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Internal Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What is the cause of mucosal bleeding in CKD?

A

Increased urea –> inhibits arginine conversion to urea and shunts it towards GSA –> nitric oxide –> decreased vWF secretion, decreased ADP and thromboxane A2, and decreased GP IIb/IIIA receptor activation –> decreased platelet adhesion, activation and aggregation

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2
Q

Membranous nephropathy - what kind? Associated secondary causes?

A

Nephrotic syndrome, subepithelial deposits, gradual podocyte damage, subacute presentation (vs acute for minimal change disease)

Malignancy
Infection (Hep B/C, syphilis)
Autoimmune (eg lupus, thyroiditis)
Drugs (NSAIDs)

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3
Q

Amyloidosis - what kind? Risks?

A

Nephrotic syndrome - glomerular amyloid deposition

Risk of restrictive cardiomyopathy

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4
Q

What does low urine chloride in metabolic alkalosis suggest?

A

Body depletion of chloride (e.g. vomiting, diuretic overuse) –> should replete with normal saline

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5
Q

Acute papillary necrosis - most causes, signs

A
  1. Analgesic overuse
  2. Sickle cell anemia

Signs:
AKI, hematuria, flank pain, fever

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6
Q

Desmopressin indications and adverse effects

A
  1. Diabetes insipidus
  2. Mild-moderate heavy menstrual bleeding associated with vWD

Adverse: Induces effects of ADH –> hypotonic hyponatremia with euvolemia (due to increased natriuretic peptide secretion)

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7
Q

Hypercalcemia symptoms

A
  1. Nausea
  2. Polyuria
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8
Q

When does hypercalcemia of immobilization occur?

A

After 4 weeks

May be as soon as 3 days in those with chronic renal insufficiency

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9
Q

How does acute rhabdomyolysis affect calcium?

A

Precipitation of calcium and phosphorus in damaged muscles –> hypocalcemia

During diuretic/recovery phase, hypercalcemia and hyperphosphatemia

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10
Q

What are paraneoplastic syndromes of renal cell carcinoma?

A
  1. EPO production
  2. Hypercalcemia
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11
Q

What should be used to relieve urine in acute bacterial prostatitis?

A

Suprapubic catheter - don’t want to spread bacteria from prostate upward or rupture prostate

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12
Q

Ureteral stone - medication?

A

Alpha blocker (e.g. tamsulosin) for stones >5 and <=10 mm to facilitate passage

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13
Q

How do kidneys respond to metabolic acidosis from non-renal etiology?

A
  1. Increased bicarbonate reabsorption (Cl excretion increases via beta-intercalated cells in collecting duct)
  2. Increased excretion of ammonium and dihydrogen phosphate
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14
Q

Oliguria definition

A

<500 mL of urine/24 hours

Often present in prerenal AKI

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15
Q

Hypocalcemia signs

A
  1. Paresthesia
  2. Hyperreflexia
  3. Trousseau sign (BP cuff inflated >SBP 3 min causes carpopedal spasm)
  4. Chvostek sign (tapping facial nerve causes ipsilateral facial muscle contraction)

Tetany, seizure, others

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16
Q

When is bicarb indicated in metabolic acidosis?

A

When pH<7.2

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17
Q

Why does DKA have hyperkalemia but total potassium deficit?

A

Osmotic diuresis, elimination of ketoacid anions as potassium salts, and secondary hyperaldosteronism from volume contraction lead to potassium deficit

Hyperkalemia due to hyperosmolarity and diminished insulin

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18
Q

Fibroblast growth factor 23

A

Lowers phosphate by decreasing intestinal absorption and increasing renal excretion

Increased in phosphate retention and secondary hyperPTH due to CKD

19
Q

What is suggested by hypercalcemia with renal injury?

A

Malignancy (eg multiple myeloma)

Normally kidney injury results in hypocalcemia due to decreased phosphate excretion

20
Q

How do loop and thiazides affect calcium and sodium in kidney

A

Loop: promote Ca wasting
Thiazide: decreases urinary excretion

21
Q

Adrenal vein sampling - purpose

A

Differentiate between adrenal hyperplasia and adenoma

22
Q

Tumor lysis syndrome prophylaxis for AKI

A

Normal saline
Allopurinol or rasburicase

Hyperuricemia and hyperphosphatemia lead to uric acid and calcium phosphate stones, respectively

23
Q

How to avoid contrast-induced AKI?

A

0.9% saline increases intravascular volume first

Do not give if already volume overloaded

Would expect to see creatinine rise 24-48h after administration

24
Q

What electrolyte disturbance in alcohol use causes refractory hypokalemia?

A

Hypomagnesemia - intracellular magnesium normally inhibits renal outer medullary potassium (ROMK) pump, preventing excessive K+ loss

25
Q

Diabetic nephropathy - injury to what part?

A

Basement membrane and adjacent structures
-Albuminuria (albumin-creatinine ratio 30-300 mg/g

Random urine test should be done at diagnosis (type 2) or 5 years after type 1

26
Q

Diabetic nephropathy - treatment

A

BP control: ACEi/ARB
Glycemic control: SGLT2 inhibitor or GLP-1 agonist

27
Q

Opioid neds to avoid in kidney disease

A

Morphine
Tramadol
Codeine
Meperidine

28
Q

How to alkalinize urine for uric acid stones?

A

Potassium citrate

29
Q

Diabetes predisposes to which stones?

A

Uric acid stones

30
Q

How does CKD affect phosphate and calcium?

A

Hyperphosphatemia
Hypocalcemia
Secondary hyperPTH

31
Q

Calcium in which direction causes seizures?

A

Severe hypocalcemia -> neuronal hyperexcitability

32
Q

When is serum osmolality possible helpful in evaluating hyponatremia?

A

When suspected hypertonicity (e.g. hyperglycemia causing translocational hyponatremia) or isotonicity (e.g. hyperlipidemia causing lab artifact pseudohyponatremia)

Otherwise, most likely hypotonic

33
Q

How does PTH affect alk phos?

A

Increased

34
Q

Nephrotic syndrome infection risk

A

Loss of IgG -> decreased humoral immunity, particularly to encapsulated organisms

35
Q

Nephrotic syndrome effect on anemia

A

Via loss of transferrin, erythropoietin

36
Q

Nephrotic syndrome effect on vitamin D

A

Deficiency due to loss of vit D-binding protein

37
Q

ADPKD effects from cyst development

A

Hypertension - cysts cause ischemia, resulting in RAAS
Polyuria/nocturia - mild, neprhogenic diabetes insipidus from cyst damage to distal tubules and receipt of vasopressin signals

38
Q

Milk-alkali pathogenesis

A

Calcium carbonate antacids:
Hypercalcemia causes renal vasoconstriction, decreased GFR

Calcium inhibits NaK2Cl cotransporter due to activation of calcium-sensing receptors in thick ascending tubule
Ca impairs ADH activity
These cause hypovolemia and increased bicarb reabsorption, compounding alkali intake

39
Q

Milk-alkali risk factors

A

CKD
Thiazide use (increased Ca retention)
ACEi, NSAIDs (decreased GFR)

40
Q

How do loop diuretics affect calcium and magnesium levels?

A

Hypocalcemia and hypomagnesemia - blocking NaK2Cl prevents K reabsorption, leading to Ca and Mg loss

41
Q

Why does metabolic alkalosis (hypochloremic hypokalemic from vomiting, NG, diuretics) benefit from normal saline?

A

Replenishes Cl to help bicarb excretion by kidneys
Restored volume to decrease RAAS signaling, reducing loss of K and H from kidneys

42
Q

What protein is proteinuria?

A

> 3.5 g/day

43
Q

Diffuse BM thickening with granular deposits (light) and IgG/C3 (IF)

A

Membranous nephropathy

Primary: anti-PLA2R Ab serology or antigen on tissue stain

Internal Medicine (23 decks)

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