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| 2689973633 | What is a diuretic? | a drug that increases the excretion of both fluids and solutes | 0 | |
| 2689974215 | What are the 2 types of diuretics? | Natriuretic: increases Na+ excretion Kaliuretic: increases K+ excretion | 1 | |
| 2689974727 | What are the 2 modes of action of diuretics? | 1) Direct action on the cells of the nephron (more common) 2) Modification of content of the filtrate | 2 | |
| 2689975361 | Two major applications of diuretic agents: | 1) Reduce circulating fluid volume 2) Removal of excess body fluid (oedema) | 3 | |
| 2689975760 | In which conditions do we use diuretics? | - hypertension - chronic heart failure - liver cirrhosis - renal disease - premenstrual oedema - toxic oedema - increase elimination of drugs - rapid weight loss (abuse) Other actions - glaucoma (reduces intra-ocular pressure) - epilepsy (reduces pressure of CSF?) | 4 | |
| 2689977230 | Overview of fluid reabsorption in the Nephron |  | 5 | |
| 2689979218 | How much water and Na+ are reabsorbed? | 99.5% 99.4% | 6 | |
| 2689979724 | What are the 5 classes of diuretics | - Carbonic anhydrase inhibitors - Osmotic diuretics - Loop diuretics - Thiazides - Potassium-sparing diuretics - Aldosterone antagonists - Non-aldosterone antagonists |  | 7 |
| 2689985908 | How (where from?) do diuretics produce their effect? | Most (not all) are secreted into the proximal tubule and then produce their actions from the luminal (urine) side of the tubule | 8 | |
| 2689982090 | Where do Carbonic Anhydrase Inhibitor act? | PT | | 9 |
| 2689982467 | Where do Osmotic Diuretics act? | PT Descending LOH (i.e. water permeable part of the nephron) | | 10 |
| 2689983009 | Where do loop diuretics act? | Ascending LOH | | 11 |
| 2689983255 | Where do Thiazides act? | Early DT | | 12 |
| 2689983820 | Where do Aldosterone antagonist Potassium sparing diuretics act? | late distal tubule | | 13 |
| 2689983821 | Where do Non-Aldosterone antagonist Potassium sparing diuretics act? | Early Collecting Tubule | | 14 |
| 2689987822 | Which diuretics are most effective? | Loop Diuretics | 15 | |
| 2689988147 | MOA of Loop Diuretics | Inhibit the Na+/K+/2Cl- transporters (NKCC2) in the thick ascending limb of loop of Henle -> this reduces reabsorption of Na+, K+ and Cl- => Reduced Na+ reabsorption leads to rapid and profound diuresis: =>Single dose: can increase urine volume from 200 to 1,200 ml over 3 h... |  | 16 |
| 2689991343 | Loop Diuretics : Route of Administration and Effects (Furosemide) | - Oral absorption: diuresis in 60 minutes and persists for 4-6 hours (called Lasix as it lasts 6h) - IV administration: diuresis begins within 5 minutes and persists for 2 hours - IM administration: diuresis begins in 30 minutes | 17 | |
| 2689992775 | Clinical uses of Loop Diuretics | Acute pulmonary oedema Chronic heart failure Cirrhosis of the liver Resistant hypertension USED FOR ACUTE CONDITIONS Nephrotic syndrome Acute renal failure REDUCED URINE PRODUCTION (OLIGURIA) | 18 | |
| 2689993839 | Unwanted effects of Loop Diuretics | - Dehydration - hypokalaemia (+can potentiate effects of cardiac glycosides ) - Metabolic alkalosis - Deafness (when used with aminoglycoside antibiotics) | 19 | |
| 2689994947 | Why can Loop Diuretics cause Hypokalaemia? | - Loop diuretics cause increased Na+ delivery to the DT - This is exchanged for K+ in the DT which is excreted in the urine => This K+ loss contributes to the hypokalaemia associated with loop diuretics |  | 20 |
| 2689996969 | MOA of Thiazide Diuretics? | - Act in the distal tubule to inhibit the apical Na+/Cl- co-transporter -> Cause moderate but sustained Na+ excretion with increased water excretion |  | 21 |
| 2689997809 | Characteristics of Thiazides | -Moderately powerful diuresis -Well absorbed from GI tract - long duration of action: up to 24 h | 22 | |
| 2689998807 | What is the most used Thiazide diuretic? | bendroflumethiazide (bendrofluazide) (Neo-NaClex®, Aprinox®) (several others available) | 23 | |
| 2690000107 | Clinical uses of Thiazide Diuretics | Hypertension Oedema Mild heart failure GENERALLY USED FOR LESS ACUTE CONDITIONS | 24 | |
| 2690004861 | Unwanted Effects of Thiazide Diuretics | Hypokalaemia Metabolic alkalosis Increased plasma uric acid - gout Hyperglycaemia Increased plasma cholesterol (with long-term use) Male impotence (reversible) | 25 | |
| 2690006720 | Why is hypokalaemia a potential problem? | Mild hypokalaemia - fatigue, drowsiness, dizziness, muscle weakness Severe hypokalaemia - abnormal heart rhythm, muscle paralysis, death | 26 | |
| 2690007687 | How to avoid hypokalaemia when using diuretics? | Potassium-sparing diuretics - Act on distal tubules to inhibit Na+ reabsorption - However, K+ is not secreted into the distal tubule Two subcategories: - Aldosterone antagonists (e.g. eplerenone, spironolactone) - Non-Aldosterone antagonists (e.g. amiloride, triamterene) | 27 | |
| 2690008271 | MOA of ALDOSTERONE ANTAGONISTS Potassium-sparing diuretics [Spironolactone & Eplerenone] | - Spironolactone and Eplerenone - Competitive antagonists of aldosterone => reduce Na+ channel formation ==>Reduces Na+ absorption from distal tubule - Limited diuretic action (not as potent as loop diuretics or thiazides) - Mechanism depends on reduction of protein expression in distal tubular cells =>effects may take several days to develop |  | 28 |
| 2690010348 | Clinical uses of Spironolactone & Eplerenone | Heart failure Oedema SHORT TERM USE Can also be used for resistant hypertension but some concerns over long-term use due to possible incidence of cancer (note: reported in rat studies only) | 29 | |
| 2690011687 | Unwanted effects of Spironolactone & Eplerenone | - HYPERkalaemia - needs to be monitored regularly - Metabolic acidosis (due to increased plasma H+) - GI upsets (peptic ulceration reported) - Gynaecomastia, menstrual disorders, testicular atrophy | 30 | |
| 2690012476 | MOA of NON-ALDOSTERONE ANTAGONISTS Potassium-sparing Diuretics [Triamterene and Amiloride] | - Weak diuretics - act on distal tubule - Blocks luminal Na+ channel by which aldosterone produces its main effects -> inhibit Na+ reabsorption + decrease K+ excretion |  | 31 |
| 2690013317 | Clinical use of Triamterene and Amiloride | - Of little therapeutic use alone - but are useful in combination with potassium-depleting diuretics as they limit hypokalaemia | 32 | |
| 2690013897 | Main unwanted effects of Triamterene and Amiloride | - hyperkalaemia - metabolic acidosis - GI disturbances - skin rashes | | 33 |
| 2690016348 | What are the advantages of using diuretics in combination? | (1) To increase diuretic effect - Some patients do not respond well to just one type of diuretic (e.g. loop diuretics) - reasons unknown, probably genetic - Combinations of diuretics with different sites of action can sometimes provide a synergistic action (2) To avoid the unwanted effects of hypokalaemia - Combinations of loop diuretics or thiazides with potassium-sparing diuretics - Diuretic preparations containing K+....... | 34 | |
| 2690017430 | List the Diuretics combinations preparations | - Loop diuretics with spironolactone Lasilactone®: furosemide + spironolactone - Loop diuretics with amiloride or triamterene Co-amilofruse: furosemide + amiloride - Thiazides with spironolactone Co-flumactone: hydroflumethiazide + spironolactone - Thiazides with amiloride or triamterene Co-amilozide: hydrochlorothiazide + amiloride | 35 | |
| 2690021070 | List Diuretics containing K+ | Burinex K®: bumetanide + K+ Centyl K®: bendroflumethiazide + K+ Lasikal®: furosemide + K+ Neo-NaClex-K®: bendroflumethiazide + K+ | 36 | |
| 2690022023 | MOA of Carbonic Anhydrase Inhibitors [azetozolamide (Diamox®)] | - Blocks sodium bicarbonate (NaHCO3) reabsorption in the PT - These were the earliest diuretic agents developed - Causes only weak diuresis so not now commonly used as diuretic agent |  | 37 |
| 2690022856 | Clinical use of Carbonic Anhydrase Inhibitors [azetozolamide (Diamox®)] | - glaucoma (reduces intraoccular pressure) - epilepsy (reduces volume and pressure of CSF) | | 38 |
| 2690023438 | Unwanted effects of Carbonic Anhydrase Inhibitors [azetozolamide (Diamox®)] | - metabolic acidosis (due to excretion of HCO3-) - enhances renal stone formation (due to alkaline urine) | 39 | |
| 2690025226 | MOA of Osmotic Diuretics [Mannitol] | - Non-reabsorbable solute which undergoes glomerular filtration -> Excreted within 30-60 min => Diuresis begins in 30-60 min and persists for 6-8 h | 40 | |
| 2690030062 | Clinical uses of osmotic diuretics [Mannitol] | - Treatment of raised intercranial pressure (cerebral oedema) - glaucoma (reduces intraoccular pressure) - If given orally, can cause 'osmotic diarrhoea' - eliminates toxins - May be useful for treatment of acute renal failure | 41 | |
| 2690030828 | Unwanted effects of osmotic diuretics [Mannitol] | Presence in blood also exerts osmotic pressure => increased plasma volume... ==> can't be used in patients with hypertension | 42 | |
| 2690032180 | Water as a diuretic | - most simple of diuretics - Under normal conditions, increased water intake leads to increase in volume of urine excreted - Process is controlled by antidiuretic hormone (ADH) | 43 | |
| 2690032599 | Characteristics of ADH | - Most important hormone regulating water balance - Normally some ADH is present in the circulation, maintaining urine volume at approximately 1.5 L/day - However, this can be adjusted in various ways... | 44 | |
| 2690033198 | What happens in increased fluid intake? | reduction in plasma osmolality ==> reduced secretion of ADH from the posterior pituitary ===> Reduced expression of AP-2 receptors on apical surface of DT and collecting duct cells ====> more water excretion [Note - there is no increased excretion of Na+ - the AP-2 channel moves water only] |  | 45 |
| 2690040576 | Give an example of an agent inhibiting ADH release What is the consequence? | Alcohol -> inhibits ADH release => increase urine excretion: (although tolerance develops rapidly so diuresis not sustained) | 46 | |
| 2690042670 | What other agents increase diuresis? How? | Xanthines [caffeine, theophylline, theobromine] - Commonly found in tea and coffee - increase cardiac output - Possibly also some vasodilatation of the glomerular afferent arteriole ==> Results in increased renal and glomerular blood flow which increases glomerular filtration rate and urine output ====> Produce a weak diuresis | 47 | |
| 2690043902 | Are Xanthines used clinically? Why? | Rarely used clinically due to gastric irritant effects (but theophylline used clinically as a bronchodilator for asthma) | 48 | |
| 2690041653 | What agents increase ADH release? What is the consequence? | Nicotine (anecdotal evidence) Ether Morphine Barbiturates ->increase ADH release => reduce urine excretion | 49 | |
| 2690035971 | What are the two non-selective ADH antagonists developed as possible New Diuretics Agents? | Two nonselective agents (orally active) - Lithium (Li+) and demeclocycline. | 50 | |
| 2690038417 | What are the problems of Lithium & demeclocycline? | Toxicity is a Problem - Can cause diabetes insipidus - Renal failure reported for both Li+ and demeclocycline - Li+ can cause tremors, mental confusion, cardiotoxicity, thyroid dysfunction and leukocytosis - Demeclocycline shouldn't be used in patients with liver disease | 51 | |
| 2690039278 | What drug is currently in fast track trial for the treatment of Polycystic Kidney Disease? | Tolvaptan (OPC-41061) - V2 receptor antagonist, - approved in US for treatment of hyponatriuraemia. - In fast track clinical trials for polycystic kidney disease | 52 |
