Hypertension Flashcards
-PRIL Drugs
Ace Inhibitors; they inhibit Angiotensin II from forming
- SARTAN Drugs
Angiotensin Receptor Blockers; they inhibit angiotensin II from binding to its receptor
Aliskiren
Renin Inhibitor
Chlorthalidone
Thiazide Diuretic which works in the Distal Tubule
Hydrochlorothiazide
Thiazide Diuretic which works in the Distal Tubule
Metolazone
Thiazide Diuretic which works in the Distal Tubule
Furosemide
Loop Diuretic which works in the Ascending LOH
Torsemide
Loop Diuretic which works in the Ascending LOH
Bumetanide
Loop Diuretic which works in the Ascending LOH
Mannitol
Osmotic Diuretic which works in the Descending LOH
Eplerenone
Potassium Sparing Diuretic
Aldosterone Antagonist
Spironolactone
Potassium Sparing Diuretic
Aldosterone Antagonist
Amiloride
Potassium Sparing Diuretic
Sodium Channel Blocker
Triamterene
Potassium Sparing Diuretic
Sodium Channel Blocker
Hydralazine
Vasodilator
Minoxidil
Vasodilator
Nifedipine
Calcium Channel Blocker
Dihydropyridine
Isradipine
Calcium Channel Blocker
Dihydropyridine
Felodipine
Calcium Channel Blocker
Dihydropyridine
Amlodipine
Calcium Channel Blocker
Dihydropyridine
Diltiazem
Calcium Channel Blocker
Non-Dihydropyridine
Verapamil
Calcium Channel Blocker
Non-Dihydropyridine
Acetazolamide
CAI which works in the Proximal Tubule
Methazolamide
CAI which works in the Proximal Tubule
Clonidine
Alpha 2 Agonist
Methyldopa
Alpha 2 Agonist
Prazosin
Alpha Blocker
Doxazosin
Alpha Blocker
Terazosin
Alpha Blocker
Fenoldopam
HTN ER
Dopamine and Alpha 2 Agonist
Nitroprusside
Vasodilator
HTN ER
Digoxin
Inhibits sodium pump and increases calcium concentration (contractility)
Positive Inotropic Agent
Milrinone
phosphodiesterase inhibitor which increases calcium
Dopamine
Beta Agonist for HF
Dobutamine
Beta Agonist for HF
Isosorbide Nitrate / Dinitrate
Vasodilator for HF
what factors control arterial BP
CO and peripheral resistance
How does the RAAS system work to control BP
a fall in BP stimulates release of renin from kidney
renin converts angiotensinogen to ATI (inactive)
ACE converts ATI to ATII (active)
ATII: vasoconstriction, release aldosterone (increases BV), release catecholamines (sym), and induce cardiac hypertrophy
What are the effects of ACE inhibitors
less ATII + more bradykinin (VD and decrease Na/H20 retention which decreases BV)
What are ACE inhibitors used for
diabetic nephropathy + patients with MI
1st line for HTN
What are the contraindications for ACE inhibitors
fetotoxic !! don’t use with k-sparing diuretics
What are the AE of ACE inhibitors?
chronic dry cough, skin rash, fever, hyperkalemia (do NOT use with k-sparing diuretics)
What are the AE of aliskiren
fetotoxic and hyperkalemia
What do diuretics do in general
induce urine production by decreasing reabsorption of sodium in nephron so that the ions will enter urine and water follows
which diuretics are most likely for treating HTN
thiazide diuretics and k-sparing diuretics + calcium channel blockers
What are the contraindications for thiazide diuretics
digoxin users
What are the contraindications for CAI
Avoid in cirrhosis (liver issues)
What are the contraindications for fenoldopam
glaucoma patients because it increases IOP
what are the contraindications for digoxin
increase risk of toxicity with amiodarone, erythromycin, quinidine, tetracycline, verapamil
Corticosteroids, thiazide and loop diuretics all decrease K levels as well
What are the effects of Thiazide Diuretics (sulfa)
inhibits the Na/Cl co-transporter: Na, K, and Mg OUT while Ca stays in
decreases peripheral resistance (decrease BP)
Takes 1-3 weeks for effects
What are the effects of loop diuretics
inhibit the nacl and K+ co transport so EVERYTHING LEAVES (Na, K, Ca, and Mg)
increases prostaglandin synthesis
RAPID ONSET (ER USE) ~ highest efficacy in diuretics
What are the uses of loop diuretics
reduce acute pulmonary edema of HF, treat hypercalcemia and hyperkalemia
What are the AE of loop diuretics
ototoxicity (aminoglycosides), hyperuricemia, acute hypovolemia (bc so many things leaving nephron)
What are the effects of potassium-sparing diuretics
inhibit Na reabsorption(decrease BV) and K excretion
What are the effects of aldosterone antagonists
aldosterone is high in edematous states – can relieve edema
What are the AE of aldosterone antagonists
GI upset, peptic ulcers, induce gynecomastia, menstrual irregularities
What are the effects of sodium channel blockers
increase uric acid, renal stones
What are the effects of CAIs
inhibits bicarbonate production and increases Na excretion
What are the therapeutic uses for CAIs
treat glaucoma by decreasing AH production and for Acute Angle Closure Glaucoma with Acetazolamide
Treat mountain sickness and pseudotumor cerebri
what are the AE of CAIs
metabolic acidosis, drowsy, k depletion, renal stones, paresthesia
What is mannitol used for
increase water retention, prevent acute renal failure, and increase intracranial pressure
What are the effects of vasodilators
relax vascular smooth muscle, decrease BP from nitric oxide, which results in release of renin and reflex tachycardia
What are the uses for hydralazine
monotherapy in pregnant women
What are the uses for Minoxidil
treats severe HTN + causes hypertrichosis
What are the uses for calcium channel blockers
negative inotropic agents (decrease calcium and contractility) + increases dilation of coronary and periphery arteries (decrease BP)
what are the AE of calcium channel blockers
the decreased contraction leads to peripheral edema, reflex tachycardia, flushing, constipation, dizzy, HA, fatigue
what are the compensatory mechanisms of heart failure
when heart failure occurs the body increases the SYM NS and RAAS which leads to hypertrophy and stiffness which ultimately decreases contraction of the heart (long-term no good)
what are the symptoms of heart failure
fatigue, fluid retention and dyspnea (SOB) due to abnormal blood volume and interstitial fluid
what happens in systolic failure
reduced contractility leading to reduced CO
what happens in diastolic failure
reduced filling and relaxation leading to reduced CO and hypertrophy (stiffness)
what are the most common causes of HF
CHD and HTN
MI, valvular disease, congenital
How do you treat HF
decrease physical activity, sodium intake, avoid NSAIDs, AVOID alcohol, AVOID calcium channel blockers and AVOID high dose BB
You want to decrease the workload of the heart and increase CO by slowing the cardiac remodeling and improve contractility
What are the AE of digoxin
low levels of K can lead to arryhthmia, angina, N, V, CNS effects, BLUR + COLOR VISION + HALOS
What are the inpatient treatments of HF
Milrinone + Beta Agonists
IV only
How do diuretics help HF
relieve the pulmonary congestion and peripheral edema by decreasing the cardiac workload
Loop Diuretics = most common for HF
How do aldosterone antagonists help HF
heart failure patients have a lot of aldosterone because of the increased activation of sym system
prevents salt retention, myocardial hypertrophy, and hypokalemia
How do ACE or ARB help HF
Heart failure patients have more RAAS bc of the sym system and so by blocking those molecules (ATII) it can decrease workload of heart
what are the effects of BB
decrease chronic activation of sym system to decrease renin, HT and remodeling
ONLY FOR CHRONIC HF
initial worsening of symptoms