acetylcholine, carbachol |
| This direct muscarinic agonist class of drug has greater effects on glands like salivary glands and an ex. is pilocarpine. | Alkaloid |
| Why can ACh, carbachol, and pilocarpine be used for eye drops without concern for other areas being stimulated? | Because they have little systemic absorption. |
| Blocks the actions of the PSNS and causes SNS symptoms? | Muscarinic antagonist |
| Cardiac PSNS- Vagus nerve innervates the heart and causes what reaction? | Releases ACh which acts M2 receptors. M2 receptors activates Gi-protein that increases K+ efflux which hyperpolarizes the cell & causes brady. Also decreases the influx of Ca++ & Na+. |
| Norepi causes what changes in the cardiac system? | Decreases the K+ efflux, increases Ca++ & Na+. SA node rapidly reaches threshold for action potential. Tachycardia |
| If you were wanting to increase the HR, what measures could you use? | Increase SNS by increasing the amount of epi, OR.. Decrease the PSNS atropine. |
| An anticholinergic drug would would be a muscarinic antagonist or.. muscarinic agonist? Give examples | Muscarinic antagonist. Ex. Atropine, glycopyrrolate (robinul), and scopolamine. |
| If you were to give an anticholinergic drug what would you expect to see? | Tachycardia, pupil dialation, dry mouth, urinary retention, blurred vision, constipation, anhidrosis. |
| Anticholinergic drugs mimics SNS or PSNS effects? | Mimics the SNS. Stops PSNS. Remember cholinergic=PSNS. |
| This drug is a quarternary ammonium salt and does not cross the BBB easily. It is completely ionized at physiologic pH, and has a MW of 398.33. | Robinul |
| Robinal's MW is 398.33. Does this have any effect on the drugs action? | Yes, it is inbetween 100-1000 and crosses between membranes easily, but since it is a quarternary amine it does not readily cross the BBB. |
| Over 80% of the IM dose of Robinal is unchanged in the urine and bile, would you want to give this to a pt with renal/liver dysfunction? | No. If it is unchanged, then it is still active when it is excreted. Renal/liver dysfunction would cause the drug to remain active in the body causing longer lasting effects. |
| If Robinal is completely ionized at physiologic pH, what is it's volume of distribution? | It is very LOW! Ionized means decreased ability to cross lipid membranes therefor decreased ability to spread to many areas in the body. |
| Why would you not want to give a pt w myasthenia gravis Robinal? | Because Myasthenia gravis destroys ACh receptors. Tx for Myasthenia gravis is to try and increase ACh at those receptors. Robinal is an antichonlinergic and decreases ACh. |
| Cholinesterase Inhibitor inhibits what? | acetylcholinesterase. Increases circulating ACh=increases PSNS |
| What are some examples of Cholinesterase inhibitors? | Razadyne, aricept, neostigmine. |
| Aricept some fun facts | 96% protein bound. Excreted in urine both intact & metabolized-2 out of 4 metabolites are active. Poor metabolizers=31% slower clearance. Ultra rapid metabolizers=24% faster clearance-CYO2D6 plays a role in metabolism. |
| If a patient is taking aricept and has hepatic disease what is this going to do to the clearance of aricept? | Decrease clearance. The liver is where there are ultra super duper fast metabolizers that = 24% faster clearance. Relies on CYP2D6 liver enzyme for this to occur. |
| Knowing that aricept is highly protein bound what things do we need to consider with this drug? | Drug displacement at inert binding sites. Aricept can be knocked off by another drug that has a higher affinty for the protein, making aricept active again. |
| Myathenic crisis | Lack of ACh, severe muscle weakness. |
| What is the tx for a myathenic crisis? | Anticholinesterase. Breaks down cholinesterase which breaks down ACh. More ACh available bc not as much is being broken down. |
| Muscarinic agonist | Selectively mimic the effects of ACh at muscarinic receptors. |
| Muscarinic antagonist | Ex. Atropine selectively blocks the effects of ACh and other agonists at muscarinic receptors. |
| Neuromuscular blocking agents | Selectively block the effects of ACh at nicotinic receptors at the neuromuscular junction. |
| When you think of sympathetic do you think of cholinergic or adrenergic? | Adrenergic |
| Sympathomimetics is another name for what type of agonist? | Adrenergic agonist. Does the same thing as the SNS |
| Sympatholytics is another name for what type of antagonist? | Adrenergic antagonist. |
| Give an example of a class of drugs in which are adrenergic antagonists? | Beta Blockers |
| The two types of actions of an adrenergic drug? | Either stimulates the sympathetic activity or blocks the sympathetic activity. |
| What happens with an adrenergic antagonist? | It blocks the sympathetic activity which leads to an increase in parasympathetic activity. |
| Clonidine (Catapres) acts where in the body? | In the brain. It is centrally active. |
| Clonidine (Catapres) is a centrally acting selective alpha 2 adrenergic agonist. How does this drug act? | It is an alpha 2 agonist, which blocks sympathetic flow. Even though it is an agonist, it does not increase sympathetic flow, but inhibits adrenergic outflow from the brainstem decreasing SNS activity. |
| Clonidine (Catapres) inhibits the outflow of what two NT that are responsible for SNS activity? | Norepi and Epi |
| Clonidine (Catapres) is effective in renin-dependent hypertension in what way? | It decreases the outflow of SNS activity which then decreases the release of renin. Decrease in renin, decrease in conversion of angiotension 1 to angiotension 2 and decrease in renin dependent HTN. |
| Clonidine (Catapres) is also effective in decreasing CO, how is this accomplished? | Decrease in sympathetic outflow decreases NE which leads to decrease in firing of sympathetic nerves to the heart decreasing HR and CO and vasodialating vessels. |
| If an alpha 2 agonist decreases the release of NE and sympathetic outflow, what action does an alpha 2 receptor have when stimulated? | Inhibits NE release, and decreases adrenergic activity. |
| Selective alpha 2 agonists has the action of opposing what receptor? | Alpha 1, because alpha 2 does opposite of alpha 1. |
| Where are alpha 2 receptors found? | Both the central and peripheral nervous system, pre and post-synaptically. |
| Presynaptic alpha 2 receptors serve what function? | They serve as an important receptor in the negative feedback control of NE release. |
| Postsynaptic alpha 2 receptors serve what function? | Liver cells, platelets, and the smooth muscle of blood vessels. Platelet aggregation, and blood vessel constriction. |
| In what ways does Clonidine work as an analgesia? | Activates postsynaptic A2 receptors in the spinal cord substantia geltinosa, which are pain pathways from sensory nerves to brain. Suppresses adenylyl cyclase (2nd messenger) in pain signal transduction. |
| What are some side effects of neuraxial clonidine? | Hypotension, sedation, dry mouth. |
| Why would we use Clonidine Pre- operative? | Reduces reflex tachycardia cause by direct larygoscopy. Reduces inoperative blood pressure and HR. Reduces plasma catecholamines levels. Can decrease anesthetic requirements, and enhances intrathecal morphine + tetracaine w/o increase in morphine SE. |
| Methyldopa (Aldomet) what type of drug? | Sympatholytic. Prodrug that is metabolized to alpha-methylnoreinephereine. |
| Methyldopa (Aldomet) has the same type of effects as what other drug? | Clonidine |
| What are the side effects of Methyldopa (Aldomet)? | Dry mouth, parkinsonian signs, bradycardia (in pt's w/ SA node abnormality) hepatotoxicity, Positive Coombs test (20%) |
| Give 3 examples of adrenergic neuron blockers? | Guanadrel (hylorel), Guanethidine (Ismelin), Reserpine |
| Guanethidine inhibits the function of postganglionic adrenergic neurons thus inhibiting what? | Inhibiting sympathetic function |
| How does Guanethidine inhibit the sympathetic function? | It uses the NE re-uptake transporter, enters cell, enters the neurosecretory vesicles & replaces NE in the vesicle & it is released instead. Cell releases inactive transmitter (Guanethidine). |
| Sympathetic blockade by Guanethidine (Ismelin) produces what effects on the body? | Venodialtion, reduction in CO, blockade of the sympathetic reflex arteriolar response to the reduction in CO, body can no longer compensate. |
| What are some SE and adverse outcomes with Guanethidine? | Symptomatic hypotension (due to sympathetic reflex blockade). Guanethidine effects are blocked by NE reuptake blockers such as trycyclic antidepressents, cocaine, ephedrine, amphetamine, chlorpromazine (Thorazine). |
| Reserpine is an adrenergic neuron blocker that inhibits what? | Inhibits the function of postganglionic adrenergic neurons. Binds to NE storage vesicles in central and peripheral nerve terminals, which makes the vesicles nonfunctionsl loosing the ability to store and concentrate NE and dopamine. |
| What are the adverse effects of Reserpine? | CNS effects predominate including sedation, inability to concentrate, and depression. |
| Flowmax is what type of antagonist? | Alpha 1 antagonist that targets receptors in the prostate. |
| Flomax acts on alpha 1 receptors in the prostate causing what action? | Relaxes smooth muscle in the bladder neck and prostate. |
| Flomax acting on alpha 1 receptors in the prostate is important why? | Because alpha 1 receptors mediate smooth muscle tone in the prostate. |
| What can happen if too much flowmax is given? | Flowmax is an alpha 1 blocker which decreases SNS activity in the prostate when given in smaller doses. If does exceeds selective receptors in the prostate then it acts systemically causing smooth muscle tone to be relaxed vascularly decreases BP. |
| Give three examples of adrenoceptor antagonist (sympatholytics) drugs. | Labetalol (trandate, Normodyne)(alpha % beta), Prazosin (minipress)(alpha), Terazosin (Hydrin)(alpha). |
| Labetalol acts on adrenergic receptors as what? | Competitive antagonist at both alpha 1 and beta 1 adrenergic receptors. |
| Labetalol acts on beta 2 receptors and has what effect? | Intrinsic sympatholytic effect |
| What effect does Labetalol have on the body when it acts on alpha 1 receptors? | Being a competitive antagonist it blocks alpha 1 receptors and results in vasodialation which is further enhanced by beta 2 receptor activation which when blocked causes vasodialation everywhere BUT bronchioles. |
| Beta 1 receptor antagonism causes what to happen to the HR? | A decrease in HR. |
| Esmolol is selective to what receptor? What happens when esmolol is given? | Esmolol is selective to beta 1 receptor. Causes decreases in HR with little decrease in BP. |
| Lopressor (Metoprolol) is selective for what receptor and has what action? | Selective at Beta 1 antagonist. Decreases CO and decreases SVR. High concentrations are found in CSF after IV injection. (central effect leading to reduced sympathetic outflow. |
| What drug would you want to give to lower BP in a patient who is an asthmatic? | Lopressor (metoprolol)- Relative selective at beta 1 lowers BP and does not block beta 2 which would cause bronchconstriction. |
| What drug would you want to give to a patient who has a high HR but a stable BP? | Esmolol- beta 1 selective causes it to decrease HR with little decrease in BP. |
| Compare Lopressor (metoprolol) to Esmolol and Labetolol. | Lopressor causes more significant decrease in BP compared to esmolol and lasts longer. Lopressor compared to labetolol causes less bronchoconstriction. |
| Minipress is what type of drug? Hint- what does it do at the receptor site? | Selective postsynaptic alpha 1 adrenergic receptor blocker. |
| What actions does Minipress produce on the body? | Vasodialates both arterial and venous. Reduces systemic vascular resistance without causing reflex tachycardia, & w/o causing increases in plasma renin (alpha 2 receptor function inhibits renin release). |
| Minipress has a greater affinity for venular alpha receptors or arteriolar alpha receptors? | Venular alpha receptors |
| What drug would you give to treat benign prostatic hypertrophy in an older male? | Minipress |
| What are some adverse effects of Minipress? | Initial dose marked orthostatic hypotension (blocks ability of body to compensate for decrease BP), fluid retention, dry mouth, urinary frequency, lethargy. |
| While giving Minipress you notice a severe decrease in BP, what drug would you choose to give to increase BP? | I would give epinephrine b/c it acts on both beta and alpha receptors & has a direct & indirect action to increase BP. I would not give phenylephrine b/c it is selective for alpha 1 receptors in which Minipress competes for & has a high affinity for. |
| Minipress and a beta blocker could result in what? | Nearly refractory hypotension having a diminished response to both beta and alpha 1 agonitst. |
| Sympathetic agonist is also called what? | Sympathomimetics |
| When would you give a sympathetic agonist? | When treating hypotension due to hemorrhage or cardiogenic shock. |
| Sympathetic agonists have a direct effect by what two ways? | Catecholoamines and analogs of catecholomines. |
| Sympathetic agonists act indirectly by...? | Increasing release or decrease reuptake of catecholoamines. Ex: amphetamine, meth, and cocaine. |
| Name some sympathomimetic drugs that are natural catecholamines or NT? Name one that is a catecholamine analog or does not occur naturally? | Dopamine, epinephrine, and norepinephrine are natural occuring catecholamines or NT. Dobutamine is not natural occuring and is a catecholamine analog. |
| Phenylephrine predominately acts on what receptor? And what is it used to treat? | Alpha 1. Used to treat hypotension, decongestant, eye drops. |
| What might you see while giving an IV bolus of phenylephrine? | Reflex bradycardia from an increase in BP. HR no longer needs to be tachycardic with an increase in BP, so HR will sometimes drop. |
| Dopamine given in low doses has what effects? | Stimulates dopaminergic receptors, renal and mesenteric vasodialation. Increases renal blood flow and urine output and preserves renal function. |
| Dopamine given in higher doses has what effect? | Stimulates Beta receptors as well as dopaminergic, and increases HR and force of contraction |
| Pseudoephedrine is a less potent version of what? | Ephedrine. Comes from the same plant. Readily absorbed from GI |
| Pseudoephedrine is used for what? | Nasal decongestants, local vasoconstriction of nasal capillaries, reduces nasal mucosa edema. Does not cause hypertension and tachycardia. |
| Dobutamine is a synthetic catecholamine that acts on Beta 1 having what effects? | Increases contractility greater than HR and having little direct effect on BP. |
| When would you give Dobutamine? | When a patient is having hypotension due to cardiac failure. Doesn't typically cause sinus tach. |
| Ephedrine is an alkaloid containing a nitrogen atom that is from an ephedra plant. What receptors does it act on alpha or beta? | Acts on alpha and beta. |
| Ephedrine acting indirectly | Acts at the norepinephrine synapse causing more norepinephrine to be released from its storage vesicles in the terminal of neurons. |
| Ephedrine acting directly | Binds to adrenergic receptors and mimics NE. |
| Hypertension is caused by what? | 1)Increased CO-factors that increase HR & factors that increase stroke volume. @)Increased total peripheral resistance-factors that increase blood viscosity & factors that reduce vessel diameter. |
| When there is an increase or decrease in BP how does our body know how to react? | Because central baroreceptors sense a decrease or increase in BP and help the body to respond appropriately. |
| With a decrease in BP the central baroreceptors respond bu stimulating what two systems? | Stimulation of B-adrenergic systems causing an increased HR (chronotropic), increased force of contraction (inotropic), increased renin secretion (renal cells). Stimulation of alpha-adrenoceptor systems (specifically a 1). |
| Essential HTN (primary) can be caused from what two things? | Excessive sympathetic activation, & elevated NE may promote through vascular endothelium injury. |
| Essential HTN through elevated NE from vascular endothelium injury can be caused from? | Vascular hypertrophy, atherogenesis, B-adrenergic receptor down-regulation, & sympathetic activation promotes enhanced peripheral vascular resistance |
| What are some classes of antihypertensives? | Diuretics, sympatholytics, vasodialators, Ca++ channel blockers, Angiotensin converting enzyme inhibitors (ACE), angiotensin receptor blockers. |
| Three types of Diuretics | Thiazides, Potassium sparring, & Loop diuretics. |
| Name some thiazide diuretics | Hydrochlorothiazide (HydroDIURIL), Chlorthalidone (Hygroton), Chlorothiazide (Diuril), Indapamide (Lozol), Metolazone (Zaroxolyn). |
| This type of diuretic acts in the distal tubule to decrease Na+ reabsorption (inhibits Na/Cl reansporter)? | Thiazide |
| Thiazide diuretics decrease the reabsorption of what two ions so that hyperosmolar diuresis ensues? What ion does it promote to reabsorb? | Decreases Na+ and Cl- reabsorption, and promotes Ca++ reabsorption. |
| What are some adverse effects of using thiazides? | Potassium depletion, hyperuricemia may occur precipitating gout (decrease in the ability to effectively secrete organic acids), hyperglycemia. |
| When using a thiazide diuretic why is hyperglycemia sometimes seen? | Because with a decrease in K+ there is a decrease in the insulin production leading to an increase in glucose. |
| Name some of the common loop diuretics. | Furosemide (Lasix), Bumetanide (Bumex), & Ethacrynic acid (Edecrin) |
| Where do loop diuretics take their action in the kidneys? | They act primarily at the ascending limb of the loop of Henle. |
| Why are loop diuretics very effective? | Because they act on the ascending limb where 30-40% of the filtered Na+ and Cl- load occurs. They act by reducing NaCl reabsorption. |
| Do loop diuretics increase or decrease urinary Ca++ in contrast to thiazides? | They increase urinary Ca++, and thiazides increase Ca++ reabsorption. |
| Loop diuretics increase renal blood flow by increasing or decreasing vascular resistance? | Decreasing |
| What are some adverse effects of loop diuretics? | Ototoxicity, Furosemide (Lasix)-block renal excretion or uric acid, & can precipitate gout, & potassium depletion. |
| This class of diuretics are weak diuretics? | Potassium sparing diuretics |
| This class of diuretics are weak diuretics? | Potassium sparing diuretics |
| How do potassium sparing diuretics work to lower BP? | They inhibit the effect of aldosterone. They compete for intracellular aldosterone receptor in the distal tubule cells, and increases the secretion of water and Na+, while decreasing the excretion of K+. |
| Do potassium sparing diuretics have an indirect or direct effect on decreasing BP? | Indirect because they are inhibiting the effect of aldosterone which in turn decreases the retention of Na+ and water. |
| What are some adverse effects of using potassium sparring diuretics? | GI problems, ataxia, drowsiness, and rashes |
| Name some common vasodilators? | Nitroglycerine, Diazoxide (Hyperstat), sodium Nitroprusside (Nipride), Hydralazine (Apresoline), Minoxidil (Loniten) |
| What are the two main actions of using a vasodilator? | Arterial vasodilator- decrease SVR = decrease afterload. Venous vasodilator- decrease venous return and CO = decrease preload. |
| This type of BP medication acts on the systemic circulation and produces cellular Nitric Oxide? | Vasodilators |
| What are some main functions of the chemical messenger nitric oxide (NO)? | Modulation of CV tone, plt regulation, neurotransmitter function in CNS, GI smooth muscle relaxation, immune regulation. |
| What happens with the inhalation of NO? | Decrease is pulmonary vascular resistance. Used for pulmonary HTN. |
| Where is NO synthesized and what is needed for this process? | Endothelial cells. Need Ca++ activated enzymes for this process. |
| What effect does NO have on the target tissue? | It increases cGMP which is a second messenger that causes vasodilation. |
| How is NO inactivated? | When it binds to iron on HGB. |
| A constant release of __ in systemic circulation maintains baseline BP and is produced more in arteries VS veins. | Nitric Oxide (NO) |
| Hypoxemia stimulates this substance to be produced in the body? | Nitric Oxide (NO) |
| Nitric Oxide has positive/negative ionotropic & chronotropic effects? | Negative Decreases HR and force of contraction. |
| What is the agent of choice to use for acute management of a hypertensive crisis or melignant hypertension? | Sodium Nitroprusside |
| What is the action of Sodium Nitroprusside that aids in acute hypertensive crisis or malignant HTN? | It is metabolized by smooth muscle cells to NO which dilates both arterial and venules. (Prodrug) NO activates guanylyl cyclase resulting in increased intracellular cGMP which then inhibits Ca++ entry into vascular smooth muscle. |
| Why would we want to inhibit Ca++ entry into vascular smooth muscle? | Because it aids in vasoconstriction which then increases HR. By inhibiting Ca++ entry we are relaxing the smooth muscle resulting in vasodilation and decrease HR. |
| Is Sodium Nitroprusside direct or indirect acting? | Direct acting |
| How does Nitroprusside increase CO? | By dilating the vessels it allows for adequate filling time (preload) and decreases peripheral vasucular resistance (afterload). Decreases both preload and afterload. |
| Nitroprusside may worsen myocardial infarction or coronary steal how? | Because it is dilating vessels and potentially causing less blood flow to an already depleted or infarcted area in which needs more blood flow. |
| Nitroprusside Toxicity may result from what? | The conversion of nitroprusside to cyanide and thiocyanate. |
| Nitroprusside can worsen arterial hypoxemia in COPD patients how? | It interferes with hypoxic pulmonary vasoconstriction and perfuses non ventilated areas instead of increasing perfusion to the well ventilated areas further increasing V/Q mismatches. |
| Why is Nitroprusside contraindicated in patients with decreased cerebral blood flow? | Because giving Nitropursside will further dilate arterial and venous vessels thus decreasing CBF in an already compromised patient. Will contribute to the problem and possible worsening. |
| Metabolism of Nitroprusside releases cyanide ions, what happens next? How can this cause toxicity? | 5 ions are released and 1 binds w methomeglobin=cyanomethemoglobin=not good in large amounts. 4 are converted to thiocyanate in liver & kidneys w the help of sulfur donors. If the 2nd system is overloaded then the first system takes over, which is BAD! |
| What would make you suspect that a patient on a cyanide gtt is developing cyanide toxicity? | If there is resistance to hypotension during administration of SNP gtt. Increased mixed venous PO2 (increase cyanide binds to cytochrome oxidase), and metabolic acidosis (anaerobic metabolism). |
| What is the treatment of cyanide toxicity? | 100% O2, sodium bicarb for metabolic acidosis, sodium thiosulfate-(sulfur donor), if severe sodium nitrate-(converts HGB to methemoglobin). e |
| Nitrogylcerin has greater effects on systemic venous or arterial dilation? | Greater effects on systemic venous system and coronary arteries. |
| Nitroglycerin requires thio-containing compounds for production of what? | Nitric Oxide |
| How can nitroglycerine cause methemoglobinemia? How do you treat this? | Because nitrates can bind with the HGB's iron in the blood to form methemoglobinemia. Tx with methylene blue to convert metheglobin to HGB. |
| Nitroglycerine has what effects on the bronchioles, biliary tract, and intra cranial pressure? | Bronchial dilation, relaxation of biliary tract, and is a cerebral vasodilator that increases ICP. |
| Nitroglycerine causes venodilation which does what to the CV system? | Decreases CO by dilating the venules. |
| Venodilation from administering Nitro can cause a mild increase or decrease in HR due to the baroreceptor response? | Mild increase in HR. |
| Nitro causes bronchial dilation, does this increase or decrease pulmonary vascular resistance? | Decreases pulmonary vascular resistance worsens V/Q mismatch |
| Nitro and bleeding | increases cGMP inhibits plt aggregation. Vasodilation increases blood flow to peripheral tissue or incision site. |
| Why would you give nitroglycerine to a patient in cardiac failure due to hypotension? | To increase coronary blood flow & decrease preload. By decreasing preload we decrease pulmonary edema, decrease myocardial O2 demands and increase CO. |
| Hydralazine and Minoxidil alters cellular Ca++ metabolism causing what to occur in the arterioles more then the venules? | Vasodilation |
| These two drugs have significant reflex mediated cardiac stimulation and water retention that increases CO, increases contractility, possible tachy, and can increase PAP if no pulmonary vascular relaxation occurs? | Hydralazine and Minoxidil |
| Name three classes of Ca++ channel blockers | 1)Dihydropyridines 2)Phenylalkylamines 3)Benzothiazepines |
| Calcium channel blockers work by blocking Ca++ from entering the cell. What are two ways in which this can be accomplished? | Reducing transmembrane movement of Ca++ (can reduce peripheral vascular resistance), Drug binding to voltage gated calcium ion channels (channels remain closed or inactive). |
| This sub type of Ca++ ion channel has 5 subunits Alpha 1 & 2, beta, gamma, & delta. | L channel |
| Is the L-type channel a slow or fast channel? | Slow channel |
| The L-type Ca++ channel has what effect in the cardiac cycle? | Phase 2 of cardiac action potential, cardiac & vascular smooth muscle excitation, depolarization of SA & AV nodal tissue. |
| Blocking the L-type Ca++ channel has what effect on the CV system? | Decreases HR, Decreases cardiac contractilitly, relaxes vascular smooth muscle. |
| What are some associated adverse effects of Ca++ channel blockers? | SA nodal inhibition (bradycardia or SA nodal arrest. Beta adrenergic antagonists increase risk), GI reflux (weakens smooth muscle control and causes reflex), negative iontropic if beta-adrenergic antagonist are used. |
| Ca++ channel blockers should be contraindicated in patients with? | SA or AV nodal abnormalities or patients with CHF. |
| Dihydropyridines- Name some common drugs that belong to this class | Amlodipine (Norvasc), Felodipine (Plendil), Nimodipine, Isradipine, Nicardipine, Nifedipine |
| Nifedipine modulates extracellular Ca++ channels and is commonly used for? | Sublingual for angina pectoris due to coronary vasospasm. |
| Why would you use Nifedipine for a patient having a coronary vasospasm? | Because it has great coronary vasodilation effects and great peripheral arterial vasodilation effects. |
| This drug has the greatest vasodilating effects of all the Ca++ channel blockers | Nicardipine |
| Nicardipine will have what type of effects on the heart? | No effect on SA or AV node, and has minimal myocardial depression. Works mainly on the Ca++ blockade in blood vessels and has minimal direct effects on the heart. |
| This Dihydropyridine drug is highly lipid soluble nefedipine analog? | Nimodipine (nimotop) |
| What advantage does Nimodipine (Nimotop)have on being highly lipid soluble? | It readily has access to the CNS to reduce large cerebral arterial contraction (Cerebral Vasospasm) |
| This drug is useful in preventing/reducing cerebral vasospasm associated with subarachnoid hemorrhage. | Nimodipine (Nimotop) |
| This drug may be used as a tocolytic? Blocks myometiral L-type Ca++ channels, and inhibits uterine contraction. | Nicardipine |
| Phenylalkylamines block Ca++ channels intra/extracellularly? | Intracellular block of Ca++ channels. Racemic mixture- Dextroisomer (fast Na+ channels) and Levoisomer (slow Ca++ channels). |
| What is Verapamil used to treat and where is its effect the greatest? | Used to treat SVT. Its effect is greatest at the AV node. |
| What are some SE of using Verapamil? | Moderate negative inotrope-avoid in the presence of heart failure, use caution if also using beta-blocker and avoid in pt with wolff-parkinson-white syndrome. |
| Diltiazem (Bensothiazepines) | Exact action unknown. Ca++ blocker, decrease Na-K pump, inhibit Ca-calmodulin binging. Primarily AV node site of action (SVT treatment) |
| Angiotensin I is formed by the action of __ on __. | 1)Renin 2)Angiotensin |
| Angiotensinogen is mainly released from where? Renin is released from where? | 1)The liver 2)The kidneys |
| Angiotensin concerting enzyme inhibitors block what from happening? | They block angiotensin I from converting to angiotensin II. |
| What properties does angiotensin II have? | Vasoactive properties |
| Angiotensin II is a potent vasocinstrictor that increases what? | Sympathetic discharge, adrenal catecholamines. Noradrenergic enhancement by decreasing reuptake and increasing the release and vascular response. |
| Angiotensin II has what effect on renal function? | Increases- Na+ reabsorption (aldosterone), noradrenergic transmission, renal sympathetic tone |
| Angiotensin II (Vascular & Cardiac changes) | Increases-growth factors, afterload & wall tension. These all contribute to cardiac hypertrophy |
| Name some ACE inhibitors | 1)Benazepril (Lotensin) 2)Captopril (Capoten) 3)Enalapril (Vasotec) 4)Fosinopril (Monopril) 5)Lisinopril (prinvivil, Zestril) 6)Moexipril (Univasc) 7)Quinapril (Accupril) 8)Ramipril (Altace) 9)Losartin (Cozaar) |
| ACE inhibitors reduce the production of what that causes an increase in BP? | Reduce the amount of angiotensin II produced. |
| This is the drug of choice in a hypertensive patient with hypertrophic left ventricles, and chemical heart disease with impaired left ventricular function. | ACE inhibitors- Because it can decrease BP w/o effecting contractility. |
| ACE inhibitors can also be used for management of diabetic patients in what way? | Reducing the development of diabetic neuropathy and glomerulosclerosis. |
| Along with decreasing the production of angiotensin II, ACE inhibitors also block what in the presence of low Na+? | ACE inhibitors also block the action of aldosterone with a loss of Na+. |
| What do you want to watch out for while administering an ACE inhibitor to a patient who is receiving high doses of diuretics? | Undersirable hypotensive reactions. A diuretic will volume deplete but still has aldosterone to hold onto some Na+ and fluid. Giving an ACE inhibitor along w a diuretic will further contribute to volume loss in the absence of the aldosterone feedback. |
| ACE inhibitors affects K+ levels how? | Decreasing aldosterone causes the body to excrete Na+ and retain K+. This could be serious in patients with renal disease or if the pt is also taking a K+ sparing diuretic. |
| Adverse effects of ACE inhibitors | Angiodema. Significant reduction in GFR=acute renal failure in pt's w renovascular hypertension & Dry cough |
| ACE inhibitors and Dry cough | Bradykinin is broken down by angiotensin converting enzyme. ACE inhibitors associated w/ increase in bradykinin levels. Bradykinin = contraction of non-vascular smooth muscle. |
| Na+ channel blockers bind to open Na+ channels also blocking what ion? | K+ channels |
| The transmembrane potential is determined by three primary ionic gradients? | Na+, K+, Ca++ |
| What are the three classes of Na+ channel blockers? | Type Ia- (Quinidine, procainamide) Type Ib, and Type Ic |
| Lidocaine (Xylocaine) is what class of Na+ channel blocker? | Class Ib |
| Lidocaine | More effective in suppressing activity in depolarized arrhythmogenic cardiac tissue (ischemic tissue not returing to resting potential). With normal resting potentials (-90)mV lidocaine rapidly dissociates from the channel & is less effective. |
| Amiodarone (Cordarone) works by | Blocking Na+ and K+ channels and prolonging the action potential. Minimal renal excretion and extensive protein binding. Long elimination halftime. |
| Complications of Amiodarone | Long term therapy is a rapidly progressive pulmonary fibrosis. Postoperative pulmonary edema in long term therapy, catecholamine responsiveness decreased due to alpha & beta receptor blocking activity. |
| K+ channel blockers work by | Delaying repolarization and prolong the action potential. Increase QT interval. Effective refractory period is increased. |
| Bretylium | A K+ channel blocker that prolongs the cardiac action potential and inhibits norepi reuptake by sympathetic nerves. |
| What can be seen after the first does of Bretylium? | Transient HTN- due to norepi release and decrease in its reuptake. |
| Bretylium possesses anti-fibrillaroty activity and can be used in management of serious ventricular arrhythmias by | Increasing ventricular fibrillation threshold (harder for V-fib to occur), prolonging action potential duration, & prolonging effective refractory period (when next contraction can take place) |
| Adenosine (Adenocard) works at the G- protein coupled adenosine receptor in which activates? | The acetylcholine-sensitive K+ current in the atrium, sinus, and A-V node. |
| How does Adenosine terminate SVT? | Decreases action potential duration, reduces automaticity. Increases A-V nodal refractoriness. Rapidly terminates re-entrant SVT arrhythmias. |
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