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Step 2 CK > Nephrology > Flashcards

Nephrology Flashcards

1
Q

The best initial test in nephrology

A

UA

BUN

Creatinine

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2
Q

Tamm-Horsfall protein

A

The name of protein that is normally secreted by the renal tubules (very tiny amount)

Normal protein is less than 300 mg per 24 hours

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3
Q

Severe proteinuria means

A

glomerular disease

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4
Q

What is transient proteinuria

A

Protein excretion increased by standing and physical activity

Present in 2-10% of the population

Mostly benign

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5
Q

Urine dipstick for protein detects

A

only albumin

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6
Q

A protein-to-creatinine (P/Cr) ratio of one is equivalent to

A

1 g of protein on a 24-hour urine

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7
Q

Define microalbuminuria

A

The presence of tiny amounts of proteins that are too small to detect on the UA

30-300 mg/24 hours

Long-term microalbuminuria leads to worsening renal function in a diabetic patient and should be treated

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8
Q

Best initial therapy for any degree of proteinuria in a diabetic patient

A

ACEi or ARB

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9
Q

True/False

Bence-Jones protein in myeloma is detectable on a dipstick

A

False

Must use immunoelectrophoresis

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10
Q

WBCs in the UA means

A

Inflammation

Infection

Allergic interstitial nephritis

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11
Q

True/False

You cannot distinguish neutrophils from eosinophils on a UA

A

True

However, if you could:

Neutrophils indicate infection

Eosinophils indicate allergic or acute intersitial nephritis

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12
Q

Persistent WBC on UA with negative culture

A

TB

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13
Q

How do you detect eosinophils in the urine?

A

Wright and Hansel stains

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14
Q

Normal UA has how many RBCs

A

<5 RBCs per high power field

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15
Q

Mild recurrent hematuria

A

think IgA nephropathy

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16
Q

False positive tests for hematuria on dipstick are caused by…

A

hemoglobin or myoglobin in the urine

They make the dipstick positive, but no red cells will be seen on microscopic examination

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17
Q

Dysmorphic red cells

A

Glomerulonephritis

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18
Q

When is cystoscopy the answer?

A

Cystoscopy is the most accurate test of the bladder

The right answer when there is hematuria w/o infection or prior trauma and:

  • renal US or CT does not show an etiology
  • bladder sonography shows a mass for possible biopsy
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19
Q

White cell casts

A

Pyelonephritis

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20
Q

Eosinophil casts

A

Acute (allergic) interstitial nephritis

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21
Q

Hyaline cast

A

Dehydration concentrates the urine and the normal Tamm-Horsfall protein precipitates or concentrates into a cast

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22
Q

Broad, waxy casts

A

Chronic renal disease

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23
Q

Granular “muddy-brown” casts

A

Acute tubular necrosis (collections of dead tubular cells)

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24
Q

Define AKI

A

A decrease in creatinine clearance resulting in a sudden rise in BUN and creatinine

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25
Q

3 types of AKI

A

Prerenal azotemia (decreased perfusion)

Postrenal azotemia (obstruction)

Intrinsic renal disease (ischemia and toxins)

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26
Q

How do NSAIDs and ACEi effect the renal arteriole?

A

NSAIDs = contriction of the afferent arteriole

ACEi = dilation of the efferent arteriole

Both can lead to prerenal azotemia

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27
Q

With completely dead kidneys, the creatinine will rise

A

about 1 mg/dL a day

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28
Q

BUN: creatinine ratio above 20:1

Clear history of hypoperfusion or hypotension

A

Prerenal azotemia

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29
Q

BUN: creatinine ratio above 20:1

Distended bladder or massive release of urine with catheter

Hydronephrosis on sonogram

A

Postrenal azotemia

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30
Q

When the cause of AKI is not clear, the next best diagnostic step is?

A

UA (order first)

UNa

FENa

Urine osmolality

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31
Q

UNa <20

FENa <1%

A

Prerenal azotemia

It is normal for urine sodium to decrease when there is decreased renal perfusion because aldosterone levels rise

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32
Q

The urine produced in ATN is similar in osmolality to

A

the bood (about 300 mOsm/L)

This is called isosthenuria and the urine osmolality is inappropriately low

AKA in ATN, the body inappropriately loses sodium (UNa > 20) and water (Uosm < 300)

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33
Q

The only significant manifestation of sickle cell trait is a defect in renal…

A

renal concentration ability or isosthenuria

these patients will continue to produce inappropriately dilute, high-volume urine despite dehydration

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34
Q

Urine specific gravity correlates to

A

urine osmolality

High UOsm = high specific gravity

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35
Q

True/False

ATN can cause proteinuria

A

False

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36
Q

What has the most proven benefit at preventing contrast-induced nephrotoxicity?

A

Saline hydration

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37
Q

What unique labs values are found in contrast-induced renal failure (a form of ATN)

A

The usual finding in ATN from nephrotoxins would be UNa > 20 and

FENa > 1% and a low specific gravity

However, contrast causes spasm of the afferent arteriole leading to tremendous reabsorption of sodium and water

High specific gravity (~1.040), UNa < 20 (~5), FENa < 1%

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38
Q

Patient with myeloma with a plasmacytoma is admitted for combination chemo. Two days later, the creatinine rises. Why?

A

Tumor lysis syndrome leading to hyperuricemia

Allopurinol, hydration, and rasburicase should be given prior to chemo to prevent renal failure from tumor lysis syndrome

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39
Q

Ethylene glycol is associated with what type of kidney injury?

A

Acute kidney injury based on oxalic acid and oxalate precipitating within the kidney tubules causing ATN

Look for hypocalcemia (precipitates as calcium oxalate - envelope shaped crystals)

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40
Q

Aminoglycoside abx

Amphotericin

Cisplatin

Vancomycin

Acyclovir

Cyclosporine

A

Cause nonoliguric renal injury

Slow onset: 5-10 days

Low magnesium level may increase risk of aminoglycoside or cisplatin toxicity

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41
Q

Contrast media causes

A

immediate renal toxicity

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42
Q

UA for rhabdo

A

UA will be positive only on dipstick for large amounts of blood, but no cells will be seen on microscopic examination

Most specific test is a urine test for myoglobin

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43
Q

Urine dipstick cannot tell the difference between

A

Hemoglobin

Myoglobin

Red blood cells

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44
Q

Lab findings in rhabdo

A

CPK markedly elevated

Hyperkalemia

Hyperuricemia (similar to tumor lysis syndrome)

Hypocalcemia (increased binding to damaged muscle)

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45
Q

Treatment for rhabdo

A

Saline hydration

Mannitol (osmotic diuretic)

Bicarbonate (drives potassium back into cells)

DO NOT TREAT HYPOCALCEMIA IF ASYMPTOMATIC

Saline and mannitol increase urine flow rates to decrease the amount of contact time between the myoglobin and the tubular cells

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46
Q

Why doesn’t hemolysis cause hyperuricemia?

A

RBCs have no nuclei

In all other cells, break down results in nucleic acids being released from the nucleus and rapidly metabolized to uric acid by xanthine oxidase

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47
Q

Most important intial step when someone presents with signs/symptoms of rhabdo

A

EKG (to detect life-threatening hyperkalemia)

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48
Q

Most common wrong answers for treatment of ATN

A

Low-dose dopamine

Diuretics

Mannitol

Steroids

Diuretics increase urine output, but do not change overall outcome

49
Q

When is dialysis the right answer for ATN?

A

Fluid overload

Encephalopathy

Pericarditis

Metabolic acidosis

Hyperkalemia

50
Q

Patient develops ATN from gentamicin. She is vigorously hydrated and treated with high dose of diuretic, low-dose dopamine, and calcium acetate as a phosphate binder. Urine output increases but she still progresses to end-stage renal failure. She also becomes deaf.

What caused the hearing loss?

A

Furosemide causes ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss (related to how fast it is injected)

51
Q

What is hepatorenal syndrome?

A

Hepatorenal syndrome is renal failure developing secondary to liver disease (d/t splanchnic arterial vasodilation and subsequent endogenous vasoconstrictors acting on renal vessels)

Look for: cirrhosis, new-onset renal failure, very low urine sodium, FENa <1%, BUN: creatinine > 20:1

Lab values in hepatorenal syndrome fit in with prerenal azotemia

52
Q

Treatment for hepatorenal syndrome

A

Midodrine

Octreotide

Albumin

goal = constriction of splachnic vessles and dilation of renal vasculature

53
Q

Etiology of Atheroemboli

A

Cholesterol plaques in the aorta or near the coronary arteries are sometimes large and fragile enough that they can be “broken off” when the vessels are manipulated during catheter procedures

Cholesterol emboli lodge in the kidney, leading to AKI, look for blue/purplish skin lesions in fingers and toes, livedo reticularis, and ocular lesions

54
Q

Diagnostic test for atheroemboli

A

Biopsy of one of the purplish skin lesions is the most accurate diagnostic test (shows cholesterol crystals)

Look for: eosinophilia, low complement levels, eosinophiluria, elevated ESR

55
Q

Define Acute (Allergic) Interstitial Nephritis

A

A form of acute renal failure that damages the tubules occurring on an idiosyncratic (idiopathic) basis

Antibodies and eosinophils attack the cells lining the tubules as a reaction to drugs (70%), infection, and autoimmune disorders

56
Q

Fever

Rash

Arthralgias

Eosinophiluria

A

AIN

57
Q

Differences between pyelonephritis and papillary necrosis

A

Pyelo: onset-few days, symptoms-dysuria, UCx-positive, CT scan-diffusely swollen kidney, Tx-abx

Papillary necrosis: onset-few hours, symptoms-necrotic material in urine, UCx-negative, CT scan-bumpy contour, Tx-none

58
Q

Summary of tubular diseases

A

Acute

Toxins

Non nephrotic

No biopsy usually

No steroids

Never additional immunosuppressive agents

59
Q

Chronic

Not from toxins/drugs

All potentially nephrotic

Biopsy sample

Steroids often

A

Characteristics of Glomerular Diseases

60
Q

In terms of diagnostic tests, all forms of glomerulonephritis have:

A
  • UA with hematuria
  • Dysmorphic red cells
  • Red cell casts
  • Low UNa and FENa
  • Proteinuria
61
Q

Difference between glomerulonephritis and nephrotic syndrome?

A

The degree/amount of proteinuria

62
Q

Difference between Goodpasture and Wegener granulomatosis

A

Goodpasture also presents with lung and kidney involvement, but unlike WG, there is no upper respiratory tract involvement

Signs of systemic vasculitis are also absent

63
Q

Best initial test for Goodpasture and treatment

A

Antiglomerular basement membrane antibodies

Treat with plasmapheresis and steroids

64
Q

The most common cause of acute glomerulonephritis in the US

A

IgA Nephropathy (Berger Disease)

Look for an Asian patient with recurrent episodes of gross hematuria 1-2 days after an upper respiratory tract infection (synpharynigitic)

65
Q

Treatment for IgA Nephropathy

A

No treatment proven to reverse the disease

Severe proteinuria is treated with ACE inhibitors and steroids

66
Q

Follows throat infection or skin infection (impetigo) by 1-3 weeks

A

PSGN

Look for dark urine, periorbital edema, HTN, and oliguria

67
Q

Complement levels in PSGN

A

Low

68
Q

How many of those with PSGN will progress to ESRD?

A

5%

69
Q

Glomerular disease +

Sensorineural hearing loss +

Visual disturbance

A

Alport Syndrome

Congenital defect of type IV collagen

No specific therapy

70
Q

Systemic vasculitis that commonly affects the kidneys, tends to spare the lungs, and can be associated with hepatitis B

A

Polyarteritis Nodosa

71
Q

In addition to the presentation of glomerulonephritis, PAN presents with:

A

nonspecific symptoms of fever, malaise, weight loss, myalgias, and arthralgia developing over weeks to months

72
Q

Stroke in a young person

A

Look for a vasculitis (e.g., PAN)

73
Q

Best initial test for PAN

A

Angiography of the renal, mesenteric, or hepatic artery showing aneurysmal dilation in association with new-onset HTN and characteristic symptoms

74
Q

Treatment of PAN

A

Prednisone and cyclophosphamide

Treat hepatitis B when it is found

75
Q

Why is kidney biopsy performed for lupus nephritis

A

To determine therapy based on the stage (not to diagnose lupus)

Mild = glucocorticoids

Severe = glucocorticoids combined with either cyclophosphamide or mycophenolate

76
Q

Large kidneys on sonogram and CT scan

A

Amyloid

HIV nephropathy

PKD

Diabetes

77
Q

Diagnosis and treatment of amyloidosis

A

Biopsy is the most accurate test (green birefringence with Congo red staining)

Control the underlying disease (myeloma, chronic inflammatory diseases, RA, IBD, chronic infection) and use melphalan and prednisone as a last resort

78
Q

Generalized edema

Hyperlipidemia

Thrombosis

A

Think nephrotic syndrome

79
Q

Most common causes of nephrotic syndrome

A

DM and HTN

  • Cancer (solid organ): membranous*
  • Children: MCD*
  • IV drug use and AIDS: focal-segmental*
  • NSAIDs: MCD and membranous*
  • SLE: any*
80
Q

By definition, nephrotic syndrome is:

A

Hyperproteinuria (>3.5 gram per 24 hours)

Hypoproteinemia

Hyperlipidemia

Edema

81
Q

Uremia is defined as the presence of:

A

Metabolic acidosis

Fluid overload

Encephalopathy

Hyperkalemia

Pericarditis

Each of these is an indication for dialysis

82
Q

Manifestations of renal failure

A

Anemia

Hypocalcemia and osteomalacia

Bleeding (platelets do not work in a uremic environment)

Pruritis

Hyperphosphatemia

Hypermagnesemia

Atherosclerosis

Endocrinopathy

83
Q

Most common cause of death in those on dialysis

A

Accelerated atherosclerosis and hypertension

The immune system helps keep arteries clear of lipid accumulation; WBCs don’t work in a uremic environment

84
Q

Calcium acetate

Calcium carbonate

Sevelamer

Lanthanum

A

Oral phosphate binders

When vitamin D is replaced to control hypocalcemia, it is critical to also give phosphate binders; otherwise vitamin D will increase GI absorption of phosphate

85
Q

Why should aluminum-containing phosphate binders be avoided

A

Aluminum causes dementia

86
Q

Intravascular hemolysis

Renal insufficiency

Thrombocytopenia

A

Think TTP and/or HUS

Hemolysis is visible on smear with schistocytes, helmet cells, and fragmented red cells

TTP is associated with neurological symptoms and fever (very similar to DIC, but does not have increased PT/PTT, decreased fibrinogen, or increased d-dimer)

87
Q

Difference in management of HUS vs TTP

A

HUS from E. coli will resolve spontaneously

Plasmapheresis (exchange transfusion) is generally urgent for TTP (associated with HIV, cancer, and drugs such as cyclosporine, ticlopidine, and clopidogrel). If plasmapheresis is not one of the choices, use infusions of FFP.

Steroids DO NOT help and platelet transfusion is never the correct choice

88
Q

Characteristics of a potentially malignant cyst

A

Mixed echogenicity

Irregular, thick

Lower density on back wall

Debris in cyst

89
Q

Pain

Hematuria

Stones

Infection

HTN

A

PCKD

90
Q

High-volume water loss from insufficient or ineffective ADH

A

DI

Nephrogenic is a loss of ADH effect (caused by lithium or demeclocycline, CKD, hypokalemia, or hypercalcemia)

Central is decreased production of ADH

91
Q

Sodium disorders vs Potassium disorders

A

Sodium = CNS symptoms

Hyperkalemia = muscular and cardiac symptoms

92
Q

Treatment of NDI

A

Correct potassium and calcium

Stop lithium or demeclocycline

Give HCTZ or NSAIDs for those still having NDI despite these interventions

93
Q

How does Addison disease cause hyponatremia?

A

Loss of aldosterone

94
Q

For every 100 mg/dL of glucose above normal, how does the sodium change

A

1.6 mEq/L decrease

95
Q

History of bipolar disorder + hyponatremia

A

psychogenic polydipsia

96
Q

Management of SIADH

A

Based on symptoms, not on sodium level

Mild = restrict fluids, Moderate = saline and loop diuretic, Severe = hypertonic saline, conivaptan, tolvaptan

Tolvaptan and conivaptan are antagonists of ADH (used for urgent treatment in the hospital). Demeclocycline treats chronic SIADH.

Correction of sodium must occur slowly: 0.5-1 mEq per hour or 12-24 mEq per day

97
Q

True/False

Hyperkalemia causes seizures

A

False

98
Q

Life-threatening management of hyperkalemia

A
  1. Calcium chloride or calcium gluconate
  2. Insulin and glucose
  3. Bicarbonate

Kayexalate and loop diuretics can be used to lower potassium when no EKG changes are present

99
Q

When replacing potassium, what should you keep in mind?

A

There is no maximum rate or oral potassium replacement (GI cannot absorb faster than the kidneys can excrete)

IV potassium replacement, however, can cause a fatal arrhythmia

100
Q

How does magnesium effect potassium?

A

Hypomagnesemia can lead to increased urinary loss of potassium (via magnesium-dependent potassium channels)

101
Q

2 most important caued of a metabolic acidosis with a normal anion gap

A
  1. RTA
  2. Diarrhea

The anion gap is normal in both of these because the chloride level rises

102
Q

Define RTA Type 1

A

AKA Distal RTA

The distal tubule is responsible for generating new bicarbonate under the influence of aldosterone. Drugs such as amphotericin and autoimmune diseases (SLE and Sjogren syndrome) can damage the distal tubule.

Result = acid cannot be excreted into the tubule, raising the pH of the urine

103
Q

Best test for RTA Type 1

A

Best initial = UA looking for high pH (> 5.5)

Most accurate = infuse acid into the blood with ammonium chloride (those with distal RTA cannot excrete acid and the urine pH will remain basic)

104
Q

Define RTA Type II

A

AKA Proximal RTA

Normally 85-90% of filtered bicarbonate is reabsorbed at the proximal tubule. Damage to the proximal tubule from amyloidosis, myeloma, Fanconi syndrome, acetazolamide, or heavy metals decreases the ability of the kidney to reabsorb most of filtered bicarbonate

Result = bicarbonate is lost in the urine until the body is so depleted that the distal tubule can absorb the rest

105
Q

Most accurate test for diagnosing RTA II

A

Give bicarbonate and test the urine

Because the kidney cannot absorb bicarb, the urine pH will rise

106
Q

Treatment for RTA II

A

Thiazide diuretics

Volume depletion will enhance bicarbonate reabsorption

107
Q

What type of RTA occurs most often in diabetics?

A

Hyporeninemia, Hypoaldosteronism (Type IV RTA)

Test by finding a persistently high urine sodium despite a sodium-depleted diet

108
Q

For RTA I, II, and IV describe the following:

Urine pH

Blood potassium

Nephrolithiasis

Diagnostic Test

Treatment

A

I: pH >5.5, low potassium, (+) nephrolithiasis d/t alkaline urine, administer acid to diagnose, treat with bicarb

II: variable pH, low potassium, (-) stones, administer bicarb to diagnose, treat with thiazides

IV: pH <5.5, high potassium, (-) stone, diagnose with urine salt loss, treat with fludrocortisone (steroid with the highest mineralocorticoid effect)

109
Q

How is the urine anion gap (UAG) used to distinguish RTA from diarrhea?

A

UAG = Na - Cl

Positive = RTA
Negative = diarrhea

The more acid excreted, the greater amount of chloride found in the urine

110
Q

Causes of metabolic acidosis with an increased anion gap

A

Lactate

Ketoacids (test acetone level)

Oxalic acids (crystals on UA d/t ethylene glycol overdose)

Formic acid (inflamed retina d/t methanol overdose)

Uremia

Salicylates

111
Q

COPD/emphysema

Drowning

Opiate overdose

Alpha 1-antitrypsin deficiency

Kyphoscoliosis

Sleep apnea/morbid obesity

A

Common causes of respiratory acidosis

112
Q

When the presentation of nephrolithiasis is clear, it is important to…

A

provide relief from pain (usually with ketorolac, an NSAID that is available orally and IV, that provides a similar level of analgesia to opiates)

113
Q

Treatment for stones 5-7 mm

A

Give nifedipine and tamsulosin

114
Q

Management for stones 0.5-2 cm

A

Lithotripsy

115
Q

Long term management of stones

A

HCTZ

Removes calcium from the urine by increasing distal tubular reabsorption of calcium

116
Q

Pregnancy safe HTN drugs

A

Labetalol (first line)

Nifedipine

Alpha methyldopa

Hydralazine

117
Q

The best initial therapy for HTN with:

CAD

DM

BPH

Depression

Hyperthyroidism

Osteoporosis

A

CAD - BB, ACEi/ARB

DM - ACEi/ARB (goal <140/90)

BPH - Alpha blockers

Depression - Avoid BBs

Hyperthyroidism - BB first

Osteoporosis - Thiazides

118
Q

Best initial therapy for hypertensive crisis

A

Labetolol or nitroprusside (nitroprusside needs monitoring with an arterial line)

Hypertensive crisis is defined as high BP in association with: confusion, blurry vision, dyspnea, or chest pain (not defined as a specific level of BP)

Step 2 CK (18 decks)

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