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Chapter 15 - Diuretic Agents - Test#3 Pharm Flashcards

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515223624Four main targets of Diuretics:1.) Membrane transport proteins 2.)Water permeability segments of nephron - Decrease amount of h20 reabsorbed regardless of Na ion concentration 3.) Enzyme Inhibition - Proximal convoluted tubule 4.) Interference with hormone receptors0
515223625Natriuretic-Increase Na ion secretion, and when Na leaves, body water will follow -Increase water secretion1
515223626A ________ is not necessarily a _________.Diuretic; natriuretic2
515716003Carbonic Anhydrase Inhibitors:-Primarily block reabsorption of NaHc03 in the PCT -Rarely used -Forerunner of modern diuretics -Acetazolamide is the prototype3
515716004Acetazolamide:Carbonic anhydrase inhibitor4
515716005Acetazolamide Pharmacokinetics:-Well absorbed orally -Effects seen in 30 minutes -Peak in 2 hours -Persists for 12 hours5
515716006Excretion of Acetazolamide-Excreted in the S2 segment of PCT -Decrease dose in someone with renal insufficiency because is a larger molecule6
515716007Acetazolamide Pharmacokinetics:-85% suppression of HCO-3; reabsorption in the PCT -Significant loss of HCO in body can lead to metabolic acidosis -Trouble with acid base balance7
515716008Clinical use of Carbonic Anhydrase Inhibitors in Glaucoma:-CA in the ciliary body can decrease IOP8
515716009Clinical use of CA Inhibitors in Alkanization of urine:-Trapping of weak acids9
515716010Clinical use of CA inhibitors in someone who has Metabolic Alkalosis:-Treat with Acetyzolamide -Will cause patient to become more acidotic10
515716011Clincal use of CA inhibitors in someone who has Acute Mountain Sickness:-Decrease cerebral edema by decreasing CSF production -Decrease in the ICP as well11
515716012Toxicity of CA inhibitors - Acetylzolamide:-Potassium wasting -Decreased buffering capacity -Drowsiness -Hypersensitivity *Contraindicated in patients with cirrhosis.12
515716013Mechanism of action of Loop Diuretics:-Selectively inhibit NaCl reabsorption in the thick ascending loop (TAL) -No development of acidosis -Most efficacious diuretics available -Ex: Furosemide ( Sulfanamide) Ethacryic acid (Not a sulfa drug)13
515716014Absorption of Loop diuretics - Lasix-Rapid (3 hours for Furosemide) -Rapid onset of action14
515716015Excretion of Lasix:-Renal secretion and glomerular filtration15
515716016Duration of action for Lasix:-2 to 6 hours - 1/2 life depends on the renal state.16
515716017Pharmacodynamics of Loop diuretics - Lasix-Inhibit the Na/K/2Cl (NKCC2) transporter17
515716018Results of loop diuretics inhibiting the NKCC2 transporter:-Reduction in NaCl absorption -Diminish lumen positive potential -Increase secretion (loss) of Mg and Ca.18
515716019How do loop diuretics induce renal prostaglandin synthesis?Participates in renal actions of diuretics19
515716020What can NSAID administration do to Loop Diuretics:Inhibit PG synthesis and interfere with the effectiveness of diuretics20
515728445What do Loop diuretics treat in the body?-Increase renal blood flow -Decrease pulmonary congestion -Decrease left ventricle filling pressure21
5157284465 indications for loop diuretic administration:1.) Acute pulmonary edema 2.) Edema - peripheral 3.) Acute hypercalcemia 4.) Hyperkalemia 5.) Acute renal failure - Increase in flow, and may flush out casts (precipitates than can build up and damage the nephron)22
515728447Loop Diuretics in treatment of anion OD:-Br, F, I all reabsorbed in the TAL -Must administer with NaCl to decrease loss Ex: Young child eating toothpaste and getting too much fluoride in their system23
515728448Toxicity of Loop diuretics:-Hypokalemia metabolic alkalosis - Reversed through K admin and fluid replacement -Ototoxicity -Hyperuricemia - Gout - Caused by a decrease in amount of uric acid being absorbed -Hypomagnesemia/Hypocalecemia -Dehydration24
515728449Allergic reactions of loop diuretics:-All are sulfonamides (Except ethacyrnic acid) -Avoid in patients with sulfa allergies - Rash -iosiniphils Nephritis Resolves rapidly25
515728450Mechanism of Action of Thiazides:-Inhibit NaCl transport in the DCT -Some inhibition of CA activity -All can be given orally -Prototype: Hydrochlorothiazide -All are suldonamides as well - avoid giving to people who have an allergy.26
515728451Pharmacokinetics of Thiazides:-Well absorbed orally -Metabolism is different within medication of this class -Excreted in the 2s segment - compete with uric acid for secretion27
515728452Pharmacodynamics of Thiazides:-Inhibit NaCl reabsorption at the DCT -Enhance Ca reabsorption (Unknown mechanism) -Enahance prostaglandin production - Same caution with NSAIDS -- Will decrease efficacy of thiazides if pt has renal failure.28
515728453What will NSAIDS do when a patient is on Thiazide?If the patient is suffering from renal failure, will decrease the efficacy of that thiazide.29
515903756Clinical indications for Thiazides:- HTN -CHF -Nephrolithiasis due to idiopathic hypercalciuria. -Nephrogenic diabetes indipidous30
515903757Toxicity of Thiazides-Hypokalemic metabolic alkalosis -Hyperuricemia -Impaired carbohydrate clearance -Hyperlipidemia -Allergic rxs in people with sulfa allergy -Weaness, fatigue -Impotence - due to volume depletion31
515903758Why do Thiazides sometimes cause hyperuricemia?-Because it is secreted in the S2 segment -Compete with uric acid for secretion32
515903759How do thiazides cause hyponatremia with toxicity?-Because thiazides inhibit the action the NCC and therefore decrease NaCl reabsorption at the DCT33
515903760Potassium sparing diuretics:-Block the aldosterone receptors -Inhibition of Na flux through ion channels in luminal membrane -Na reabsorption couples to K and H secretion -Acts on the ENaC channe;34
515903761Pharmacokinetics of Aldactone:-Is a K sparing diuretic -Onset and duration determined by kinetics of aldosterone response in individual Ex: Depends on patients hormone levels, such as SIADH Effect takes place in the COLLECTING TUBULE35
515903762Aldactone is inactivated in the:Liver36
515903763Aldactone has a ________ onset, and can take ______ ________ to take full effect.Slow onset; several days37
515903764Pharmacodynamics of Aldactone:-Reduce Na absorption in collecting tubules and ducts (mainly the ducts) -Na absorption regulated by aldosterone -Rate of K secretion related with Aldosterone levels38
515903765Clinical indications for a potassium sparing diuretic - Primary-Most useful in states of mineralcorticoid excess -Conn syndrome -Ectopic ACTH production39
515903766Secondary clinical indications for K sparing diuretic:-CHF -Nephrotic syndrome -Use of other diuretics40
515903767Toxicity of K sparing diuretic:-Hyperkalemia -Increase with renal disease -Most common is K sparing agent is the sole diuretic -Gynecomastia -Acute renal failure (Rare) -Kidney stones41
515903768Hyperchloremic metabolic acidosis:-Results from toxicity in K sparing diuretics -Inhibits H secretion in parallel with K secretion42
515903769This K sparing diuretic blocks the Aldosterone receptors:Aldactone (Spironolactone)43
515903770This K sparing diuretic causes inhibition of Na flux through ion channels in the luminal membrane:-Amiloride44
515903771Contraindications to someone taking a K sparing Diuretic:-Patient taking K -Patient on drugs affecting K -Liver disease impairs metabolism45
515903772Osmotic diuretics-Target the Proximal convoluted tubule (PCT) and descending loop of Henle -These areas are freely permeable to water -Osmotic agents that are NOT transported cause water retention in tubule46
515903773Mannitol-Osmotic diuretic -Used mainly to reduce Intracranial pressure -Promote removal of renal toxins through acute hemolysis and after use of radiocontrast agents -USeful for hyperproteinuria or RHABDO -Help flush out the system47
515903774Absorption of mannitolPoor - can induce diarrhea48
515903775Metabolism of mannitolNot metabolized49
515903776Excretion of Mannitol-Glomerular filtration (30-60 minutes) -No significant reabsorption -No significant secretion *If patients have issues with their GFR, these meds may not have much of an effect50
515903777Pharmacodynamics of osmotic diuretics:-Counter osmotic force -Result : Urine volume increases -Reduced Na reabsorption51
515903778Clinical indications for Osmotic diuretics:-Increase urine output -Reduce ICP - 60 to 90 minutes after administration.52
515903779Toxicity of osmotic diuretics:-Extracellular volume expansion -Rapidly distributed to extracellular compartments -Can lead to congestion and hyponatremia prior to diuresis -If pt has renal problems, it will slowly go to the EC compartments and lead to edema53
515903780Toxicity of osmotic diuretics:-Dehydration - excessive use without water replacement -Hypernatremia -Hyperkalemia -In patients with real failure, will cause HYPOnatremia (Stay in system longer, and therefore more Na loss )54
515903781Administration of Osmotic Diuretics:-Caution : Mannitol can crystalize (Penetrate through blood vessels) -In line filter set should always be used with higher concentrations (>20%)55
515903782Antidiuretic hormone - Agonist-Vasopressin -Desmopressin *Both increase ADH levels and increase blood volume and BP56
515903783ADH - Antagonist-Conivaptin -Non selective - Lithium57
515903784Which drug is useful for patients refractory to loop agents?-Metolazone (Thiazide)58
515903785Diabetes Insipidous-Excessive thirst -Excessive urination59
515903786Use of Thiazide diuretics in tx of Diabetes Insipidous:-Decrease plasma volume -Decreased GFR -Water and NaCl reabsorption (PCT)60

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