kidney

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What drugs are associated with with acute interstitial nephritis?

5 P'S 1. Pee ( diuretics- e.g loop diuretics) 2. pain free ( NSAIDs) 3. PCNs and Cephalosporins 4. PPIs 5. rifamPin S-sulfa drugs

A 75-year-old man with endstage kidney disease presents to his primary care physician because of right leg pain. He states the pain began yesterday after he hit his right leg on his kitchen table. He states that he has had episodes of bone pain, joint pain, and multiple fractures since becoming dialysis-dependent 3 years ago. On examination, the patient is able to pinpoint the leg pain to the middle of his right femur. An X-ray of the right leg shows a fracture. There is an elevated serum parathyroid hormone level and hypocalcemia. A deficit in which of the following renal functions is most likely contributing to this patient's findings?

Ability to excrete phosphate. An increase in parathyroid hormone production in CKD (secondary hyperparathyrodism) is caused primarily by the reduction in phosphate excretion. reduced glomerular filtration rate in CKD leads to the accumulation of phosphate, and retained phosphate directly stimulates parathyroid hormone (PTH) production, causing secondary hyperparathyroidism. Additionally, increased serum phosphate binds free calcium, which can lead to hypocalcemia, which also increases PTH production. CKD also affects α1-hydroxylation of vitamin D2, the second hydroxylation step necessary to produce active vitamin D3. PTH also binds to osteoblasts and stimulates osteoblast expression of RANKL and inhibits osteoblast expression of osteoprotegerin. This stimulates osteoclast production and increases bone resorption. All these changes contribute to alterations in bone metabolism in CKD.

A 6-year-old boy is brought to his pediatrician's office by his mother. The primary complaint is "swelling in his face and legs" over the past day. His medical history includes no significant ailments, and he takes no medications on a regular basis. He does have severe food allergies to peanuts, tree nuts, milk, and eggs but no allergies to medication. His mother strongly opposes vaccination, and the child has not received any vaccinations in accordance with her wishes. His temperature is 98.7° F (37° C), pulse is 128/min, respiratory rate is 20/min, and blood pressure is 132/81 mm Hg. Physical examination is significant for edema in the periorbital area and bilateral lower extremities. Blood work is done, and urinalysis reveals the following: Color: dark yellow Clarity: cloudy pH: 4.6 Specific gravity: 1.013 Glucose: negative Ketones: negative Nitrites: negative Leukocyte esterase: negative Blood: negative Protein: 3+ Which of the following findings are most likely on microscopic immunofluorescence? most common in what group

Absence of complement or immunoglobulin deposits Minimal change disease is the most common cause of childhood nephrotic syndrome. Typical signs and symptoms include periorbital and peripheral edema, massive proteinuria, hypoalbuminemia, and hyperlipidemia. A kidney biopsy specimen appears normal (because of the absence of complement and immunoglobulin deposits) on light microscopy and immunofluorescence, but effacement of podocyte foot processes is visible on electron microscopy. Nephrotic sxs- fatty casts, (hyperlipidemia) sever pronteinuria usually (but in MCD only hypoalbuminuria) and periorbital edema from decreased ontotic Pressure. patient, presenting with peripheral and periorbital edema, is found to have proteinuria on urinalysis. He most likely has minimal change disease signs and symptoms include massive proteinuria, hypoalbuminemia, and hyperlipidemia.

what would the deposition/ presentation look like in PSGN? compare and contrast with IgA nephropathy? -Goodpasteur's syndrome?

Acute poststreptococcal glomerulonephritis (PSGN) can be confused with IgA nephropathy. Although the presentation of PSGN is similar to that of IgA nephropathy, PSGN occurs 2-4 weeks after a group A streptococcal pharyngitis or skin infection.Granular or linear IgG deposits can be seen in poststreptococcal glomerulonephritis. aside*** Deposition of IgM in the mesangial matrix is nonspecific. IgA nephropathy (also called Berger disease occurs concurrently with or shortly after an upper respiratory tract infection. Anti-glomerular basement membrane antibodies can be found in Goodpasture syndrome presents with hematuria and pulmonary hemorrhage.

A 36-year-old man presents to the clinic for an annual flu shot. He has been treated for hypertension with an angiotensin-converting enzyme inhibitor since age 30. He denies smoking and alcohol use. Family history is notable for his father requiring dialysis at age 50 and an older brother who recently underwent unilateral nephrectomy to decompress intra-abdominal organs. Vital signs are significant for a blood pressure of 135/90 mm Hg. An abdominal ultrasound reveals multiple cysts within the liver. Which of the following is this patient most at risk to develop?

Autosomal dominant polycystic kidney disease (ADPKD) typically manifests in adulthood with hypertension and cysts in the kidneys. It is associated with other systemic pathologies, such as berry aneurysms, liver cysts, diverticulosis, and mitral valve prolapse. wrong answers to not confuse with Hemangioblastomas are vascular malformations found in patients with von Hippel Lindau syndrome. Retinal hamartomas are characteristic tissue growths seen in patients with tuberous sclerosis.

A 22-year-old female college student is rushed to the emergency department by her roommate, who found her lying unconscious on her bed. The roommate is not familiar with the medical history of the patient but notes that she had been having excruciating menstrual cramps for several days, during which time she was taking an unspecified pain medication. A careful examination reveals no signs of trauma. Vital signs include a temperature of 38.2°C (100.8°F), respiratory rate of 37/min, blood pressure of 145/59 mm Hg, and pulse of 110/min. Selected laboratory test results show:Hematocrit: 34%Hemoglobin: 12.9 g/dL White blood cells: 8000/mm3Sodium: 145 mEq/LPotassium: 3.2 mEq/LAST: 20 IU/LALT: 30 IU/LChloride: 112 mEq/L Bicarbonate: 13 mEq/L Blood urea nitrogen: 14 mg/dL Creatinine: 0.9 mg/dL Glucose: 137 mg/dL Arterial blood gas analysis reveals a pH of 7.32, PCO2 of 24 mm Hg, and PO2 of 99 mm Hg. Qualitative analysis of β-human chorionic gonadotropin is negative. Which of the following is the most likely diagnosis? A.Acetaminophen toxicity B.Diabetic ketoacidosis C.Ethanol toxicity D.Opiate toxicity E.Pelvic inflammatory disease checkF.Salicylate toxicit

Common causes of anion gap metabolic acidosis include Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets or Isoniazid, Lactic acidosis, Ethylene glycol/ethanol toxicity, and Salicylate toxicity (MUDPILES). Her arterial blood gas test results reveal that she is experiencing metabolic acidosis (as indicated by the low pH and bicarbonate level). Additionally, this patient has an anion gap of 20 mEq/L (normal range is 8-16; anion gap = Na+ - [Cl- + HCO3- Salicylates, in particular, also cause a respiratory alkalosis by promoting hyperventilation (not solely compensatory but also a direct effect of salicylates), creating a mixed anion gap metabolic acidosis and respiratory alkalosis. This will result in a decreased PCO2. Using Winters formula, PCO2 = 1.5 × [HCO3-] + 8 ± 2, one can calculate that in appropriate respiratory compensation, the PCO2 would be 27.5 ± 2 mm Hg.

A 24-year-old woman with type 2 diabetes mellitus comes to her primary care physician's office for a follow-up visit. She does not report any concerns. Her daily blood sugars range from 100 to 130 mg/dL, and she follows a carbohydrate-restricted diet. The patient's last eye examination was 4 months ago, and findings were unremarkable. Her medications include lisinopril, metformin, and oral contraceptives. She denies changes in weight, excessive thirst or urination, peripheral neuropathy, and changes in vision. She does not smoke, drink alcohol, or use illicit substances. On physical examination, her temperature is 37.1° C (98.7° F), pulse is 82/min, respiratory rate is 14/min, and blood pressure is 133/80 mm Hg. She is 152.4 cm (5 ft) tall and weighs 85.3 kg (188 lb), with a body mass index of 36.7 kg/m2. Her heart rate is regular without murmurs, rubs, or gallops; and lungs are clear to auscultation bilaterally. All pulses are normal, and sensation is intact in all extremities. Which of the following is most appropriate means of monitoring for early renal disease in this patient? A.Measurement of fasting glucose concentration B.Measurement of hemoglobin A1c concentration C.Measurement of serum creatinine concentration D.Renal biopsy E.Serial blood pressure measurements F.Urinalysis G.Urine albumin concentration

DN is the leading cause of end-stage renal failure in the United States. The best test to screen for early-stage DN is measurement of the urine albumin concentration, which will reveal loss of GMB integrity leading to hyperfiltration.

What is the most common cause of chronic kidney disease in the US?

Diabetic nephropathy is the most common cause of chronic kidney disease in the US. Advanced disease shows nephrotic range proteinuria (>3.5 grams/24 hours) and progresses to end-stage renal disease, requiring renal replacement therapy.

A 51-year-old homeless woman is found unconscious and brought to the emergency department by paramedics. She is lethargic and difficult to arouse. She is admitted to the hospital and intravenous fluids are started. Several hours later, she is alert and reports no significant personal or family medical history; she takes no medications. She admits drinking alcohol earlier in the day and observed blood in her urine several hours later. Her temperature is 38° C (100.4° F ), blood pressure is 119/75 mm Hg, pulse is 105/min, and respiratory rate is 22/min. On physical examination. extraocular movements are intact and her pupils are equal, round, and reactive to light and accommodation. Laboratory studies show: Blood alcohol content: 205 mg/dL Glucose: 68 mg/dL BUN: 16 mg/dL Creatinine: 1.6 mg/dL Sodium: 135 mEq/L Potassium: 3.5 mEq/L Chloride: 98 mmol/L Bicarbonate: 17 mEq/L Which of the following is the most likely cause of the patient's presentation? A.Acetaminophen B.Aspirin C.Cocaine D.Ethylene glycol E.Heroin F.Methanol

Ethylene glycol is a main component of antifreeze and is converted to glycolic and oxalic acid by alcohol dehydrogenase. It results in a high anion gap metabolic acidosis and oxalate anions combine with calcium to produce calcium oxalate crystals that obstruct the renal tubules, causing renal failure and hematuria Methyl alcohol (ie, methanolThe patient does not present with any vision problems. Formic acid damages the optic nerve, causing optic neuritis and the potential for permanent blindness. Methyl alcohol consumption is not associated with hematuria and would not explain this patient's lab results. This patient presents with altered mental status, hematuria, elevated creatinine, and anion gap metabolic acidosis (AG =20 Meq/L). The patient admits to drinking alcohol earlier in the day but the type of alcohol has yet to be determined. Ethanol would explain her mental state, but is not the most likely cause. The patient's elevated creatinine indicates a kidney injury, which suggests ethylene glycol intoxication. Clinical manifestations of ethylene glycol poisoning include central nervous system sedation, high anion gap metabolic acidosis, flank pain, hematuria, and formation of oxalate crystals. Oxalate anions combine with calcium to produce calcium oxalate crystals that obstruct the renal tubules, causing acute tubular necrosis secondary to nephrotoxic injury, which explains the patient's creatinine and BUN levels. Calcium oxalate crystals also cause hematuria Ethylene glycol poisoning can be treated with sodium bicarbonate if severely acidotic, however, fomepizole and hemodialysis are the primary treatment options to remove toxic metabolites .

A 22-year-old man comes to the emergency department because of hemoptysis, increasing fatigue and breathlessness for three weeks. He has no history of prior medical illness. His temperature is 37.0C (98.6F), pulse is 84/min and blood pressure is 151/96 mm Hg. On examination, he has bilateral inspiratory crackles and bilateral pitting edema in his feet.Urinalysis shows:Protein: +2Blood: +3Red blood cells: 75-100/hpfDysmorphic red blood cells +Casts: noneChest X-ray shows diffuse opacities in both lower lung fields. Which of the following is the most likely diagnosis?

Goodpasture syndrome is a rare autoimmune disorder in which antibodies directed against glomerular basement membrane antigen cause a rapidly progressive glomerulonephritis. The clinical presentation includes acute hematuria, pallor, edema, dyspnea, cough, and hemoptysis. 22-year-old man presents with an initial episode of hemoptysis, high blood pressure, bilateral edema and diffuse opacities in both lungs seen on an x-ray. Urinalysis shows a high red blood cell (RBC) count with dysmorphic RBCs, pointing to inflammation of the kidney. This finding and the patient's other symptoms support a diagnosis of Goodpasture syndrome, a rare autoimmune disorder in which antibodies directed against glomerular basement membrane (GBM) antigen cause a rapidly progressive glomerulonephritis. Hemoptysis occurs if antibodies are deposited in the alveolar basement.

what are causes of normal anion gap metabolic acidosis?

HARDASS H-yperchloremia/hyperalimentation A-ddison disease R-enal tubular acidosis D-iarrhea A-cetazolamide S-pironolactone S-aline infusion

A 55-year-old man is admitted to the hospital because of complications of alcoholic cirrhosis and concurrent hepatitis Cinfection. Vital signs are: temperature 99° F (37.2° C); pulse, 80/min; blood pressure, 110/80 mm Hg; respiratory rate, 24/min; oxygen saturation, 98% on room air. Basic metabolic panel and urine electrolyte values are as follows: Glucose: 121 mg/dL Sodium: 132 mEq/L Potassium: 4.5 mEq/L Chloride: 90 mEq/L CO2: 38 mEq/L BUN: 121 mg/dL Creatinine: 3.8 mg/dL Calcium: 7.8 mEq/L Urine sodium: 5 mEq/L Urine potassium: 29 mEq/L Urine creatinine: 53 mg/dL Urine osmolality: 641 mOsm/kg Total urine output for the day has decreased to less than 300 mL. There is no evidence of proteinuria or hematuria. Which of the following would most likely be present on imaging of this patient's kidneys? A.Enlarged cystic kidneys B.Enlarged kidneys with severe hydronephrosis C.Horseshoe kidneys D.Normal kidneys with a "flea-bitten" infarcted appearance E.Normal size and shape

Hepatorenal syndrome is a progressive functional renal failure caused by a reduction in the glomerular filtration rate due to declining liver function. Kidney anatomy is completely unaffected, and thus visualization of the kidneys with use of most modalities would reveal normal size and shape. Horseshoe kidneys are usually an isolated finding and asymptomatic. This condition is not associated with hepatorenal disease nor does it put a patient with liver cirrhosis at higher risk for developing hepatorenal syndrome. causes a prerenal type of azotemia, evidenced by the patient's blood urea nitrogen/creatinine ratio > 21 and a fractional excretion of sodium (FeNa) of 0.3% Enlarged cystic kidneys are seen in patients with polycystic kidney disease, which can present with flank pain, hematuria, hypertension, urinary tract infections, and progressive kidney failure. Systemic manifestations include berry aneurysms, mitral valve prolapse, and hepatic cysts, none of which are manifest in this patient. Enlarged kidneys with severe hydronephrosis can be present in patients with an obstruction caused by benign prostatic hypertrophy or a stone in the calyxes. Normal kidneys with a "flea-bitten" infarcted appearance are characteristic of patients with malignant hypertension.

A previously healthy 63-year-old man comes to his primary care doctor for an initial evaluation. He has a history of hypertension well controlled in the past with amlodipine. He also has hyperlipidemia managed with atorvastatin. His temperature is 36.9°C (98.4°F), pulse is 78/min, respirations are 18/min, and blood pressure is 170/110 mm Hg. On physical examination, an abdominal bruit is heard left of the midline. Which of the following laboratory abnormalities is most likely to be seen in this patient as a result of his underlying medical condition? Describe the pathogenesis mechanism.

Hypokalemia Renal artery stenosis can lead to resistant hypertension and hypokalemia caused by activation of the renin-angiotensin-aldosterone system. sudden increase in well-controlled blood pressure or new hypertension in a patient over 60 suggests secondary hypertension. bruit (blowing vascular sounds resembling heart murmurs that are perceived over partially occluded blood vessels) is heard left of the midline on auscultation of the abdomen, raising concern for renal artery stenosis(RAS). RAS inhibits blood flow to the kidney. decreased perfusion causes juxtaglomerular cells to release renin, which cleaves angiotensinogen into angiotensin I. Angiotensin-converting enzyme (ACE) in the alveolar capillaries converts angiotensin I to angiotensin II, which stimulates vasoconstriction, sympathetic activity, tubular reabsorption of sodium and water, and secretion of aldosterone from the adrenal cortex. Aldosterone leads to sodium reabsorption and potassium excretion (potassium wasting). All of these mechanisms lead to hypertension and potential development of hypokalemia I incorrectly chose hypernatremia patient has a condition that would increase sodium reabsorption, but not usually cause hypernatremia since water is absorbed as well.

What charachterizes Bergers' disease? Lab presentations (2) Deposition in golmeruli?

IgA nephropathy (Berger disease) is characterized by glomerulonephritis, shortly after or concurrently with an upper respiratory tract infection. Patients present with hematuria, RBC casts in the urine, and mild proteinuria. IgA immune-complex deposits are found in the mesangium on immunofluorescence. we would find IgA a.b in glomeruli.

A 27-year-old male medical student, with no significant medical history, presents to his physician complaining of periodic pain in his abdomen and sides and of several intermittent episodes of passing foamy, cola-colored urine. He denies fever, dysuria, and flank pain but says that he has had a cough and nasal congestion for the past week. His temperature is 100.0°F (37.7°C), blood pressure is 150/90 mm Hg, pulse is 68/min, and respiratory rate is 16/min. Urinalysis reveals proteinuria and gross hematuria with numerous red blood cell (RBC) casts. A renal biopsy is performed. Which of the following is likely to be found on the patient's glomeruli? close A.Anti-glomerular basement membrane antibodies B.C3 C.IgA D.IgG E.IgM

In a young patient presenting with hematuria, RBC casts, and proteinuria on urinalysis, as well as a current upper respiratory tract infection, the most likely diagnosis is IgA nephropathy (also called Berger disease), a nephritic syndrome. IgA nephropathy occurs directly after or at the same time as an upper respiratory tract infection.

A 22-year-old woman presents to the office of her new primary care physician because of increases in both urinary frequency and urine volume over the previous 2 weeks. She also reports increased thirst over this period of time. The patient's medical history is significant for psychiatric illness, but she cannot remember her diagnosis. She states that she takes oral contraceptive pills, multivitamins, and "some psychiatric drugs," the names of which she cannot recall. She denies tobacco, alcohol, and drug use. The patient has no known drug allergies, and her surgical history is negative. In the office, a dipstick urinalysis is found to be negative for glucose. The patient's fasting glucose is later found to be 87 mg/dL. A qualitative β-hCG test is performed and found to be negative. A 24-hour urine collection demonstrates a urine osmolarity of 240 mOsm/L and specific gravity of 1.005 in a total volume of 4 L. A water deprivation test shows an increased specific gravity and slightly decreased urine production, but does not change further upon administration of a single dose desmopressin test. Which of the following is the most likely diagnosis?

In nephrogenic diabetes insipidus (NDI), the kidney is unable to concentrate urine, leading to increased urinary frequency and volume with low osmolarity that does not improve with water restriction or administration of desmopressin. Extreme thirst is another hallmark symptom of NDI.

An 18-year-old woman is admitted to the hospital because of a purulent, infected puncture wound in the right foot. She is given piperacillin-tazobactam, gentamicin, and acetaminophen. She improves, but five days later as she is prepared for discharge, the patient develops fatigue, a diffuse rash, and fever. The vital signs and findings on examination are otherwise normal. The BUN concentration is 45 mg/dL and the serum creatinine concentration is 3.1 mg/dL. Urinalysis shows WBC casts and eosinophils. Which of the following most likely led to her new findings?

In the presence of fever, rash, and deteriorating renal function following antibiotic use, consider acute interstitial nephritis. Common culprits include penicillins, cephalosporins, and sulfonamides. One would expect to see WBC casts and eosinophils in the urine. in Q stem used Piperacillin. her lab findings show eosinophils and WBC casts in the urine (the appearance of WBC casts is shown in the image), the most likely diagnosis is acute interstitial nephritis

A 30-year-old woman comes for evaluation because of a 3-week history of increased thirst and urination. She was diagnosed with bipolar I disorder 6 months ago and began treatment with lithium. Her pulse is 105/min and her blood pressure is 105/62 mm Hg. On physical examination, there are dry mucous membranes and poor skin turgor. Which of the following laboratory values will most likely correlate with this patient's presentation? A.Decreased aldosterone B.Decreased sodium C.Increased antidiuretic hormone (ADH) D.Increased potassium E.Increased urine osmolality

Increased antidiuretic hormone (ADH) Nephrogenic diabetes insipidus (DI) is a rare condition caused by a variety of different mechanisms, one of which is a side effect of lithium. Nephrogenic DI is characterized by a minimal change in urine osmolality after water deprivation test, which determines the diagnosis.

A 25-year-old man is referred to a nephrology clinic after his primary care doctor diagnosed him with heavy proteinuria. He has a history of hepatitis B infection and type 1 diabetes mellitus, which was diagnosed 10 years ago. His pulse is 80/min, respiratory rate is 12/min, and blood pressure is 149/82 mm Hg. His most recent hemoglobin A1c test took place 2 months ago, and the concentration was 6.2%. Repeat urinanalysis confirms proteinuria, and microscopy shows dysmorphic RBCs. A renal biopsy specimen is eventually obtained, and light microscopy reveals large, hypercellular glomeruli with mesangial proliferation, along with thickening and splitting of the basement membrane, as shown in the image. Immunofluorescent staining shows granular deposits of C3 and IgG. Electron microscopy reveals subendothelial deposits.

MPGN can cause either nephritic or nephrotic syndrome. In MPGN type I, immunofluorescence reveals subendothelial deposits of C3 and IgG. MPGN type II is caused by C3 nephritic factor, which stabilizes C3 convertase, leading to dense deposit disease. hepatitis B infection and type 1 diabetes mellitus, presents with heavy proteinuria and dysmorphic RBCs on urine microscopy (remember the RBC are associated with nephritic The disease is classified as a nephritic syndrome but often presents with nephrotic syndrome as well). glomerular hypercellularity, increased mesangial matrix, and thickening of the peripheral capillary walls (double contour), which are classic signs of membranoproliferative glomerulonephritis (MPGN). I should have known from the question stem saying mesangial proliferation that it was referring to MPGN. although Goljan says Membrano nephropathy ( membrano Glomerulonephritis) associated with Hep B and MPGN is associated with with Hep C apparently here it could be associated with both. Additionally Membrano nephropathy ( membrano Glomerulonephritis) would have Subepithelial deposits (spike and dome appearance -think MemBranco= Hep B and Blue shell-spike and dome shaped. also membranoproliferative glomerulonephritis (MPGN). type 2 would be dense deposit disease and be intramembraneous, IC, and C3 nephritic factor.

A 42-year-old woman comes to her physician because of leg swelling for the past several weeks. She has a history of systemic lupus erythematosus (SLE) and hypertension. She takes lisinopril and hydroxychloroquine. Temperature is 98.9° F (37° C), blood pressure is 114/73 mm Hg, pulse is 76/min, and respiratory rate is 20/min. Physical examination shows 2+ pitting edema in the both lower extremities. Laboratory studies show:Glucose: 86 mg/dLBUN: 12 mg/dLCreatinine: 1 mg/dLAlbumin: 2.2 g/dLUrinalysis shows 3+ protein. Based on these findings, she undergoes renal biopsy. Histopathologic findings are shown. Which of the following is the most likely diagnosis in this patient? A.Amyloidosis B.Focal segmental glomerulosclerosis C.Membranoproliferative glomerulonephritis D.Membranous nephropathy E.Minimal change disease

Membranous nephropathy is defined as a thick GBM without proliferative change. The clinical presentation includes: an insidious onset with loss of GFR over the course of years, a normal serum creatinine, and proteinuria. Membranous nephropathy is a diagnosis that causes nephrotic syndrome defined as a thick glomerular basement membrane (GBM) without proliferative changes. Clinical presentation includes a slow onset with loss of GFR over the course of years, normal serum creatinine, and proteinuria. Lupus is a secondary cause, along with chronic infection of HCV, HBV, or syphilis, solid tumors, or medications (NSAIDs, penicillamine, gold compounds).

What are symptoms of MCD? How is it treated?

Minimal change disease presents with the abrupt onset of edema and severe proteinuria. Specifically (hypoalbuminuria) Empiric treatment with steroids should be initiated based on these findings. Renal biopsy is not necessary before treatment begins.

A 56-year-old woman with advanced cervical cancer who began treatment with radiation and chemotherapy 2 weeks ago is admitted to the hospital for worsening abdominal pain and continuous vomiting over a 4-day period. The patient′s blood pressure is 108/75 mm Hg supine and 85/60 mm Hg standing. Her pulse is 98/min, respiratory rate is is 10/min, and temperature is 98.2°F (36.8°C). Cardiorespiratory examination is unremarkable. Capillary refill time is 4 seconds. Skin tenting is evident. Laboratory studies show: Serum pH: 7.47 BUN: 31 mg/dL Na+: 141 mEq/L K+: 3.3 mEq/L Cl-: 90 mEq/L HCO3-: 35 mEq/L Creatinine: 1.2 mg/dL Urine pH: 5.3 (normal 4.5-8) UrineNa+: 18 mEq/L Which of the following is the most likely cause of the patient's serum and urine electrolyte abnormalities? Which of the following is the most likely cause of the patient's serum and urine electrolyte abnormalities?

Prolonged episodes of vomiting can result in hypochloremic metabolic alkalosis due to excessive loss of chloride and hydrogen ions in vomitus. Early in metabolic alkalosis, bicarbonate is lost in urine, producing a high urine pH. Several days later, bicarbonate is more efficiently reabsorbed and urine becomes paradoxically acidic. patient demonstrates several signs of dehydration, including orthostatic hypotension (ie, variation of ≥20 mm Hg systolic blood pressure with positional change), tachycardia, delayed capillary refill, and skin tenting as well as pre-renal azotemia on laboratory testing. S alos chloride <97mEq/=hypochloremic If renal perfusion is particularly compromised, prerenal failure progresses to acute tubular necrosis, which is characterized by a normal BUN:Cr ratio (10-15), high fractional excretion of sodium, and muddy brown granular, epithelial cell casts. Tumor lysis syndrome results as a complication of chemotherapy, and is associated with elevated uric acid, elevated potassium, elevated phosphorous, and decreased calcium on serum chemistry profile.

A 37-year-old woman comes to her primary care physician with concerns that she may have diabetes based on a 2-week history of frequent urination. She reports voiding large volumes of clear, dilute urine at least 10 times a day but denies urgency, dysuria, discharge, or incontinence. She describes feeling thirsty "all the time" and estimates drinking at least 8 liters of water a day. She denies changes in vision or appetite, peripheral neuropathy, seizures, nausea, vomiting, or chest pain. Her medical history is significant for schizoaffective disorder, which is well managed with paliperidone and lithium. On examination, her temperature is 37.1° C (98.7° F), blood pressure is 125/78 mm Hg, pulse is 80/min, respiratory rate is 16/min, and oxygen saturation is 99% on room air. Her heart rate is regular and lungs are clear to auscultation bilaterally. Capillary refill is < 3 seconds. Sensation is intact in all extremities. A water deprivation test (patient was water-restricted and desmopressin was administered at hour 5). is ordered and results are provided below, alongside additional laboratory findings. Sodium: 127 mEq/L Potassium: 4.1 mEq/L Chloride: 102 mEq/L CO2: 35 mEq/LBUN: 20 mg/dL Cr: 1.1 mEq/L Glucose: 102 mg/dL Calcium: 9.8 mEq/L Serum lithium level: pending Serum osmolality: 270 mOsm/L Which of the following is the most likely diagnosis in this patient?

Psychogenic polydipsia Primary polydipsia is characterized by excessive water intake in the setting of normally functioning kidneys. It is commonly seen in psychiatric patients. With water deprivation, the urine osmolality should immediately and robustly increase as the kidneys begin to retain water. .

What would the differences be between Psychogenic polydipsia? central DI ? Partial nephrogenic DI? Complete nephrogenic DI? Syndrome of inappropriate antidiuretic hormone secretion (SIADH?

Psychogenic polydipsia-Primary polydipsia is characterized by excessive water intake in the setting of normally functioning kidneys. It is commonly seen in psychiatric patients.With water deprivation, the urine osmolality should immediately and robustly increase as the kidneys begin to retain water. In central DI urine osmolality would be expected to remain constant until the administration of desmopressin. Upon administration of desmopressin, urine osmolality should rapidly increase to maximal levels (~800). Partial nephrogenic DI would be associated with a mild increase in urine osmolality throughout water deprivation and attenuated response to desmopressin. Complete nephrogenic DI would have no change of urine osmolality during water deprivation or after desmopressin administration Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a cause of hyponatremia that occurs secondary to excessive ADH and inappropriate water retention. Typically, serum osmolality is less than 270 mOsm/L from excessive water retention, and urine is inappropriately concentrated prior to water deprivation or desmopressin administration.

A 59-year-old woman who has a 5-year history of type 2 diabetes mellitus comes to her primary care physician for a routine visit. Her last Hb A1c 1 year ago was 9% and she was told to improve her diet and to exercise regularly. She was also started on metformin 1500 mg daily; however, she has not taken her medication consistently. Today, she notes that she was recently in the emergency department for a humeral fracture; she states that she is still confused because she "didn't fall that far." On evaluation today, her temperature is 37.7° C (99° F), blood pressure is 130/90 mm Hg, pulse is 75/min, and respiratory rate is 18/min. Routine laboratory results show a creatinine of 2.1 mg/dL. Her last creatinine 1 year ago was 1 mg/dL. Given the patient's laboratory findings, she is most likely developing which of the following conditions?

Renal osteodystrophy occurs in chronic kidney disease due to the kidneys' inability to excrete phosphate or synthesize 1-alpha-hydroxylase to maintain vitamin D production. Poor management of diabetes causes significant damage to the kidneys, and secondary hyperparathyroidism is a common complication in these patients. Renal osteodystrophy is a form of secondary hyperparathyroidism caused by chronic kidney disease. CKD is associated with decreased phosphate excretion, which in turn results in hyperphosphatemia. The elevated serum phosphate levels directly depress serum calcium levels and thereby stimulate parathyroid gland activity. In addition, loss of renal substance reduces the availability of 1-alpha-hydroxylase necessary for the synthesis of the active form of vitamin D, which in turn reduces intestinal absorption of calcium.

Why would you not measure serum creatinine to try and diagnose earliest signs of renal disease in a patient>

Those with early DN may initially have a normal creatinine level despite ongoing kidney damage because of the kidneys' ability to compensate with hyperfiltration in certain healthy glomeruli. Patients with uncontrolled diabetes may have elevated serum creatinine levels in the middle to late stages of renal disease. Serum creatinine rises in the setting of renal damage and is a reflection of decreased GFR

What are features of VHL (ways to not confuse with ADPKD)?

Von Hippel-Lindau (VHL) syndrome hemangioblastomas of the retina, spine, or cerebellum; renal cell carcinoma; and pheochromocytoma. This patient does not have any of these tumors. In addition, VHL syndrome does not cause hepatic cysts, early-onset hypertension, or kidney disease as observed in this patient?

What test do you use to differentiate distinguish central versus nephrogenic DI? What calues would you get?

Water deprivation studies help distinguish central versus nephrogenic DI. After water deprivation, urine osmolality (UOsm) is decreased in both central DI and nephrogenic DI (less than 300 mOsm/kg). After injection of desmopressin acetate (ADH), UOsm is greater than 800 mOsm/kg in central DI (indicating concentration), whereas in nephrogenic DI, it is still less than 300 mOsm/kg.

Name 2 genitourinary cancers that one could present with and compare and contrast their presentation. Biggest risk factors to develop.

invasive transitional cell carcinoma (TCC), also known as urothelial carcinom- invasive transitional cells and prominent, atypical nuclei.. -presents with painless hematuria (No casts) and significant unintentional weight loss. Prostate cancer is a consideration, but his prostate gland is not enlarged most significant risk factor for TCC is an extensive history of cigarette smoking RCC- Renal cell carcinoma is asymptomatic in about one third of patients. Hematuria (40% of patients), flank pain (40%), and a palpable mass in the flank or abdomen (25%) are common; but only about 10% of patients present with all three findings. RCC is asymptomatic in about one third of patients. Hematuria (40% of patients), flank pain (40%), and a palpable mass in the flank or abdomen (25%) are common; but only about 10% of patients present with all three findings.

Compare and contrast presentation of Nephrogenic diabetes insipidus (DI)? 4 clinical presentations? 4 lab values? What med can precipitate this?

nephrogenic diabetes insipidus (DI), which typically presents with increased thirst, polydipsia, polyuria, hypernatremia, and urine osmolarity less than 500 mOsm/kg. Serum osmolarity is typically greater than 295 mOsm/kg, and urine osmolarity is typically less than 500 mOsm/kg. Laboratory values will show either increased antidiuretic hormone (ADH) levels or values within the reference ranges (see table) since ADH is stimulated in the setting of volume depletion, as seen in this patient with hypotension and tachycardia. Chronic lithium ingestion can lead to resistance to ADH, resulting in polyuria and polydipsia. Lithium enters the principal cells of the collecting duct through epithelial sodium channels in the luminal membrane.

A 30-year-old woman is brought to the emergency department after neighbors saw her collapse on her front lawn. On arrival in the emergency department, her pulse is 108/min, blood pressure is 104/54 mm Hg, and oxygen saturation is 92% on room air. On physical examination, the patient awakens to painful stimuli. Bowel sounds are present, and there is moderate abdominal tenderness to palpation. The remainder of the examination findings are unremarkable. Initial laboratory analysis reveals the following: Na+: 140 mEq/L K+: 3.6 mEq/L Cl-: 116 mEq/L HCO3-: 15 mEq/L Arterial blood gas pH: 7.32 PCO2: 30 mm Hg Which of the following is most likely to explain these laboratory abnormalities? A.Bulimia B.Diabetic ketoacidosis C.Diarrheal illness D.Furosemide use E.Heroin overdose

patient presents with syncope, likely as a result of hypotension, and her labs indicate she has a non-anion gap metabolic acidosis. diarrheal illness. we would expect to see metabolic acidosis caused by bicarbonate loss in the gastrointestinal tract, dehydration also causes contraction alkalosis, which can normalize the pH or even drive the pH up causing alkalosis. Diarrhea leads to excess HCO3- excretion, resulting in a non-anion gap metabolic acidosis.

A mother brings her 9-year-old boy to the pediatrician for an annual check-up. She is concerned that he has gained 4.5 kg (10 lb) over the past 2 months. On questioning, it is revealed that the patient had a viral upper respiratory tract infection 2 weeks ago, which resolved without treatment. On examination, his lungs are clear, and his pulse is regular. However, he has 2+ pitting edema in his lower extremities bilaterally and bilateral periorbital edema. Urinalysis demonstrates 4.5 g protein in a 24 hour specimen but is otherwise normal. In addition to close monitoring of his renal function and proteinuria, which of the following is the most appropriate next step in the management of this patient?

patient presents with weight gain, 2+ pitting edema, and significant proteinuria, all of which suggest a diagnosis of nephrotic syndrome, which is also characterized by hypoalbuminemia and hyperlipidemia remember MCD is also called Lipoid Nephrosis). In the pediatric population, nephrotic syndrome is most commonly caused by minimal change disease (MCD). MCD presents with the abrupt onset of edema and weight gain accompanied by significant proteinuria, as seen in this patient. Immediate treatment with corticosteroids should be initiated based on clinical findings that suggest MCD. Renal biopsy is not necessary before treatment. Although up to 30% of children experience spontaneous remission, all children should be treated with prednisone or a similar corticosteroid.


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