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Muscles of the Back and Suboccipital Triangle
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Name: Marco Ramirez - āI Am Not Batmanā TW: language Itās the middle of the night. And the sky is glowing like mad radioactive red. And if you squint, you could maybe see the moon through a thick layer of cigarette smoke and airplane exhaust that covers the entire city like mosquito net that wonāt let the angels in. And if you look up high enough you could see me-standing on the edge of a eighty seven story building. And up there-a place for gargoyles and broken clock towers that have stayed still and dead for maybe like a hundred years-up there is me. And Iām freakin Batman. And I gots Bat-mobiles and Bat-a-rangs and freakin Bat-caves like for real, and all it takes is a broom closet or a back room or a fire escape and Dannyās hand-me-down jeans are gone. And my navy blue polo shirt? ā The one that looks kinda good on me but has a hole on it near the butt from when it got snagged on the chain linked fence behind Arturoās but it isnāt even a big deal cause I tuck that part in and its like all good? āthat blue polo shirt? ā Itās gone too. And I get like, like transformational. And nobody pulls out a belt and whips Batman for talking back ā-Or for not talking back āAnd nobody calls Batman simple ā- Or stupid ā- Or skinny ā- And nobody fires Batmanās brother from the Eastern Taxi Company ācause they was making cutbacks, neither, ācause they got nothing but respect, and not like afraid-respect. Just like respect-respect. āCause nobodyās afraid of you. Cause Batman doesnāt mean nobody harm. Ever. Cause all Batman really wants to do is save people and maybe pay Abuelaās bills one day and die happy and maybe get like mad famous. For real.ā¦And kill the Joker. Tonight, like most nights, Iām all alone. And Iām watchingā¦And Iām waitingā¦ Like a eagle. Or like a āno, yea, like a eagle. And my cape is flappinā in the wind (ācause itās freakinā long), and my pointy ears are on, and that mask that covers like half my face is on too, and I got like bulletproof stuff all in my chest so no one could hurt me and nobody ā nobody ā is gonna come between Batman, And Justice. From where I am I could hear everything. Somewhere in the city thereās a old lady picking Styrofoam leftovers up outta a trash can and sheās putting a piece of sesame chicken someone spit out into her own mouth. And somewhere thereās a doctor with a whack haircut in a black lab coat trying to find a cure for the diseases that are gonna make us all extinct for real one day. And somewhere thereās a man, a man in a janitorās uniform, stumbling home drunk and dizzy after spending half his paycheck on forty-ounce bottles of twist-off beer and the other half on a four hour visit to some ladyās house on a street where the lights have all been shot out by people whoād rather do what they do, in this city, in the dark. And half a block away from JanitorMan thereās a group of good-for-nothings who donāt know no better waiting to beat JanitorMan with rusted bicycle chains and imitation Lousiville Sluggers, and if they donāt find a cent on him ā which they wonāt ā theyāll just pound at him till the muscles in their arms start burning, till thereās no more teeth to crack out. But they donāt count on me. They donāt count on no dark night (with a stomach full of grocery store brand macaroni-and-cheese and cut up Vienna sausages), Cause theyād rather believe I donāt exist, And from eighty-seven stories up I could hear one of the good-for-nothings say āGimmethecashā real fast (like that) just āGimmethefuckingcashā and I see JAnitorMan mumble something in drunk language and turn pale and from eighty-seven stories up I could hear his stomach trying to hurl its way out of his Dickies. So I swoop down like and fast and Iām like darkness. Iām like SWOOSH ā- And I throw a Bat-a-rang at the one naked lightbulb ā- And theyāre all like āwhoa-motherfucker-who-just-turned-out-the-lights?ā āāWhatās that over there?ā ā-āWhat?ā ā- āGimme whatchou got old manā ā- āDid anybody hear that?!ā ā- āNo, reallyā ā- āThere aināt. No. Bat.ā ā But then ā- One out of three good-for-nothings gets it to the head! And number Two swings blindly into the dark cape before him but before his fist hits anything I grab a trash can lid and ā-- Right into the gut, and number One comes back with a jump-kick but I know judo-karate too so Iām like ā-- Twice ā-- but before I can do any more damage suddenly we all hear a CLIC ā CLIC āAnd suddenly everything gets quiet And the one good-for-nothing left standing grips a handgun and aims straight up, like heās holding Jesus hostage, like heās threatening maybe to blow a hole in the moon. And the good-for-nothing who got it to the head who tried to jump-kick me and the other good-for-nothing who got it in the gut is both scrambling back away from the dark figure before him. And the drunk man the JanitorMan is huddled in a corner, praying to Saint Anthony ācause thatās the only one he could remember. And thereās me, Eyes glowing white, cape blowing softly in the wind. Bulletporoof chest heaving. My heart beating right through it in a Morse code for āfuck with me, just once, come on, just try.ā And the one good-for-nothing left standing, the one with the handgun, he laughs he lowers his arm, and he points it at me and gives the moon a break, and he aims it right between my pointy ears, like goalposts and heās special teams. And JanitorMan is still calling Saint Anthony but he aināt pickinā up, And for a second it seems likeā¦maybe Iām gonna lose. Naw. SHOO ā SHOO! FUACATA! --āDonāt kill me man!ā āāSNAP! ā Wrist CRACK ā Neck ā SLASH! ā Skin ā meets ā acid ā āAHH!!ā āAnd heās on the floor. And Iām standing over him. And I got the gun in MY hands now. And I hate guns, I hate holding āem cause Iām Batman, and āBatman donāt like guns ācause his parents got iced by guns a long time ago ā but for just a second, my eyes glow white, and I hold this thing, for I could speak to the good-for-nothing in a language he maybe understandsā¦CLIC ā CLICā¦And the good-for-nothings become good-for-disappearing into whatever toxic-waste-chemical-sludge-shit-hole they crawled out of. And itās just me and JanitorMan. And I pick him up. And I wipe sweat and cheap perfume off his forehead. And he begs me not to hurt him and I grab him tight by his JanitorMan shirt collar and I pull him to my face, and heās taller than me, but the cape helps so he listens when I look him straight in the eyes and I say two words to him: āGo home.ā And he does, checking behind his shoulder every ten feet. And I SWOOSH from building to building on his way there, ācause I know where he lives. And I watch his hands where he lives. And I watch his hands tremble as he pulls out his keychain and opens the door to his building. And Iām back in bed before he even walks in through the front door. And I hear him turn on the faucet and pour himself a glass of warm tap water And he puts the glass back in the sink. And I hear his footsteps, And they get slower as they get to my room. And he creaks my door open like mad slow. And he takes a step in, which he never does. And heās staring off into nowhere, his face the color of sidewalks in summer, and I act like Iām just waking up, and I say, āWhatās up, Pop?ā And JanitorMan says nothing to me. But I see, in the dark, I see his arms go limp and his head turns back, like towards me, and he lifts it for I could see his face, For I could see his eyes, And his cheeks is dripping but not with sweat. And he just stands there, breathing, like he remembers my eyes glowing white. Like he remembers my bulletproof chest. Like he remembers heās my pop. And for a long time I donāt say nothing. And he turns around, hand on the doorknob, and he aināt looking up my way but I hear him mumble two words to me. āIām sorry.ā And I lean over and open my window just a crack.ā¦ If you look up high enough you could see me. And from where I am? I could hear everything.A Brief History of Washingtonās Crossing of the Delaware River, Christmas Night 1776... In the fall of 1776, General George Washington and his army had suffered a series of defeats at the hands of the British Army. The Continental Army had lost every battle with the British in the New York campaign: Long Island, Manhattan, Brooklyn Heights, Harlem and White Plains and had surrendered Fort Washington and Fort Lee. At Fort Lee, the army barely escaped and was forced to leave behind its store of provisions, ammunition, and many of its weapons. A sense of defeat had settled around Washington as he was forced to retreat across New Jersey in November and finally to Pennsylvania on December 8, 1776. The British, at least, considered the war over. By December 11th, the only reason the British had not taken Philadelphia, the seat of the Continental Congress, was that Washington had ordered every boat in the Delaware River on the New Jersey side to be brought to the Pennsylvania side, thus denying the British army transportation. Washington knew that the British would be capable of resuming an offensive by crossing the Delaware once it iced over. As the harsh winter set in, the morale of the American troops was at an all-time low. The soldiers were forced to deal with a lack of both food and warm clothing, while Washington watched his army shrink because of desertions and expiring enlistments. Now, more than ever, a victory was desperately needed. Washington devised a courageous plan to take the offensive and cross the Delaware River on Christmas night and attack the Hessian garrison at Trenton, New Jersey, nine miles south of his encampment near McConkey's Ferry. The original plan called for three divisions to cross the Delaware under the cover of darkness. Lt. Col. John Cadwalader's division was to cross at Bristol and engage the southern most contingent of British forces ā Hessian troops under the command of Colonel von Donop. General James Ewing's division was to cross at Trenton Ferry and take a position south of Assunpink Creek below Trenton and hold the bridge over that stream. Washington's division was to cross at McConkey's Ferry and then divide into two corps under General Nathanael Greene and General John Sullivan. Their point of attack was Trenton and the Hessian troops quartered there under the command of Colonel Johann Gottlieb Rall. The boats to be used for the crossing were gathered earlier in the month in compliance with General Washington's orders, primarily as a defensive measure. Various types of boats had been collected, most notably the large Durham boats used to carry pig iron down the Delaware to the Philadelphia markets. There were a number of problems in moving a large number of men, cannons, and supplies in an age when overland transportation was by foot and animal power. The roads were rutted and winding. There were no bridges over major rivers because the technology did not exist to span great distances. A river like the Delaware was crossed by ferry, sometimes out of service because of ice floes or floods, and certainly not designed to carry masses of men and equipment across quickly. A river could be a formidable natural barrier to an army on the move. Washington had several logistical concerns for the crossing. In addition to the troops were the cannon; each of which required at least two horses to pull it. The heavier twelve pounders, and probably the eight pounders, had four horses. There would have been between four and six ammunitions wagons. Officers of the rank of colonel or higher may have had horses. In sum, Washington had to move 2,400 men, eighteen cannons, at least four ammunition wagons and fifty to seventy-five horses across the Delaware River the night of December 25, 1776. Fully expecting to be supported by Cadwalader's and Ewing's divisions south of Trenton, Washington assembled his own troops near McKonkey's Ferry in preparation for the crossing. By 6:00 pm, 2,400 men had begun crossing the ice-chocked river. There was an abrupt change in the weather, forcing the men to fight their way through sleet and a blinding snowstorm. The river was flooded with sheets of ice moving at eleven or twelve miles per hour. These obstacles proved to be too much for the two supporting divisions led by Generals Cadwalader and Ewing, who did not cross at their assigned points along the river. It was Washington's pure force of will and determination that led to his troops' successful crossing of the river. Increasing Washington's odds were the sailors of Marblehead, Massachusetts. This group of hardened seamen, led by Col. John Glover, were used to the Nor'easters of New England. Sheer determination and muscles conditioned to the demands of rowing under the weather conditions now facing the Continental army enabled the Marbleheaders to row back and forth across the Delaware countless times. During the time of the Revolution, American soldiers marched single file along the margins of the roads. They were only assembled into a battle line (three deep) when they reached the battlefield. The battle plan had Washington's army marching in two divisions... General Greene's and General Sullivan's. They made a night march in two columns on separate roads, a very tricky operation that was prone to failure since the columns needed to arrive at the battlefield at the same time to carry out the surprise attack planned by Washington. The American army carried out the march flawlessly. Against all odds, Washington and his men successfully completed the crossing and marched to Trenton on the morning of December 26th and, in the resulting battle, achieved a resounding victory over the Hessians. By moving ahead with his bold and daring plan, General Washington reignited the cause of freedom and gave new life to the American Revolution.LESSON 4. Cellular Respiration ā¢ Define cellular respiration ā¢ Identify the stages of clan respiration You have just learned how the energy from the sun is captured, processed, and stored in the form of glucose. Cellular respiration, another important life process, is the means by which cells release the stored energy in glucose to make adenosine triphosphate (ATP). The primary goal of this life process is to convert stored energy into usable form, such as ATP, for the cells to carry out their functions. Cellular respiration involves several chemical reactions. The reactions can be summed up in the following equation: C6 H12 O6 + 602 -----ļ 6 COā +6HāO + ATP Glucose oxygen carbon dioxide water energy Aerobic respiration reactions, or cellular respiration that takes place in the presence of oxygen, can be grouped into three stages glycolysis, Krebs cycle, and electron transport chain (ETC). Stage 1: Glycolysis Glycolysis is the process that breaks down one molecule of 6-C glucose into 3-C pyruvates or pyruvic acids. It also releases four molecules of ATP. This process occurs in the cytoplasm of the cell. The following is the step-by-step process of glycolysis. Take note that several enzymes are involved in this process. 1. The first step of glycolysis requires energy. It can only proceed when the two ATP molecules donate energy to the glucose by transferring a phosphate group with the help of an enzyme, producing glucose 6-phosphate 2. Then, a specific enzyme promotes the rearrangement of the atoms, producing the fructose 6-phosphate. 3. The action of the enzyme in step 2 promotes the transfer of a phosphate group from another ATP molecule, forming fructose 1,6-bisphosphate. 4. The resulting fructose 1,6-bisphosphate molecules, with the help of another enzyme, splits into two molecules, each with three carbon backbones. These two sugars are dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. 5. Another important enzyme then rapidly interconverts the molecules of dihydro-xyacetone phosphate and glyceraldehyde 3-phosphate. This produces two molecules of glyceraldehyde 3-phosphate or 3-phosphoglyceraldehyde (PGAL) 6. The succeeding step involves another enzyme-mediated action. The hydrogen (H) from PGAL is transferred to the oxidizing agent, nicotinamide adenine dinucleotide (NAD), which forms NADH. A phosphate (P) is also added from the cytosol of the cell to oxidize the two molecules of PGAL, forming two 1.3-bisphosphoglycerate. 7. A phosphate (P) from 1,3-biphosphoglycerate is transferred to ADP to form ATP. This happens for each of the two 1,3-bisphosphoglycerate. resulting to a yield of two ATP and two 3-phosphoglycerate molecules. 8. A phosphate is transferred from 3-phosphoglycerate molecules from the third carbon to the second carbon, forming 2-phosphoglycerate molecules A hydrogen atom and a hydroxyl ((OH) group is released, which then combines to form water (H2O). The removal of H2O from 2-phosphoglycerate results in the formation of 2- phosphoglycerate molecules. 9. A hydrogen atom and a hydroxyl ((OH) group is released, which then combines to form water (H2O). The removal of H2O from 2-phosphoglycerate results in the formation of two phosphoenolpyruvic acid (PEP) 10. Phosphate (P) from PEP is transferred to ADP (and forms ATP) and the final product, pyruvic acid. This reaction yields two molecules of pyruvic acid and two ATP molecules In summary, a single glucose molecule that undergoes the process of glycolysis produces two molecules of pyruvic acid, four molecules of ATP, two molecules of NADEL and two molecules of H.O. However, only two molecules of ATP are counted as net products since two molecules of ATP are spent throughout the process. Stage II: Krebs Cycle The Krebs cycle, named after its proponent Sir Hans Adolf Krebs, is a cyclical series of enzyme-controlled reactions. This stage of cellular respiration occurs in the matrix of the mitochondria. It is sometimes. called the citric acid cycle (CAC) since it produces citric acid. Citric acid contains three carboxyl (COOH) groups; hence, it is also called the tricarboxylic acid cycle (TCA). This requires the pyruvic acids produced during glycolysis. The main function of this cycle is to produce high-energy-yielding molecules, namely, NADH and flavin adenine dinucleotide (FADH) that will later on be used in the electron transport chain reaction. Figure 6-7. Summary of glycolysis and corresponding products in each reaction presented (See Appendix F on page 285 for an enlarged and complete version of the image.) An initial process is needed for the Krebs cycle to begin. As a pyruvate molecule from glycolysis enters the mitochondrion, it undergoes an important preliminary ate to form acetyl-CoA reaction. Coenzyme-A (COA) combines with pyruvate help of an enzymatic complex. This conversion also produces CO, and NADH. The Krebs cycle is summarized as follows. Take note that several enzymes are involved in this process. 1. The Krebs cycle technically begins when the acetyl-CoA combines with oxaloacetic acid (OAA), a 4-C molecule, to produce citric acid, a 6-C molecule. 2. With the aid of an enzyme, the citric acid now goes through a series of reactions that releases energy. Water molecule is removed from the citric acid and is returned in a different location. The-OH group is repositioned, forming the molecule isocitrate. 3. Isocitrate is then oxidized, forming the a-ketoglutarate, a 5-C molecule. The byproducts of this reaction are NADH and CO, 4 The a-ketoglutarate loses its CO, and a coenzyme-A is added in its place. The decarboxylation occurs with the help of NAD, which then becomes NADH. The resulting molecule is called succinyl-CoA. 5. Succinyl-CoA is converted into succinate. Also in this reaction, a molecule of guanosine triphosphate (GTP) is synthesized. The GTP molecule has similar structure and energy properties to that of ATP and is used by cells the same way. The free phosphate group attacks the succinyl-CoA molecule, which detaches the COA. Then, phosphate is attached to GDP to come up with GTP, similar to the process that occur in ATP synthesis (from ADP to ATP). 6. Two hydrogens are removed from succinate, A molecule of flavin adenine dinucleotide (FAD), a coenzyme similar to NAD, is reduced to FADH, as it takes the hydrogens from the succinate. This reaction produces the fumarate. 7. Fumarate is then converted into malate as the addition of a water molecule is catalyzed. The final reaction is the regeneration of oxaloacetate. The resulting byproduct of this regeneration is NADH Recall that two pyruvate molecules were produced during glycolysis, causing the Krebs cycle to turn twice. Each tuts produces three molecules of NADH, single ATH one FADIH, and the by-product CO, which is exhaled. Stage III: Electron Transport Chain The electron transport chain (ETC) is a series of photon pumps on the inner membrane of the mitochondrion. Electron transport is the last stage of the cellular respiration. In this stage, the energy from NADH and FADH, from the Krebs cycle is transferred to ADP to produce ATP. This process is generally known as oxidative phosphorylation. This energy coupling mechanism in the cell was revealed by the work of Peter stored energy in the form of proton (1) gradient to phosphorylate (add phosphate) ADP and produce ATP. The pumping of hydrogen sons across the inner membrane creates higher concentration ions in the inner membrane than on the outside of the membrane. This chemiosmotic gradient causes the ions to flow back across the membrane where the concentration of ions is lower. ATP synthase lined in the matrix serve as a channel protein, helping the ions to move across the membrane. The chemiosmotic gradient powers the phosphorylation of ADP to ATP, which also occurs in the ATP synthase. After passing through the ETC, the oxygen, being the final hydrogen acceptor, combines with two electrons and two protons, forming a water molecule. Water is a by-product of cellular respiration and is excreted. MINI TEST 6-3 1. Which energy-releasing pathway yields the most ATF in each glucose molecule? 2. Briefly describe the two stages of aerobic respiration that follow glycolysis: (a) Krebs cycle (b) Electron transport chain Anaerobic Respiration Most cells carry out arrobic respiration when oxygen is present. Aerobic respiration is an efficient process that yields a lot of ATP. However, many organisms thrive in mud, marshes, animal gut, canned goods, sewage treatment pond, and deep oceans where oxygen is scarce. Organisms that can live without oxygen are called anaerobes. Cellular respiration that proceeds without the presence of oxygen is called anaerobic respiration. In the event that the oxygen supply becomes low, aerobic cells also perform fermentation and lactic acid fermentation anaerobic pathways. There are two common anaerobic pathways in these cells, alcoholic fermentation and lactic acid fermentation. In alcoholic fermentation, ethyl alcohol and carbon dioxide are produced by some cells using the pyruvate from glycolysis. Each pyruvate molecule is rearranged into acetaldehyde and carbon dioxide, which is eventually released. NADII gives up electrons to acetaldehyde to form ethanol Fermentation is widely used in the industry. Yeast, a fungus used in making bread. can undergo anaerobic respiration. Bakers aux sugar, flour, water, and yeast to form the bread dough. The dough rises due to the carbon dioxide and alcohol released by the yeast cells trapped in air bubbles. Beer and wine manufacturers, we yeast to ferment the sugars in wheat and grape juice, forming alcoholic beverages such as beer and wine. In some cells, glycolysis produces two pyruvates, two NADH molecules, and two ATP molecules. Pyruvate itself becomes the final acceptor of the electrons from the NADH that produces the final product: lactate. Oftentimes, this product is called lactic acid. Human skeletal muscles can carry out fermentation when the blood cannot supply the cells with adequate oxygen during strenuous activities. When lactic acid builds up in the muscles, fatigue, burning sensation, and cramps result. Lactic acid will continue to build up until there is adequate supply of oxygen. Lactic acid is then converted back into pyruvate in the liver. Muscles also restore normal functions. Have you ever wondered why milk or cream turns sour after some time? Bacterial cells that undergo fermentation are responsible in producing lactate that turns the milk sour. These bacteria are used in manufacturing yogurt and sour milk products. Fermentation pathways do not breakdown and utilize the glucose completely. ATP is no longer produced beyond the process of glycolysis. Thus, energy produced is just enough for some single-celled organisms, or the energy can only be used by multicellular organisms for a short period.1. SA node sends an impulse causing the atria to contract 2. Blood moves from the right atrium into the right ventricle past the tricuspid valve 3. Blood moves from the left atrium into the left ventricle past the mitral or bicuspid valve 4. Impulse pauses at AV node to allow for maximum blood to be squeezed into the ventricles 5. Impulse travels to the AV bundle (or bundle of His) and down the bundle branches 6. Impulse travels out Purkinje fibers causing the apex to contract 7. The apex contraction increases the blood pressure in the ventricles causing the Mitral and Tricuspid (AV) valves to close. 8. Atria repolarize and begin to fill 9. Purkinje fibers cause the ventricle walls and papillary muscles to depolarize (contract) 10. Papillary muscles hold the AV valves shut (keep them from prolapsing) through the chordae tendineae connection 11. The aortic and pulmonary semilunar valves open when the pressure is higher in the ventricles than in the major arteries 12. Blood moves from right ventricle to pulmonary trunk/arteries past the pulmonary semilunar valve 13. Blood moves from left ventricle to aorta past the aortic semilunar valve 14. Blood pathway is arteries to arterioles, to capillaries (or capillary bed), to venules, veins and vena cava back to the right atrium 15. The ventricles start to repolarize (relax) which decreases the pressure in the ventricles 16. When the pressure is lower in the ventricles than in the major arteries, blood moves back toward heart shutting semilunar valves 17. When the aortic valve closes, the openings to the coronary arteries are exposed 18. Back pressure in the aorta pushes blood out the left and right coronary arteries supplying the heart with oxygenated blood 19. The AV valves open and blood moves from the atria into the ventricles when the ventricular pressure falls below atrial pressure. 20. The process starts again when the SA node fires causing the atria to contract.Chapter 22 Antihypertensive Drugs Hypertension Defined (JNC-8) Pharmacology Overview 7 main categories of drugs to treat HTN Adrenergic drugs (old friend) Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers (ARBs) Calcium channel blockers (CCBs) Diuretics Vasodilators Direct renin inhibitors A. Adrenergic Drugs: 5 Subcategories and where they act A1. Adrenergic neuron blockers (central and peripheral)- we wonāt talk about this A2. Alpha1 receptor blockers (peripheral) A3. Alpha2 receptor agonists (central) A4. Beta receptor blockers (peripheral) A5. Combined Ī± and Ī² receptor blockers (peripheral) A2. Peripherally Acting Adrenergic Drug Alpha1 Blockers (weāve met these) Doxazosin, prazosin, alfuzosin Block alpha1-receptors which causes BP to decrease Reduces peripheral vascular resistance and BP by dilating both arterial and venous blood vessels Main Use: benign prostatic hyperplasia (BPH) Alpha1 Blockers REMEMBER Tamsulosin (Flomax)* is an Ī±1 blocker BUT *Tamsulosin is not used to control BP, just for BPH. A3. Centrally Acting Adrenergic Drugs Alpha 2 agonist Clonidine and methyldopa 1- Stimulate alpha2-adrenergic receptors. in the brain Decreases sympathetic outflow from the CNS which decreases NE production 2. Stimulate alpha2-adrenergic receptors in kidneys remember alpha 2 opposes alpha 1 Dilates peripheral blood vessels ā lowers peripheral resistance āĀ Results in decreased BP So ā¦.Clonidine (Catapres) Used primarily for its ability to decrease blood pressure in an urgent setting Also use in opioid withdrawal as previously discussed Oral (multiple times a day), and topical patch formulations Do not stop abruptly as it may lead to rebound hypertension In reality, Clonidine and methyldopa Not prescribed as first-line home antiHTN drugs High incidence of unwanted adverse effects: orthostatic hypotension, fatigue, and dizziness MIGHT be uses as adjunct drugs after other drugs have failed, in conjunction with other antiHTN such as diuretics A4. Adrenergic Drugs Selective Beta 1 Blockers Metoprolol, Atenolol Reduction of HR through Ī²1 receptor blockade (remember adrenergic blocking of this receptor???) HR results in BP Cause reduced secretion of renin = BP A4. Adrenergic Drugs Selective Beta1 Blockers Nebivolol (Bystolic) Uses: hypertension and HF Action: blocks Ī²1 receptors and produces vasodilatation, which results in a decrease in SVR High doses loses selectivity and blocks both Ī²1 and Ī²2 Less sexual dysfunction All BB- Do not stop abruptly; must be tapered over 1 to 2 weeks A4. Adrenergic Drugs NONSelective Beta Blockers Propranolol Acts equally on Ī²1 and Ī²2 Other uses include situational anxiety associated with public speaking, test taking As mentioned on previous slide, nebivolol at high doses becomes beta nonselective A5. Dual-Action Adrenergic Drugs Ī±1 and Ī² Receptor Blockers Dual antihypertensive effects of reduction in heart rate (beta1 receptor blockade) and vasodilation (alpha1 receptor blockade) Examples are carvedilol (common) and labetalol (not as common) A5. Dual-Action Adrenergic Drugs Ī±1 and Ī² Receptor Blockers Carvedilol (Coreg) Widely used drug that is well tolerated Uses: HTN, mild to moderate HF in conjunction with digoxin, diuretics, and ACE inhibitors Contraindications: severe bradycardia or unstable HF, bronchospastic conditions such as asthma, and various cardiac conduction problems Adrenergic Drugs Indications - HTN But also for Glaucoma (topical) BPH: doxazosin, prazosin, and terazosin (2 for 1) Management of severe HF when used with cardiac glycosides and diuretics Contraindications Acute HF- have to stabilize first MOAIs- yeah doesnāt everything interact with MAOIs? Peptic ulcers Severe liver/kidney disease Asthma (with beta blockers) Adrenergic Drugs: Adverse Effects Orthostatic hypotension 1st-dose syncope Rebound hypertension with abrupt discontinuation Most common: Dry mouth, drowsiness, constipation, sedation Interactions- always check for specific drug interactions Can cause additive CNS depression with alcohol, benzodiazepines, opioids Question #1 When administering an alpha-adrenergic drug for hypertension, it is most important for the nurse to assess the patient for the development of what response? Hypotension Hyperkalemia Oliguria Respiratory distress Answer A Hypotension This is a key point in patient education These drugs have strong vasodilating properties and may cause severe hypotension, especially at the beginning of therapy. B. Angiotensin-Converting Enzyme Inhibitors aka ACE Inhibitors or ACEi Large group of safe and effective drugs Currently are 10 ACEi Often used as first-line drugs for HF and hypertension May be combined with a thiazide diuretic, loop diuretic, or Calcium Channel Blocker (CCB) You need to understand the basics ACE Inhibitors: Review RAAS ACE converts angiotensin I, formed through the action of renin, to angiotensin II Angiotensin 2 is a potent vasoconstrictor and also induces aldosterone secretion by the adrenal glands Aldosterone stimulates sodium resorption (H20 follows Na Both act to raise BP which causes kidneys to reduce renin production ACEi= Great drug to treat HTN BUT contraindicated in pregnancy (2nd,3rd trimester due to fetal renal damage) and breastfeeding first few weeks after birth B. ACE Inhibitors - PRIL Lisinopril (Prinivil) super common, often the 1st drug Enalapril (Vasotec) also common Captopril (Capoten) great if liver disease present Benazepril (Lotensin) Fosinopril (Monopril) Perindopril (Aceon) Quinapril (Accupril) Ramipril (Altace) Trandolapril (Mavik) Primary Effects of the ACE Inhibitors Prevent Na (and H2O) resorption by inhibiting aldosterone secretion (volume reduction) (GO BACK TO RAAS DIAGRAM) blood volume decreases work of the heart preload, or the left ventricular end-diastolic volume which is important in HF ACE SUMMARY OF ACTIVITY 1) Prevent vasoconstriction caused by angiotensin 2 (2) Prevent aldosterone secretion ļØ less sodium and water resorption Cardioprotective Effects of ACEi They slow progression of left ventricular hypertrophy (ventricular remodeling) after MI so considered cardioprotective ACE inhibitors have been shown to decrease morbidity and mortality in patients with HF Renal Protective Effects of ACEi ACE inhibitors: reduce glomerular filtration pressure by volume reduction Cardiovascular drug of choice for patients with diabetes since it helps protect kidneys by reducing pressure. Sometimes used low dose for kidney protection with DM without HTN B. ACEi Enalapril (Vasotec) Only ACEi available in both oral and IV Enalapril IV does not require cardiac monitoring Oral enalapril: prodrug (metabolized in liver) Improves patientās chances of survival after an MI Reduces the incidence of HF B. ACEi Captopril (Capoten) Uses: prevention of ventricular remodeling after MI; reduce the risk of HF after MI Shortest half-lifeļØ Must be administered multiple times throughout the day so this limits its use Not a prodrug so good for patient with liver disease Question #2 A patient with diabetes has a new prescription for the ACE inhibitor lisinopril. She questions this order because her provider has never told her that she has hypertension. What is the best explanation for this order? The doctor knows best The patient is confused This medication has cardioprotective properties This medication has a protective effect on the kidneys for patients with diabetes Answer D ACE inhibitors have been shown to have a protective effect on the kidneys because they reduce glomerular filtration pressure. This property makes them the cardiovascular drug of choice for patients with diabetes. Question #3 A patient with a history of pancreatitis and cirrhosis is also being treated for hypertension. Which drug will most likely be ordered for this patient? Clonidine Prazosin Diltiazem Captopril Answer D Captopril Captopril is not a prodrug; therefore, it does not need to be metabolized by the liver to be effective. This is an advantage in patients with liver disease. ACE Inhibitors: Adverse Effects *Dry, nonproductive cough, which reverses when therapy is stopped. This is a class effect Dizziness- Note: First-dose hypotensive effect may occur Headache & Fatigue Possible hyperkalemia ** Angioedema: rare but potentially fatal Not safe in pregnancy-areĀ contraindicated during the second and third trimesters of pregnancyĀ because of increased risk of fetal renal damage C. Angiotensin II Receptor Blockers (ARB) Considered an alternative to ACEi Less likely to cause a dry cough and hyper K+ that is common with ACE inhibitors Angiotensin II Receptor Blockers: Mechanism of Action Go back to RAAS diagram! ARBs affect primarily 2 places 1. Vascular smooth muscle - blocks vasoconstriction 2. Adrenal gland -Selectively blocks the binding of Ang 2 to certain Ang 2 receptors inhibiting secretion of aldosterone Lowers volume retention and BP Angiotensin II Receptor Blockers -ARTAN Losartan (Cozaar)- very common Eprosartan (Teveten) Valsartan (Diovan) Irbesartan (Avapro) Candesartan (Atacand) Olmesartan (Benicar) Telmisartan (Micardis) Azilsartan (Edarbi) C. ARB Losartan (Cozaar) Beneficial in patients with HTN and HF Used with caution in patients with kidney or liver dysfunction and in patients with renal artery stenosis ***Not safe for breastfeeding women and should not be used in pregnancy (Cat C 1st trimester, Cat D 2nd-3rd trimester), potential fetal toxicity Appear to be equally effective for the treatment of hypertension and well tolerated ARBs less likely to cause cough and hyperK+ but can still happen Evidence that ARBs are associated with lower mortality after MI than ACE inhibitors Never take ACEi and ARBs at the same time* 5. Calcium Channel Blockers (CCB) Primary use: HTN, angina, some dysrhythmias Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction Results in: Relaxed blood vessels to the heart Decreased peripheral smooth muscle tone Decreased SVResistance Decreased BP E. Diuretics First-line antiHTN in JNC 8 guidelines Decreases fluid volume The results from diuresis: preload, Peripheral resistance Overall effect ļ Decreased workload of the heart and decreased BP Thiazide diuretics are the most commonly used diuretics for HTN Ie hydrochlorothiazide (HCTZ), chlorthalidone We will discuss diuretics further in the chapter on diuretics F. Vasodilators Directly relax arterial or venous smooth muscle (or both) Results in: Decreased SVR Decreased afterload Peripheral vasodilation Indicated for treatment of HTN May be used in combination with other drugs F. Vasodilators Hydralazine (Apresoline) Orally: routine cases of essential hypertension Injectable: hypertensive emergencies BiDil: specifically indicated as an adjunct for treatment of HF in African-American patients F. Vasodilators Sodium Nitroprusside (Nitropress) *Sodium nitroprusside and IV diazoxide are reserved for the management of hypertensive emergencies. Contraindications: severe HF, known inadequate cerebral perfusion (especially during neurosurgical procedures) F. Vasodilators Adverse Effects Hydralazine: dizziness, headache, tachycardia, edema, dyspnea, N/V/D, vitamin B6 deficiency, rash Sodium nitroprusside: hypotension, bradycardia, decreased platelet aggregation, rash G. Direct Renin Inhibitors Aliskirin (Tekturna) Blocks theĀ RASĀ pathway at the point of activation. Inhibiting renin production prevents the downstream production of Ang II (potent vasoconstrictor) Adverse effects: N/V, severe hypotension, hyponatremia, hyperkalemiaā¦ Contraindicated in patients with DM taking ACEi or ARB Miscellaneous Antihypertensives Eplerenone (Inspra) Newer class of drugs called selective aldosterone blockers (remember RAAS?) Reduces BP by blocking the actions of aldosterone at its corresponding receptors in the kidney, heart, blood vessels, and brain Indications: routine treatment of hypertension and for post-MI HF Contraindicated if serum potassium levels are high (above 5.6 mEq/L) A Special Form of HTN Treatment of Pulmonary Hypertension Sildenafil and Tadalafil Commonly used for erectile dysfunction Used for pulmonary hypertension but with different trade names Sildenafil: Revatio* (Viagra for ED) Tadalafil: Adcirca* (Cialis for ED)Muscles of the wrist and elbowMuscles of the body and antagonistic pairsMuscles of the feet