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Internal Medicine Boards 2018 > Nephrology > Flashcards

Nephrology Flashcards

First Aid and NEJM Knowledge+

1
Q

Rate by which to raise Na in acute vs. chronic symptomatic hyponatremia

A 
Acute symptomatic (seizing!?): raise until symptoms resolve
1-2 mEq/L/hr

Chronic symptomatic: slower raise, 0.5-1.0 mEq/L/hr

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2
Q

Clinical features of hyponatremia

A

Symptoms typically correlate to rate and severity of decline

Seizure, coma
AMS- confusion, lethargy
Nausea/vomiting

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3
Q

Overcorrection of hyponatremia raises risk for what?

A

Overcorrecting hyponatremia (raising blood Na too fast- drawing water out of brain) => CPM (central pontine myelinolysis)

Do not correct Na by more than 10-12 mEq/L over 24 hrs

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4
Q

Overcorrection of hypernatremia raises risk for what?

A

Cerebral edema- drop sodium fast, water goes into brain

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5
Q

Main three causes of SIADH

A
  1. CNS pathology: SAH, subdural, meningitis, tumor, CVA
  2. Pulmonary: SCLC, Tb, pneumonia
  3. Drugs: typically psychotropic meds (TCAs, haldol, SSRIs)
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6
Q

Urine osmolality in SIADH vs. psychogenic polydipsia

A

SIADH- high urine osms (over 100, UNa over 20) b/c body holding onto water

Psychogenic polydipsia- low urine osms (below 50) b/c body trying to get rid of as much water as possible

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7
Q

Prototypical clinical vignette for hypernatremia

A

Hypernatremia- due to hypovolemia (almost always from free water deficit and not due to high salt)

Old demented bedridden pt who can’t get up and respond to thirst reflex

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8
Q

When to think of diabetes insipidus in hypernatremic pt

A

DI = either not producing (central) or not responding to (nephrogenic) ADH => have dilute urine despite hypernatremia

So when hypernatremic with Uosm low consider DI

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9
Q

Name a cause of hypervolemic hypernatremia

A

Rare that hypernatremia is in s/o hypervolemia- consider primary hyperaldosteronism = mineralocorticoid excess (aldo prompts holding onto Na)

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10
Q

Name causes of hyperkalemia due to extracellular K+ shift

A 
K+ pushed out of cells
metabolic acidosis (ex: DKA)
tumor lysis
rhabdo
digitalis overdose
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11
Q

EKG changes of mild, moderate, severe hyperkalemia

A

Mild- normal, peaked T-waves
Moderate- (pulling the string)- prolonged QRS, flattened P-waves
Severe- VF

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12
Q

Mechanism of type I (distal) RTA

A

Distal RTA due to inability to secrete acid load in distal part of nephron (collecting duct)

Most commonly due to reduced activity of H/K ATPase that secretes H+ ions => also results in hypokalemia (b/c K left in urine)

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13
Q

Mechanism of type II (proximal) RTA

A

Proximal inability to reabsorb bicarb => lose bicarb in urine

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14
Q

2 main etiologies of non-anion gap metabolic acidosis

(a) How to distinguish

A

Non-anion gap metabolic acidosis due to loss of bicarb containing solutions (from kidneys (type II RTA) or GI (diarrhea)) or inability to excrete H+ (type I RTA)

  1. Diarrhea
  2. RTA

(a) Clinically (duh) and also by urine anion gap
if positive urine AG then RTA present

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15
Q

Type I (distal) RTA

(a) Clinical distinguishing feature

A

Type I RTA = inability to secrete H+ ions into urine => hypokalemia and metabolic acidosis

(a) often presents w/ recurrent kidney stones or hypercalciuria
- acidemia increases CaPO4 release from bone during buffering
- alkaline urine promotes stone formation

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16
Q

Causes of type II (proximal) RTA

A

Proximal RTA (type II) = bicarb wasting- means that the bicarb filtered can’t be reabsorbed in the proximal tubule

Causes
M-protein disorders: multiple myeloma, amyloid
Heavy metal poisoning: Pb, Cu
Acetazolamide

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17
Q

Liddle syndrome

A

Liddle syndrome = psudeohyperparathyroidism- autosomal dominant mutation in ENac that mimics high aldo b/c increased Na reabsorption and decreased K reabsorption =>

refractory HTN and hypokalemia, and metabolic alkalosis

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18
Q

Bartter’s vs. Gitelman’s syndrome

A

Both autosomal recessive genetic defects that cause hypokalemia and mimic loop diuretic (Barter’s) and thiazide diuretic (Gitelman’s) use

Differentiate by urine Ca
Bartter’s- high urine Ca
Gitelman’s- low urine Ca

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19
Q

Name some etiologies of renal K+ loss (hypokalemia due to something at level of kidney)

A 
Diuresis
Mineralocorticoid excess: licorice, Hyperaldo, Cushing's disease- at high levels cortisol has mineralocorticoid properties
Liddle syndrome (pseudohyperaldo due to genetic ENac mutation)
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20
Q

Etiologies of type I RTA

A

Type I (distal) RTA = inability of kidney to secrete acid in collecting duct

Main causes

  • Sjogrens
  • amphotericin
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21
Q

Two main ways by which kidneys maintain acid/base status

A
  1. Reabsorption of bicarbonate that is filtered into the proximal tubule
  2. Secretion of daily acid load (from sulfur-containing amino acids) in collecting duct
22
Q

Mechanism of hypokalemia in type I (distal) RTA

A

Distal RTA = reduced ability to excrete H in collecting system

Renal potassium wasting- b/c H/K ATPase isn’t doing its thing to pump out H and bring in K
- diminished H-ATPase activity is the most common cause of distal RTA

23
Q

Main cause of type IV RTA

A

Hypoaldo => hyperkalemia and metabolic acidosis

24
Q

Explain concept of delta-delta (or delta gap)

A

Delta gap- use this when you have an anion-gap metabolic acidosis to see if there is a concomitant non-anion-gap metabolic acidosis present

If (AG - 12) / (24 - bicarb) is less than one: suggests presence of concomitant non-anion gap metabolic acidosis

D/D over 2 c/w concomitant metabolic alkalosis (HCO3 much higher than expected for degree of acidosis)

25
Q

On an ABG once you find an anion-gap metabolic acidosis, what are the two next steps

A
  1. Check delta-delta to see if concomitant non-anion gap metabolic acidosis is present
  2. Use winter’s formula pCO2 = (HCO3 x 1.5) + 8 +/- 2 to check for adequate respiratory compensation
26
Q

Explain rationale behind winter’s formula

A

Winter’s formula- used to calculate respiratory compensation for metabolic acidosis

pCO2 = (HCO3 x 1.5) + 8 +/- 2

If pCO2 is over expected value- concomitant respiratory acidosis

if pCO2 under expected value- concomitant respiratory alkalosis

27
Q

Lab tests to distinguish three main types of RTA

A

Hyperkalemia = type IV RTA

Hypokalemia or normkalemia seen in type I and type II, to differentiate use urine pH
Urine pH over 5.5 = distal (type I) RTA
Urine pH under 5.0 = proximal (type II) RTA

Degree of low bicarb
Lowest in type I (distal)
Moderately low in type II (14-20)
Usually over 15 in type IV

28
Q

Other lab findings typically found in type II RTA

A

Any cause of type II (proximal) RTA can also cause Fanconi’s syndrome where nothing gets reabsorbed proximally => hypophosphatemia, glycosuria despite normal serum glucose, low-grade proteinuria

29
Q

Bicarb compensation for acute vs. chronic respiratory acidosis

A

Respiratory acidosis (pCO2 over 45)

For every 10 mmHg increase in pCO2

  • acute: 1 mEq/L raise in bicarb
  • chronic: 3-5 mEq/L raise in bicarb
30
Q

Bicarb compensation for acute vs. chronic respiratory alkalosis

A

Respiratory alkalosis (pCO2 under 35)

For every 10 mmHg decrease in pCO2

  • acute: 2 mEq/L drop in bicarb
  • chronic: 4 mEq/L drop in bicarb
31
Q

Which acid base disturbances are present 27 y/oF w/ type I diabetes p/w intractable vomiting/abdominal pain

pH 7.52, pCO2 30, pO2 260 on RA
AG 40
Bicarb 15

A

Mixed:

  1. anion-gap metabolic acidosis (probs from DKA)
  2. delta/delta = (40-12) / (24-15) > 2 c/w concomitant metabolic alkalosis (likely from the vomiting)
  3. Compensatory respiratory alkalosis
32
Q

What acid/base disorder is caused by salicylate toxicity

A

Triple

Anion-gap metabolic acidosis (from the salicylic acid), metabolic alkalosis (from vomiting) and primary respiratory alkalosis (salicylate directly stimulate the respiratory center causing tachypnea)

33
Q

Typical clinical presentation of nephrolithiasis

(a) UA findings

A

Kidney stones typically present w/ flank/back pain radiating to the groin
Also often w/ cystitis features of frequency, dysuria, urgency

(a) Hematuria on UA (at least 10 RBCs)

34
Q

Most common form of kidney stones

(a) Other types

A

Calcium oxalate stones account for about 80% of kidney stones

(a) Other types include uric acid stones, struvite stones, and cysteine stones

35
Q

Utility of AXR in finding kidney stones

(a) Gold standard diagnostic imaging

A

KUB can see calcium oxalate stones (most common type) but miss uric acid stones

(a) Gold standard is non-con abdominal CT

36
Q

3 types of urine abnormalities that increase risk of calcium oxalate kidney stones

A

Increase risk of calcium oxalate kidney stones

  1. Hypercaliuria seen in hyperparathyroidism
  2. Hyperoxalaturia seen in short-gut syndrome/IBD
  3. Hypocitraturia seen in metabolic acidosis (RTA, CKD, chronic diarrhea)
37
Q

2 types of urine abnormalities that increase risk of uric acid kidney stones

A

Increased risk of uric acid kidney stones

  1. Acidic urine (pH below 5.5): diets high in animal protein (b/c urine excretes daily H+ load from sulfur-containing amino acids
  2. Hyperuricosuria: gout, tumor lysis syndrome
38
Q

Medical treatment of calcium oxalate kidney stones

A

Calcium restriction does NOT help b/c can lead to hyperoxaluria (calcium binds oxalate in the gut to promote excretion)

  • tons of PO hydration
  • thiazides (reduce Ca excreted in urine)
  • K citrate
39
Q

Type of kidney stone more likely to be seen in acidic vs alkaline urine

A

Acidic urine (pH under 5.5) predisposes to uric acid kidney stones

Alkaline urine (pH over 6.5) predisposes to struvite stones

40
Q

The following clinical history increases risk of which type of kidney stone

(a) Recurrent UTI
(b) Malignancy in current treatment
(c) IBD

A

(a) Recurrent UTIs w/ urease producing organisms increases risk for struvite stones
(b) Consider tumor lysis syndrome => hyperuricosuria => uric acid kidney stone
(c) IBD predisposes to hyperoxaluria (b/c oxalate excreted by gut) which increases risk of calcium oxalate kidney stones

41
Q

2 conditions that make checking a FeNA useless

A
  1. Pt on diuresis

2. Pt not oliguric!!! Remember FeNa is only of use if the pt is oliguric

42
Q

Urine osmolality expected in

(a) Prerenal azotemia
(b) ATN

A

Urine osms in

(a) Prerenal azotemia- very high osms, urine concentrated b/c kidneys are functionally able to hold onto water
(b) ATN- usually similar to plasma, intrinsic kidney issue so that tubules cannot concentrate

43
Q

UA findings (casts/cells) seen in the following causes of acute renal failure

(a) Pre-renal
(b) Atheroembolism to renal artery
(c) ATN due to ischemia
(d) AIN from drug

A

UA findings

(a) Pre-renal: low SG, nonspecific hyaline casts
(b) Atheroembolism: eosinophiluria (eos in urine)
(c) ATN from ischemia (ex: sepsis, shock)- muddy brown casts
(d) AIN from drug or contrast- white cell casts

44
Q

Key diagnoses for the following clues on UA

(a) Muddy brown casts
(b) Dysmorphic RBCs and RBC casts
(c) WBC casts
(d) Hyaline casts

A

UA findings

(a) Muddy brown cast = ATN, typically from ischemia (ex: ATN after bout of sepsis)
(b) Dysmorphic RBC/RBC casts seen in glomerulonephritis/vasculitis
(c) WBC casts seen in AIN in response to contrast or nephrotoxic drugs
(d) Hyaline casts are nonspecific, can be seen in dirty UAs or pre renal azotemia

45
Q

Treatment options for HRS before liver transplant

A
  • albumin
  • splanchnic vasoconstrictors = vasopressin analogus = octreotide, midodrine
  • TIPS
  • RRT as bridge to transplant
46
Q

27 y/oF w/ worse HTN after starting ACEi

Next best test

A

Renal artery duplex to assess renal artery flow- worsening of HTN after initiation of ACEi is suspicious for renovascular HTN (ex: renal artery stenosis in s/o fibromuscular dysplasia?

47
Q

Urge incontinence vs. stress incontinence

A

Urge incontinence = overactive bladder, feel the need to go right before involuntary leakage of urine

Stress incontinence = involuntary leakage w/ increases in abdominal pressure (sneezing, vagal maneuver)

48
Q

Urge incontinence vs. stress incontinence

A

Urge incontinence = overactive bladder, feel the need to go right before involuntary leakage of urine

Stress incontinence = involuntary leakage w/ increases in abdominal pressure (sneezing, vagal maneuver)

49
Q

Elderly M w/ post-renal obstruction 2/2 prostate requiring foley: start on finasteride or tamsulosin

A

Tamsulosin (alpha blocker) in acute setting b/c finasteride (PDE5 inhibitors take weeks to kick in)

50
Q

Acid/base disturbance seen in aspirin toxicity

A

Elevated salicylate level => primary respiratory alkalosis w/ secondary metabolic acidosis

51
Q

When is EPO indicated in ESRD?

A

EPO indicated when Hb under 10 despite adequate iron stores
EXCEPT in cancer pts, actually increases risk of tumor progression

So cancer pt w/ ESRD and Hb 8- give IV Iron, NOT EPO

52
Q

Workup of painless hematuria in 65 y/o smoker

A

Need to evaluate both upper and lower GU tract for cancer

  1. CT urography to look for RCC, urolithiasis, ureteral mass/stone (CT urogram w/ contrast, better than IV pyelogram)
  2. Cystoscopy for bladder CA

Internal Medicine Boards 2018 (13 decks)

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