Chapter 15 - Diuretic Agents - Test#3 Pharm Flashcards
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| 515223624 | Four 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 receptors | 0 | |
| 515223625 | Natriuretic | -Increase Na ion secretion, and when Na leaves, body water will follow -Increase water secretion | 1 | |
| 515223626 | A ________ is not necessarily a _________. | Diuretic; natriuretic | 2 | |
| 515716003 | Carbonic Anhydrase Inhibitors: | -Primarily block reabsorption of NaHc03 in the PCT -Rarely used -Forerunner of modern diuretics -Acetazolamide is the prototype | 3 | |
| 515716004 | Acetazolamide: | Carbonic anhydrase inhibitor | 4 | |
| 515716005 | Acetazolamide Pharmacokinetics: | -Well absorbed orally -Effects seen in 30 minutes -Peak in 2 hours -Persists for 12 hours | 5 | |
| 515716006 | Excretion of Acetazolamide | -Excreted in the S2 segment of PCT -Decrease dose in someone with renal insufficiency because is a larger molecule | 6 | |
| 515716007 | Acetazolamide 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 balance | 7 | |
| 515716008 | Clinical use of Carbonic Anhydrase Inhibitors in Glaucoma: | -CA in the ciliary body can decrease IOP | 8 | |
| 515716009 | Clinical use of CA Inhibitors in Alkanization of urine: | -Trapping of weak acids | 9 | |
| 515716010 | Clinical use of CA inhibitors in someone who has Metabolic Alkalosis: | -Treat with Acetyzolamide -Will cause patient to become more acidotic | 10 | |
| 515716011 | Clincal use of CA inhibitors in someone who has Acute Mountain Sickness: | -Decrease cerebral edema by decreasing CSF production -Decrease in the ICP as well | 11 | |
| 515716012 | Toxicity of CA inhibitors - Acetylzolamide: | -Potassium wasting -Decreased buffering capacity -Drowsiness -Hypersensitivity *Contraindicated in patients with cirrhosis. | 12 | |
| 515716013 | Mechanism 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 | |
| 515716014 | Absorption of Loop diuretics - Lasix | -Rapid (3 hours for Furosemide) -Rapid onset of action | 14 | |
| 515716015 | Excretion of Lasix: | -Renal secretion and glomerular filtration | 15 | |
| 515716016 | Duration of action for Lasix: | -2 to 6 hours - 1/2 life depends on the renal state. | 16 | |
| 515716017 | Pharmacodynamics of Loop diuretics - Lasix | -Inhibit the Na/K/2Cl (NKCC2) transporter | 17 | |
| 515716018 | Results of loop diuretics inhibiting the NKCC2 transporter: | -Reduction in NaCl absorption -Diminish lumen positive potential -Increase secretion (loss) of Mg and Ca. | 18 | |
| 515716019 | How do loop diuretics induce renal prostaglandin synthesis? | Participates in renal actions of diuretics | 19 | |
| 515716020 | What can NSAID administration do to Loop Diuretics: | Inhibit PG synthesis and interfere with the effectiveness of diuretics | 20 | |
| 515728445 | What do Loop diuretics treat in the body? | -Increase renal blood flow -Decrease pulmonary congestion -Decrease left ventricle filling pressure | 21 | |
| 515728446 | 5 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 | |
| 515728447 | Loop 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 system | 23 | |
| 515728448 | Toxicity 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 -Dehydration | 24 | |
| 515728449 | Allergic reactions of loop diuretics: | -All are sulfonamides (Except ethacyrnic acid) -Avoid in patients with sulfa allergies - Rash -iosiniphils Nephritis Resolves rapidly | 25 | |
| 515728450 | Mechanism 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 | |
| 515728451 | Pharmacokinetics of Thiazides: | -Well absorbed orally -Metabolism is different within medication of this class -Excreted in the 2s segment - compete with uric acid for secretion | 27 | |
| 515728452 | Pharmacodynamics 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 | |
| 515728453 | What 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 | |
| 515903756 | Clinical indications for Thiazides: | - HTN -CHF -Nephrolithiasis due to idiopathic hypercalciuria. -Nephrogenic diabetes indipidous | 30 | |
| 515903757 | Toxicity of Thiazides | -Hypokalemic metabolic alkalosis -Hyperuricemia -Impaired carbohydrate clearance -Hyperlipidemia -Allergic rxs in people with sulfa allergy -Weaness, fatigue -Impotence - due to volume depletion | 31 | |
| 515903758 | Why do Thiazides sometimes cause hyperuricemia? | -Because it is secreted in the S2 segment -Compete with uric acid for secretion | 32 | |
| 515903759 | How do thiazides cause hyponatremia with toxicity? | -Because thiazides inhibit the action the NCC and therefore decrease NaCl reabsorption at the DCT | 33 | |
| 515903760 | Potassium 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 | |
| 515903761 | Pharmacokinetics 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 TUBULE | 35 | |
| 515903762 | Aldactone is inactivated in the: | Liver | 36 | |
| 515903763 | Aldactone has a ________ onset, and can take ______ ________ to take full effect. | Slow onset; several days | 37 | |
| 515903764 | Pharmacodynamics 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 levels | 38 | |
| 515903765 | Clinical indications for a potassium sparing diuretic - Primary | -Most useful in states of mineralcorticoid excess -Conn syndrome -Ectopic ACTH production | 39 | |
| 515903766 | Secondary clinical indications for K sparing diuretic: | -CHF -Nephrotic syndrome -Use of other diuretics | 40 | |
| 515903767 | Toxicity 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 stones | 41 | |
| 515903768 | Hyperchloremic metabolic acidosis: | -Results from toxicity in K sparing diuretics -Inhibits H secretion in parallel with K secretion | 42 | |
| 515903769 | This K sparing diuretic blocks the Aldosterone receptors: | Aldactone (Spironolactone) | 43 | |
| 515903770 | This K sparing diuretic causes inhibition of Na flux through ion channels in the luminal membrane: | -Amiloride | 44 | |
| 515903771 | Contraindications to someone taking a K sparing Diuretic: | -Patient taking K -Patient on drugs affecting K -Liver disease impairs metabolism | 45 | |
| 515903772 | Osmotic 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 tubule | 46 | |
| 515903773 | Mannitol | -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 system | 47 | |
| 515903774 | Absorption of mannitol | Poor - can induce diarrhea | 48 | |
| 515903775 | Metabolism of mannitol | Not metabolized | 49 | |
| 515903776 | Excretion 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 effect | 50 | |
| 515903777 | Pharmacodynamics of osmotic diuretics: | -Counter osmotic force -Result : Urine volume increases -Reduced Na reabsorption | 51 | |
| 515903778 | Clinical indications for Osmotic diuretics: | -Increase urine output -Reduce ICP - 60 to 90 minutes after administration. | 52 | |
| 515903779 | Toxicity 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 edema | 53 | |
| 515903780 | Toxicity 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 | |
| 515903781 | Administration of Osmotic Diuretics: | -Caution : Mannitol can crystalize (Penetrate through blood vessels) -In line filter set should always be used with higher concentrations (>20%) | 55 | |
| 515903782 | Antidiuretic hormone - Agonist | -Vasopressin -Desmopressin *Both increase ADH levels and increase blood volume and BP | 56 | |
| 515903783 | ADH - Antagonist | -Conivaptin -Non selective - Lithium | 57 | |
| 515903784 | Which drug is useful for patients refractory to loop agents? | -Metolazone (Thiazide) | 58 | |
| 515903785 | Diabetes Insipidous | -Excessive thirst -Excessive urination | 59 | |
| 515903786 | Use of Thiazide diuretics in tx of Diabetes Insipidous: | -Decrease plasma volume -Decreased GFR -Water and NaCl reabsorption (PCT) | 60 |