Pharm 1 Exam 3 Chart PDF

Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects Hypertension overview BP=CO x PVR Baroreceptors (like in carotid sinus) are l...

Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects Hypertension overview BP=CO x PVR Baroreceptors (like in carotid sinus) are located in arteries and they detect changes in BP and send signals to the brain when BP is too high or too low for the brain to process the info and decide if BP needs to be adjusted. If it does, the brainstem sends signals through ANS (which controls HR and BV constriction/dilation) to either the sympathetic if BP needs to be increased or the parasympathetic system if BP needs to decrease. The signals act on the alpha and beta receptors in BVs and the heart to adjust BP When there is a decrease of BP in the renal arteries, the kidneys release renin (stimulated by beta receptors) which helps produce angiotensin 1, which can get converted to angiotensin 2 by ACE in the lungs ○ The angiotensin 2 can then induce vasoconstriction of BVs increasing PVR, and stimulating the production of aldosterone which leads to sodium retention increasing the volume and raising BP more 4 main sites of antihypertensive drugs include brain, heart, blood vessels, and kidneys Categories of antihypertensives include diuretics, agents that block production or action of angiotensin, direct vasodilators, and sympathoplegic agents Generally, ACEis end in pril and inhibit ACE, ARBs end in sartan and block angiotensin 2 receptors, alpha blockers end in osin and block alpha receptors, BBs end in lol and block beta receptors, CCBs end in dipine and block calcium channels, and diuretics end in ide and facilitate diuresis First line hypertensive agents include ACEs, ARBs, CCBs, and thiazide diuretics and remember the general 4 steps/stages of HTN treatment  Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects Meds that can affect blood pressure (prolly do not have to know specifics of these) ○ Sympathomimetic agents like amphetamines, phenylpropanolamine, ephedrine, etc ○ NSAIDs and COX2 inhibitors like ibuprofen, naproxen, diclofenac, etc ○ CNS stimulants like caffeine ○ Estrogens and progestins like oral contraceptives, ERT/HRT ○ Dietary supplements like ginseng, natural licorice, and yohumbine Thiazide Diuretics (ide) First line for black adults with HTN (with or without DM) that These generally increase the One of the first line Gout Hyperglycemia do not have HR or CKD excretion of NaCl which induces agents for HTN DM especially in DM pts Good for pts with osteoporosis water to follow it resulting in Also helps reduce fluid Hypokalemia increased calcium reabsorption build up in conditions like Hyperuricemia which Blocks the transporter that would HF and liver disease (not can trigger a gout attack otherwise bring NaCl back into the as effective as loop Sulfonamide sensitivity distal convoluted tubule diuretics tho) and toxicity Prevents hypercalcinuria Hyponatremia preventing kidney stone Orthostatic hypotension formation Hyperlipidemia Sexual dysfunction Renin Angiotensin Aldosterone Three types of drugs include ACEis which block the enzyme System acting drugs ACE that converts angiotensin 1 to 2, ARBs which block angiotensin 2 from binding to receptors, and direct renin inhibitors which decrease production of renin Refer to renal response to decreased blood pressure  Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects ACE and ARBs are first line as they are cheap, affordable, effective, and easy to use Angiotensin converting enzyme Main meds (that are all available orally) include lisinopril, Blocks angiotensin 1 from being hypertension Absolute include a history Dry cough due to (ACE) inhibitors (pril) ramipril, captopril, enalapril, fosinopril, and quinapril converted to angiotensin 2 in the of angioedema, bilateral increased bradykinin Can be helpful in DM and kidney disease patients, as well as lungs renal artery stenosis, and which is usually broken pts with a hx of CHF and MI pregnancy down by ace ○ Really good for CKD patients with albuminuria or Relative (monitor closely) hyperkalemia creatinine >300 mg/d if there is unilateral renal Angioedema (swelling ○ A chart said all first line classes are useful and artery stenosis or renal of face, lips, tongue, effective in adults with HTN and DM but ACE for sure insufficiency and throat) as well as ARBs are considered in the presence of Teratogenic in albuminuria pregnancy Hypotension Renal insufficiency Dysgeusia Angiotensin Receptor Blockers Common arbs include candesartan, irbesartan, losartan, and These block the action of Hypertension pregnancy hyperkalemia ARBS (sartan) valsartan angiotensin 2 by binding to the AT Heart failure Remember that ACEs Good alternative to ACEs and these do not induce a cough type 1 receptor in the heart, kidneys, Diabetic nephropathy and ARBs are not and there is less risk of angioedema and BVs which prevents angiotensin combined together as Good for pts with history of MI and HF 2 from vasoconstricting and they can induce kidney increasing BP damage and hyperkalemia Direct Renin Inhibitors (aliskiren) This is aliskiren (tekturna) This directly blocks and inhibits the hypertension Pregnancy Similar toxicity to ACEi This is more costly than ACEs or ARBs effects of renin which is the enzyme although less common that starts the production of Hyperkalemia angiotensin 1 which eventually leads (especially in combo to angiotensin 2. By blocking renin, with ACE or ARB) there is a decrease amount of Dry cough angiotensin 2 which helps lower BP Angioedema Vasodilators These are not first line Example 1 from lil chart Meds like nitroprusside, hydralazine, nitrates, histamine, and Release nitric oxide from drug or maybe nebivolol endothelium which relaxes blood  Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects vessels Example 2 from lil chart Meds like verapamil, diltiazem, amlodipine, and nifedipine These are calcium channel blockers that reduce calcium influx preventing calcium from entering smooth muscle cells which reduce contraction and promote relaxing Example 3 from lil chart Meds like minoxidil and diazoxide These open potassium channels causing the inside of smooth muscle cells to become more negatively charged (hyperpolarized) inhibiting contraction and promoting relaxation Hydralazine (apresoline) This is given either orally or through IV with a short duration Triggers the release of NO which HTN in general but not Headache of about 6 hours helps relax and widen arterioles but first line Flushing no veins Can be used in HTN Nasal congestion emergency Tachycardia and Commonly used in people palpitations which can with very resistant HTN lead to myocardial and/or who are getting ischemia ready for dialysis Lupus like syndrome Sodium Nitroprusside IV only but can result in cyanide toxicity from thiocyanate Similar to hydralazine but this HTN Headache that can accumulate (especially in renal dysfunction) and relaxes both arterial and venous HTN emergencies Flushing cause psychosis and delirium blood Nasal congestion Tachycardia and palpitations that can lead to myocardial ischemia Risk of cyanide toxicity Minoxidil and Diazoxide Minoxidil is available through oral Both drugs activate potassium Minoxidil is indicated for Similar to hydralazine as Diazoxide is IV only channels and open them up which severe or resistant HTN they can cause helps relax and hyperpolarize the Diazoxide is indicated tachycardia and smooth muscle in blood vessels for HTN emergencies palpitations Dilates arteries but not veins Minoxidil can lead to hypertrichosis (excessive hair growth) ○ That is why this is also formulated as rogaine Calcium Channel Blockers (pine) These relax blood vessels which allows blood to flow more Heart disease / Hypotension freely which also decreases blood pressure conduction issues Coronary hypoperfusion Good for pts with angina HF Reflex tachycardia edema Edema Worsening CHF  Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects constipation Dihydropyridines (FANN) These include meds like amlodipine, felodipine, nifedipine, These focus on the relaxation of hypertension Bradycardia and nicardipine (FANN) blood vessels and are more AV node block selective as vasodilators This leads to the dilation of coronary arteries which increases blood flow to the heart, increases the capacity of the veins which reduces the volume of blood returning to the heart which decreases preload, and they decrease the arterial resistance which reduces the workload of the heart which leads to a decrease in afterload Non-dihydropyridines (DV) These include meds like verapamil and diltiazem These are more cardiac active Hypertension Pedal edema These are not recommended in treatment of HTN in patients helping to decrease HR and CO May also be used to treat with HFrEF These have a more chronotropic arrhythmias Good for pts with cardiac arrhythmias and migraines effect May be preferred in Same effects as the dihydropyridines asthmatics and diabetics but they also decrease the strength of heart contractions and depress heart rate in addition to relaxing blood vessels Hypertensive emergency This is a BP over 180/120 that shows signs of end organ damage Need to lower BP more progressively to prevent ischemia Use parenteral (IV) drugs that can easily be titrated Choose meds based on other health conditions and the organs that are impacted by the HTN Treatment options… ○ BB Labetalol (good for pregnant pts) Esmolol (iv only) ○ CCB Nicardipine (dihydro; IV available) ○ Direct Vasodilators Nitroglycerin and nitroprusside Adrenoreceptor Antagonists Alpha 1 Blockers (sin) Includes meds like prazosin, doxazosin, and terazosin Alpha one These meds block alpha one HTN These are not first line but may be considered second line in adrenergic receptors which usually BPH patients with concomitant BPH lead to vasoconstriction These block alpha one receptors  Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects which then blocks sympathetic stimulation reducing vascular resistance by allowing relaxation of blood vessels and reducing venous return Beta Blockers Includes nonselective BB like propranolol and nadolol, beta 1 Beta 1 in heart These decrease CO (lowers amount HTN Asthma Can worsen an acute selective like metoprolol and atenolol, and mixed antagonists of blood pumped from heart which Depression exacerbation of HF if like labetalol and carvedilol lowers helps lower blood pressure) DM being taken for HTN Not recommended as first line agents for HTN unless the These also decrease HR and the Heart disease / patient has IDH or HF or post MI or cardiac arrhythmias or force of contraction of the heart conduction issues angina Carvedilol and labetalol also have an Propranolol specifically can be used for essential tremors and alpha 1 blockade therefore they migraines induce vasodilation Drugs that alter sympathetic Sympathoplegics are drugs that alter sympathetic function by Depression function (sympathoplegics) interfering and reducing the activity of the sympathetic nervous system which lead to an reduction in venous tone (reducing blood returning to the heart), heart rate, contractile force of the heart, and total peripheral resistance There are several types… ○ Those that work in the CNS like clonidine and methyldopa These are centrally acting drugs that work on alpha 2 selective agonists that lead to a decrease in sympathetic outflow which leads to a decrease in blood pressure by reducing CO and/or vascular resistance They are lipid soluble meaning they can readily enter the brain They are rarely used for HTN ○ Adrenoreceptor blockers like alpha one blockers (prazosin, doxazosin, and terazosin) and beta blockers (metoprololis , atenolol, carvedilol) Clonidine Can be taken orally or as a transdermal patch This is an alpha 2 selective agonist HTN Rebound effect may that inhibits sympathetic outflow occur with abrupt discontinuation of the drug Dry mouth Sedation Sexual dysfunction Marked bradycardia Contact dermatitis Methyldopa This is a prodrug meaning it enters the brain where it is then Same as above HTN Sedation  Hypertension Name General Info Receptors Mechanism Uses Contraindications Adverse Effects converted into an active methylnorepinephrine which is the ○ May be preferred Dry mouth active form that reduces sympathetic activity helping lower for HTN in Hemolytic anemia (rare) blood pressure pregnancy Sexual dysfunction Lower incidence of rebound HTN Heart Failure Name General Info Receptors Mechanism Uses Contraindications Adverse Effects Heart failure info This is a condition where the heart can not pump enough Treatment consists of a blood to meet the oxygen demands of the body use of… About 50% of people diagnosed with HF die within five years ○ Diuretics Most common cause of HF in USA is CAD with HTN also ○ Inhibitors of RAAS being a big contributing factor such as ACEI, Some basic risk factors include HTN, obesity, prediabetes or ARBS, ARNIs, DM, and ASCVD spironolactone Systolic HF (HFrEF) is when the heart’s ability to contract and and eplerenone pump blood is reduced leading to a reduced left ventricular ○ BB ejection fraction lower than 40% ○ Digitalis Diastolic HF (HFpEF) is when the heart can not fill because glycosides the left ventricle is stiff or thickened ○ Nitrates and Responses to reduced CO hydralazine ○ Sympathetic outflow increases meaning the SNS ○ Ivabradine becomes more active leading to tachycardia, ○ Combination of increased contractility, and increased vascular tone therapies (narrowing blood vessels through angiotensin 2 and ○ SGLT2 inhibitors endothelin which is a potent vasoconstrictor) in DM pts ○ Parasympathetic outflow is decreased Drugs that can worsen HF ○ The vasoconstriction increases afterload (the pressure (implied not on the heart must pump against) which then further quiz/exam) reduces EF and CO which then leads to cardiac ○ Non- remodeling dihydropyridine Preload is the volume of blood in the heart before it pumps CCBs and this is increased in HF because increased blood volume ○ Classic IC Afterload is the resistance the heart has to pump against and antiarrhythmic this is increased in HF due to heightened sympathetic tone ○ NSAIDS and the RAAS effects If diuresis isn’t working, Contractility is the heart’s ability to contract and pump blood use… and this is decreased in HF with pts with low CO ○ Nitroprusside Heart rate is the speed at which the heart beats and this is ○ Nesiritide increased in HF by sympathetic tone ○ IV nitroglycerin Signs and symptoms of HF ○ Decreased exercise tolerance resulting from decreased CO, tachycardia, SOB, edema,  Heart Failure Name General Info Receptors Mechanism Uses Contraindications Adverse Effects cardiomegaly, etc Goals of therapy include removal of retained salt and water, reduction of afterload and salt and water retention and excessive sympathetic stimulation and preload, direct augmentation of depressed cardiac contractility, correct underlying precipitating factors, relieve patient symptoms, improve hemodynamics, optimize pharmacotherapy, and educate pt on disease and management strategies 4 main pillars include ACE/ARNI, BB, MRA, and SGLT2is ACE inhibitors (pril) These are the gold standard as patients on them have longer Lowers resistance in blood vessels which term survival as it slows progression of HF therefore reduces afterload as it makes it All patients with CHF should be on an ACEi unless there easier for the heart to pump blood is a contraindication or a severe intolerance Reduce sodium and water retention by ○ Especially if LVEF is less than 40% helping the kidneys get rid of it in urine which lowers the preload easing the heart’s workload Stimulates release of vasodilator bradykinin to reduce preload further Lowers level of angiotensin which reduces the activation of the SNS Reduces long term remodeling of cardiac tissue Helps inhibit the RAAS system ARBs (sartans) This may be equally effective in reducing hospitalizations for Block angiotensin 1 (AT1) receptors HF, sudden cardiac death, and all causes of mortality but preventing the effects of angiotensin 2 ACEis have more clinical experience making them the such as vasoconstriction, release of preferred agents aldosterone, and cellular growth These should for sure be used in patients with a recent MI promoting effects and LVEF lower than 40% who are intolerant to ACEis ARNI (sacubitril/valsartan) Also called entresto (which is made up of sacubitril and Similar to ACE and ARBs valsartan) Risk of angioedema We can not do an ACE plus an ARB or ARNI in patients hypotension This is more effective than ACE inhibitors in reducing death and hospitalizations in HF pts but this is more expensive  Heart Failure Name General Info Receptors Mechanism Uses Contraindications Adverse Effects This is considered to be a new first line drug in the treatment of HF This can replace an ACE but can not be combined with an ACE Sacubitril This is a prodrug that blocks neprilysin (which is an enzyme that normally breaks down natriuretic peptides) therefore there is an increase in natriuretic peptides that lead to an increase in vasodilation, and diuresis Neprilysin inhibition Valsartan This is just an ARB therefore it blocks the effects of angiotensin 2 RAS inhibition Beta Blockers Main three include carvedilol (B1,2 and A1), metoprolol Help prevent arrhythmias and especially Toxic in HF that is not (B1), and bisoprolol (B1) and only these have proven to ones triggered by stress hormones like stable especially if patient have mortality benefits in CHF catecholamines has volume overload These are recommended for all stable HF patients only Reduce cardiac remodeling Starting dose should be low and gradual Decrease heart rate giving the heart more time to fill and pump effectively Diuretics Focused on loop diuretics as it induces more diuresis Reduce extracellular fluid volume and Have not shown to improve mortality, but they do lower ventricular filling pressures improving and managing symptoms (preload) making it easier for the heart to Given when patients with HF have fluid retention and pump blood congestive symptoms Little to no change in CO The main goal of diuretic use is to eliminate all fluid retention Sometimes, HF patients can be maxed using the lowest dose possible while maintaining euvolemia out on diuretic doses and they eventually (normal fluid balance) reach a threshold where the body can not pump out anymore sodium or water ○ That is when we add another diuretic, usually a thiazide Loop Diuretics (ide) Includes bumetanide, furosemide, and torsemide These are stronger and are more commonly used in general for HF and are used for more severe fluid retention Thiazide Diuretics Includes HCTZ and metolazone Milder and used for less severe fluid build up Aldosterone Antagonists (MRA) This includes spironolactone which is a potassium sparing These block the effects of aldosterone Primary use is advanced Gynecomastia diuretic and eplerenone (which induces the body to retain sodium heart failure stages where These help reduce fluid build up and prevent heart damage and water) by competitively binding to the heart is very weak associated with HF while improving heart function and aldosterone receptors in the collecting  Heart Failure Name General Info Receptors Mechanism Uses Contraindications Adverse Effects improving symptoms ducts of the kidneys Shows improvement in mortality Eplerenone may be preferred as it tends to have a better side effect profile however it does not usually happen because it is much more expensive than spironolactone Cardiac Glycosides - Digoxin This is an older drug that comes from the foxglove plant This inhibits the Na/K ATPase transporter Toxic responses include 65-80% bioavailability so most is absorbed into blood and it is (sodium pump) leading to increased N/V, confusion, spread widely throughout the body calcium and sodium inside the heart hallucinations, and It is not extensively metabolized and mostly excreted muscle cells helping the heart contract visual changes (we unchanged by the kidneys more strongly and efficiently and should be concerned; Long half life of 36-40 hours in normal renal function increasing the EF they might see yellow (elimination is significantly decreased in renal impairment This leads to positive mechanical inotropic halos; think of painting which can lead to some yucky side toxic effects) effects like increased intracellular sodium emily made in ○ In the event of digoxin toxicity, digoxin immune fab which reduces calcium expulsion by the bathroom), electrolyte (digiband) is used to treat it by selectively binding to Na/Ca antiporter so more calcium stays in abnormalities, and digoxin making it inactive and preventing it from the cell. This also leads to increased arrhythmias such as atrial affecting the heart and other organs and then removes calcium entry through Na and Ca voltage tachycardia or fibrillation, itself with digoxin through the kidneys gated channels as well as increased AV node tachycardia or Narrow therapeutic window making the drug hard to work release of calcium from storage sites block, or premature with and use ○ Said to focus more on this side ventricular contractions This also leads to electrical effects like through purkinje system decrease heart rate and a decreased conduction velocity via the AV node Vasodilators Isosorbide dinitrate is a long acting oral medication used to These drugs release NO within smooth dilate blood vessels over time muscle which result in smooth muscle Nitroglycerin is a patch that provides long lasting treatment or relaxation as a fast acting form The NO also stimulates the production of Nitroprusside is only used for acute treatment cGMP which causes vasodilation with veins being more sensitive than arteries Hydralazine Hydralazine along with isosorbide dinitrate has been Triggers release of NO to lead to smooth shown to reduce mortality in blacks already taking ACEis muscle relaxation and dilation as well as a ○ This is expensive? reduction in afterload and renal vascular ○ Only recommended for blacks resistance and an increase in renal blood flow along with some direct inotropic activity SGLT2 Inhibitors (flozin) Includes canagliflozin, dapagliflozin, empagliflozin, and These inhibit SGLT2 protein in the Used in pts with HFrEF ertugliflozin kidneys which is responsible for Also is the only therapy Initially designed to treat diabetes reabsorbing glucose from the urine back known to reduce CV Pretty sure this helps with mortality into the blood. Therefore, by blocking this death or HF protein, they increase glucose excretion in hospitalization in pts with the urine lowering blood sugar which can HFpEF  Heart Failure Name General Info Receptors Mechanism Uses Contraindications Adverse Effects help manage weight In terms of heart failure, it can help decrease some BP, improve LV function and pumping, and help with stiffness Acute decompensated HF Treat with morphine for pain and pulmonary edema, O2 for hypoxia, IV diuretic, nitrate therapy, nesiritide IV if symptomatic after diuretics and nitrates Inodilator Milrinone is a PDE-3 inhibitior Increases cAMP levels inside heart cells Only used for acute HF Hypotension ○ IV only as it is for acute decompressed HF which leads to the activation of a protein or severe exacerbation Ventricular arrhythmias that phosphorylates calcium channels of chronic failure Sudden death allowing more calcium to enter the cells leading to stronger heart contractions which also improves CO and dilation of blood vessels Adrenergic agonists Hypertension (noted on slides that this would Tachycardia not be on quiz) Arrhythmias Dopamine Beta 1 receptor agonist Increases heart contractility helping the Limited use in HF heart pump more efficiently Dopamine receptor activation causes vasodilation in renal, mesenteric, and cardiac vascular beds lowering peripheral resistance and afterload Little to no change in HR Dobutamine Beta 1 and 2 agonist Net effect is increased contractility with Mild alpha 1 effects minimal increase in HR Vasodilation as well leading to decreased peripheral resistance decreasing afterload to a small degree