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Rxs that enhance elimination of water (& salt) by kidneys

Diuretics

Five groups of Diuretics

COLT PC
Carbonic Anhydrase inhibitors
Osmotic diuretics
Loop diuretics
Thiazides
Potassium-sparing diuretics
Conivaptan

Carbonic anhydrase inhibitor location, mechanism & eg

AT PCT; When enzyme is inhibited, [HCO3] increases--> alkaline urine--> diuresis;
Acetazolamide (Diamox)

Loop diuretics location, mechanism & eg

MOST EFFECTIVE gp, so used most often.
Ascending Limb; Active transport at PCT forces Rx into Loop. Here, a Na/K/2Cl (NKCC2) transporter is blocked, so Na & K are not reabsorbed -- > H2O retained;
Furosemide (Lasix) [lasso loop!]

Loop diuretic strength & weakness

Strength: BEST at WATER removal;
Weakness: POOR at lowering BP

Loop diuretics competitor & SEs

Uric acid competition-> hyperuremia;
HYPOs: volemia, natremia, kalemia, calcemia;
HYPERs: uricemia (GOUT), glycemia;
TOXICITY: OTOTOXIC
Rx Iax: Sulfonamides (<5% cross reactive)

Thiazide diuretics location, mechanism & eg

DCT; Often used as SYNERGIST w/ Loops Block Na/Cl cotransport (NCCT), so Na is not reabsorbed -->H2O retained;
Hydrochlorothiazide, Chlorthalidone, & Metolazone ("thiazide-like")
NB: TAKES UP TO 6 WKS TO HIT Css

Class of Diuretics listed as 1st line in JNC VII

Thioazides (Hydrochlorothiazide, Chlorothalidone)

Diuretics that take up to 6 wks to hit effective conc.

Thiazides

POS SEs of thiazide diuretics

Increased Ca reabsorption --> Osteoporosis Tx;
Decreased peripheral vasc resistance--> edema Tx

SEs of thiazides

HYPOs: volemia, natremia, kalemia (arrhythmia)
HYPERs: CALCEMIA, uricemia (GOUT), glycemia;
TOXICITY: small increase in LDL

Diuretic that causes 5-10% Impotence in men

Aldosterone analog K-sparing diuretics (Spironolactone=Aldactone)

Potassium sparing diuretics location, mechanism & eg

DCT/Collecting duct; block a Na pump (ENaC) that is UNCOUPLED from K. Allows DIURESIS WITHOUT K LOSS;
Amiloride (Midamor), & Triamterene (Dyrenium)

Weak diuretics w/ mortality benefits for CLASS II & CLASS IV heart failure pts (RALES) and low ejection frction post MI

Spironolactone & Eplerenone. Belong to K-sparing

Potassium sparing diuretic SEs

Hyperkalemia, Gynecomastia (spironolactone is a steroid), Dysmenorrhea

Estrogen analog diuretics & their larger class

Aldosterone Antagonists: Aldactone & Spironolactone-- belong to K-sparing diuretics

Diuretic class used with Thiazides to protect against potassium loss

Potassium-sparing: Triamterene & Amiloride

ADH inhibitor location mechanism & eg

Block V2 receptors for ADH in the collecting duct. Without ADH, aquaporins can't be inserted & H2O can't exit. Conivaptan (Vaprisol)

Osmotic Diuretics location, mechanism & eg

PCT & Descending limb; Enter @ glomerulus but are not reabsorbed-->increases osmotic pull on H2O; eg: Mannitol(Osmitrol), glycerol

SE Osmotic diuretics

Edema

Clinical indications for diuretics

HTN, CHF, Hepatic ascites, Pulmonary edema, RF/nephrotic syn, Hyperaldosteronism (Spironolactone)

Hypercalcemia Tx

Loop diuretics

Hypocalcemia Tx

Thiazides (Hydrochlorothiazide)

SIADH Tx

Loop diuretic (Furosemide = Lasix) & ADH inhibitor (Conivaptan = Vaprisol)

Intracranial pressure Tx

Mannitol

Glaucoma & Epilepsy Tx

Acetazolamide

Hyperaldosteronism Tx

Spironolactone

Hyperkalemia Tx

Loop diuretic (Furosemide = Lasix)

Hypokalemia Tx

K-Sparing diuretic (Amiloride = Midamor)

Diuretic that may cause Gynecomastia or Dysmenorrhea

Spironolactone (K-sparing steroid)

Diuretics that exacerbate gout

Loops & Thiazides

Act at the ascending limb

Loop diuretics

Act at the descending limb

Osmotic diuretics

Act at the PCT

Carbonic anhydrase inhibitors (Acetazolamide)

Act at the DCT & CT

K-sparing diuretics (Spironolactone & Amiloride) and ADH inhibitors (Conivaptan)

"Gates" blocked by CCBs

Voltage sensitive slow Ca channels

Effect of CCBs

Reduces plateau phase of cardiomyocyte contractions in SA & AV nodes; Vasodilation -> lowered BP

Area of heart not affected (much) by CCBs

Ventricles

Two most common CCBs & their effects, tropic summary

Verapamil & Diltiazem;
DDPRR: Dilate ALL coronary vessels, Dilate peripherial arterioles (NOT venules), Prolong AV conduction time, Reduce myocardial contractility, Reduce heart rate;
NEG inotrope/NEG chronotrope

Dihydropyridines gp, members, & effects

CCBs; Nifedipine (Procardia), Nicaripine (Cardene), Amlodipine (Norvasc); such strong vasodilators that AV conduction is reduced, Heart rate is increased, Contractility is increased; POS inotrope/POS chronotrope

Clinical indicators for CCBs

PSVT (slows both SA & AV);
A-flutter/A-fib (slowing AV reduces ventricular rate);
Angina (coronary arterioles dilate);
HTN, Cerebral vasospasm, Migraine

CCB SEs

CHEAR:
Constipation, hTN, Exacerbates CHF (esp verapamil!), AV block/brady, Red (flushing)

Indicators for anti-HTN Rx

CHF, CAD, TIA/stroke, MI, HTN

When to initiate anti-HTN

BP >140/90

BP determinants

(Cardiac output) (Peripheral resistance);
CO = (Rate) (SV);
SV = (Contractility) (Preload-Afterload)

Two BP effectors

Baroreceptors & RAAS

Baroreceptor mechanism & effects

Monitor sudden BP drop; stimulate SNS/inhibit PNS

RAAS mechanism & effects

Low BP-> low perfusion->JGA stimulation->Renin->converts Angiotensinogen to Angiotensin I->(lungs/ACE) converts to Angiotensin II-->vasoconstriction & Aldosterone release-->Na reabsorption/K excretion

1st line anti-HTN Rxs

1. Thiazide (Hydrochlorothiazide)
2. Beta Blockers (esp Metoprolol)
3. ACEIs (Captopril or Enalopril)

BB indications; Contraindications

IND: Tachy, PSVT, Exertion Angina, Hyperthyroid crisis, HTN, Glsaucoma, Migraine;
C-IND: Heart block, CHF, Resting Angina, Asthma, DM, Peripheral Vasc Dz

BB SEs

Bronchospasm, h-glycemia, CNS depression, Insomnia/nightmares, Sexual dysfx

Side effects of Aldosterone antagonists

Hyperkalemia, Gynecomastia (Spironolactone), GI upset

The cardiotherapies that alter RAAS

ACEIs, ARBs, ß blockers, Aldosterone inhibitors, Direct Renin Inhibitors

Rx class that ALL CHF pts MUST be on unless there's a documented reason

ACEI's

MOA for ACEI's

Prevents conversion of Angiotensin I to Angiotensin II

ACEI effects

Prevent vasoconstriction; decrease aldosterone- reduce Na & H2O retention

Heart Rx that preserves renal fx in DM pys

ACEI's

ACEI primary SEs & CIx

1. Cough
2. hTN*
3. Angioedema* (Severe Type I immune rxn, may block breathing) in mucus membranes
4. Hyperkalemia**
5. Taste disturbance (sulfurus)
CIx: Pregnancy

ACEI monitoring issues

BP, Hyperkalemia, Renal fx-- and warn of angioedema

ACEI w/ shortest half-life

Captopril

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