Term
| Acetazolamide (Diamox)excretory and renal hemodynamic effects |
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Definition
1. Na+: +
2. K+: ++
3. H+: -
4. Ca2+: NC
5. Mg2+: V
6. Cl: (+)
7. HCO3-: ++
8. RBF: -
9. GFR: -
10. TGF: + |
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Term
| acetazolamide (diamox) diagram basics |
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Definition
1. secreted into proximal tubule by anion transporter
2. less water is absorbed at proximal tubule
3. bicarbonate concentration is higher which leads to lower H+ and higher pH
4. Macula densa sense increased HCO3-
5. trapped bicarb increases luminal positive charge which attracts Na+ and K+ and repels Cl- |
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Term
| Acetazolamide (diamox)uses |
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Definition
| for pharmacological actions since more efficacious diuretics are currently available |
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Term
| Acetazolamide (diamox)site of actions |
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Definition
| proximal tubule where 85% of bicarb is absorbed , collecting duct intercalated cells, and other sites where CA is found (eye, RBC, and gastric mucosa) |
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Term
| Acetazolamide (diamox) mechanism |
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Definition
| inhibits CA in the lumen and in epithelial cells, reduces the amount of bicarb reabsorbed and decreases secretion of H+ (can create acidotic conditions), decreases production of aqueous humor in the eye |
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Term
| acetazolamide (diamox) urine |
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Definition
| pH 8, decrease in RBF and GFR due to increased solutes at the macula densa |
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Term
| acetaxolamide (diamox) plasma |
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Definition
| decreased bicarb, NA, K and increase in Cl, H, and CO2; hyperchloremic acidosis due to increased reabsorption of Cl in CD as a result of increased negative charge in lumen |
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Term
| acetazolamide (diamox) therapeutic uses |
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Definition
absorbed orally, 90% bound to plasma proteins, secreted into lumen at prox. tubule by organic acid transporter and is excreted unchanged, can be given IV or IM
1. 2nd line treatment of open-angle glaucoma (beta antagonists are first line)
2. urinary alkalinization: renal excretion of uric acid and other weak acids can be enhanced by increasing the pH of the urine – prolonged therapy requires bicarb administration
3. Metabolic alkalosis: can correct the alkalosis due to excessive use of loop or thiazide diuretics (cause excessive H+ secretion), especially useful in patient with heart failure
4. Acute mountain sickness: prophylactically to help prevent this form of respiratory alkalosis
5. adjunct therapy for epilepsy: sometimes given in conjunction with antiepileptic meds to treat generalized and partial seizure – metabolic acidosis slows down synaptic transmission |
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Term
| acetazolamide (diamox) adverse effects |
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Definition
1. large doses produce drowsiness and paresthesia, does needs to be decreased in the elderly and those with renal failure
2. Hyperchloremic metabolic acidosis: bicarb wasting limits effectiveness to 2-3 days, contraindicated in COPD and hepatic cirrhosis
3. Nephroliathiasis: more common since calcium salts precipitate out of solution at alkaline pH
4. reduction in urinary excretion of weak organic bases, NH3, due to increased pH
5. cross-hypersensitivity with sulfonamides |
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Term
| hydrochlorothiazide excretory and renal hemodynamic effects |
|
Definition
1. Na+: +
2. K+: ++
3. H+: +
4. Ca2+: V(-)
5. Mg2+: V(+)
6. Cl-: +
7. HCO3-: +
8. RBF: NC
9. GFR: V(-)
10. TGF: NC |
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Term
| hydrochlorothiazide diagram basics |
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Definition
1. transported via the organic acid transporter
2. inhibits NaCl cotransporter in DCT
3. increases Ca reabsorption
4. cortico-medullary osmotic gradient intact |
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Term
| hydrochlorothiazide mechanism |
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Definition
| inhibit the electroneutral NaCl cotransporter |
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Term
| hydrochlorothiazide urine |
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Definition
| increase the urinary excretion of Na, Cl, and K; decrease the excretion of Ca; urine is hyperosmolar |
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Term
| hydrochlorothiazide plasma |
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Definition
| may lead to hypokalemia and hypochloremic alkalosis |
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Term
| hydrochlorothiazide therapeutic uses |
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Definition
well absorbed orally, benzothiadiazine derivative are bound to plasma proteins and secreted by the acid transport system of the prox. tubule
1. HTN: reduces BP by reducing volume and producing mild vasodilation
2. CHF
3. Hypercalciuria: prevention of renal stones
4. Nephrogenic diabetes insipidus: in the absence of appropriate ADH response, thiazides can reduce urine outflow |
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Term
| hydrochlorothiazide adverse effects |
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Definition
1. fluid and electrolyte imbalance: hypochloremia, hyponatremia, hypercalcemia, hypokalemic alkalosis, cardiac arrhythmias
2. HypoTN: volume depletion
3. hyperglycemia
4. increase in the levels of LDL, total cholesterol, and total TGs
5. Hypersensitivity |
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Term
| furosemide excretory and renal hemodynamic effects |
|
Definition
1. Na+: ++
2. K+: ++
3. H+: +
4. Ca2+: ++
5. Mg2+: ++
6. Cl-: ++
7. HCO3-: +
8. RBF: V(+)
9. GFR: NC
10. TGF: - |
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Term
| furosemide diagram basics |
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Definition
1. Loop diuretics are secreted into the tubule by the anion transporter
2. knocks out the NaK2Cl cotransporter which effectively abolishes the corticomedullary osmotic gradient
3. K+ recycling decreased |
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Term
| Furosemide site of action |
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Definition
| TAL, NaK2Cl- cotransporter |
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Term
|
Definition
| by inhibiting the transporter less K+ is available for recycling which reduces the positive potential and decreases the paracellular reabsorption of Mg and Ca, impair the ability to concentrate urine, decrease renal vascular resistance and increase renal blood, acts as weak CA inhibitor, dilates large veins when given IV |
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Term
|
Definition
| increases the excretion of NaCl, K, H, Mg, Ca, and HCO3- |
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Term
|
Definition
| can lead to hypokalemic alkalosis and hypochloremia |
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Term
| furosemide therapeutic uses |
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Definition
orally absorbed, IV admin shows effects within 5 min, 1-3 hour window of action, 60% is excreted in the urine and the rest is metabolized, extensively bound to plasma proteins and are secreted by the organic acid transporter
1. acute pulmonary edema
2. edema of cardiac, hepatic , or renal origin which do not respond to thiazides
3. hyperkalemia, hypercalcemia
4. acute renal failure – to increase urine flow and potassium excretion |
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Term
| furosemide adverse effects |
|
Definition
1. electrolyte imbalance: hyeruricemia, hypchloremia, hypomagnesemia, hypokalemic metabolic alkalosis
2. cardiac arrhythmias: loop and thiazide diuretics can have a potentially fatal interaction with quinidine causing torsades de pointes
3. hypotension due to volume depletion
4. ototoxicity: ethacrynic acid
5. hypersensitivity reaction in persons allergic to sulfonamides |
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Term
| Potassium sparing diuretics basics |
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Definition
| lead to the inhibition of Na reabsorption and K and H secretion, usually used in conjunction with thiazide diuretics, can produce hyperkalemia (plasma K levels should be monitored) |
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Term
| spironolactone diagram basics |
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Definition
| a. canrenone, the active metabolite of spironolactone, blocks the action of aldosterone at the level of principal cells – it take hours to days to reach its peak effect |
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Term
| spironolactone site of action |
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Definition
| CD by competing with aldosterone for its receptor and blocking its action |
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Term
|
Definition
| competes with aldosterone receptor which upon activation upregulate Na channels and pumps on the luminal surface, has no effect if there is no circulating aldosterone |
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Term
|
Definition
| excretion of Na, Cl and water is increased while secretion of K is decreased |
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Term
|
Definition
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Term
| spironolactone therapeutic uses |
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Definition
takes days to hrs to reach peak effect, absorbed orally and induce P-450
a. given in conjunction with thiazide or loop diuretics to prevent some of the K excretion that would occur with these drugs
b. primary hyperaldosteronism
c. secondary hyperaldosteronism resulting from CHF, hepatic cirrhosis, and nephrotic syndrome |
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Term
| spironolactone adverse effects |
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Definition
a. hyperkalemia: concomitant use of drugs that suppress the RAA system, i.e. ACE inhibitor, increases the likelihood of developing hyperkalemia, patient K levels must be measured
b. gynecomastia in males and menstrual irregularities in females |
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Term
|
Definition
| a. blocks Na channel at the principal cells |
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Term
|
Definition
| Na channels, principal cells, CD |
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Term
|
Definition
| block Na channels decreasing Na-K exchange, independent of the presence of aldosterone |
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Term
|
Definition
| decrease the excretion of K |
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Term
|
Definition
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Term
| amiloride therapeutic uses |
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Definition
| given in conjunction with thiazides and loop diuretics to prevent the loss of K, are bound to plasma proteins and secreted by the organic base transporters |
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Term
| amiloride adverse effects |
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Definition
| a. hyperkalemia, especially in the presence of renal disease |
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Term
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Definition
| nonelectrolytes, freely filterable, poorly reabsorbed, pharmacologically inert |
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Term
| mannitol excretory and renal hemodynamic effects |
|
Definition
a. Na+: ++
b. K+: +
c. H+: I
d. Ca2+: +
e. Mg2+: ++
f. Cl-: +
g. HCO3-: +
h. RBF: +
i. GFR: NC
j. TGF: I |
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Term
|
Definition
a. increases renal blood flow, freely filterable at the glomerulus
b. less water is absorbed in PCT
c. decreased corticomedullary gradient because of increased blood flow |
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Term
|
Definition
| segments of the tubule that are permeable to water – proximal tubule, descending loop of Henle, CD |
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Term
|
Definition
a. increases osmolality of filtrate, decrease water reabsorption
b. increases renal blood flow, decreased corticomedullary gradient |
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Term
|
Definition
| increase in electrolyte excretion due to the lowered tubule Na concentration and increased tubular flow rate |
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Term
|
Definition
| admin of mannitol to the vascular compartment will cause a transfer of fluid from intracellular compartment to extracellular compartment causing hyponatremia, water diuresis is greater than natriuresis which can lead to hypernatremia |
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Term
| mannitol therapeutic uses |
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Definition
must be given IV
a. maintenance of urine flow in prophylaxis and treatment of acute renal failure
b. short term reduction in intracranial or intraocular pressure before and after surgery
c. acute glaucoma attacks
d. dialysis disequilibrium: to reduce hypoTN and CNS symptoms after over dialysis (decreased plasma osmolality) |
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Term
|
Definition
a. before diuresis, increased extracellular volume may cause pulmonary edema and congestive heart failure, initial hyponatremia can cause HA, nausea, and vomiting
b. prolonged use without water replacement will lead to dehydration, free water loss, and hypernatremia
c. active cranial bleeding is a contraindication |
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Term
| conivaptan diagram basics |
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Definition
a. less water is reabsorbed
b. decreased corticomedullary gradient due to less urea
c. nonpeptide antagonist o f ADH receptor at basolateral membrane of principal cell in CD |
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Term
| conivaptan site of action |
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Definition
|
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Term
|
Definition
| acts at ADH receptors (V1a and V2) as antagonist |
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Term
|
Definition
| increase in dilute urine volume |
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Term
|
Definition
| increase in Na concentration (needs to be monitored) |
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Term
| conivaptan therapeutic uses |
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Definition
a. used to treat SIADH, only IV preps
b. euvolemic and hypervolemic hyponatremia as a result of hypothyroidism, adrenal insufficiency, and certain pulmonary disorders
c. CHF |
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Term
| conivaptan adverse effects |
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Definition
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