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pharm exam 2
HTN and diuretics
| Question | Answer |
|---|---|
| BP = | CO x TPR |
| CO = | cardiac output (heart rate x stroke volume) |
| TPR = | total peripheral resistance |
| some meds target | CO and others TPR |
| primary HTN | unknown cause, referred to as essential or primary HTN |
| what percent of hypertensive diagnoses fall into this category | >90% |
| causes of primary HTN | specific cause is unknown, many theories which implicate structural, neural and hormonal factors |
| genetic basis of primary HTN | Rather than a single gene, likely multiple genes involved Sodium balance or other BP regulating pathways |
| secondary HTN | comorbid condition or drug (or other product) induced |
| what percent of hypertensive diagnoses fall into this category | Up to 10% of HTN |
| secondary HTN characteristics | most common renal dysfunction from severe chronic kidney disease or renovascular disease, drugs or other products, remove or treat cause |
| HTN category: normal | SBP: <120 DBP: <80 |
| HTN category: stage I HTN | SBP: 130-139 DBP: 80-89 |
| HTN category: elevated | SBP: 120-129 DBP: <80 |
| HTN category: stage II HTN | SBP: >140 DBP: >90 |
| drugs associated with HTN | abrupt stop of beta blockers, alcohol, think about secondary causes of HTN |
| cardiovascular risk pearls | Starting at BP of 115/75 mmHg, risk doubles with every 20/10 mmHg increase |
| SBP elevations are a stronger predictor in | adults 50 or older |
| isolated systolic HTN | SBP >130 mmHg and normal DBP |
| wider pulse pressure believed to reflect | extent of atherosclerotic disease, arterial stiffness |
| why control BP? | stroke death by ~50-60% CAD related death by ~40-50% heart failure by ~50% |
| kidneys play a large role in | BP, heart controls CO |
| diuretics classes | Loop Thiazide Potassium-sparing Carbonic anhydrase inhibitors |
| most often used diuretics | Loop Thiazide Potassium-sparing |
| carbonic anhydrase inhibitors do not have much of a | role |
| loop diuretics | work in loop of henle, when a lot of edema, CHF, or ascites watch electrolytes with this! |
| loop diuretics examples | Furosemide (Lasix), Bumetanide (Bumex) Torsemide (Demadex) Ethacrynic acid (Edecrin) |
| Ethacrynic acid is used in | sulfa allergies |
| loop diuretics site of action | Thick ascending loop of Henle Blocks Na+/K+/2Cl- transporter |
| adverse effects of loop diuretics | decreased K and Na dehydration, hypotension increased uric acid (gout) |
| clinical uses for loop diuretics | Heart failure (HF) or other conditions with volume overload |
| thiazide diuretics examples | Hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide (Lozol), Metolazone (Zaroxolyn) |
| thiazide diuretics site of action | Distal convoluted tubule Blocks Na+/Cl- transporter |
| thiazide diuretics adverse affects | decreased K and Na dehydration, hypotension increased uric acid (gout) |
| thiazide diuretics clinical | Hypertension (HTN) in combination with other classes (i.e., K+-sparing diuretic) Adjunct to loop diuretic for HF |
| thiazide vs loop | less potent, don't move fluid out as quickly but more modestly, long acting so effective |
| potassium sparing diuretics site of action | collecting duct |
| potassium sparing diuretics adverse effects | increased K+, decreased Na+ androgenic effects (i.e., gynecomastia) with spironolactone due to non-selectivity of effect |
| if potassium sparing diuretics adverse effects occur | then switch to a selective med |
| potassium sparing diuretics clinical uses | Myocardial infarction (MI), HF, HTN in combination with other classes, Chronic kidney disease/diabetes (finerenone), Primary aldosteronism, acne (spironolactone) |
| aldosterone antagonists diuretics examples | Spironolactone (Aldactone), Eplerenone (Inspra), Finerenone (Kerendia) |
| Spironolactone is non- selective, unlike | eplerenone & finerenone it affects kidneys but has other SE because structure is related to sex hormones |
| aldosterone antagonists diuretics site of action | Prevent aldosterone from causing Na+ reabsorption by binding to mineralocorticoid receptor |
| aldosterone antagonists diuretics adverse effects | increased K+, decreased Na+ androgenic effects (i.e., gynecomastia) with spironolactone due to non-selectivity of effect |
| aldosterone antagonists diuretics clinical uses | Myocardial infarction (MI), HF, HTN in combination with other classes, Chronic kidney disease/diabetes (finerenone), Primary aldosteronism, acne (spironolactone) |
| sodium blockers diuretics examples | Amiloride, Triamterene *Combination with HCTZ (Dyazide, Maxzide) |
| why is the combination of sodium blockers and HCTZ helpful | because HCTZ will offset the K loss |
| sodium blockers diuretics site of action | inhibits epithelial Na channels |
| sodium blockers diuretics adverse affects | increased K+, decreased Na+ androgenic effects (i.e., gynecomastia) with spironolactone due to non-selectivity of effect |
| sodium blockers diuretics clinical uses | HTN in combination with thiazide diuretic |
| carbonic anhydrase inhibitors diuretics examples | Acetazolamide (Diamox), Dorzolamide (Trusopt) |
| carbonic anhydrase inhibitors diuretics site of action | inhibit carbonic anhydrase in the proximal tubule |
| carbonic anhydrase inhibitors diuretics adverse affects | decreased Na+, decreased HCO3- dehydration, hypotension ↑ uric acid (gout) |
| carbonic anhydrase inhibitors diuretics clinical uses | Glaucoma (decreased intraocular pressure) Acute mountain sickness Metabolic alkalosis |
| Acute mountain sickness: carbonic anhydrase inhibitors diuretics | helps acclimate to high altitudes |
| Metabolic alkalosis: carbonic anhydrase inhibitors diuretics | bicarbonate is high so using carbonic anhydrase inhibitors diuretics to help the loss of bicarb |
| other agents with diuretic like properties | Sodium glucose co-transporter 2 inhibitors (SGLT2i) |
| Sodium glucose co-transporter 2 inhibitors (SGLT2i) | work within PCT, bind to SGLT2, prevent reabsorption of Na, glucose and H2O |
| Multiple proposed mechanisms of cardiovascular benefit (beyond diuresis & natriuresis): | Anti-inflammatory Inhibit sympathetic nervous system Improve cardiac energy metabolism Prevent adverse cardiac remodeling Reduce oxidative stress Improve vascular function |
| PCT = | proximal convoluted tubule |
| Sodium glucose co-transporter 2 inhibitors (SGLT2i) examples | Dapagliflozin (Farxiga), Empagliflozin (Jardiance) |
| Sodium glucose co-transporter 2 inhibitors (SGLT2i) site of action | Inhibits SGLT2i in proximal tubule |
| Sodium glucose co-transporter 2 inhibitors (SGLT2i) adverse affects | Urinary tract infection, genital yeast infection Dehydration Hypoglycemia Diabetic ketoacidosis (rare) |
| Diabetic ketoacidosis (rare) as a SE from SGLT2i are more a problem for | T1D, you may have to increase the insulin dose |
| Dehydration, hypoglycemia, diabetic ketoacidosis (rare) as SE from SGLT2i are | uncommon |
| SGLT2i clinical uses | HF and diabetes mellitus |
| SGLT2i important hygienal care | perineal care because increased chance of UTI or genital yeast |
| diuretics effects on BP | decreases amount of extracellular fluid volume because its causing an increase in urine volume, overtime the body learns to function at a lower pressure |
| what two things are inversely related in the diuretic cascade | extracellular fluid volume and urine volume |
| overtime, what will a pt who has been on a diuretic need? | another med that interferes with the RAS pathway |
| diuretics effects on BP: kidneys | kidneys sense volume and pressure loss so renin is released |
| activation of the RAS system by diuretics will cause | volume loss |
| angiotensin II does | the stuff we don't want aka aldosterone release and vasoconstriction which contributes to high BP |
| ACE inhibitors examples | Captopril (Capoten),Benazepril (Lotensin), Enalapril (Vasotec), Fosinopril (Monopril), Lisinopril (Prinivil, Zestril), Moexipril (Univasc), Quinapril (Accupril), Ramipril (Altace) |
| ACE inhibitors mechanism of action | Bind to and inhibit ACE & prevent formation of angiotensin II from angiotensin I (prevents ACE ability to convert I to II) |
| ACE inhibitors adverse affects | Increased K+ Increased serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury Cough Decreased BP Angioedema (rare) |
| when using ACEi, its important to | monitor labs |
| ACEi high potassium inhibits | aldosterone |
| ACEi: Increased serum creatinine (SCr) | lowers filtration, do not use if SCr is 2.5-3! |
| how do you know if the ACEi is working or if you need a lower dose? | if lower than 30%, working if higher than 30%, need to lower dose |
| Angioedema is rare when using an ACEi BUT | most significant, medical emergency, lips/tongue/throat walls swell which may result in intubation |
| ACEi affect | bradykinin |
| Angiotensin Receptors Blockers (ARBs) are similar to | ACEi |
| when do you use an Angiotensin Receptors Blockers (ARBs) | after the use of an ACEi, but never together because they are similar |
| ARB examples | Losartan (Cozaar),Candesartan (Atacand), Eprosartan (Teveten), Irbesartan (Avapro), Telmisartan (Micardis), Valsartan (Diovan), Olmesartan (Benicar), Azilsartan (Edarbi) |
| ARB mechanism of action | Bind to and inhibit angiotensin II from binding to its receptor - they sit on the receptor and prevent II from binding |
| ARB adverse effects | Increased K+ Increased serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury Decreased BP |
| what is the difference btwn ARB and ACEi side effects | ARBs have no cough or angioedema, don't affect bradykinin |
| ARB clinical uses | HTN HF MI CKD with or without DM |
| ARBs are often used as an alternative to what | an ACEi in patients who experience cough or angioedema |
| direct renin inhibitor example | Aliskiren (Tekturna) |
| direct renin inhibitor mechanism of action | Bind to and inhibit renin from binding to angiotensinogen |
| direct renin inhibitor adverse effects | Increased K+ Increased serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury Decreased BP |
| what is the difference btwn direct renin inhibitor and ACEi side effects | no cough and no angioedema |
| clinical uses of direct renin inhibitors | HTN - only approved use and narrower use (more money) |
| Angiotensin Receptor-Neprilysin Inhibitor (ARNi) example | Sacubitril/Valsartan (Entresto) Sacubitril = heproylisn inhibitor valsartan = ARB |
| ARNi used in combination with an ARB to | block vasoconstrictions like angiotensin II |
| ARNi mechanism of action | Angiotensin-neprilysin inhibitor ARB (valsartan) combined with a neprilysin inhibitor (sacubtril) Neprilysin is an enzyme that degrades vasoactive peptides Sacubitril leads to increases in important vasodilators (but also some vasoconstrictors) |
| ARNi adverse affects are | just like ACEi |
| ARNi adverse affects | Increased K+ Increased serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury Cough Decreased BP Angioedema (rare) |
| ARNi affect on BP | decreases BP even more so because there are two components so some pts can't handle that and may need just an ACEi or an ARB |
| clinical uses of ARNI | HF - first line therapy for pts with HF |
| RAAS Inhibitors – Effects on BP | block aldosterone causing less Na and water reabsorption |
| ACEi - hemodynamic effects | prevent Angiotensin II formation and relax vascular smooth muscle (vasodilators) |
| Beta (β)-one selective (Cardio-selective) - beta blocker examples | Metoprolol tartrate (Lopressor), Metoprolol succinate (Toprol XL), Atenolol (Tenormin), Bisoprolol (Zebeta), Esmolol (Brevibloc) |
| Beta (β)-one selective (Cardio-selective) - beta blocker site of action | Block β1 receptors on the heart leading to decrease heart rate (HR) & stroke volume (SV) which lowers cardiac output (CO) |
| non selective Beta blockers examples | Propranolol (Inderal), Timolol, Nadolol |
| non selective Beta blockers site of action | Block β1 and β2 receptors |
| Non-selective with alpha(α)-one antagonism examples | Labetalol, Carvedilol (HF) - IV, PO, bolus, drip |
| Non-selective with alpha(α)-one antagonism site of action | Block β1 and β2 receptors Block α-1 receptors on the arteries (vasorelaxation) |
| when alpha receptors are stimulated | there is constriction so meds are used to dilate |
| Cardio-selective with nitric oxide (NO)-mediated vasodilation - beta blockers | Nebivolol (Bystolic) - newer and more expensive |
| adverse affects of all beta blockers | Decreased HR Heart block (slows AV nodal conduction) Fatigue Dizziness Bronchospasm (avoid in asthma) Sedation, disturbed sleep, depression - if crosses BBB Sexual dysfunction Avoid abrupt withdrawal due to rebound HTN |
| clinical uses of all beta blockers | MI Chronic stable angina HF HTN many “off-label” uses (i.e., migraine prophylaxis, essential tremor, anxiety, hyperthyroidism) |
| beta blocker users tire more easily because | the drug is preventing peak heart rate, especially effects younger pts but will go away because body starts to produce more beta receptors |
| Beta Blocker – Effects on BP | decrease CO, HR and SV |
| what drugs decrease TPR | vasodilators |
| centrally active agents (very old) examples | Clonidine (Catapres), Methyldopa - seen with pregnant pts |
| centrally active agents site action action | Bind to and stimulate α-2 receptors in the brain (medulla) leading to decrease sympathetic outflow to body |
| where do centrally active agents work | centrally in the brain, essentially putting brakes on SNS |
| adverse effects of centrally active agents | Sedation!!!!! Dry mouth Sudden withdrawal canlead to hypertensive crisis Lactation (methyldopa) due to increased prolactin (uncommon) |
| clinical uses of centrally active agents | HTN (adjunct/refractory) many “off-label” uses for clonidine (i.e., analgesic, withdrawal) - used in the ICU for pts with withdrawal symptoms |
| centrally active agents effect on BP | prevents release of NE from neuron |
| alpha receptor blockers aka | alpha blockers |
| alpha blockers are located in | vessels (a-10 |
| alpha blockers examples | Prazosin (Minipress), Terazosin (Hytrin), Doxazosin (Cardura), |
| alpha blockers site of action | Block α-1 receptors on the arteries and veins (vasorelaxation) |
| adverse effects of alpha blockers | First-dose hypotension/orthostasis Dizziness SE due to abrupt drop in BP if you stand up fast because all a-1 are blocked |
| clinical uses for alpha blockers | HTN (adjunct) Benign prostatic hypertrophy - 'claim to fame' - decrease size of prostate |
| alpha blockers are | not as effective and have more SE |
| calcium channel blockers (CCBs) are split into | Dihydropyridines (DHPs) and Non-dihydropyridines (Non-DHPs) |
| Dihydropyridines (DHPs) - CCBs examples | Amlodipine (Norvasc), Felodipine, Nifedipine (Procardia, Adalat), Isradipine, Nimodipine |
| Dihydropyridines (DHPs) - CCBs site of action | Reduce contractile state of vascular smooth muscle cells by binding to L-type calcium channels (vasorelaxation of arteries) vasodilators, prevents early entry of Ca into the cell |
| adverse effects of Dihydropyridines (DHPs) - CCBs | Peripheral edema Constipation Increase HR (reflex tachycardia) Dizziness |
| clinical uses of Dihydropyridines (DHPs) - CCBs | HTN and chronic stable angina |
| Non-dihydropyridines (Non-DHPs) examples | Diltiazem (Cardizem), Verapamil (Calan, Isoptin) |
| Non-dihydropyridines (Non-DHPs) site of action | In addition to above effect on vasculature, this sub- class also decreases HR & SV, which lowers CO also works on the heart which is much of what B blockers do |
| Non-dihydropyridines (Non-DHPs) adverse effects | Decreases HR Heart block (slows AV nodal conduction) Mainly: Hypotension Fatigue Dizziness |
| clinical uses of Non-dihydropyridines (Non-DHPs) | Slow heart rate (rate control) in atrial arrhythmias such as Afib HTN |
| what pts should Non-dihydropyridines (Non-DHPs) not be used for | HF pts |
| all Dihydropyridines (DHPs) - CCBs end in | -dipine suffix |
| Dihydropyridines (DHPs) - CCBs deal with | structure and are primarily HTN drugs |
| Non Dihydropyridines (non DHPs) - CCBs are primarily | rate control drugs |
| CCBs pharmacology | prevent Ca from entering, all vasodilators differ between DHPs and non DHPs |
| CCBs effects of BP | binding to calcium channels leads to reduced intracellular calcium leads to reduced contraction |
| direct acting vasodilators | hydralazine and minoxidil |
| hydralazine site of action | Interferes with release of calcium from the sarcoplasmic reticulum in vascular smooth muscle (arterial vasorelaxation) |
| hydralazine adverse effects | increased HR, Rash/lupus-like syndrome - 'butterfly rash' and happens with long term use or high dose |
| clinical uses of hydralazine | HTN (adjunct/refractory) HF (used with nitrate as an alternative to RAAS inhibitor in certain patients) |
| minoxidil is only used if | truly refractory HTN |
| minoxidil site of action | Binds to and stimulates potassium channels in vascular smooth muscle (arterial vasorelaxation) |
| minoxidil adverse effects | increased HR, hair growth (hypertrichosis) |
| minoxidil clinical uses | HTN (adjunct/refractory) |
| Nitrates and Nitroprusside work on | NO pathway, increase amount of NO, all vasodilators |
| Nitrates and Nitroprusside: Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate- release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin transdermal, sublingual, spray, IV - MECHANISM OF ACTION | Metabolism leads to intracellular production of nitric oxide (NO), Venodilator (works on veins) |
| Nitrates and Nitroprusside: Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate- release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin transdermal, sublingual, spray, IV - ADVERSE AFFECTS | ha, dizziness, hypotension - all very common |
| Nitrates and Nitroprusside: Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate- release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin transdermal, sublingual, spray, IV - CLINICAL USES | CAD and ACS |
| Nitrates and Nitroprusside: Sodium nitroprusside - only IV: MECHANISM OF ACTION | Metabolism leads to intracellular production of NO and cyanide Potent arterial and venous vasodilator (veins and arteries) |
| Nitrates and Nitroprusside: Sodium nitroprusside - only IV: only used in | ICU in arterial line for HF or HTN emergency |
| Nitrates and Nitroprusside: Sodium nitroprusside - only IV: ADVERSE AFFECTS | cyanide and thiocyanate toxicity with high doses or prolonged use (confusion, metabolic acidosis, bradycardia, seizures, low oxygen) hypotension |
| Nitrates and Nitroprusside: Sodium nitroprusside - only IV: CLINICAL USES | hyptertensive emergency |
| Nursing Considerations: Anti- hypertensives | Do not discontinue abruptly Monitor BP, weight, edema, labs (BUN, SCr, K+) Positional changes (orthostasis) |
Created by:
leh195