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 |
Chapter 15 - Diuretic Agents - Test#3 Pharm Flashcards
Primary tabs
Need Help?
We hope your visit has been a productive one. If you're having any problems, or would like to give some feedback, we'd love to hear from you.
For general help, questions, and suggestions, try our dedicated support forums.
If you need to contact the Course-Notes.Org web experience team, please use our contact form.
Need Notes?
While we strive to provide the most comprehensive notes for as many high school textbooks as possible, there are certainly going to be some that we miss. Drop us a note and let us know which textbooks you need. Be sure to include which edition of the textbook you are using! If we see enough demand, we'll do whatever we can to get those notes up on the site for you!