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Step 2 UWORLD > Renal > Flashcards

Renal Flashcards

1
Q

Whats on ddx when patient has Hypokalemia, Alkalosis, Normal BP

A

Low Urine Chloride
1. Bulimic (surreptious) vomiting

High Urine Chloride

  1. Diuretic abuse
  2. Bartters syndrome (reab defect in TAL NaK2Cl)
  3. Gittelmans syndrome (reab defect of NaCl in DCT)
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2
Q

Hyponatremia with Serum osmolality >300

A

Glucose, Mannitol, Contrast Agents

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3
Q

Hyponatremia with low serum Osm and Urine osm >100

A

SIADH
hypothyroid
glucorticoid def
drugs

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4
Q

Hyponatremia with low serum Osm and Urine osm <100

A

Primary polydipsia, Beer drinker potomania

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5
Q

Hyponatremia in schizophrenic patient

A

Psych hx –> Primary polydipsia

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6
Q

T/F: Hypercoagulation is commonly seen in nephrotic syndrome

A

True, especially renal vein thrombosis

->loss of Antithrombin III, changes to protein C and S, liver make more fibrinogen,

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7
Q

Earliest sign of diabetic nephropathy?

A

Glomerular hyperfiltration

Ultimately leads to GBM thickening, mesangial expansion, and the characteristic nodular sclerosis

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8
Q

Nephrotic syndrome in blacks/mexicans

A

FSGS

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9
Q

Nephrotic syndrome in heroin users, HIV, sickle cell, obesity

A

FSGS

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10
Q

Nephrotic syndrome in whites

A

Membraneous

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11
Q

How to remember nephrotic syndrome in whites vs blacks/mexicans

A

Blacks/Mexicans are segregated: FSGS

Whites are always members: Membraneous

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12
Q

T/F: Amitryptiline has anticholinergic side effects, including urinary retention

A

True. This TCA drug, used for pain/neuropathy, can cause atropine like sxs: dry mouth, urinary retention, etc.

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13
Q

Intramembraneous deposits that stain for C3 + proteinuria

A

Membraneoproliferative glomerulopathy

  • -> caused by persistent activation of alternate pathway
  • ->IgG Ab = C3 nephritic factor
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14
Q

Renal vascular lesions seen in hypertension

A

Arterio sclerotic of afferent and efferent arterioles and glomerular capillary

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15
Q

Characteristics of diabetic nephropathy

A

increased extracellular matrix, BM thickening, mesangial expansion, fibrosis

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16
Q

T/F: Diabetic nephropathy is characterized by nodular (or sometimes diffuse) glomerulosclerosis and GBM thickening

A

True, with Kimmelstiel-Wielstein lesion

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17
Q

Envelope-shaped rectangular crystals on UA

A

Calcium stones

  • -> acidic low pH = calcium oxalate
  • ->basic high pH = calcium phosphate

–Tx = hydration, thiazides, citrate

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18
Q

Causes of calcium oxalate stones (acidic low pH)

A

Ethylene glycol (antifreeze)
vitamin C abuse
malabsorption (Crohns)

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19
Q

Oliguria, hypertension, increased Creatinine/BUN a few days after renal transplant

A

Renal transplant dysfunction: causes = ureteral obstruction (look for dilated calcyces), cyclosporine toxicity (high levels), vascular obstruction, ATN, acute rejection

–>Acute rejection Tx with IV STEROIDS

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20
Q

How do you prevent contrast-induced nephropathy?

A

Pre-tx with IV hydration is the big one. can also pretx with sodium bicarb. can give acetylcysteine on top of one of those.

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21
Q

Signs of aspirin toxicity

A

Gastric ulcer, tinnitus. Causes hyperventilation and mixed respiratory alkalosis and anion gap metabolic alkalosis

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22
Q

T/F: Thiazides decrease uric acid

A

False. Toxicity can cause hyperuricemia

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23
Q

Tx for uric acid stones

A

Alkalinization of the urine (POTASSIUM CITRATE), low-purine diet, hydration. Or Allopurinol.

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24
Q

Hematuria, unilateral flank pain, palpable renal mass in a smoker

A

Renal cell carcinoma

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25
Q

best imaging for renal cell carcinoma?

A

abdominal CT

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26
Q

why might RCC present with polycythemia?

A

paraneoplastic EPO. can also have paraneoplastic ACTH, PTHrP

hyperaclcemia, thrombocytosis, erythrocytosis

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27
Q

Patient has hyperkalemia and ECG changes (no p waves, wide QRS, bradycardia). Mgmt?

A

So need the Calcium Gluconate first now.
After you can give the measures to decrease K
(Insulin = temporary; then Dialysis/cation exchange = perm)

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28
Q

Hyalinosis of afferent and efferent arterioles

A

Diabetic nephropathy (pathognomonic)

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29
Q

Patient with rheumatoid arthritis that develops nephrotic syndrome

A

strongly consider Amyloidosis

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30
Q

Urine sediment microscopy shows no or few rbcs, but UA shows large amounts of blood

A

Rhabdomyolysis secondary to myoglobulinuria

standard UA can’t distinguish btwn myoglobin and hemoglobin

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31
Q

What metabolic state would you expect after a seizure?

A

Anion Gap Metabolic Acidosis

  • ->postictal rise in Lactic Acid (due to skeletal mm hypoxia)…self-resolves in about 2 hours
  • ->esp seen with GTC seizures
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32
Q

wbc casts on UA

A

Pyelonephritis and Interstitial Nephritis (i.e. AIN)

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33
Q

broad and waxy casts on UA

A

Chronic renal failure

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34
Q

Fatty casts on UA

A

Nephrotic syndrome

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35
Q

Muddy brown granular casts on UA

A

ATN

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36
Q

What kind of casts on UA would you expect to see after MVA/hypovolemic shock?

A

Muddy brown –> ATN

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37
Q

What is ADPKD associated with?

A

Berry aneurysms (intracranial bleeding), MVP, benign hepatic cysts

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38
Q

Hypertension, bilateral palpable flank masses, microhematuria

A

ADPKD

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39
Q

electrolyte effects of Addison’s dz

A

= Primary Adrenal Insuff –> no Aldosterone.
Aldosterone normally saves sodium, secretes K and H+.

Addisons–>Hyponatremia, Hyperkalemia, non-gap metabolic acidosis

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40
Q

How do you use Winter’s formula?

A

arterial pCO2 should = 1.5 (HCO3) + 8…+/- 2.

So use this whenever trying to figure out what normal respiratory compensation is. based on this, you determine if there is respiratory disorder or appropriate compensation

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41
Q

How do you differentiate btwn glomerular and non-glomerular hematuria using UA?

A

Glomerular: Blood + Protein; rbc casts, dysmorphic rbc
(even if they say 3+ protein, don’t think “glomerulonephritis means less than 2+ protein…the bleeding still from glomerulus)

Nonglomerular: Blood + no protein, normal rbc

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42
Q

Hematuria/proteinuria after strep throat

A

Within 5 days: IgA nephropathy
Around 2 weeks: PSGN
don’t be a peasant kid

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43
Q

acid-base changes from Loops

A

Hypokalemia, Metabolic alkalosis, Pre-renal kidney injury (not called AKI, b/c this typically causes hyperkalemia and AG metab acidosis)

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44
Q

which dzs results in hyper-oxaluria and predisposes to stones?

A

Crohns or any malabsorption disorder.

oxalate is obtained from diet; normally bound by calcium in gut and absorption prevented. in fat malabsorption, calcium is bound to fat and leaves oxalate open.

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45
Q

causes of AIN (wbc casts, eosinophils in urine)

A

Drugs: Penicillin, Bactrim, Cephalosporins, NSAIDs

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46
Q

Features of AIN (wbc casts, eosinophils in urine)

A

Maculopapular rash (don’t pick gonorrhea), Fever, New drug exposure i.e. bactrim/nsaid/ABx +/- arthralgias

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47
Q

most common renal malignancy in childhood

A

Wilms (does not cross midline)

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48
Q

What is the biggest association with Wilms tumor?

A

BECKWIDTH-WIEDMANN

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49
Q

cancer in the 1st year of life, presents as abdominal mass that crosses midline with systemic sxs

A

Neuroblastoma (SNS chain; typically involves adrenal glands)

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50
Q

Who gets renal cell carcinoma?

A

Men 50-80 years old

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51
Q

What is the etiology of Hypernatremia?

A

Renal or GI losses (of water)

(less common: can be hypervolemic hypernatremia if excess sodium intake or mineralicorticoid excess from hyperaldosterone)

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52
Q

Hematuria with normal rbc suggests: (general)

A

extra-glomerular pathology i.e. not GN

53
Q

T/F: Sickle cell trait patients can have spontaneous painless hematuria, UTI and renal medullary cancer

A

True, hematuria secondary to renal papillary necrosis/ischemia

54
Q

common causes of metabolic alkalosis

A
  1. Vomiting!!!!
  2. Meds (thiazides/loops)
  3. Hyperaldosteronism (Hypokalemia)
55
Q

whats the relationship btwn aldosterone and potassium

A

Normally, aldosterone saves sodium by pushing out K and H+(distal renal tubule).

  • ->Aldosterone def: Hyperkalemia
  • ->Aldosterone excess: Hypokalemia
56
Q

Acid base status of Addisons dz (note: can be caused by TB in endemic areas, autoimmune or mets)

A

Primary Adrenal Insuff: Low Cortisol/T/ALDOSTERONE

–> Kidney loses sodium and retains K and H = Normal gap metabolic acidosis + Hyperkalemia and Hyponatremia

57
Q

Tx of choice for hypovolemic hyponatremia

A

Normal Saline (replenishes depleted salt stores, restores euvolemia, shuts off nonosmotic stimuli for ADH release)

58
Q

T/F: Protein and gross blood are present in both glomerular and non-glomerular hematuria

A

False.
Glomerular: Protein + Microscopic blood (dysmorphic)
Non-glomerular: Gross blood, no protein (normal rbcs)

59
Q

causes of non-glomerular hematuria

A 
Nephrolithiasis
Cancer (RENAL/prostate/bladder)
ADPKD 
Infection (cystitis)
RENAL Papillary Necrosis
60
Q

Most common glomerulonephritis in adults

A

IgA Nephropathy…5 days after URI or pharyngeal illness

61
Q

causes of Renal Papillary Necrosis

A 
Nsaids
Sickle cell
Analgesics
Infx
DM
62
Q

Whats the major cause of refractory hypokalemia (despite trying to aggressively replenish K, level does not increase significantly)?

A

Hypomagnesemia (leads to excessive renal loss)

63
Q

features of drug-induced interstitial nephritis (AIN)

A
  • Fever, Rash, Arthalgia, Hematuria

- Sterile pyuria + Eosinophiluria. can have wbc casts

64
Q

tx for drug-induced interstitial nephritis

A

remove offending agent habibi

65
Q

flank pain and +urinary cyanide nitroprusside test

A

Cystinuria: Hexagonal crystals, impaired amino acid transport (Cystine, Ornithine, Lysine, Arginina aka COLA); radioopaque

66
Q

Why does a patient with severe liver cirrhosis have decreased UOP despite resuscitative fluids?

A

Hepatorenal syndrome: systemic and renal hypoperfusion (NO in splanchnic circulation causes vasodilation). Patients have ARF with low Urine sodium (<10) and absence of casts, blood or protein in urine

67
Q

Hyponatremia with low serum Osm (<280), high urine Osm (>100), and elevated Urine Na (>40)

A

SIADH

68
Q

Drugs implicated in SIADH

A 
SSRIs
Carbamazepine 
NSAIDs
Cyclophosphamide
Sulfonylureas
69
Q

Protocol for investigating VUR post febrile UTI’s in peds

A

First febrile UTI 2mo-24mo: Renal US (eval for anatomic abnormal)
Second/recurrent UTI: Voiding cystourethrogram (eval for VUR)

70
Q

Dietary recommendations for patients with renal calculi

A
  1. Decrease sodium
  2. normal calcium
  3. lots of fluids
  4. increase citrate (fruits/veggies. Potassium citrate alkalinizes urine, good for uric stones etc)
71
Q

leading cause of death in ESRD/dialysis patients

A

CVD son

72
Q

Why does lymphoma patient getting treatment have arrythmia and EKG changes?

A

Tumor Lysis Syndrome –> Hyperkalemia

73
Q

Treatment in hyperkalemia to stabilize cardiac membranes

A

Calcium carbonate

74
Q

Treatment to rapidly lower serum potassium in a patient with hyperkalemia and EKG changes

A

you need to Temporize!
Give Insulin and Glucose (the calcium carbonate is to stabilize cardiac mem). This lowers SERUM k…vs kayexolate which decreases total potassium

75
Q

Is there a difference between decreasing serum K and decreasing total body K in the treatment of a patient with hyperkalemia?

A

Yup!
Decrease serum K: Insulin and Glucose (hide it intracellularly)

Reduce total body K: Kayexelate (rids via stool). can also use Loops (urine) but not as common

76
Q

What other options on top of Insulin/Glucose exist for rapidly decreasing serum K in a hyperkalemic patient?

A
  • beta 2 agonists

- sodium bicarbonate (NaHCO3)

77
Q

EKG changes of hyperkalemia

A 
Prolonged PR interval
Wide QRS interval
PEAKED T WAVES
loss of p wave
Worse: can go to a sine wave
78
Q

How do you do a UA/culture in a patient in diapers? i.e babies/elderly

A

Straight catheterization (avoid clean-catch, which is appropriate for majority of patients, b/c skin and stool flora contaminants)

79
Q

what are the indications for dialysis

A

Acidosis (pH <7.1 refractory to medical tx)
Electrolytes (hyper K)
Ingestions (methanol, ethylene glycol, salicylate, Li, sodium valproate, carbamazepine)
Overload (V)
Uremia (encephalopathy/asterixis, pericarditis, bleeding)

80
Q

Toxicity of thiazides (chlorthalidone/HZT)

A
  • hypokalemic metab acidosis
  • hyponatremia
  • HYPER GLUC: Glycemia, Lipidemia, Uremia, Calcemia
81
Q

options for removal of total body K in hyperkalemics

A

Kayexelate (med ed)
Diuretics (CI in ESRD pts)
Cation exchange resins (i.e. sodium polystyrene sulf)
Hemodialysis

82
Q

How do you manage post-ictal lactic acidosis?

A

Observe and recheck in a few hours. Transient AG metabolic acidosis that resolves in 90 minutes

83
Q

most common kidney stones

A

Calcium oxalate (radioopaque)

84
Q

which stones are radioopaque?

A

Calcium and Ammonium Magnesium Phosphoate (aka Struvite). visible

85
Q

features of cyanide toxicity (secondary to nitroprusside)

A

HA, confusion, AMS, arrythmia, flushing, respiratory depression

86
Q

T/F: AIN typically presents with leukocyte casts/eosinophils, hematuria, and a RASH

A

True RASH

87
Q

Most common cause of obstructive uropathy

A

BPH. Postrenal azotemia

88
Q

best way to screen diabetics for development of nephropathy?

A

Spot (random) or time measurement of urine microalbumin to creatinine ratio (all about the MICROALBUMINURIA…so looking at creatinine clearance is the wrong answer)

89
Q

T/F: Squamous cell lung cancer causes SIADH

A

False. SMALL CELL

90
Q

Why does patient that comes in vomiting have low chloride?

A

Vomiting = Hypochloremic Hypokalemic Metabolic Alkalosis = GI LOSSES. CL, K, and H all present in gastric contents

91
Q

In which 3 patients should you stop/not use Metformin?

A

Acute Renal Failure, Liver failure, Sepsis

92
Q

Hypertension, Bilateral palpable flank masses and microscopic hematuria in a 50 year old

A

ADPKD…watch out for intracranial hem (Berry aneurysm leading to SAH). Hepatic cysts are actually most common extra renal manifestation. colonic diverticula and MVP/AR can also happen.

93
Q

Leading cause of euvolemic hypernatremia

A

Diabetes Insipidus (SIADH is HYPOnatremia)

94
Q

Increased thirst, polyuria, mild hypernatremia

A

Diabetes Insipidus. Inability to concentrate the urine b/c lack (central) or failure to respond (nephrogenic) to ADH

95
Q

causes of central diabetes insipidus

A

Pituitary tumor, trauma, hemorrhage, infx

96
Q

causes of nephrogenic diabetes insipidus

A
  • Hypercalcemia
  • severe hypokalemia
  • meds: Lithium, Demeclocycline (ADH antagonist used in SIADH), Amphotericin, foscarnet/cidofivir (both for CMV retinitis, acyclovir-resistant HSV)
97
Q

serum osm diff in central vs nephrogenic DI

A

Central <300 (closer to 100)

Nephrogenic: >300 (300-600)

98
Q

Drug therapy that can help reduce nephrolithiasis

A
  • calcium stones: Thiazides
  • Uric acid: Allopurinol
  • Urine alkalinization by Potassium Citrate
99
Q

Why does patient with 4+ proteinuria have renal vein thrombosis (sudden development of pain)

A

Hypercoaguble state in nephrotic syndrome due to loss of Antithrombin III

100
Q

Increased extracellular matrix, mesangial expansion, fibrosis, BM thickening of renal arterioles

A

Diabetic Nephropathy

101
Q

Intimal thickening and luminal narrowing of renal arterioles with sclerosis

A

Arteriosclerotic lesions secondary to hypertension Habibi

102
Q

Potassium sparing diuretics

A

Spironolactone, Epelrenone, Triamterene, Amiloride

–>potassium high when he EATS bananas

103
Q

Papillary Necrosis and Tubulointerstitial Nephritis are caused by:

A

Analgesic-induced Nephropathy (chronic back pain patient on opioids/nsaids/etc)
–>painless hematuria, sterile pyuria, wbc casts, trace proteinuria

104
Q

T/F: US is the best initial test for kidney stones

A

False! First get UA obvi but best test is NON-CONTRAST CT!!! Pregnant patients get US

105
Q

how is a KUB used in dx of kidney stone?

A

Not used for Dx!!! Can be used to track dz progression of a known stone

106
Q

Size rules for tx of stone

A

<5mm: passes spontaneously. Just fluids/pain meds
<7mm: medical CCB (Amlodipine), Alpha blocker (-zosin)
<1.5cm: break stone down… lithiotripsy (proximal) or ureteroscopy (Distal)
>1.5cm: Surgical resection (ex lap)
if ever SEPTIC: emergent decompression with Nephrostomy (proximal) or Stent (distal)

107
Q

Patient comes in with bones, stones, groans, psychic moans. Management?

A

Hypercalcemia, first thing to do is VOLUME VOLUME VOLUME VOLUME VOLUME VOLUME. can augment with Calcitonin (short term/quick) and furesomide and BISPHOSPHENATES (long term)

108
Q

Brown tumors/fibrosa cystica. Dz and mgmt

A

Primary hyperparathyroidism (hypercalcemic state). Single autonomous gland secreted PTH w/o feedback

  • ->resection (after radionucleotide scan to ID which gland)
  • ->monitor for hypocalcemia after surg
109
Q

Why does early renal failure lead to secondary hyperparathyroidism?

A

Vit D not converted to active form = hypocalcemia = increased PTH (and hypertrophy)

110
Q

Why does persistent renal failure lead to tertiary hyperparathyroidism?

A

Hypertrophied, autonomous parathyroid glands (initially hypertrophy due to vit d deficiency 2ndary hyperPTH)

111
Q

How does imaging differentiate primary vs tertiary hyperparathyroidism

A

Sestamibi scan!

1: One huge gland
3: all the glands have some hypertrophy

112
Q

weight loss, decrease PTH, increase Ca, increase P

A

bone mets (or granuloma…look for increase vit d)

113
Q

weight loss, decrease PTH, increase Ca, decrease P

A

squamous cell, PTHrP

114
Q

T/F: You order 1,25 vit D to see if granulomatous dz, you order 25, vit D in Vit D deficiency

A

true

115
Q

Increase PTH, decreased Ca and decreased P

A

Pseudohypoparathyrodisim: PTH end organ resistance (low yield)

116
Q

flank pain, flank mass, hematuria

A

likely cancer (RCC)

117
Q

Why do nephrotic syndrome and cirrhosis lead to prerenal AKI?

A

Decreased albumin = third spacing

118
Q

How do fibromuscular dysplasia and renal artery stenosis lead to prerenal AKI?

A

“Clog” = narrowing of vessels = decreased perfusion

119
Q

Drugs that cause AIN

A

nsaids, bactrim, PCN, cephalosporins

120
Q

how do you assess/rule out a postrenal obstruction?

A

US!!!! better than CT usually. Tx with foley/stent/remove obstruction/nephrostomy

121
Q

what’s the creatinine level where you begin to dialyze?

A

NOT BASED ON Cr. AEIOU bruh

122
Q

Hemoptysis, Hematuria, rbc casts, +Anti-basement membrane with linear deposits

A

Goodpastures. Tx with plasmapharesis and steroids

123
Q

Sinusitis/otitis, lung problems, renal involvment with rbc casts + random systemic vasculitis signs

A

Wegeners. Tx with cyclophosphamide and steroids

124
Q

Joint paint, purpuric lesions, +Hep C with renal involvement, high levels immunoglobulins

A

Cryoglobulinemia. Tx the Hep C with interferon, ribavirin, and protease inhibitor (-vir)

125
Q

Tx of lupus nephritis

A

steroids, mycophenolate mofetil

126
Q

Asthma, hematuria, eosinophils

A

Churg strauss. Tx with steroids, cyclophosphamide

127
Q

Tx for secondary hyperparathyroidism

A

due to early renal failure and not converting vit d. Give phosphate binders (sevelamer) and calcimimeics (cinacalcet…sensitizes CaSR) . Can also give vit d and ca supplements

128
Q

does CKD results in alkalosis or acidosis?

A

Acidosis (i.e. lactic acidosis). give bicarb supplement in CKD. also not saving sodium and swithcing with K/H

129
Q

Synchronized vs unsynchronized cardioversion?

A

Synchronized = shock –> use for any tachyrrythmias (narrow/atrial or wide/ventricular) w/hemodynamic instability.

Unsynchronized = defribillation –> for pulseless cardiac arrest = VFIB, pulseless VTach

Step 2 UWORLD (17 decks)

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