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258 Cards in this Set
- Front
- Back
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What is Lx - best initial - in nephrology?
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What is Lx - best initial - in nephrology? 1 Urinalysis, 2 BUN and Creatinine
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In Uninalysis, what does Nitrites show?
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In Uninalysis, hat does Nitrites show? Nitrites is Gram Negative organism
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In Uninalysis, what does Leukocyte Esterase show?
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In Uninalysis, what does Leukocyte Esterase show? Leukocyte Esterase shows Infection
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What does severe proteinuria tells?
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What does severe proteinuria tells? Severe Proteinuria tells Glomerular Damage
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What is orthostatic proteinuria?
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What is orthostatic proteinuria? Orthostatic proteinuria is prolonged standing cause proteinuria and it is normal.
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What is Lx for total amount of protein in a day?
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What is Lx for total amount of protein in a day? 1 Single Protein to Creatinine ratio (Better), 2 24-hour Urine Collection
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What is microalbuminuria? Dx? Tx?
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What is microalbuminuria? 50 to 300 mg per 24 hour. It is present in early Diabetic. Tx - ACEI or ARB
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Bence-Jones protein. Dx? How to detect?
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Bence-Jones protein. Dx? Multiple Myeloma. How to detect? Not detectable on a urine dipstick. Use ImmunoElectrophoresis.
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In UA, what does WBC represents?
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In UA, what does WBC represents? 1 Inflammation, 2 Infection, 3 Allergic Interstitial Nephritis
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In nephrology, what does Eosinophil represent? Lx?
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In nephrology, what does Eosinophil represent? Eosinophil is Allergic or Acute Interstitial Nephritis. Eosinophils is very specific. Lx - 1 Wright Stains, 2 Hansel Stains.
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In UA, what does RBC represents?
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In UA, what does RBC represents? RBC represent Hematuria - 1 Stones (Bladder, Ureter, Kidney), 2 Infection (Cystitis, Pyelonephritis), 3 Cancer (Bladder, Ureters, or Kidney), 4 Trauma, 5 Glomerulonephritis, 6 Hematologic disorders that cause bleeding (Coagulopathy), 7 Drugs (Cyclophosphamide gives Hemorrhagic Cystitis)
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What cause false positive tests for hematuria on UA?
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What cause false positive tests for hematuria on UA? 1 Hemoglobin, or 2 Myoglobin in urine
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How to differential RBC from Hemoglobin or Myoglobin in UA?
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How to differential RBC from Hemoglobin or Myoglobin in UA? RBC, Hemoglobin, and Myoglobin causes positive dipstick for blood. Hemoglobin and Myoglobin will have No RBC on Microscopic Examination of urine.
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Dysmorphic RBC. Dx?
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Dysmorphic RBC. Dx? Glomerulonephritis
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Does NSAIDs induce renal disease show Eosinophil?
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Does NSAIDs induce renal disease show Eosinophil? No
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Bladder Lx - Most Accurate?
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Bladder Lx - Most Accurate? Cystoscopy
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When is cystoscopy done?
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When is cystoscopy done? 1 Hematuria without Infection or Prior Trauma, and 2 Renal Ultrasound or CT does NOT show an etiology, 3 Bladder Sonography shows a Mass for possible Biopsy.
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What are casts?
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What are casts? Casts are collections of material Clogging up the Tubules and being excreted in urine.
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Urinary cast - Red cell . Association?
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Urinary cast - Red cell . Association? Glomerulonephritis
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Urinary cast - White cell . Association?
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Urinary cast - White cell . Association? Pyelonephritis
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Urinary cast - Eosinophil . Association?
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Urinary cast - Eosinophil . Association? Acute (Allergic) Interstitial Nephritis
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Urinary cast - Hyaline . Association?
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Urinary cast - Hyaline . Association? Dehydration concentrates urine and normal Tamm-Horsfall protein precipitates or concentrates into a cast
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Urinary cast - Broad, Waxy . Association?
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Urinary cast - Broad, Waxy . Association? Chronic renal disease
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Urinary cast - Granular, or Muddy-Brown . Association?
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Urinary cast - Granular, or Muddy-Brown . Association? Acute tubular necrosis. they are collections of dead tubular cells
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Glomerulonephritis . What cast Association?
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Glomerulonephritis . What cast Association? Red cell
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Pyelonephritis . What cast Association?
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Pyelonephritis . What cast Association? White cell
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Acute (Allergic) Interstitial Nephritis . What cast Association?
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Acute (Allergic) Interstitial Nephritis . What cast Association? Eosinophil
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Dehydration. Tamm-Horsfall protein . What cast Association?
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Dehydration. Tamm-Horsfall protein . What cast Association? Hyaline
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Chronic renal disease . What cast Association?
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Chronic renal disease . What cast Association? Broad, Waxy
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Acute tubular necrosis. Dead tubular cells . What cast Association?
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Acute tubular necrosis. Dead tubular cells . What cast Association? Granular, or Muddy-Brown
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What is another name for AKI?
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What is another name for AKI? Acute Kidney Injury is same as Acute Renal Failure
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What is AKI? Types?
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What is AKI? Aka ARF. Defined as a Decrease in Creatinine Clearance resulting in a sudden rise in BUN and Creatinine. Types? 1 PreRenal Azotemia (Decreased Perfusion), 2 PostRenal Azotemia (Obstruction), 3 Intrinsic Renal Disease (Ischemia and Toxins).
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What are causes of Prerenal Azotemia?
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What are causes of Prerenal Azotemia? 1 Hypotension (Systolic Below 90) - aaa Sepsis, bbb Anaphylaxis, ccc Bleeding, ddd Dehydration. 2 Hypovolemia - aaa Diuretics, bbb Burns, ccc Pancreatitis. 3 Renal Artery Stenosis. 4 Relative Hypovolemia from Decreased Pump Function - aaa CHF, bbb Constrictive Pericarditis, ccc Tamponade. 5 HypoAlbuminemia. 6 Cirrhosis. 7 NSAIDs - Constrict Afferent Arteriole. 8 ACEI - Efferent arteriole vasodilation.
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What is NSAIDs affect on renal capillary?
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What is NSAIDs affect on renal capillary? NSAIDs Constrict Afferent Arteriole
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What is ACEI affect on renal capillary?
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What is ACEI affect on renal capillary? ACEI Vasodilate Efferent Arteriole
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What are causes of PostRenal Azotemia?
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What are causes of PostRenal Azotemia? Obstruction cause damages to kidney by blocking filtration at glomerulus. 1 Prostate Hypertropy or Cancer. 2 Stone in Ureter. 3 Cervical Cancer. 4 Urethral Stricture. 5 Neurogenic (Atonic) Bladder. 6 Retroperitoneal Fibrosis (Bleomycin, Methylsergide, or Radiation)
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What medication cause retroperitoneal fibrosis?
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What medication cause retroperitoneal fibrosis? 1 Bleomycin, 2 Methylsergide, 3 Radiation
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What is the managment of PreRenal and PostRenal Azotemia?
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What is the managment of PreRenal and PostRenal Azotemia? Correcting the underlying cause. Majority are Reversible. They cause 80 perc of AKI
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What is the most common cause of Intrinsic Renal disease?
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What is the most common cause of Intrinsic Renal disease? MCC is Acute Tubular Necrosis from 1 Toxins, or 2 Prolonged Ischemia of kidney. Glomerulonephritis is rarely acute, but when kidney is injured from any cause, there is always a greater risk of AKI.
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What is the cause of Intrinsic Renal disease?
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What is the cause of Intrinsic Renal disease? MCC is 1 Acute Tubular Necrosis from aaa Toxins, or bbb Prolonged Ischemia of kidney. 2 Glomerulonephritis is rarely acute, but when kidney is injured from any cause, there is always a greater risk of AKI. 3 Acute (Allergic) Interstitial Nephritis - Penicillins. 4 Rhabdomyolysis and Hemoglobinuria. 5 Contrast Agents, Aminoglycosides, Cisplatin, Amphotericin, Cyclosporine, and NSAIDs(Most common toxins causing AKI from ATN). 6 Crystals - HyperUricemia, HyperCalcemia, or HyperOxaluria. 7 Proteins - Bence-Jones protein from Multiple Myeloma. 8 PostStreptococcal Infection.
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Enlargement of Bladder, Massive Diuresis after Foley catheter placement. Dx?
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Enlargement of Bladder, Massive Diuresis after Foley catheter placement. Dx? PostRenal Azotemia - Obstruction
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Complete dead kidney. What changes?
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Complete dead kidney. What changes? Creatinine Rises 1 per day.
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PreRenal. Lx - BUN over Creatinine?
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PreRenal. Lx - BUN over Creatinine? More than 20 over 1
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PostRenal. Lx - BUN over Creatinine?
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PostRenal. Lx - BUN over Creatinine? More than 20 over 1
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Intrinsic Renal Disease. Lx - BUN over Creatinine?
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Intrinsic Renal Disease. Lx - BUN over Creatinine? Around 10 over 1
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Who should not get Contrast?
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Who should not get Contrast? No Contrast for Renal Insufficiency
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When AKI with unclear etiology. Next step?
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When AKI with unclear etiology. Next step? 1 Urinalysis, 2 Urine sodium (UNa), 3 Fractional Excretion of Sodium (FeNa), or 4 Urine Osmolality. Urinalysis is First
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Prerenal azotemia. Lx - UNa and FeNa?
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Prerenal azotemia. Lx - UNa and FeNa? Low UNa (Less than 20) equal to Low FeNa (Less than 1 perc)
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What kidney cell reabsorb water?
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What kidney cell reabsorb water? Tubule cells reabsorb water. In ATN, Urine cannot be contrated because tubule cells are damaged. Urine osmolality is same as blood. Body loses Sodium (UNa Above 20), and Water (UOsm Below 300) into Urine.
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What renal problem causes Sodium and Water loss in Urine?
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What renal problem causes Sodium and Water loss in Urine? Kidney Tubule cells reabsorb water. In ATN, Urine cannot be contrated because tubule cells are damaged. Urine osmolality is same as blood. Body loses Sodium (UNa Above 20), and Water (UOsm Below 300) into Urine.
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UNa Above 20. UOsm Below 300. Dx?
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UNa Above 20. UOsm Below 300. Dx? Kidney Tubule cells reabsorb water. In ATN, Urine cannot be contrated because tubule cells are damaged. Urine osmolality is same as blood. Body loses Sodium (UNa Above 20), and Water (UOsm Below 300) into Urine.
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20 yo African American man comes for a screening test for sickle cell. He is found to be heterozygous (Trait or AS) for sickle cell. What is best advice for him?
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20 yo African American man comes for a screening test for sickle cell. He is found to be heterozygous (Trait or AS) for sickle cell. What is best advice for him? --- Avoid Dehydration. Sickle cell trait has a Defect in Renal Concentrating ability or Isosthenuria. They will continue to produce inappropriately Dilute, High-Volume Urne despite Dehydration.
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What is Urine Specific Gravity?
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What is Urine Specific Gravity? Urine Osmolality. High Specific Gravity is High UOsm.
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What is Urine Osmolality?
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What is Urine Osmolality? Urine Specific Gravity. High Specific Gravity is High UOsm.
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BUN to Creatinine More than 20 to 1. UNa Less than 20. FeNa Less than 1 p. UOsm More than 500. Dx?
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BUN to Creatinine More than 20 to 1. UNa Less than 20. FeNa Less than 1 p. UOsm More than 500. Dx? PreRenal Azotemia
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BUN to Creatinine Less than 20 to 1. UNa More than 20. FeNa More than 1 p. UOsm Less than 300. Dx?
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BUN to Creatinine Less than 20 to 1. UNa More than 20. FeNa More than 1 p. UOsm Less than 300. Dx? Acute Tubular Necrosis
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PreRenal Azotemia. Lx - BUN to Creatinine. UNa. FeNa. UOsm.?
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PreRenal Azotemia. Lx - BUN to Creatinine. UNa. FeNa. UOsm.? --- BUN to Creatinine More than 20 to 1. UNa Less than 20. FeNa Less than 1 p. UOsm More than 500. PreRenal Azotemia
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Acute Tubular Necrosis. Lx - BUN to Creatinine. UNa. FeNa. UOsm.?
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Acute Tubular Necrosis. Lx - BUN to Creatinine. UNa. FeNa. UOsm.? --- BUN to Creatinine Less than 20 to 1. UNa More than 20. FeNa More than 1 p. UOsm Less than 300. Acute Tubular Necrosis
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What kidney cell reabsorb water and Na?
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What kidney cell reabsorb water and Na? Tubule cell
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What kidney cell damage causes proteinuria?
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What kidney cell damage causes proteinuria? Gomeruli
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What happen when kidney tubule cell damage?
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What happen when kidney tubule cell damage? Cannot reabsorb Na and Water
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What happen when kidney Glomerulil damage?
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What happen when kidney Glomerulil damage? Proteinuria
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What is the difference between Contrast and Aminoglycoside causing ATN?
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What is the difference between Contrast and Aminoglycoside causing ATN? Contrast cause Creatinine to rise Next day. Aminoglycoside causes Creatinine to rise after 5 to 10 days.
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How to prevent contrast induced nephrotoxicity?
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How to prevent contrast induced nephrotoxicity? Give Saline Hydration.
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Contrast induced nephropathy. Lx - UNa, FeNa, Urine Specific Gravity?
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Contrast induced nephropathy. Lx - UNa, FeNa, Urine Specific Gravity? --- Contrast induced nephropathy. Lx - UNa Less than 20, FeNa Less than 1p, Urine Specific Gravity - Very high. Contrast causes spasm of afferent arteriole that leads to renal tubular dysfunction. There is tremendous reabsorption of sodium and water, leading the specific gravity of urine to become very high.
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A pt with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later, the creatinine rises. What is the most likely cause?
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A pt with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later, the creatinine rises. What is the most likely cause? --- Hyperuricemia. Two days after chemotherapy, the creatinine rises in a person with a hematologic malignancy. This is most likely from Tumor Lysis Syndrome leading to Hyperuricemia.
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What does tumor lysis syndrome cause? how to prevent?
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What does tumor lysis syndrome cause? how to prevent? TLS causes HyperUricemia. Prevent this with 1 Allopurinol, 2 Hydration, and 3 Rasburicase given Prior to chemotherapy to prevent renal failure from TLS.
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What is Rasburicase Tx for?
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What is Rasburicase Tx for? Tumor Lysis Syndrome causes HyperUricemia. Prevent this with 1 Allopurinol, 2 Hydration, and 3 Rasburicase given Prior to chemotherapy to prevent renal failure from TLS.
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A pt who is suicidal ingests an unknown substance and develops renal failure 3 days later. Her calcium level is also low and the urinalsis shows an abnormality. What did she take?
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A pt who is suicidal ingests an unknown substance and develops renal failure 3 days later. Her calcium level is also low and the urinalsis shows an abnormality. What did she take? --- Ethylene Glycol. Ethylene Glycol is associated with AKI based on Oxalic acid and Oxalte precipitating within kidney tubules causing ATN. Oxalate crystal appears as Envelope-shaped crystals. The Calcium level is Low because it precipitates as calcium Oxalate.
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Envelope-shaped crystals. Dx?
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Envelope-shaped crystals. Dx? Ethylene Glycol. Envelope shaped crystal is Oxalate crystals. Oxalic acid and oxalate precipitating within Kidney tubules causing ATN. Calcium level is Low because it precipitates as calcium oxalate.
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Inflammation of retina. Ingestion of something. Dx?
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Inflammation of retina. Ingestion of something. Dx? Methanol.
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What makes toxins more likely to cause ATN?
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What makes toxins more likely to cause ATN? 1 Hypoperfusion, 2 Underlying renal insufficiency (Hypertension, or Diabetes), 3 Increasing age (Body loses 1 perc of renal function every year past age 40)
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What are causes of ATN summary?
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What are causes of ATN summary? 1 Drugs (aaa Aminoglycoside, bbb Amphotericin, ccc Cisplatin, ddd Vancomycin, eee Acyclovir, and fff Cyclosporine) - Slower onset - 5-10 days - dose dependent. Low Magnesium INcrease Risk of Aminoglycoside, or Cisplatin Toxicity. 2 Contrast - Immediate renal toxicity - prevented with Saline Hydration and N-acetylcysteine. 3 Pigments - Hemoglobin and Myoglobin (Rhabdomyolysis). 4 HyperUricemia - Tumor Lysis Syndrome (Chemotherapy with Cisplatin). Long standing HyperUricemia from Gout can cause Chronic Renal Failure. 5 Calcium Oxalate in Renal Cortex from Ethylene Glycol overdose. 6 Bence-Jones protein. 7 NSAIDs.
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What is etiology of Rhabdomyolysis? Lx? Tx?
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What is etiology of Rhabdomyolysis? Lx? Tx? --- Rhabdomyolysis is caused by 1 Trauma, 2 Prolonged Immobility, 3 Crush Injuries, 4 Snake bites, 5 Seizures. Lx confirm - Urinalysis. UA will be Positive only on Dipstick for large amount of Blood, but No Cell on Microscopic exam. Most specific test is Urine Test for Myoglobin. High Creatine Phosphokinase (CPK, Hyperkalemia, HyperUricemia, and HypoCalcemia. Tx - 1 Saline Hydration, 2 Mannitol, 3 Bicarbonate (Drives Potassium into cells). Myoglobin is a severe oxidant stress on tubular cells. Saline and Mannitol Increase urine flow rates to Decrease amount of Contact Time
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Why hemolysis does not cause hyperUricemia?
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Why hemolysis does not cause hyperUricemia? RBC has no Nuclei
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What does dipstick not able to differentiate?
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What does dipstick not able to differentiate? 1 Hemoglobin, 2 Myoglobin, 3 RBC
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A man comes to ER after a triathlon, followed by status epilepticus. He takes Simvastatin at triple recommended dose. His muscles are tender and urine is dark. IV fluids are started. Next best step in management?
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A man comes to ER after a triathlon, followed by status epilepticus. He takes Simvastatin at triple recommended dose. His muscles are tender and urine is dark. IV fluids are started. Next best step in management? --- EKG. EKG is done to detect Life-Threatening HyperKalemia.
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ATN Tx?
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ATN Tx? Correct the underlying cause. Hydration if pt is Volume depleted. Correction of Electrolyte abnormalities. Wrong answer - 1 Low-Dose dopamine, 2 Diuretics, 3 Mannitol, 4 Steroids
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When to use Dialysis?
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When to use Dialysis? 1 Fluid Overload, 2 Encephalopathy, 3 Pericarditis, 4 Metabolic Acidosis, 5 HyperKalemia. Remember CNS, Heart, H+, K+, H2O. Dialysis is based on these Life Threatening condition.
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Prolonged QT interval. Dx? Tx?
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Prolonged QT interval. Dx? Hypocalcemia. It can lead to Arrhythmia. Tx - Vitamin D and Calcium.
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What is Furosemia AE?
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What is Furosemia AE? Ototoxicity. Deaf.
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What is Aminoglycoside AE?
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What is Aminoglycoside AE? Oxtotoxicity. Deaf
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What is hepatorenal syndrome? Lx? Tx?
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What is hepatorenal syndrome? Renal failure developing secondary to Liver disease. Severe liver Disease (Cirrhosis). Hepatorenal syndrome fit in with PreRenal Azotemia. Lx? 1 UNa Low (Less than 10-15), 2 FeNa Low (Below 1p), 3 BUN to Creatinine Greater than 20. Tx? 1 Albumin, 2 Midodrine, 3 Octreotide
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What are Atheroemboli? Dx? Tx?
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What are Atheroemboli? Cholesterol Plaques in Aorta or near Coronary arteries are sometimes large and fragile can Break Off when these vessels are manipulated during catheter procedures. Cholesterol Emboli lodge in kidney, leading to AKI. Px - Blue_Purplish skin lessions in Finger and Toes, Livedo Reticularis, and Ocular lesions. Dx? 1 Eosinophilia, 2 Low Complement levels, 3 Eosinophiluria, 4 Elevated ESR. 5 MA - Biopsy of Purplish skin lesions - Cholesterol Crystals. Tx? None
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What is another name for Acute Interstitial Nephritis?
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What is another name for Acute Interstitial Nephritis? Allergic Interstitial Nephritis
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What is another name for Allergic Interstitial Nephritis?
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What is another name for Allergic Interstitial Nephritis? Acute Interstitial Nephritis
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What is AIN? Etiology? Px? Lx? Tx?
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What is AIN? Acute Interstitial Nephritis is a form of Acute Renal Failure that Damages Tubules. Idiopathic. Antibodies and Eosinophils attack cells lining tubules as a Reaction to 1 Drugs, 2 Infection, and 3 Autoimmune Disorders (SLE, Sjogren, and Sarcoidosis). Etiology? Most Common Allergenic medications - 1 Penicillins and Cephalosporins, 2 Sulfa (Diuretics - Furosemide and Thiazides), 3 Phenytoin, 4 Rifampin, 5 Quinolones, 6 Allopurinol, 7 PPI. The medications that cause AIN are same as cause of 1 Drug allergy and rash, 2 Stevens Johnson syndrome, 3 Toxic Epidermal Necrolysis, 4 Hemolysis. They affect 1 Skin, 2 Kidney, 3 RBC. Px? 1 Acute Renal Failure (Rising BUN and Creatinine), 2 Fever, 3 Rash, 4 Arthralgias, 5 Eosinophilia and Eosinophiluria. Lx? 1 BUN to Creatinine Below 20, 2 WBC and RBC in Urine. MA - Hansel or Wright Stain for Eosinophils. Tx? AIN usually Resolves Spontaneously with Stopping drug or Controlling Infection. Severe Disease - Dialysis - Temporary. If Creatinine Continues to Rise after Stopping Drug - Glucocorticoids (Prednisone, Hydrocortisone, Methylprednisolone).
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What are Most Common Allergenic medications?
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AIN Most Common Allergenic medications - 1 Penicillins and Cephalosporins, 2 Sulfa (Diuretics - Furosemide and Thiazides), 3 Phenytoin, 4 Rifampin, 5 Quinolones, 6 Allopurinol, 7 PPI. The medications that cause AIN are same as cause of 1 Drug allergy and rash, 2 Stevens Johnson syndrome, 3 Toxic Epidermal Necrolysis, 4 Hemolysis. They affect 1 Skin, 2 Kidney, 3 RBC. Px? 1 Acute Renal Failure (Rising BUN and Creatinine), 2 Fever, 3 Rash, 4 Arthralgias, 5 Eosinophilia and Eosinophiluria. Lx? 1 BUN to Creatinine Below 20, 2 WBC and RBC in Urine. MA - Hansel or Wright Stain for Eosinophils. Tx? AIN usually Resolves Spontaneously with Stopping drug or Controlling Infection. Severe Disease - Dialysis - Temporary. If Creatinine Continues to Rise after Stopping Drug - Glucocorticoids (Prednisone, Hydrocortisone, Methylprednisolone).
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How can Analgesic nephropathy present?
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How can Analgesic nephropathy present? NSAIDs is the main cause. Analgesic Nephropathy Px - 1 ATN, 2 AIN, 3 Membranous Glomerulonephritis, 4 Vascular Insufficiency of Kidney from Inhibiting Prostaglandins (Prostaglandins Dilate Afferent Arteriole. NSAIDs Constrict afferent arteriole and Decrease renal perfusion. Renal insufficiency from Diabetes and Hypertension get problem). 5 Papillary Necrosis (Acute). 6 Chronic Tubular Interstitial Nephritis (Chronic).
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How does Prostaglandins affect renal capillary? What medication is related to it?
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How does Prostaglandins affect renal capillary? What medication is related to it? Prostaglandins Dilate Afferent Arteriole. NSAIDs Constrict afferent arteriole and Decrease renal perfusion. Renal insufficiency from Diabetes and Hypertension get problem
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What is Papillary Necrosis? Px? Lx? Tx?
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What is Papillary Necrosis? Papillary Necrosis is a Sloughing Off of Renal Papillae. Caused by 1 Toxins (like NSAIDS), or 2 Sudden Vascular Insufficiency (Death of cells in papillae). Pt has Underlying Renal Damage. BUN and Creatinine may be Normal (Must lose at least 60 to 70 perc of renal function before creatinine begins to rise). Look for Extra NSAIDs Use with History of - 1 Sickle Cell Disease, 2 Diabetes, 3 Urinary Obstruction, 4 Chronic Pyelonephritis. Px? Papillary Necrosis can be Very hard to distinguish from Pyelonephritis. Look for 1 Sudden Onset of Flank Pain, 2 Fever, and 3 Hematuria, 4 History of Renal damage. Lx? 1 UA (RBC, WBC, and may show Necrotic Kidney tissue). 2 Urine Culture - Normal. MA - CT Scan - Abnormal Internal Structures of kidney from Loss of Papillae. Tx? None.
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Contrast Pyelonephritis and Papillary Necrosis. Onset, Symptoms, Urine Culture, CT Scan, Treatment.
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Contrast Pyelonephritis and Papillary Necrosis. Pyelonephritis - Onset (Few Days), Symptoms (Dysuria), Urine Culture (Positive), CT Scan (Diffusely Swollen Kidney), Treatment (Antibiotics - Ampicillin_Gentamicin or Fluoroquinolones). Papillary Necrosis - Onset (Few Hours), Symptoms (Necrotic material in Urine), Urine Culture (Negative), CT Scan (Bumpy Contour of interior where papillae were lost), Treatment (None).
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What are Renal Toxins?
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What are Renal Toxins? What are causes of ATN summary? 1 Drugs (aaa Aminoglycoside, bbb Amphotericin, ccc Cisplatin, ddd Vancomycin, eee Acyclovir, and fff Cyclosporine) - Slower onset - 5-10 days - dose dependent. Low Magnesium INcrease Risk of Aminoglycoside, or Cisplatin Toxicity. 2 Contrast - Immediate renal toxicity - prevented with Saline Hydration and N-acetylcysteine. 3 Pigments - Hemoglobin and Myoglobin (Rhabdomyolysis). 4 HyperUricemia - Tumor Lysis Syndrome (Chemotherapy with Cisplatin). Long standing HyperUricemia from Gout can cause Chronic Renal Failure. 5 Calcium Oxalate in Renal Cortex from Ethylene Glycol overdose. 6 Bence-Jones protein. 7 NSAIDs.
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What is Tubular Disease summary?
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What is Tubular Disease summary? Quick - Acute, Toxin, None Nephrotic, No Biopsy, No Steroids, No Immunosuppressive. 1 Tubular disease - Acute, 2 Tubular disease cause by - Toxins (Drugs, Myoglobin, Hemoglobin, Oxalate, Urate, NSAIDs, Contrast), 3 No Nephrotic Syndrome, or Massive Proteinuria. 4 Biopsy Not Needed for Dx, 5 No Steroids. 6 No Immunosuppressive drugs (Cyclophosphamide, Mycophenolate). 7 Tx - Correct Hypoperfusion, and Remove Toxin.
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Acute Tubular disease quick memory?
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Acute Tubular disease quick memory? Acute - Tubular - Toxin
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Glomerular disease quick memory?
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Glomerular disease quick memory? Glomerular - Slow - Sample - Steroids - ImmunoSuppressives
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What is Glomerular Disease Summary?
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What is Glomerular Disease Summary? 1 Chronic, 2 Not from Toxin_Drugs, 3 All Potentially Nephrotic, 4 Biopsy Sample, 5 Steroids often
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What is the difference between Glomerulonephritis and Nephrotic syndrome?
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What is the difference between Glomerulonephritis and Nephrotic syndrome? The degree or amount of Proteinuria is the main difference between Glomerulonephritis and Nephrotic syndrome.
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Glomerular disease Lx?
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Glomerular disease Lx? 1 UA with Hematuria, 2 Dysmorphic Red cell (Squeeze through abnormal glomerulus), 3 Red Cell Casts, 4 Proteinuria, 5 UNa and FeNa are Low
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What are individual glomerular disease? Their general presentation?
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What are individual glomerular disease? 1 Goodpasture Syndrome, 2 IgA Nephropathy (Berger disease), 3 PostInfectious Glomerulonephritis, 4 Alport Syndrome, 5 Polyarteritis Nodosa, 6 Lupus Nephritis, 7 Amyloidosis. Their general presentation? 1 Proteinuria, 2 RBC, 3 RBC Cast in Urine, 4 Edema, 5 Hypertension.
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What is Goodpasture Syndrome? Px? Lx? Tx?
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What is Goodpasture Syndrome? Glomerular disease. Px? 1 Lung (No Upper Respiratory Tract involvement). No Skin, Joint, GI, Eye, or Neurological involvement. Lx? Best Initial - 1 AntiGlomerular Basement Membrane Antibodies. MA - 2 Lung or Kidney Biopsy - Linear Deposits in Kidney biopsy. Anemia is often present from chronic blood loss from hemoptysis. Tx? 1 Plasmapheresis, and 2 Steroids. 3 Cyclophosphamide can be helpful.
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What is IgA Nephropathy? Px? Lx? Tx?
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What is Goodpasture Syndrome? Aka Berger Disease. Most Common Cause of Acute Glomerulonephritis. Px? 1 Asian, 2 Recurrent Episodes of Gross Hematuria 1-2 Days after Upper Respiratory Tract Infection (Synpharyngitic). Lx? 1 IgA Increased in only 50 perc. MA - 2 Kidney Biopsy. Tx? None. 30 perc resolves completly. 50 perc slowly progress to End-Stage Renal Disease. Severe Proteinuria Tx - 1 ACEI and 2 Steroids. 3 Fish Oil might help. More Proteinuria - Worse Progression.
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Contrast IgA nephropathy and Post-Streptococcal Glomerulonephritis.
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Contrast IgA nephropathy (Follows Upper Respiratory Tract infection by 1-2 Days) and Post-Streptococcal Glomerulonephritis (follows Pharyngitis by 1-2 Weeks).
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Kidney Biopsy shows Linear Deposit. Dx?
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Kidney Biopsy shows Linear Deposit. Dx? Goodpasture syndrome
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What is the most common cause of acute glomerulonephritis?
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What is the most common cause of acute glomerulonephritis? IgA Nephropathy (Berger Disease)
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What is PostInfectious Glomerulonephritis? Px? Lx? Tx?
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What is PostInfectious Glomerulonephritis? Most Common organism - Streptococcus. Any infection can lead to abnormal activation of immune system. Post Strep Glomerulonephritis (PSGN) follows 1 Throat Infection or 2 Skin Infection (Impetigo) by 1-3 Weeks. Px? 1 Dark (Cola-Colored) Urine, 2 Edema - Often Periorbital, 3 Hypertension, 4 Oliguria. Lx? 1 UA with Proteinuria, Red cells, Red Cell Casts - Glomerulonephritis. PSGN - Group A Beta Hemolytic Strep (Pyogenes) - confirmed by 2 AntiStreptolysin O (ASO) Titers, and 3 Anti-DNAse Antibody Titers. MA - Biopsy. Complement levels are Low in PSGN. Tx? Supportive - 1 Antibiotics, 2 Diuretics - Control fluid overload.
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What is Alport syndrome? Px? Lx? Tx?
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What is Alport syndrome? Congenital Defect of Type 4 Collagen. Px? 1 Sensorineural Hearing Loss, 2 Visual Disturbance - defect holding the Lens of eye in place. Tx? None.
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What is Polyarteritis Nodosa? Px? Lx? Tx?
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What is Polyarteritis Nodosa? Systemic Vasculitis of Small and Medium Sized arteries. Most Commonly affects Kidney. Every organ can be affected, but Spare the Lung. Associate wtih Hepatitis B. Px? 1 Glomerulonephritis, 2 NonoSpecific symptoms (Fever, Malaise, Weight Loss, Myalgias, and Arthralgia developing over Weeks to Months). 2 Common organ involved - aaa GI (Abdominal Pain, Nausea, Pain worsen by Eating), bbb Neurologic - More than One Large peripheral Nerve involved - MonoNeuritis Multiplex. Stroke in Young person. ccc Skin - Purpur, Petechiae, Ulcers, Digital gangrene, livedo reticularis. ddd Cardiac Disease. Lx? 1 Blood test - Anemia, Elevated ESR and C-reactive protein, ANCA (not present in most cases), ANA and Rheumatoid factor (Sometimes present in Low titer). 2 Best Initial - Angiography (Renal, Mesenteric, or Hepatic Artery showing aneurysmal dilation asso with new-onset Hypertension). 3 MA - Biopsy - symptomatic site (Skin, Nerves, or Muscles). Tx? 1 Prednisone, and 2 Cyclophosphamide. Tx Hepatitis B when found.
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What disease is polyarteritis nodosa associated with?
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What disease is polyarteritis nodosa associated with? Hepatitis B
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Stroke or MI in a Young person. Dx?
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Stroke or MI in a Young person. Dx? Polyarteritis Nodosa.
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What is Lupus Nephritis? Px? Lx? Tx?
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What is Lupus Nephritis? SLE can give Any Degree of Renal Involvement. Px? Mild - asymptomatic proteinuria. Severe - Membranous Glomerulonephritis. Long-standing SLE - Scar kidney - Glomerulosclerosis - Reuire Dialysis. Lx? MA - Biopsy - guide Tx. Mild Inflammatory changes - Tx 1 Glucocorticoids. Severe - Proliferative disease (Membranous Nephropathy) - Tx 2 Glucocorticoids and 3 Cyclophosphamide or 4 Mycophenolate.
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What is the purpose of biopsy in Lupus?
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What is the purpose of biopsy in Lupus? Guide intensity of Tx
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What is Amyloidosis? Px? Lx? Tx?
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What is Amyloidosis? Amyloid is Abnormal Portein. Produced in asso with - 1 Myeloma, 2 Chronic Inflammatory Diseases, 3 Rheumatoid Arthritis, 4 Inflammatory Bowel disease, 5 Chronic Infections. There is also a Primary form - protein is produced for unknown reasons. Kidney is primary target of protein. Lx? MA - 1 Biopsy - Green Birefringence with Congo Red Staining. Tx? 1 Control Underlying disease. If No Primary disease to Control - 1 Melphalan and 2 Prednisone
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What diseases is Amyloid associated with?
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What diseases is Amyloid associated with? 1 Myeloma, 2 Chronic Inflammatory Diseases, 3 Rheumatoid Arthritis, 4 Inflammatory Bowel disease, 5 Chronic Infections
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What disease gives Large Kidney on Sonogram and CT?
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What disease gives Large Kidney on Sonogram and CT? 1 Amyloid, 2 HIV Nephropathy, 3 Polycystic Kidneys, and 4 Diabetes
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Biopsy shows Green Birefringence with Congo red staining. Dx?
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Biopsy shows Green Birefringence with Congo red staining. Dx? Amyloidosis
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What does massive proteinuria leads to?
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What does massive proteinuria leads to? 1 Edema, 2 Hyperlipidemia, 3 Thrombosis (Urinary loss of natural anticoagulants Protein C and S, and AntiThrombin)
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What is the most common cause of nephrotic syndrome?
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What is the most common cause of nephrotic syndrome? 1 Diabetes, and 2 Hypertension
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What kind of kidney disease does SLE has?
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What kind of kidney disease does SLE has? Mild - asymptomatic proteinuria. Severe - Membranous Glomerulonephritis. Long-standing SLE - Scar kidney - Glomerulosclerosis - Reuire Dialysis.
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Cancer of solid organ . Neprotic syndrome Association?
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Cancer of solid organ . Neprotic syndrome Association? Membranous
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Children . Neprotic syndrome Association?
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Children . Neprotic syndrome Association? Minimal Change Disease
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Injection Drug Use . Neprotic syndrome Association?
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Injection Drug Use . Neprotic syndrome Association? Focal-Segmental
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AIDS . Neprotic syndrome Association?
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AIDS . Neprotic syndrome Association? Focal-Segmental
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NSAIDs . Neprotic syndrome Association?
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NSAIDs . Neprotic syndrome Association? Minimal Change Disease
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SLE . Neprotic syndrome Association?
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SLE . Neprotic syndrome Association? Any of them
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Membranous . Characteristic Association?
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Membranous . Characteristic Association? Cancer of solid organ
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Minimal Change Disease . Characteristic Association?
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Minimal Change Disease . Characteristic Association? Children
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Focal-Segmental . Characteristic Association?
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Focal-Segmental . Characteristic Association? Injection Drug Use
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Focal-Segmental . Characteristic Association?
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Focal-Segmental . Characteristic Association? AIDS
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Minimal Change Disease . Characteristic Association?
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Minimal Change Disease . Characteristic Association? NSAIDs
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Any of them . Characteristic Association?
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Any of them . Characteristic Association? SLE
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What is the difference between Nephritic and Nephrotic?
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What is the difference between Nephritic and Nephrotic? The amount of Proteinuria
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What is nephrotic syndrome? Etiology? Px? Lx? Tx?
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What is nephrotic syndrome? Nephrotic syndrome is a measure of Severity of Proteinuria in asso with any form of glomerular disease. Nephrotic syndrome occurs when Proteinuria is So Massive that Liver can No longer Increase Production of Abuminto Compensate for Urinary losses. Nephrotic syndrome - 1 HypoProteinuria (More than 3.5 grams per 24 hours), 2 HypoProteinemia, 3 HyperLipidemia (proteins to signal stop production loss), 4 Edema. Massive proteinuria leads to 1 Edema, 2 Hyperlipidemia, 3 Thrombosis (urinary loss of Anticoagulants Protein C, and S, and Antthrombin. Etiology? Diabetes and Hypertension are most common causes of nephrotic syndrome. Any Glomerular disease can lead to massive proteinuria. Cancer of Solid organ asso Membranous. Children asso Minimal Change Disease. Injection Drug Use and AIDS asso Focal-Segmental. NSAIDs asso Minimal Change Disease and Membranous. SLE asso with any of them. Px? 1 Generalized Edema, 2 Infection - frequent (Increase urinary loss of Ig and Complemnt). 3 Clots - more common (Loss of Antithrombin, Protein C and S). Lx? 1 UA, 2 Urine Albumin to Creatinine Spot Urine ratio (Equal to 24-Hour Urine). MA - 3 Renal Biopsy. Tx? 1 Glucocorticoids. If No response after several weeks, 2 Cyclophosphamide. 3 ACE or ARB - Control Proteinuria. Edema - 4 Salt Restriction, and 5 Diuretics. Hyperlipidemia - 6 Statins.
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What is nephrotic syndrome defined?
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What is nephrotic syndrome defined? Nephrotic syndrome - 1 HypoProteinuria (More than 3.5 grams per 24 hours), 2 HypoProteinemia, 3 HyperLipidemia, 4 Edema.
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Periorbital edmea. Dx?
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Periorbital edmea. Dx? Nephrotic Syndrome
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Contrast CHF and Nephrotic pt?
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Contrast CHF and Nephrotic pt? CHF (Edema of Dependent area - legs). Nephrotic pt (Edema every where)
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What is Maltese crosses?
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What is Maltese crosses? Maltese crosses are lipid deposits in sloughed-off tubular cells on UA.
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What is the most common cause of ESRD?
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What is the most common cause of ESRD? 1 Diabetes, and 2 Hypertension
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What is Uremia?
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What is Uremia? Uremia - CNS, Heart, H+, K+, H2O. 1 Encephalopathy, 2 Pericarditis, 3 Metabolic Acidosis, 4 HyperKalemia, 5 Fluid Overload
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ESRD manifestation - Anemia . Tx?
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ESRD manifestation - Anemia . Tx? 1 Erythropoietin Replacement, and 2 Iron Supplementation
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ESRD manifestation - Hypocalcemia and Osteomalacia . Tx?
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ESRD manifestation - Hypocalcemia and Osteomalacia . Tx? 1 Replace Vitamin D, and 2 Calcium
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ESRD manifestation - Bleeding . Tx?
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ESRD manifestation - Bleeding . Tx? 1 DDAVP Increases Platelet function. Use only when bleeding.
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ESRD manifestation - Pruritus . Tx?
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ESRD manifestation - Pruritus . Tx? 1 Dialysis, and 2 Ultraviolet Light
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ESRD manifestation - Hyperphosphatemia . Tx?
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ESRD manifestation - Hyperphosphatemia . Tx? Oral Binders - 1 Calcium Acetate, 2 Calcium Carbonate, 3 Sevelamer, 4 Lanthanum
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ESRD manifestation - Hypermagnesemia . Tx?
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ESRD manifestation - Hypermagnesemia . Tx? Restriction of 1 High-Magnesium food, 2 Laxatives, and 3 Antacids
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ESRD manifestation - Atherosclerosis . Tx?
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ESRD manifestation - Atherosclerosis . Tx? Dialysis
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ESRD manifestation - Endocrinopathy . Tx?
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ESRD manifestation - Endocrinopathy . Tx? 1 Dialysis, 2 Estrogen, and 3 Testosterone replacement
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What are manifestations of Renal failure?
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What are manifestations of Renal failure? 1 Anemia, 2 Hypocalcemia, 3 Osteodystrophy, 4 Bleeding, 5 Infection, 6 Pruritus, 7 Hyperphosphatemia, 8 Hypermagnesemia, 9 Accelerated Atherosclerosis, and Hypertension, 10 Endocrinopathy. Detail - 1 Anemia (Loss of Erythropoietin), 2 Hypocalcemia (kidney convert Vitamin D to more active form - calcium absorb from gut), 3 Osteodystrophy (Low calcium leads to Secondary hyperparathyroidism), 4 Bleeding (Platelets do Not work normally in Uremia), 5 Infection (Neutrophils can degranulate), 6 Pruritus (urea in skin is itchy), 7 Hyperphosphatemia (High PTH release phosphat from bone, but kidney cannot excrete), 8 Hypermagnesemia (loss of excretory ability), 9 Accelerated Atherosclerosis, and Hypertension (lipid accumulation cause HTN. Most common cause of death on dialysis), 10 Endocrinopathy (Women Anovulatory. Men have Low Testosterone. Erectile dysfunction. Insulin levels goes up because insulin is excreted renally).
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What is most common cause of death on dialysis?
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What is most common cause of death on dialysis? Accelerated Atherosclerosis, and Hypertension (lipid accumulation cause HTN. Most common cause of death on dialysis
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What is ESRD? Etiology? Px?
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What is ESRD? ESRD or Chronic Renal Failure - form of kidney failure so Severe as to need Dialysis or Renal Transplantation. ESRD - loss of renal function leading to a collection of symptoms and abnormalities - Uremia. Etiology? Any form of 1 Tubular or 2 Glomerular damage can cause ESRD. Diabetes and Hypertension are more common than all other causes. Chronic - disease present for years. Rapidly Progressive Glomerulonephritis can lead to ESRD over weeks. Px? Uremia - 1 Encephalopath, 2 Pericarditis, 3 Metabolic Acidosis, 4 Hyperkalemia, 5 Fluid Overload.
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What can lead to ESRD over weeks?
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What can lead to ESRD over weeks? Rapidly Progressive Glomerulonephritis can lead to ESRD over weeks.
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When is Erythropoietin the only
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When is the only time Erythropoietin always used as Tx? Anemia from ESRD is the only time Erythropoietin is always used
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Hyperphosphatemia Tx?
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Hyperphosphatemia Tx? Hyperphosphatmia due to Hypocalcemia, which lead to Hyperparathyroidism that causes increased phosphate release from bone. When Vitamin D is replaced to control hypocalcemia, it is critical to also give phosphate binders. Vitamin D will increase GI absorption of phosphate. Oral Phosphate binders - 1 Calcium acetate, 2 Calcium carbonat, 3 Sevelamer, 4 Lanthanum. Sevelamer and Lanthanum are used when Calcium is High.
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What is Aluminum containing phosphate binders AE?
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What is Aluminum containing phosphate binders AE? Dementia.
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What phosphate binders to used when High calcium?
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What phosphate binders to used when High calcium? Sevelamer, or Lanthanum
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How long does HLA-identical, Related donor kidneys last on average?
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How long does HLA-identical, Related donor kidneys last on average? 24 years
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Contrast Simple and Complex cyst. Echogenicity, Walls, Demarcation, Transmission.
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Contrast Simple and Complex cyst. Simple Cyst - Echogenicity (Echo Free), Walls (Smooth, Thin), Demarcation (Sharp), Transmission (Go through to back). Complex - potential malignancy. Complex cyst - Echogenicity (Mixed echogenicity), Walls (Irregular, Thick), Demarcation (Lower Density on back wall), Transmission (Debris in cyst).
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Polycystic kidney disease Px? Most common cause of death? organs affected? Tx?
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Polycystic kidney disease Px? PCKD - 1 Pain, 2 Hematuria, 3 Stones, 4 Infection, 5 Hypertension. Most common cause of death - Renal Failure due to recurrent episodes of Pyelonephritis and Nephrolithiasis causing progressive scarring and loss of renal function. Extra Renal manifestation - 1 Cerebral Aneurysms, 2 Liver cysts (most common site outside kidney), 3 Ovarian cysts, 4 Mitral Valve prolapse, 5 Diverticulosis. Tx - None
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High volume nocturia. Dx?
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High volume nocturia. Dx? Diabetes Insipitus
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Sodium disorder Px - general?
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Sodium disorder Px - general? Sodium disorder - CNS problem.
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HyperKalemia Px - general?
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HyperKalemia Px - general? 1 Muscular and 2 Cardiac symptoms
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Increased urine volume despite dehydration and hyperosmolality. Dx?
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Increased urine volume despite dehydration and hyperosmolality. Dx? Diabetes Insipitus
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What does Positive Water Deprivation test means?
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What does Positive Water Deprivation test means? Positive Water Deprivation test means Urine Volume stays High despite Withholding Water.
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Hypernatremia Etiology? Px? Lx? Tx?
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Hypernatremia Etiology? Hypernatremia - Loss of Free Water. 1 Sweating, 2 Burns, 3 Fever, 4 Pneumonia (Hyperventilation loss), 5 Diarrhea, 6 Diuretics, 7 Diabetes Insipidus (CDI - Decreased ADH, and NDI - ADH resistance). Px? Sodium - CNS. Confusion, Disorientation, Lethargy, Seizures, Coma, and Brain damage. Lx? High serum sodium - Hyperosmolality. 1 Water Deprivation Test (DI - Urine Volume High without Drinking water, Urine Osmolality Low.), 2 Response to ADH given (CDI - Sharp Decrease in urine volume). MA - ADH level (CDI - Low ADH. NDI - High ADH). Tx? 1 Correct Underlying cause of Fluid Loss, 2 CDI - Replace ADH (Vasopressin - DDAVP), 3 NDI - Correct Potassium and Calcium, Stop Lithium or Demeclocycline, Give HCTZ or NSAIDs resistance. Complication of Tx - if sodium level is brought down too rapidly, Cerebral Edema will occur. Fluid goes from vascular space into breain cells. Cerebral Edema Px - worsening confusion and seizures.
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What are causes of NDI?
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What are causes of NDI? 1 Lithium, 2 Demeclocycline, 3 Chronic Kidney disease, 4 Hypokalemia, 5 Hypercalcemia. They make ADH ineffective on tubule.
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Contrast CDI and NDI. Polyuria and Nocturia, Urine Osmolality and Sodium, Positive Water Deprivation test, Response to ADH, ADH level
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Contrast CDI and NDI. CDI - Polyuria and Nocturia (Yes), Urine Osmolality and Sodium (Low), Positive Water Deprivation test (Yes), Response to ADH (Yes), ADH level (Low). NDI - Polyuria and Nocturia (Yes), Urine Osmolality and Sodium (Low), Positive Water Deprivation test (Yes), Response to ADH (No), ADH level (High)
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Polyuria and Nocturia (Yes), Urine Osmolality and Sodium (Low), Positive Water Deprivation test (Yes), Response to ADH (Yes), ADH level (Low). Dx?
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Polyuria and Nocturia (Yes), Urine Osmolality and Sodium (Low), Positive Water Deprivation test (Yes), Response to ADH (Yes), ADH level (Low). Dx? CDI
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Polyuria and Nocturia (Yes), Urine Osmolality and Sodium (Low), Positive Water Deprivation test (Yes), Response to ADH (No), ADH level (High). Dx?
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Polyuria and Nocturia (Yes), Urine Osmolality and Sodium (Low), Positive Water Deprivation test (Yes), Response to ADH (No), ADH level (High). Dx? NDI
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What complication of Hypernatremia Tx?
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What complication of Hypernatremia Tx? If sodium level is brought down too rapidly, Cerebral Edema will occur. Fluid goes from vascular space into breain cells. Cerebral Edema Px - worsening confusion and seizures.
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What is Hyponatremia? Px? Lx? Tx?
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What is Hyponatremia? Hyponatremia is grouped based on Body volume status. 1 Hypervolemia, 2 Hypovolemia, 3 Euvolemia. 1 Hypervolemia (aaa CHF, bbb Nephrotic syndrome, ccc Cirrhosis) - Intravascular volume depletion leads to Increased ADH levels. 2 Hypovolemia (aaa Sweating, bbb Burns, ccc Fever, ddd Pneumonia, eee Diarrhea, fff Diuretics) - also causes hypernatremia, but Chronic Replacement with Free Water - depletes body sodium. ggg Addison Disease - loss of adrenal function - loss of Aldosterone - lose Sodium. 3 Euvolemia (aaa Pseudohyponatremia - hyperglycemia, bbb Psychogenic polydipsia, ccc Hypothyroidism, ddd SIADH). aaa Pseudohyponatremia - Hyperglycemia - High glucose draw on fluid inside cell. Free water leaves cells to correct hyperosmolar serum - this drops sodium level. Every 100 glucose above normal, there is 1.6 decrease in sodium. Tx - Correct Glucose level. bbb Psychogenic polydipsia - massive ingestion of free water above 12 to 24 liters a day. Minimum urine osmolality is 50. Look for Bipolar disorder for Psychogenic polydipsia. ccc Hypothyroidism - thyroid hormone is needed to excrete water. If thyroid hormone level is low, free water excretion is decreased. ddd SIADH - Lung or Brain Disease, or drugs (SSRI, Sulfonylureas, Vincristine, Cyclophosphamide, or Tricyclic antidepressants). Small cell lung cancer produce ADH. Pain causes SIADH. Px? Sodium - CNS symptoms - Confusion, Lethargy, Disorientation, Seizures, Coma, Seizure. Lx? SIADH - 1 High Urine Osmolality. MA - 2 High ADH level. Tx? Hyponatremia Tx based on Symptom or Severity. 1 Mild Hyponatremia - No Symptoms - Tx - Restrict Fluids. 2 Moderate hyponatremia - Minimal Confusion - Tx - Saline and Loop Diuretic. 3 Severe Hyponatremia - Lethargy, Seizures, Coma - Tx - Hypertonic Saline, ADH antagonist (Conivaptan, Tolvaptan). In SIADH, Saline without Diuretic makes it worse. 4 Chronic SIADH - underlying disorder that cannot be corrected (Metastatic cancer) - Tx Demeclocycline for Chronic SIADH (Demeclocyline block action of ADH at Collecting duct of kidney tubule). Complications of Tx - Correction of Sodium must occur slowly (0.5 to 1 per hour, or 12 to 24 per day). If sodium level is brought up to normal too rapidly, CNS disorder - Central Pontine Myelinolysis or Osmotic Demyelinization occurs.
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How does hyperglycemia affect sodium level?
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How does hyperglycemia affect sodium level? Pseudohyponatremia - Hyperglycemia - High glucose draw on fluid inside cell. Free water leaves cells to correct hyperosmolar serum - this drops sodium level. Every 100 glucose above normal, there is 1.6 decrease in sodium.
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What are ADH antagonist meds?
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What are ADH antagonist meds? 1 Conivaptan, 2 Tolvaptan. They Tx Severe SIADH - Hyponatremia.
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What is Conivaptan? Tx for?
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What are ADH antagonist meds? 1 Conivaptan, 2 Tolvaptan. They Tx Severe SIADH - Hyponatremia.
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What is Tolvaptan? Tx for?
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What are ADH antagonist meds? 1 Conivaptan, 2 Tolvaptan. They Tx Severe SIADH - Hyponatremia.
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What is kidney collecting duct ADH blocker? Tx for?
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What is kidney collecting duct ADH blocker? Demeclocycline. Tx for Chronic SIADH
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What is cerebral edema a complication of?
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What is cerebral edema a complication of? Tx for Hypernatremia by bringing Sodium down too fast (giving fluid too fast.)
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What is Central Pontine Myelinolysis a complication of?
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What is Central Pontine Myelinolysis a complication of? Tx for Hyponatremia by bringing Sodium up too fast.
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What is Osmotic demyelinization a complication of?
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What is Osmotic demyelinization a complication of? Tx for Hyponatremia by bringing Sodium up too fast.
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What drugs cause SIADH?
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What drugs cause SIADH? 1 SSRI, 2 Sulfonylureas, 3 Vincristine, 4 Cyclophosphamide, 5 Tricyclic Antidepressants
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How fast can Sodium be brought up in Hyponatremia?
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How fast can Sodium be brought up in Hyponatremia? Slowly - 0.5 to 1 mEq per hour, or 12-24 mEq per day.
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What makes SIADH Tx worse?
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What makes SIADH Tx worse? Saline without a Diuretic makes it worse
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What is Hyponatremia?
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What is Hyponatremia? Hyponatremia is grouped based on Body volume status. 1 Hypervolemia, 2 Hypovolemia, 3 Euvolemia. 1 Hypervolemia (aaa CHF, bbb Nephrotic syndrome, ccc Cirrhosis) - Intravascular volume depletion leads to Increased ADH levels. 2 Hypovolemia (aaa Sweating, bbb Burns, ccc Fever, ddd Pneumonia, eee Diarrhea, fff Diuretics) - also causes hypernatremia, but Chronic Replacement with Free Water - depletes body sodium. ggg Addison Disease - loss of adrenal function - loss of Aldosterone - lose Sodium. 3 Euvolemia (aaa Pseudohyponatremia - hyperglycemia, bbb Psychogenic polydipsia, ccc Hypothyroidism, ddd SIADH). aaa Pseudohyponatremia - Hyperglycemia - High glucose draw on fluid inside cell. Free water leaves cells to correct hyperosmolar serum - this drops sodium level. Every 100 glucose above normal, there is 1.6 decrease in sodium. Tx - Correct Glucose level. bbb Psychogenic polydipsia - massive ingestion of free water above 12 to 24 liters a day. Minimum urine osmolality is 50. Look for Bipolar disorder for Psychogenic polydipsia. ccc Hypothyroidism - thyroid hormone is needed to excrete water. If thyroid hormone level is low, free water excretion is decreased. ddd SIADH - Lung or Brain Disease, or drugs (SSRI, Sulfonylureas, Vincristine, Cyclophosphamide, or Tricyclic antidepressants). Small cell lung cancer produce ADH. Pain causes SIADH.
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What is Hyponatremia Px? Lx? Tx?
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Hyponatremia Px? Sodium - CNS symptoms - Confusion, Lethargy, Disorientation, Seizures, Coma, Seizure. Lx? SIADH - 1 High Urine Osmolality. MA - 2 High ADH level. Tx? Hyponatremia Tx based on Symptom or Severity. 1 Mild Hyponatremia - No Symptoms - Tx - Restrict Fluids. 2 Moderate hyponatremia - Minimal Confusion - Tx - Saline and Loop Diuretic. 3 Severe Hyponatremia - Lethargy, Seizures, Coma - Tx - Hypertonic Saline, ADH antagonist (Conivaptan, Tolvaptan). In SIADH, Saline without Diuretic makes it worse. 4 Chronic SIADH - underlying disorder that cannot be corrected (Metastatic cancer) - Tx Demeclocycline for Chronic SIADH (Demeclocyline block action of ADH at Collecting duct of kidney tubule). Complications of Tx - Correction of Sodium must occur slowly (0.5 to 1 per hour, or 12 to 24 per day). If sodium level is brought up to normal too rapidly, CNS disorder - Central Pontine Myelinolysis or Osmotic Demyelinization occurs.
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What is Hyponatremia Tx?
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Hyponatremia Tx? Hyponatremia Tx based on Symptom or Severity. 1 Mild Hyponatremia - No Symptoms - Tx - Restrict Fluids. 2 Moderate hyponatremia - Minimal Confusion - Tx - Saline and Loop Diuretic. 3 Severe Hyponatremia - Lethargy, Seizures, Coma - Tx - Hypertonic Saline, ADH antagonist (Conivaptan, Tolvaptan). In SIADH, Saline without Diuretic makes it worse. 4 Chronic SIADH - underlying disorder that cannot be corrected (Metastatic cancer) - Tx Demeclocycline for Chronic SIADH (Demeclocyline block action of ADH at Collecting duct of kidney tubule). Complications of Tx - Correction of Sodium must occur slowly (0.5 to 1 per hour, or 12 to 24 per day). If sodium level is brought up to normal too rapidly, CNS disorder - Central Pontine Myelinolysis or Osmotic Demyelinization occurs.
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What is cause of Hyponatremia - Hypervolemia?
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What is cause of Hyponatremia - Hypervolemia? 1 Hypervolemia (aaa CHF, bbb Nephrotic syndrome, ccc Cirrhosis) - Intravascular volume depletion leads to Increased ADH levels.
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What is cause of Hyponatremia - Hypovolemia?
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What is cause of Hyponatremia - Hypovolemia? 2 Hypovolemia (aaa Sweating, bbb Burns, ccc Fever, ddd Pneumonia, eee Diarrhea, fff Diuretics) - also causes hypernatremia, but Chronic Replacement with Free Water - depletes body sodium. ggg Addison Disease - loss of adrenal function - loss of Aldosterone - lose Sodium.
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What is cause of Hyponatremia - Euvolemia?
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What is cause of Hyponatremia - Euvolemia? 3 Euvolemia (aaa Pseudohyponatremia - hyperglycemia, bbb Psychogenic polydipsia, ccc Hypothyroidism, ddd SIADH). aaa Pseudohyponatremia - Hyperglycemia - High glucose draw on fluid inside cell. Free water leaves cells to correct hyperosmolar serum - this drops sodium level. Every 100 glucose above normal, there is 1.6 decrease in sodium. Tx - Correct Glucose level. bbb Psychogenic polydipsia - massive ingestion of free water above 12 to 24 liters a day. Minimum urine osmolality is 50. Look for Bipolar disorder for Psychogenic polydipsia. ccc Hypothyroidism - thyroid hormone is needed to excrete water. If thyroid hormone level is low, free water excretion is decreased. ddd SIADH - Lung or Brain Disease, or drugs (SSRI, Sulfonylureas, Vincristine, Cyclophosphamide, or Tricyclic antidepressants). Small cell lung cancer produce ADH. Pain causes SIADH.
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What to look for in Psychogenic polydipsia?
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What to look for in Psychogenic polydipsia? Bipolar disorder
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Mild Hyponatremia - No Symptoms. Tx?
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Hyponatremia Tx based on Symptom or Severity. 1 Mild Hyponatremia - No Symptoms - Tx - Restrict Fluids. 2 Moderate hyponatremia - Minimal Confusion - Tx - Saline and Loop Diuretic. 3 Severe Hyponatremia - Lethargy, Seizures, Coma - Tx - Hypertonic Saline, ADH antagonist (Conivaptan, Tolvaptan). In SIADH, Saline without Diuretic makes it worse. 4 Chronic SIADH - underlying disorder that cannot be corrected (Metastatic cancer) - Tx Demeclocycline for Chronic SIADH (Demeclocyline block action of ADH at Collecting duct of kidney tubule). Complications of Tx - Correction of Sodium must occur slowly (0.5 to 1 per hour, or 12 to 24 per day). If sodium level is brought up to normal too rapidly, CNS disorder - Central Pontine Myelinolysis or Osmotic Demyelinization occurs.
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Moderate hyponatremia - Minimal Confusion. Tx?
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Hyponatremia Tx based on Symptom or Severity. 1 Mild Hyponatremia - No Symptoms - Tx - Restrict Fluids. 2 Moderate hyponatremia - Minimal Confusion - Tx - Saline and Loop Diuretic. 3 Severe Hyponatremia - Lethargy, Seizures, Coma - Tx - Hypertonic Saline, ADH antagonist (Conivaptan, Tolvaptan). In SIADH, Saline without Diuretic makes it worse. 4 Chronic SIADH - underlying disorder that cannot be corrected (Metastatic cancer) - Tx Demeclocycline for Chronic SIADH (Demeclocyline block action of ADH at Collecting duct of kidney tubule). Complications of Tx - Correction of Sodium must occur slowly (0.5 to 1 per hour, or 12 to 24 per day). If sodium level is brought up to normal too rapidly, CNS disorder - Central Pontine Myelinolysis or Osmotic Demyelinization occurs.
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Severe Hyponatremia - Lethargy, Seizures, Coma. Tx?
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Hyponatremia Tx based on Symptom or Severity. 1 Mild Hyponatremia - No Symptoms - Tx - Restrict Fluids. 2 Moderate hyponatremia - Minimal Confusion - Tx - Saline and Loop Diuretic. 3 Severe Hyponatremia - Lethargy, Seizures, Coma - Tx - Hypertonic Saline, ADH antagonist (Conivaptan, Tolvaptan). In SIADH, Saline without Diuretic makes it worse. 4 Chronic SIADH - underlying disorder that cannot be corrected (Metastatic cancer) - Tx Demeclocycline for Chronic SIADH (Demeclocyline block action of ADH at Collecting duct of kidney tubule). Complications of Tx - Correction of Sodium must occur slowly (0.5 to 1 per hour, or 12 to 24 per day). If sodium level is brought up to normal too rapidly, CNS disorder - Central Pontine Myelinolysis or Osmotic Demyelinization occurs.
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Hyperkalemia Etiology? Px? Lx? Tx?
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Hyperkalemia Etiology? 1 Pseudohyperkalemia, 2 Decreased Excretion, 3 Release of Potassium from Tissues. 1 Pseudohyperkalemia (aaa Hemolysis, bbb Repeated fist clenching with Tourniquet in place, ccc Thrombocytosis or Leukocytosis) - do not need workup, 2 Decreased Excretion (aaa Renal Failure, bbb Aldosterone Decrease [bba ACEI, bbb RTA type 4, bbc Aldosterone inhibitors[Spironolactone, and Eplerenone], bbd Potassium-Sparing diuretics[Triamterene and Amiloride], bbe Addison disease]. 3 Release of Potassium from Tissues (aaa Tissue destruction [hemolysis, rhabdomyolysis, or tumor lysis syndrome.], bbb Decreased Insulin - insulin drives potassium into cell, ccc Acidosis, ddd BB and Digoxin - inhibit sodium_potassium ch that normally brings potassium into cell, eee Heparin - increase tissue release of potassium) . Px? Potassium disorder interfere with Muscle contraction and Cardiac Conductance. 1 Weakness, 2 Paralysis when Severe, 3 Ileus (paralyzes gut muscles), 4 Cardiac Rhythm disorders. Lx? 1 EKG - Severe Hyperkalemia - Peaked T Waves, Wide QRS, PR interal prolongation. Tx? Life-Threatenging Hyperkalemia (Abnormal EKG). 1 Calcium Chloride or Calcium Gluconate, 2 Insulin and Glucose - to drive potassium back into cells, 3 Bicarbonate - drives potassium into cell (should be used most when acidosis causes hyperkalemia). 4 Removing Potassium from body - Sodium Polystyrene Sulfonat - Kayexalate. Other methods to lower potassium - 5 Inhaled Beta Agonists (albuterol), 6 Loop diuretics, 7 Dialysis.
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Hyperkalemia Etiology?
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Hyperkalemia Etiology? 1 Pseudohyperkalemia, 2 Decreased Excretion, 3 Release of Potassium from Tissues. 1 Pseudohyperkalemia (aaa Hemolysis, bbb Repeated fist clenching with Tourniquet in place, ccc Thrombocytosis or Leukocytosis) - do not need workup, 2 Decreased Excretion (aaa Renal Failure, bbb Aldosterone Decrease [bba ACEI, bbb RTA type 4, bbc Aldosterone inhibitors[Spironolactone, and Eplerenone], bbd Potassium-Sparing diuretics[Triamterene and Amiloride], bbe Addison disease]. 3 Release of Potassium from Tissues (aaa Tissue destruction [hemolysis, rhabdomyolysis, or tumor lysis syndrome.], bbb Decreased Insulin - insulin drives potassium into cell, ccc Acidosis, ddd BB and Digoxin - inhibit sodium_potassium ch that normally brings potassium into cell, eee Heparin - increase tissue release of potassium) .
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Hyperkalemia Px?
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Hyperkalemia Px? Potassium disorder interfere with Muscle contraction and Cardiac Conductance. 1 Weakness, 2 Paralysis when Severe, 3 Ileus (paralyzes gut muscles), 4 Cardiac Rhythm disorders.
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Hyperkalemia Lx?
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Hyperkalemia Lx? 1 EKG - Severe Hyperkalemia - Peaked T Waves, Wide QRS, PR interal prolongation.
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Hyperkalemia Tx?
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Hyperkalemia Tx? Life-Threatenging Hyperkalemia (Abnormal EKG). 1 Calcium Chloride or Calcium Gluconate, 2 Insulin and Glucose - to drive potassium back into cells, 3 Bicarbonate - drives potassium into cell (should be used most when acidosis causes hyperkalemia). 4 Removing Potassium from body - Sodium Polystyrene Sulfonat - Kayexalate. Other methods to lower potassium - 5 Inhaled Beta Agonists (albuterol), 6 Loop diuretics, 7 Dialysis.
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Life Threatening Hyperkalemia with Abnormal EKG. Tx?
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Hyperkalemia Tx? Life-Threatenging Hyperkalemia (Abnormal EKG). 1 Calcium Chloride or Calcium Gluconate, 2 Insulin and Glucose - to drive potassium back into cells, 3 Bicarbonate - drives potassium into cell (should be used most when acidosis causes hyperkalemia).
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What does EKG for severe Hyperkalemia show?
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What does EKG for severe Hyperkalemia show? Peaked T Waves, Wide QRS, PR interal prolongation.
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What is Hypokalemia Etiology? Px? Lx? Tx?
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What is Hypokalemia Etiology? 1 Decreased Intake, 2 Shift into cells, 3 Renal Loss, 4 GI loss. 1 Decreased Intake (uncommon), 2 Shift into cells (aaa Alkalosis, bbb Increased Insulin, 3 Beta Adrenergic Stimulation), 3 Renal Loss (aaa Loop Diuretics, bbb Increased Aldosterone [bba Primary Hyperaldosteronism, bbb Volume depletion raises aldosterone, bbc Cushing syndrome, bbd Bartter syndrome [salt loss in loop of Henle], bbe Licorice], ccc Hypomagnesemia, ddd RTA type 1 and 2) , 4 GI loss (aaa Vomiting, bbb Diarrhea, ccc Laxative abuse). Px? Problem with musclar contraction and cardiac conduction. 1 Weakness, 2 Paralysis, 3 Loss of Reflexes. Lx? EKG - U waves - hypokalemia. Ventricular ectopy (PVC), Flattened T waves, and ST depression. Tx? 1 Oral Potassium replacement. IV potassium replacement - slowly (can cause fatal arrhythmia)
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What is Hypokalemia Etiology?
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What is Hypokalemia Etiology? 1 Decreased Intake, 2 Shift into cells, 3 Renal Loss, 4 GI loss. 1 Decreased Intake (uncommon), 2 Shift into cells (aaa Alkalosis, bbb Increased Insulin, 3 Beta Adrenergic Stimulation), 3 Renal Loss (aaa Loop Diuretics, bbb Increased Aldosterone [bba Primary Hyperaldosteronism, bbb Volume depletion raises aldosterone, bbc Cushing syndrome, bbd Bartter syndrome [salt loss in loop of Henle], bbe Licorice], ccc Hypomagnesemia, ddd RTA type 1 and 2) , 4 GI loss (aaa Vomiting, bbb Diarrhea, ccc Laxative abuse).
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What is Hypokalemia Px?
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What is Hypokalemia Px? Problem with musclar contraction and cardiac conduction. 1 Weakness, 2 Paralysis, 3 Loss of Reflexes.
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What is Hypokalemia Lx?
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What is Hypokalemia Lx? EKG - U waves - hypokalemia. Ventricular ectopy (PVC), Flattened T waves, and ST depression.
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What is Hypokalemia Tx?
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What is Hypokalemia Tx? 1 Oral Potassium replacement. IV potassium replacement - slowly (can cause fatal arrhythmia)
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EKG shows Peaked T wave. Dx?
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EKG shows Peaked T wave. Dx? Hyperkalemia
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EKG shows U wave. Dx?
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EKG shows U wave. Dx? Hypokalemia
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Hyperkalemia and abnormal EKG. Next Step?
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Hyperkalemia and abnormal EKG. Next Step? Protect the heart with Calcium Chloride or Gluconate. Instantaneous
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Pt is admitted with Vomiting and diarrhea from gastroenteritis. His volume status is corrected with intravenous fluids and the diarrhea resolves. His pH is 7.4 and his serum bicarbonate has normalized. Despite vigorous oral and intravenous replacement, his potassium level fails to rise. Next Step?
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Pt is admitted with Vomiting and diarrhea from gastroenteritis. His volume status is corrected with intravenous fluids and the diarrhea resolves. His pH is 7.4 and his serum bicarbonate has normalized. Despite vigorous oral and intravenous replacement, his potassium level fails to rise. Next Step? --- Check Magnesium level. Hypomagnesemia can lead to increased urinary loss of potassium. If magnesium is replaced, it will close up the magnesium-dependent potassium channels and stop urinary loss.
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Hypokalemia. Potassium replacement not correcting Hypokalemia. Next step?
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Hypokalemia. Potassium replacement not correcting Hypokalemia. Next step? Check Magnesium level. Magnesium dependent K channel problem.
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How long does it take for Kayexalate and dialysis to remove potassium in Hyperkalemia?
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How long does it take for Kayexalate and dialysis to remove potassium in Hyperkalemia? Hours to remove potassium
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How long does it take for Bicarbonate and Insulin to reduce Hyperkalemia?
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How long does it take for Bicarbonate and Insulin to reduce Hyperkalemia? 15 to 20 minutes
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What is formula for Anion Gap?
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What is formula for Anion Gap? AG is (Na+) - (Cl- and HCO3-). Normal AG is 6-12
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What disease is Metabolic Acidosis with Normal anion gap?
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What disease is Metabolic Acidosis with Normal anion gap? AG is (Na+) - (Cl- and HCO3-). UAG is (Na+) - (Cl-). Metabolic acidosis with a Normal anion gap - 1 RTA (UAG Positive), 2 Diarrhea (UAG Negative). They are normal anion gap because Cl- level rises. They are Hyperchloremic metabolic acidosis.
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What disease is Hyperchloremic metabolic acidosis?
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What disease is Metabolic Acidosis with Normal anion gap? AG is (Na+) - (Cl- and HCO3-). UAG is (Na+) - (Cl-). Metabolic acidosis with a Normal anion gap - 1 RTA (UAG Positive), 2 Diarrhea (UAG Negative). They are normal anion gap because Cl- level rises. They are Hyperchloremic metabolic acidosis.
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What is the function of Distal tubule in kidney?
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What is the function of Distal tubule in kidney? Excrete Acid (H+) into tubule. RTA type 1 has damaged Distal Tubule (Urine is Basic).
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What is the function of Proximal tubule in kidney?
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What is the function of Proximal tubule in kidney? Reabsorb Bicarbonate. RTA type 2 has damaged Proximal Tubule (beginning - Urine Basic. later - Urine Acidic)
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What is RTA type 1? Etiology? Px? Lx? Tx?
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What is RTA type 1? RTA 1 is Distal RTA. Distal Tubule is responsible for Excreting Acid (H+). Acid cannot be excreted, so Urine pH Rise. Etiology? Drugs (Amphotericin), and Autoimmune Diseases. 1 Amphotericin, 2 SLE, 3 Sjogren Syndrome. Px? 1 Urine pH High (Alkaline Urine), 2 Increased Formation of Kidney Stones (from Calcium Oxalate). Lx? 1 UA (High pH Above 5.5). MA - 2 Infuse Acid into Blood (Ammonium Chloride) - Urine pH High (Normal - healthy person Excrete Acid and Decrease Urine pH). Tx? 1 Replace Bicarbonate (Absorbed at proximal tubule) - Relatively easy to correct.
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What is RTA type 1? Etiology?
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What is RTA type 1? RTA 1 is Distal RTA. Distal Tubule is responsible for Excreting Acid (H+). Acid cannot be excreted, so Urine pH Rise. Etiology? Drugs (Amphotericin), and Autoimmune Diseases. 1 Amphotericin, 2 SLE, 3 Sjogren Syndrome.
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What is RTA type 1 Px?
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What is RTA type 1? RTA 1 is Distal RTA. Px? 1 Urine pH High (Alkaline Urine), 2 Increased Formation of Kidney Stones (from Calcium Oxalate).
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What is RTA type 1 Lx?
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What is RTA type 1? RTA 1 is Distal RTA. Lx? 1 UA (High pH Above 5.5). MA - 2 Infuse Acid into Blood (Ammonium Chloride) - Urine pH High (Normal - healthy person Excrete Acid and Decrease Urine pH).
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What is RTA type 1 Tx?
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What is RTA type 1? RTA 1 is Distal RTA. Tx? 1 Replace Bicarbonate (Absorbed at proximal tubule) - Relatively easy to correct.
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What is RTA type 2? Etiology? Px? Lx? Tx?
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What is RTA type 2? RTA 2 is Proximal RTA. Proximal tubule Reabsorb Bicarbonate. Proximal RTA has Decreased ability of kidney to Reabsorb Bicarbonate. Urine pH is High at beginning. Urine pH becomes Low later. Etiology? 1 Amyloidosis, 2 Myeloma, 3 Fanconi Syndrome, 4 Acetazolamide, or 5 Heavy Metals. Chronic metabolic Acidosis leaches Calcium out of Bones, and they become Soft (Osteomalacia). Px? Chronic metabolic Acidosis leaches Calcium out of Bones, and they become Soft (Osteomalacia). Lx? 1 Urine pH is variable (First - basic Above 5.5, Later Low Below 5.5). MA - 2 Evaluate Bicarbonate Malabsorption - give Bicarbonate and Testing Urine pH - Urine pH will Rise (Normal - Urine pH will Not Rise). Tx? Bicarbonate is not absorbed well in Proximal RTA - Difficult to Tx - 1 Give massive doses of Bicarbonate. 2 Thiazide Diuretics cause Volume Depletion - enhance bicarbonate reabsorption.
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What is RTA type 2? Etiology?
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What is RTA type 2? RTA 2 is Proximal RTA. Proximal tubule Reabsorb Bicarbonate. Proximal RTA has Decreased ability of kidney to Reabsorb Bicarbonate. Urine pH is High at beginning. Urine pH becomes Low later. Etiology? 1 Amyloidosis, 2 Myeloma, 3 Fanconi Syndrome, 4 Acetazolamide, or 5 Heavy Metals. Chronic metabolic Acidosis leaches Calcium out of Bones, and they become Soft (Osteomalacia).
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What is RTA type 2? Px?
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What is RTA type 2? RTA 2 is Proximal RTA. Px? Chronic metabolic Acidosis leaches Calcium out of Bones, and they become Soft (Osteomalacia).
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What is RTA type 2? Lx?
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What is RTA type 2? RTA 2 is Proximal RTA. Lx? 1 Urine pH is variable (First - basic Above 5.5, Later Low Below 5.5). MA - 2 Evaluate Bicarbonate Malabsorption - give Bicarbonate and Testing Urine pH - Urine pH will Rise (Normal - Urine pH will Not Rise).
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What is RTA type 2? Tx?
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What is RTA type 2? RTA 2 is Proximal RTA. Tx? Bicarbonate is not absorbed well in Proximal RTA - Difficult to Tx - 1 Give massive doses of Bicarbonate. 2 Thiazide Diuretics cause Volume Depletion - enhance bicarbonate reabsorption.
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What is RTA type 4? Etiology? Px? Lx? Tx?
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What is RTA type 4? RTA type 4 is HypoReninemia, HypoAldosteronism. RTA type 4 has Decreased amount or Effect of Aldosterone at kidney tubule. This leads to Loss of Sodium and Retention of Potassium and hydrogen ions. Etiology? 1 Addison disease, 2 Diabetes Nephropathy, 3 Renal Insufficiency, 4 Drugs (Spironolactone, ACEI, Amiloride, NSAIDs). Px? High Urine Sodium despite a Sodium depleted diet. Hyperkalemia. Lx? 1 Hyperkalemia. 2 High Urine Sodium. Tx? Fludrocortisone.
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What is RTA type 4? Etiology?
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What is RTA type 4? RTA type 4 is HypoReninemia, HypoAldosteronism. RTA type 4 has Decreased amount or Effect of Aldosterone at kidney tubule. This leads to Loss of Sodium and Retention of Potassium and hydrogen ions. Etiology? 1 Addison disease, 2 Diabetes Nephropathy, 3 Renal Insufficiency, 4 Drugs (Spironolactone, ACEI, Amiloride, NSAIDs).
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What is RTA type 4? Px?
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What is RTA type 4? RTA type 4 is HypoReninemia, HypoAldosteronism. Px? High Urine Sodium despite a Sodium depleted diet. Hyperkalemia.
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What is RTA type 4? Lx?
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What is RTA type 4? RTA type 4 is HypoReninemia, HypoAldosteronism. Lx? 1 Hyperkalemia. 2 High Urine Sodium.
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What is RTA type 4? Tx?
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What is RTA type 4? RTA type 4 is HypoReninemia, HypoAldosteronism. Tx? Fludrocortisone.
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What steroid has highest mineralocorticoids?
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What steroid has highest mineralocorticoids? Steroid has highest mineralocorticoids or Aldosteronelike effect - Fludrocortisone.
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How is Fludrocortisone unique in steroids?
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How is Fludrocortisone unique in steroids? Fludrocortisone has Highest Mineralocorticoids.
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What steroid has highest aldosterone like effect?
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What steroid has highest mineralocorticoids? Steroid has highest mineralocorticoids or Aldosteronelike effect - Fludrocortisone.
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What RTA has hypokalemia?
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What RTA has hypokalemia? RTA 1 (Distal), and RTA 2 (Proximal)
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What RTA has hyperkalemia?
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What RTA has hyperkalemia? RTA 4 Hyporeninemia, Hypoaldosteronism
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What is UAG on RTA?
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What is UAG on RTA? RTA has Positive UAG
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What is UAG on Diarrhea?
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What is UAG on Diarrhea? Diarrhea has Negative UAG
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What are metabolic acidosis with anion gap?
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What are metabolic acidosis with anion gap? Anion gap is Above 12. Metabolic acidosis with anion gap - LA MUD PIE. L - Lactate, A - Aspirin (Salicylate), M - Methanol (Formic Acid), U - Uremia, D - DKA (Ketoacids), P - (none), I - INH, E - Ethylene Glycol (Oxalic acid).
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Substance - Lactate . Cause? Lx? Tx?
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Substance - Lactate . Cause? Lx? Tx?1 Hypotension or 2 Hypoperfusion Lx? Blood Lactate level. Tx? Correct Hypoperfusion.
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Substance - Ketoacids . Cause? Lx? Tx?
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Substance - Ketoacids . Cause? Lx? Tx?1 DKA, 2 StarvationLx? Acetone level. Tx? Insulin and Fluids
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Substance - Oxalic acid . Cause? Lx? Tx?
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Substance - Oxalic acid . Cause? Lx? Tx?1 Ethylene Glycol overdoseLx? Crystals on UA. Tx? Fomepizole, Dialysis.
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Substance - Formic acid . Cause? Lx? Tx?
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Substance - Formic acid . Cause? Lx? Tx?1 Methanol overdoseLx? Inflamed Retina. Tx? Fomepizole, Dialysis.
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Substance - Uremia . Cause? Lx? Tx?
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Substance - Uremia . Cause? Lx? Tx?Renal failureLx? BUN, Creatinine. Tx? Dialysis.
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Substance - Salicylates . Cause? Lx? Tx?
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Substance - Salicylates . Cause? Lx? Tx?Aspirin overdoseLx? Aspirin level. Tx? Alkalinize Urine.
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Cause -Hypotension . Substance? Lx? Tx?
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Cause -Hypotension . Substance? Lx? Tx?LactateLx? Blood Lactate level. Tx? Correct Hypoperfusion.
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Cause -Hypoperfusion . Substance? Lx? Tx?
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Cause -Hypoperfusion . Substance? Lx? Tx?LactateLx? Blood Lactate level. Tx? Correct Hypoperfusion.
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Cause -DKA . Substance? Lx? Tx?
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Cause -DKA . Substance? Lx? Tx?KetoacidsLx? Acetone level. Tx? Insulin and Fluids
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Cause -Starvation . Substance? Lx? Tx?
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Cause -Starvation . Substance? Lx? Tx?KetoacidsLx? Acetone level. Tx? Insulin and Fluids
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Cause -Ethylene Glycol overdose . Substance? Lx? Tx?
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Cause -Ethylene Glycol overdose . Substance? Lx? Tx?Oxalic acidLx? Crystals on UA. Tx? Fomepizole, Dialysis.
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Cause -Methanol overdose . Substance? Lx? Tx?
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Cause -Methanol overdose . Substance? Lx? Tx?Formic acidLx? Inflamed Retina. Tx? Fomepizole, Dialysis.
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Cause -Renal failure . Substance? Lx? Tx?
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Cause -Renal failure . Substance? Lx? Tx?UremiaLx? BUN, Creatinine. Tx? Dialysis.
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Cause -Aspirin overdose . Substance? Lx? Tx?
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Cause -Aspirin overdose . Substance? Lx? Tx?SalicylatesLx? Aspirin level. Tx? Alkalinize Urine.
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What is ABG finding in Metabolic Acidosis?
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What is ABG finding in Metabolic Acidosis? pH, pCO2, Bicarb. 1 Decreased pH below 7.4, 2 Decreased pCO2 - Respiratory Alkalosis as compensation, 3 Decreased Bicarbonate
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What is Metabolic alkalosis - general?
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What is Metabolic alkalosis - general? Metabolic Alkalosis - Elevated Serum Bicarbonate level. Compensation - Respiratory Acidosis - Relative Hypoventilation - Increase pCO2
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"What is Metabolic alkalosis? Etiology? Lx?
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What is Metabolic alkalosis? Metabolic Alkalosis - Elevated Serum Bicarbonate level. Compensation -
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"What is Metabolic acidosis? Etiology? Lx?
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What is Metabolic alkalosis? 1 Normal Anion Gap (6-12) - RTA and Diarrhea. 2 Elevated Anion Gap (Above 12. AG increased if unmeasured anions driving bicarbonate level down) - LA MUD pIE. Etiology? L - Lactate, A - Aspirin (Salicylate), M - Methanol (Formic Acid), U -
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What is minute ventilation?
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What is minute ventilation? Minute Ventilation is (Respiratory rate) x (Tidal Volume)
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What is respiratory acidosis and alkalosis? Etiology?
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What is respiratory acidosis and alkalosis? Respiratory acid and base disturbances are easy to understand because they come down to single pathway of effect on Minute Ventilation. Etiology? 1 Respiratory Alkalosis - aaa Decreased pCO2, bbb Increased Minute Ventilation, ccc Metabolic acidosis as compensation. - 1 Anemia, 2 Anxiety, 3 Pain, 4 Fever, 5 Interstitial lung disease, 6 Pulmonary emboli. 2 Respiratory acidosis - aaa Increased pCO2, bbb Decreased Minute Ventilation, ccc Metabolic alkalosis as compensation. 1 COPD or Emphysema, 2 Drowning, 3 Opiate overdose, 4 Alpha 1-antitrypsin deficiency, 5 Kyphoscoliosis, 6 Sleep apnea or Morbid obesity
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