Nephro

Question 1

How to reduce contrast induced kidney injury?

Answer 1

Vigorous intravenous hydration has proven to reduce risk of contrast induced nephropathy

Question 2

what is side effect of giving EPO in ESRD?

Answer 2

Erythopoitein is given to patients on dialysis in order to correct anemia of chronic kidney disease. EPO can worsen hypertension though.

Question 3

When should EPO be given to ESRD patients?

Answer 3

EPO therapy is indicated for ESRD patients w/ Hgb <10

Question 4

African American and AIDS nephropathy?

Answer 4

Focal Segmental glomerular sclerosis (FSGS)

Question 5

IgA nephropathy:

Answer 5

Hx of strep infx (pharyngitis/URI/ skin infx)

Question 6

Kimmelstiel- wilson Nodules:

Answer 6

Associated it Diabetes

Question 7

Calcium oxalate stone in kidney treatment:

Answer 7

Most common type of kidney stone

1) Reduce calcium w/ thiazide diuretics
2) Reduce oxolate by decreasing meat consumption & VITAMIN C
3) Increase citrate levels by eating more fruit

Question 8

If you suspect kidney stone.. what is best test for size and location?

Answer 8

Non-contrast CT scan

U/S in pregnant patient

Question 9

Treatment for kidney stone <5mm

Answer 9

Stone will pass spontaneously. Hydration (IVF) and pain control is all that is needed

Question 10

Treatment for kidney stone <7mm

Answer 10

Use medical expulsive therapy: CCB (amlodipine) and Alpha blockers (terazosin) to dilate the ureters.

Question 11

Treatment for kidney stone <1.5cm

Answer 11

Stone will need to be broken down in order to pass. Use ureteroscopy for distal stones and lithotripsy for proximal stones

Question 12

Treatment for kidney stone >1.5cm

Answer 12

Stone will need to be resected.
Proximal stones w/ laparoscopic exploration

Distal stones w/ percutaneous anterograde nephrolithotomy

Question 13

Treatment for kidney stone w/ sepsis, kidney failure etc

Answer 13

Use nephrostomy tube for proximal stone and stent for distal stone until pt is stabilized and ready for surgery.

Question 14

Old man w/ frequent UTIs and alkaline urine. What kind of kidney stone?

Answer 14

Alkaline environment is perfect for magnesium ammonium phosphate stones (struvite stones) staghorn calculi throughout renal pyramids

Question 15

Management of hyperkalemia WITHOUT ECG changes:

Answer 15

1) Furosemide diuresis- renally excreting the potassium

2) Kayexalate - Excreting it thru the stool

Question 16

Management of hyperkalemia WITH ECG changes:

Answer 16

Intravenous calcium carbonate is used to stabilize the myocardium in hyperkalemia with abnormal ECG findings.

Question 17

Person with hypokalemia due to HCTZ. What can you add to manage HTN and prevent hypokalemia?

Answer 17

Add Ace-inhibitor or ARb which are K sparing. Will help with BP and hypokalemia

Question 18

what is used to replete potassium?

Answer 18

Potassium chloride

Question 19

what are the 3 phases of treating symptomatic hyperkalemia with EKG changes?

Answer 19

1) Stabilization of the myocardial membrane (IV Ca carbonate or gluconate)
2) Temporizing the potassium out of the blood (Na bicarbonate, insulin D50 & Beta-2 agonists (albuterol)
3) Eliminate K from blood (Furosemide, kayexalate, hemodialysis

Question 20

Young man with a family history of calcium disorders who has an asymptomatic hypercalcemia. He has a modestly elevated calcium, modestly elevated PTH, and a barely low phosphorous.

Answer 20

familial hypocalciuric hypercalcemia-Diagnosis is made by urinary calcium

Question 21

Patient is older, has a smoking history, and has a lung mass.
PTH is undetectable, the calcium elevated and the phosphorous is low. How to diagnose?

Answer 21

Serum PTH-rp

Question 22

Sestamibi scan of neck showing a single adenoma definitively means

Answer 22

primary hyperparathyroidism- high calcium, low phos, and high PTH in the setting of normal renal function- biopsy would be prudent to confirm it is non malignant, but the treatment is still resection, parathyroidectomy.

Question 23

Treatment for acute, severe, and symptomatic hypercalcemia as a temporizing measure while fluids are being given

Answer 23

Calcitonin (calci-tone-down)

Question 24

Hungry Bone syndrome

Answer 24

Hungry bone syndrome occurs after a parathyroidectomy; a parathyroid adenoma resection. As the adenoma autonomously secretes PTH the calcium rises and phos falls. The high calcium activates the calcium sensing receptor and turns off endogenous production of PTH, leading to atrophy of the normal parathyroid glands. When the adenoma is removed the normal parathyroid glands need time to “turn back on,” presenting with low phos, low calcium, and low PTH immediately post-operatively. Unlike the total loss of parathyroid glands that can accompany thyroidectomy, hungry bone syndrome will resolve as the parathyroid glands come back on line.

Question 25

If symptomatic hypocalcemia, give

Answer 25

intravenous calcium (Ca gluconate)

Question 26

When is Intravenous calcitriol used to treat hypocalcemia in patients?

Answer 26

Calcitriol is 1, 25-Vit D analogue. Intravenous calcitriol is used to treat hypocalcemia in patients where the impairment of 25-Vit D to 1, 25-Vit D is so severe is causes hypocalcemia. This would be in chronic kidney disease patients.

Question 27

How is hypercalcemia due to sarcoid treated?

Answer 27

Prednisone can be used to quell inflammatory diseases like sarcoid. Granulomatous diseases can increase Vit D and cause a hypercalcemia through hypervitaminosis D. Steroids decrease the inflammation, decrease the granulomatous disease, and decrease the hypercalcemia.

Question 28

Patient with high calcium and low phosphorous with normal kidneys. Diagnosis?

Answer 28

The most common cause of hypercalcemia in the outpatient setting is primary hyperparathyroidism. Regardless, with an elevated calcium and a low phos, that speaks to PTH activity in the kidney (which works). To ensure this is true a PTH level should be measured.

Question 29

Management of hypercalcemia of malignancy

Answer 29

Vigorous fluids and bisphosphonates (Alendronate) are the treatment of choice for sustained reduction in the calcium level.

Question 30

Diagnosis of hyperparathyroidism is obvious: high calcium, low phosphorous, and very high PTH. The difficulty is separating WHICH hyperparathyroidism it is - Primary or tertiary?

Answer 30

multiple adenomas in multiple places and the history of chronic kidney disease nearing end-stage renal disease, that is certainly to be tertiary hyperparathyroidism. Primary hyperparathyroidism will present WITHOUT renal failure and with a SINGLE nodule.

Question 31

Type I (Distal) Renal tubular acidosis

Answer 31

Impaired distal acid secretion Urine pH >5.5 Serum Potassium- Low Positive urine anion gap

Question 32

Type II (Proximal) Renal tubular acidosis

Answer 32

Impaired proximal bicarbonate reabsorption Urine pH < 5.5 Serum Potassium- Low Negative urine anion gap

Question 33

Type IV

Answer 33

Hypoaldosteronism or aldosterone resistance Urine pH < 5.5 Serum Potassium- high Positive urine anion gap

Question 34

What is Alport syndrome?

Answer 34

Usually in boys aged 5-20 Defect in alpha chain of type 4 collagen Glomerulonephritis, deafness, eye disorder Glomerular basement splitting (hematuria) Nephritic- mild proteinuria of 1 to 2 g/24 hours.

Question 35

Hypercalcemia affects:

Answer 35

Renal- it causes afferent arteriole vasoconstriction (polyuria, polydipsia, kidney stones, nephrogenic DI, Distal renal tubular acidosis Cardic- shorterned QT interval , bradycardia, hypertension

Question 36

Urinalysis of a diabetic patient

Answer 36

1st sign on urinalysis is proteinuria Nephrotic syndrome (Kimmelstiel-Wilson) that is characterized by a protein loss > 3.5 g/day Kimmelstiel-Wilson disease because of the presence of pink nodules of hyaline in the glomerular capillaries

Question 37

Urinalysis of a Acute Tubular necrosis

Answer 37

Muddy brown casts Can result from ischemia due to shock or chronic renal artery stenosis or nephrotoxic agents, such as cisplatin, aminoglycosides, and ethylene glycol ingestion.

Question 38

Liddle syndrome

Answer 38

Autosomal dominant condition that causes genetic mutation causing the epithelial sodium channel (ENaC) in the distal tubule to become constitutively active. This causes hypernatremia (HTN) and hypokalemia (metabolic alkalosis) Look for HTN in young patient Tx: Amiloride

Question 39

Bartter syndrome (Mimics loop diuretics)

Answer 39

Autosomal recessive mutation that causes reabsorption defect at thick ascending loop. Affects Na/K/2Cl cotransporter. Results in hypokalemia and metabolic alkalosis w/ hypercalciuria

Question 40

Gitelman syndrome (Mimics thiazide diuretics)

Answer 40

Autosomal recessive mutation causing reabsorption defect of NaCl at DCT Leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria.

Question 41

Treatment for severe (<120 mEQ/L) hyponatremia

Answer 41

Raising the serum sodium by 4-6 mEq/L should result in relief of symptoms while preventing herniation. Use 100-mL bolus of 3% saline. If symptoms persist, 2 additional 100-mL doses (total of 300 mL) can be given over 10 minutes

Question 42

Nail changes and diseases

Answer 42

Koilonychia- Spoon shaped nail- Iron deficiency anemia Onychorrhexis- Vertically ridged or split nail- Physiologic in elderly Paronychia- Painful redness and swelling of nail folds- Local bacterial, fungal, or viral infection Onycholysis- Splitting of distal nail plate from nail bed- Psoriasis, atopic dermatitis, trauma Pitting- Indentations of nail plate- Psoriasis, alopecia areata

Question 43

Risk factors for Pancreatic cancer

Answer 43

1) smoking Male gender Age > 60 years Being African American.

Question 44

Acute interstitial nephritis (AIN) secondary to chronic NSAID exposure

Answer 44

Unlike other etiologies of AIN, NSAID-induced AIN can present months, rather than days, after exposure Urinalysis is often negative for eosinophils, and patients have significant proteinuria

Question 45

Diagnosis for acute interstitial nephritis

Answer 45

Renal biopsy provides the definitive diagnosis Biopsy often reveals mononuclear, eosinophilic cellular infiltrate within the renal parenchyma with sparing of the glomeruli.