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cardio and antihtn
pharm exam 2
| Question | Answer |
|---|---|
| what is hypertension defined as? | BP ≥ 130/80 mm Hg, or receiving antihypertensive therapy |
| overall prevalance of hypertension among US adults | ~ 45-50% (~115 million) |
| what percent of US adults have BP controlled (<130/80)? | less than 25% |
| BP= | CO x TPR |
| TPR | total peripheral resistance |
| CO | heart rate x stroke volume |
| primary hypertension cause | unknown |
| what is primary hypertension referred to as? | essential or primary |
| what percent of hypertension is primary? | >90% |
| what do theories implicate as the cause of hypertension? | structural, neural, and hormonal factors |
| genetic basis of hypertension | Rather than a single gene, likely multiple genes involved Sodium balance or other BP regulating pathways |
| secondary hypertension | comorbid condition or drug (or other product) induced |
| what percent of hypertension is secondary? | up to 10% |
| most common causes of secondary hypertension? | renal dysfunction from severe chronic kidney disease or renovascular disease |
| other causes of secondary hypertension | drugs or other products |
| what to do for secondary hypertension? | remove or treat cause |
| examples of drugs associated with hypertension | NSAIDS, abrupt DC, withdrawal, amphetamines, decongestants, etc. |
| what is BP categorized based on> | average BP measurements: normal, elevated, and stage 1 or 2 hypertension |
| normal BP | <120/<80 |
| elevated BP | 120-129/<80 |
| stage 1 hypertension | 130-139/80-89 |
| stage 2 hypertension | > or = to 140/>= 90 |
| what happens to risk starting at BP 115/75 mmHg? | risk doubles with every 20/10 mmHg increase |
| Who are SBP elevations stronger predictors in? | adults >or= 50 |
| what is wider pulse pressure believed to reflect? | extent of atherosclerotic disease, arterial stiffness |
| Why control BP? | decrease: stroke death by ~50-60% CAD related death by ~40-50% heart failure by ~50% |
| what largely controls BP? | kidneys |
| How do kidneys regulated BP? | RAAS (renin angiotensin aldosterone system) |
| how does heart control BP? | increased contractility= increased cardiac output |
| classes of diuretics | Loop Thiazide Potassium-sparing Carbonic anhydrase inhibitors |
| what diuretics are used most commonly? | Loop Thiazide Potassium-sparing |
| where do loop diuretics work? | loop of henle |
| what do loop diuretics cause? | block transport of Na, K, 2Cl leading to less Na+ absorbed |
| how do loop diuretics work? | water follows NA causing water loss |
| when giving loop diuretics what should you be checking? | labs because you can also lose electrolytes |
| thiazides and thiazide-like diuretics | binds to NaCl transporter and blocks resporption of Na+ |
| where do thiazides and thiazide like diuretics work? | distal tubule |
| where do potassium sparing diuretics work? | collecting tubule |
| how do potassium sparing diuretics work? | blocks aldosterone, leading to fewer channels, less Na+ absorbed, and therefore K+ is not eliminated in exchange |
| examples of loop diuretics | Furosemide (Lasix), Bumetanide (Bumex), Torsemide (Demadex), Ethacrynic acid (Edecrin) |
| site of action of loop diuretics | Thick ascending loop of Henle -Blocks Na+/K+/2Cl- transporter |
| adverse effects of loop diuretics | -↓ K+, ↓ Na+ -Dehydration, hypotension -↑ uric acid (gout) |
| lclinical uses of loop diuretics | Heart failure (HF) or other conditions with volume overload |
| what do you usually need to take with loop diuretics? | supplemental K |
| why do you need to take supplemental K with loop diuretics? | decreased K+, loss of K can cause cramps and arrythmias |
| 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 effects | -↓ K+, ↓ Na+ -Dehydration, hypotension -↑ uric acid (gout) |
| thiazide diuretics clinical uses | -Hypertension (HTN) in combination with other classes (i.e., K+-sparing diuretic) -Adjunct to loop diuretic for HF |
| when do we use loop diuretics? | when there is a lot of fluid and we want to get rid of it fast |
| thiazide diuretics are less potent so? | they don't move fluid out as quickly-> longer acting |
| potassium sparing diuretics site of action | collecting duct |
| potassium sparing diuretics adverse effects | -↑ K+, ↓ Na+ -Androgenic effects (i.e., gynecomastia) with spironolactone due to non-selectivity of effect |
| 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 examples | Spironolactone (Aldactone), Eplerenone (Inspra), Finerenone (Kerendia) |
| spirinolactone is ______ unlike eplerenone and finerenone | non-selective |
| aldosterone antagonists site of action | Prevent aldosterone from causing Na+ reabsorption by binding to mineralocorticoid receptor |
| aldosterone antagonists adverse effects | -↑ K+, ↓ Na+ -Androgenic effects (i.e., gynecomastia) with spironolactone due to non-selectivity of effect |
| aldosterone antagonists clinical uses | -Myocardial infarction (MI) -HF -HTN in combination with other classes -Chronic kidney disease/diabetes (finerenone) -Primary aldosteronism; acne (spironolactone) |
| sodium blockers examples | Amiloride, Triamterene *Combination with HCTZ (Dyazide, Maxzide) |
| sodium blockers site of action | inhibits epithelial Na+ channels |
| sodium blockers adverse effects | -↑ K+, ↓ Na+ -Androgenic effects (i.e., gynecomastia) with spironolactone due to non-selectivity of effect |
| sodium blockers clinical uses | -HTN in combination with thiazide diuretic |
| spironolactone | non-selective, has other off target side effects |
| what is spirinolactone closely related to? | sex hormones-> can have androgenic effects |
| why do you combine sodium blockers with HCTZ | to offset K+ loss |
| carbonic anhydrase inhibitors examples | Acetazolamide (Diamox), Dorzolamide (Trusopt) |
| carbonic anhydrase inhibitors site of action | Inhibit carbonic anhydrase in the proximal tubule |
| carbonic anhydrase adverse effects | -↓ Na+, ↓ HCO3- -Dehydration, hypotension -↑ uric acid (gout) |
| carbonic anhydrase clinical uses | -Glaucoma (↓ intraocular pressure) -Acute mountain sickness -Metabolic alkalosis |
| acetazolamide | not very effective diuretic by itself; if metabolic alkalosis could use to cause loss of bicarb |
| other agents with diuretic-like properties | Sodium glucose co-transporter 2 inhibitors (SGLT2i) |
| Sodium glucose co-transporter 2 inhibitors (SGLT2i) prevent | reabsorption of Na, glucose, water |
| where does Sodium glucose co-transporter 2 inhibitors (SGLT2i) work? | PCT |
| where does Sodium glucose co-transporter 2 inhibitors (SGLT2i) bind? | SGLT1 |
| proposed mechanisms of cardiovascular benefit of sodium glucose co-transporter 2 inhibitors (SGLT2i) (beyond diuresis and natriuresis) | Anti-inflammatory Inhibit sympathetic nervous system Improve cardiac energy metabolism Prevent adverse cardiac remodeling Reduce oxidative stress Improve vascular function |
| SGLT2 inhibitors exampels | Dapagliflozin (Farxiga), Empagliflozin (Jardiance) |
| SGLT2 inhibitors site of action | Inhibits SGLT2i in proximal tubule |
| SGLT2 adverse effects | -Urinary tract infection, genital yeast infection -Dehydration -Hypoglycemia -Diabetic ketoacidosis (rare) |
| SGLT2 clinical uses | -HF -Diabetes mellitus (DM) |
| what suffix do SGLT2 inhibitors have? | -liflozin |
| what is important when taking SGLT2 inhibitors? | perineal hygiene to prevent UTIs |
| how do diuretics affect BP? | increased urine volume, decreased extracellular fluid volume; activate RAAS |
| what does the RAAS system cause? | angiotensin II causes aldosterone release, causing NA reabsorption and increased blood volume, and vasoconstriction which lead to increased BP |
| Strategies used to block the renin angiotensin system | Beta one receptor blockade. Inhibition of renin. Inhibition of angiotensin converting enzyme. Angiotensin receptor blockade |
| ACE inhibitors examples | Captopril (Capoten),Benazepril (Lotensin), Enalapril (Vasotec), Fosinopril (Monopril), Lisinopril (Prinivil, Zestril), Moexipril (Univasc), Quinapril (Accupril), Ramipril (Altace) |
| what do ACE inhibitors end in? | -pril |
| ACE inhibitors mechanism of action | Bind to and inhibit ACE & prevent formation of angiotensin II from angiotensin I |
| ACE inhibitors adverse effects | -↑ K+ -↑ serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury -Cough -↓ BP -Angioedema (rare) |
| ACE inhibitors clinical uses | -HTN -HF -MI -Chronic kidney disease (CKD) with or without DM |
| why do ACE inhibitors cause a cough and angioedema? | bradykinin |
| angioedema | oropharynx, tongue, lips all swell up |
| Angiotensin receptors blockers examples | Losartan (Cozaar), Candesartan (Atacand), Eprosartan (Teveten), Irbesartan (Avapro), Telmisartan (Micardis), Valsartan (Diovan), Olmesartan (Benicar), Azilsartan (Edarbi) |
| angiotensin receptors blockers mechanism of action | Bind to and inhibit angiotensin II from binding to its receptor |
| angiotensin receptors blockers adverse effects | -↑ K+ -↑ serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury -↓ BP |
| angiotensin receptors blockers clinical uses | -HTN -HF -MI -CKD with or without DM |
| when are ARBs often used? | n alternative to an ACEi in patients who experience cough or angioedema |
| what do ARBs end in? | -sartan |
| 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 | -↑ K+ -↑ serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury -↓ BP |
| direct renin inhibitor clinical uses | HTN |
| renin | 1st step of RAAS |
| Angiotensin Receptor-Neprilysin Inhibitor (ARNi) example | Sacubitril/Valsartan (Entresto) |
| Angiotensin Receptor-Neprilysin Inhibitor (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) |
| Angiotensin Receptor-Neprilysin Inhibitor (ARNi) adverse effects | -↑ K+ -↑ serum creatinine (SCr); caution with advanced chronic kidney disease & avoid in acute kidney injury -Cough -↓ BP -Angioedema (rare) |
| Angiotensin Receptor-Neprilysin Inhibitor (ARNi) clinical uses | HF |
| first line therapy for treatment of patients with HF | Angiotensin Receptor-Neprilysin Inhibitor (ARNi) |
| what does sacubitril need to be comined with? | ARBs |
| ACE inhibitors- hemodynamic effects | prevent all formation, relax vascular smooth muscle (decreased TPR) |
Created by:
camrynfoster