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Internal Medicine Boards 2018 > Nephrology > Flashcards

Nephrology Flashcards

First Aid and NEJM Knowledge+ (52 cards)

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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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

Hypoaldo => hyperkalemia and metabolic acidosis

24
Q

Explain concept of delta-delta (or delta gap)

Study These Flashcards
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
On an ABG once you find an anion-gap metabolic acidosis, what are the two next steps
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
Explain rationale behind winter's formula
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
Lab tests to distinguish three main types of RTA
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
Other lab findings typically found in type II RTA
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
Bicarb compensation for acute vs. chronic respiratory acidosis
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
Bicarb compensation for acute vs. chronic respiratory alkalosis
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
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
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
What acid/base disorder is caused by salicylate toxicity
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
Typical clinical presentation of nephrolithiasis (a) UA findings
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
Most common form of kidney stones (a) Other types
Calcium oxalate stones account for about 80% of kidney stones (a) Other types include uric acid stones, struvite stones, and cysteine stones
35
Utility of AXR in finding kidney stones (a) Gold standard diagnostic imaging
KUB can see calcium oxalate stones (most common type) but miss uric acid stones (a) Gold standard is non-con abdominal CT
36
3 types of urine abnormalities that increase risk of calcium oxalate kidney stones
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
2 types of urine abnormalities that increase risk of uric acid kidney stones
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
Medical treatment of calcium oxalate kidney stones
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
Type of kidney stone more likely to be seen in acidic vs alkaline urine
Acidic urine (pH under 5.5) predisposes to uric acid kidney stones Alkaline urine (pH over 6.5) predisposes to struvite stones
40
The following clinical history increases risk of which type of kidney stone (a) Recurrent UTI (b) Malignancy in current treatment (c) IBD
(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
2 conditions that make checking a FeNA useless
1. Pt on diuresis | 2. Pt not oliguric!!! Remember FeNa is only of use if the pt is oliguric
42
Urine osmolality expected in (a) Prerenal azotemia (b) ATN
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
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
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
Key diagnoses for the following clues on UA (a) Muddy brown casts (b) Dysmorphic RBCs and RBC casts (c) WBC casts (d) Hyaline casts
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
Treatment options for HRS before liver transplant
- albumin - splanchnic vasoconstrictors = vasopressin analogus = octreotide, midodrine - TIPS - RRT as bridge to transplant
46
27 y/oF w/ worse HTN after starting ACEi | Next best test
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
Urge incontinence vs. stress incontinence
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
Urge incontinence vs. stress incontinence
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
Elderly M w/ post-renal obstruction 2/2 prostate requiring foley: start on finasteride or tamsulosin
Tamsulosin (alpha blocker) in acute setting b/c finasteride (PDE5 inhibitors take weeks to kick in)
50
Acid/base disturbance seen in aspirin toxicity
Elevated salicylate level => primary respiratory alkalosis w/ secondary metabolic acidosis
51
When is EPO indicated in ESRD?
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
Workup of painless hematuria in 65 y/o smoker
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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