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[h] Nephrology System Flashcards

[i] Master this session in just 5 minutes.

[q] ………….. is a common cause of Acute Renal Failure that occurs due to decreased blood flow to kidneys. Lab findings show: serum BUN:Cr ratio> 20, urine Na (mEq/L): <20, EENa: <1%, and urine osmolarity (mOsm/kg): ˃ 500?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFByZXJlbmFsIGF6b3RlbWlhLg==[Qq]

[q] …………. is a common cause of Acute Renal Failure that occurs due to obstruction of urinary tract downstream from the kidney (bilateral). Lab findings show: serum BUN:Cr ratio> 20, urine Na (mEq/L): <20, EENa: <1%, and urine osmolarity (mOsm/kg): ˃ 500?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFBvc3RyZW5hbCBhem90ZW1pYSAoZWFybHkgc3RhZ2UpLg==[Qq]

[q] …………. is a common cause of Acute Renal Failure that occurs due to acute tubular necrosis . Lab findings show: serum BUN:Cr ratio <15, urine Na (mEq/L): >40, EENa: >2%, and urine osmolarity (mOsm/kg): <350?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEludHJhcmVuYWwgYXpvdGVtaWEu[Qq]

[q] Patients with intravascular volume depletion (congestive heart failure, diarrhea, excessive diuresis) and chronic kidney disease depend on renal prostaglandin production to dilate the afferent glomerular arteriole and maintain the glomerular filtration rate. Nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis, which can cause ………….. in at-risk patients.

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[q] ………. is the most common cause of acute renal failure (intrarenal azotemia).

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[f]IEFjdXRlIHR1YnVsYXIgbmVjcm9zaXMu[Qq]

[q] When the cause of prerenal azotemia persists, it can presents with clinical findings of ……….?

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[f]IElzY2hlbWljIEFjdXRlIHR1YnVsYXIgbmVjcm9zaXMu[Qq]

[q] Renal ischemia triggers hypoxic changes in tubular epithelial cells especially in …………….. decreasing their functional capacity.

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[f]IHByb3hpbWFsIHR1YnVsZXMgYW5kIHRoZSB0aGljayBhc2NlbmRpbmcgbGltYiBvZiBIZW5sZSYjODIxNztzIGxvb3Au

[q] Toxic agents (aminoglycosides, lead, myoglobinuria, ethylene glycol, radiocontrast dye, and urate) to renal tubules are particularly susceptible to …………?

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[q] The ………… phase of acute tubular necrosis corresponds to the original insult (ischemia or toxicity). In this phase renal tubule cell damage begins to evolve, but is not yet established, during this phase GFR starts to fall, and urine output decreases.

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[f]IFRoZSBpbml0aWF0aW9uIHBoYXNlLg==

[q] The ………… phase of acute tubular necrosis corresponds to established injury. In this phase the GFR stabilizes at a level well below normal, and urine output is low/absent. This phase usually lasts for 1 – 3 weeks. There is a risk of hyperkalemia, metabolic acidosis, and uremia. Light microscopy in this stage shows granular casts in the tubular lumina.

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[f]IFRoZSBtYWludGVuYW5jZSAob2xpZ3VyaWMpIHBoYXNlLg==

[q] The ………… phase of acute tubular necrosis corresponds to tubular re-epithelization and regain of renal function. This phase is characterized by abnormal diuresis due to increased GFR with abnormal tubular activity —-> volume and electrolytes depletion (polyuria, hypokalemia, and dehydration).

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[f]IFRoZSByZWNvdmVyeSAocG9seXVyaWMpIHBoYXNlIG9mIEFUTi4=

[q] Ethylene glycol is rapidly absorbed from the Gl tract and metabolized to:
…………… → precipitates as calcium oxalate crystals in the renal tubules.
…………… → toxic to renal tubules.

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[q] Positive blood on urine dipstick (a reaction that detects the heme pigment in both hemoglobin and myoglobin) in the absence of red blood cells on microscopic urinalysis of patient exposed to crush injury suggests ………………?

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[q] Whats is the most likely diagnosis?

32 years old patient present with fever, maculopapular rash and symptoms of acute renal failure one to three weeks after beginning treatment with sulfonamides + increased levels of eosinophils and IgE in serum + Lab findings show: serum BUN:Cr ratio <15, urine Na (mEq/L): >40, EENa: >2%, and urine osmolarity (mOsm/kg): <350?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEFjdXRlIGludGVyc3RpdGlhbCBuZXBocml0aXMu[Qq]

[q] NSAID-associated chronic renal injury is morphologically characterized by …………………..?

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[f]IHBhcGlsbGFyeSBuZWNyb3NpcyBhbmQgY2hyb25pYyBpbnRlcnN0aXRpYWwgbmVwaHJpdGlzLg==

[q] Acute colicky flank pain with abrupt onset of gross hematuria in a patient with family history of sickle cell disease suggests …………….?

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[q] ………………. is generalized dysfunction of proximal tubule cells of unclear cause. It presents with polyuria, polydipsia, dehydration, hypophosphatemia, hypokalemia and hypocalcemia and type II renal tubular acidosis. Abnormal bone formation with resultant growth impairment and failure to thrive. The bone defects result from acidosis, hypophosphatemia, and hypocalcemia.

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[f]IEZhbmNvbmkgU3luZHJvbWUu[Qq]

[q] …………….. is an inherited (Autosomal recessive) tubular defect of the sodium and chloride reabsorption in the thick ascending limb of the Henle loop (Affects Na/K/2Cl) cotransporter. Presents similarly to chronic loop diuretic use. Activated RAAS due to hypovolemia causes an increase in potassium and hydrogen ion secretion, leading to hypokalemia and metabolic alkalosis with hypercalciuria.

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[f]IEJhcnR0ZXIgc3luZHJvbWUu

[q] …………….. is an inherited (Autosomal recessive) tubular defect of the NaCl in DCT. Presents similarly to lifelong thiazide diuretics. Activated RAAS due to hypovolemia causes an increase in potassium and hydrogen ion secretion, leading to hypokalemia and metabolic alkalosis. Other electrolytes abnormalities are hypomagnesemia, and hypocalciuria.

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[q] …………….. is an inherited (Autosomal dominant) tubular defect that lead to ↑ activity of epithelial Na channel in collecting tubules —> ↑ Na reabsorption. Presents like hyperaldosteronism, but aldosterone is nearly undetectable (hypertension, hypokalemia, metabolic alkalosis, ↓ aldosterone). It can be treated with amiloride (by blocking Na channels in the cortical collecting tubule).

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

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[q] …………….. results from mutations in the gene which encodes the kidney isozyme of 11β-hydroxysteroid dehydrogenase (11β-HSD) that normally inactivates circulating cortisol to the less-active metabolite cortisone (inactive on the mineralocorticoid receptors). Presents with symptoms of hyperaldosteronism although low aldosterone level (hypertension, hypokalemia, metabolic alkalosis).

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[f]IFN5bmRyb21lIG9mIEFwcGFyZW50IE1pbmVyYWxvY29ydGljb2lkIEV4Y2Vzcy4gQ29ydGlzb2wgdHJpZXMgdG8gYmUgdGhlIFNBTUUgYXMgYWxkb3N0ZXJvbmUu[Qq]

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