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ABIM > Nephrology > Flashcards

Nephrology Flashcards

1
Q

what is a normal 24-hour urine protein?

A

less than 150 mg

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2
Q

how much protein w/i 24 hours indicates significant GLOMERULAR pathology?

A

more than 2 g/day (or 40-50 mg/kg/d)

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3
Q

how much protein w/i 24 hours indicates significant INTERSTITIAL pathology?

A

less than 1 g/day

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4
Q

the only exceptions in which there can be pathology and a NORMAL URINE SEDIMENT with MINIMAL proteinuria (2)

A
  1. medullary cystic disease

2. obstructive uropathy

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5
Q

will urinary light chains in myeloma be picked up on a urine dipstick?

A

NO

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6
Q

causes of false-positive urine albumin on urine dipstick: (6)

A
  1. very alkaline urine with a pH > 8
  2. fever
  3. heart failure (HF)
  4. urinary tract infection (UTI)
  5. hematuria
  6. very concentrated urine
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7
Q

common in people during a febrile illness, after strenuous exercise, and in pts w/ HF and COPD

A

transient proteinuria

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8
Q

first step in a pt w/ transient proteinuria

A

recheck UA (if negative; benign)

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9
Q

proteinuria reverts to near-normal when pt is SUPINE

A

BENIGN ORTHOSTATIC PROTEINURIA

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10
Q

what equates to 24-hour urinary protein?

A

spot protein:creatinine ratio

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11
Q

proteinuria ranges using spot ratio:

  • normal
  • microalbuminuria
  • overt proteinuria, usually d/t interstitial disease
  • nephrotic range
A
  • less than 0.15 (150 mg)
  • 0.03 - 0.3 (30 - 300 mg)
  • 0.3 - 1 (300 mg - 1 g)
  • 3 - 3.5 (3 - 3.5 g)
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12
Q

EARLIEST indicator of diabetic and hypertensive nephropathy

A

microalbuminuria

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13
Q

indicate probable glomerulonephritis/nephritic syndrome

A

RBC casts, or “dysmorphic” RBCs

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14
Q

FEW RBCs on microscopic analysis, BUT urine dipstick is POSITIVE for blood

A

HEMOglobinuria or MYOglobinuria (rhabdomyolysis)

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15
Q

hematuria associated w/ proteinuria, especially if dysmorphic cells and/or RBC casts are present in the urine, is ALWAYS d/t

A

glomerular bleeding

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16
Q

MCC of ISOLATED GLOMERULAR HEMATURIA (normal renal function, NO proteinuria)

A
  • IgA nephropathy
  • thin basement membrane disease
  • early Alport syndrome
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17
Q

can cause transient hematuria

A

strenuous exercise

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18
Q

pts w/ sickle cell TRAIT may also have

A

hematuria

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19
Q

isolated microscopic or gross hematuria is more likely what in origin?

A

urologic

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20
Q

in older pts, complete GU imaging must be done to exclude what?

A

renal cell or GU tract carcinomas

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21
Q

what GU imaging must be done to r/o renal cell or GU tract carcinomas?

A

US, MRI, or CT

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22
Q

w/ EOSINOPHILURIA, think of

A

drug-induced interstitial nephritis

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23
Q

w/ COARSE GRANULAR casts, or “MUDDY BROWN” casts, think

A

acute tubular injury

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24
Q

w/ OVAL FAT BODIES (“maltese crosses” under polarized light) may be seen in

A

nephrotic syndrome

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25
Q

what suggests rhabdomyolysis-induced renal failure?

A

unusually rapid rise in serum creatinine (more than 1.5 mg/dL over 24H)

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26
Q

in the elderly, what will be normal despite reduced renal function?

A

creatinine

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27
Q

serum creatinine (sCr) is artificially INCREASED by these medications (4)

A
  1. cimetidine
  2. probenecid
  3. tenofovir
  4. trimethoprim
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28
Q

interfere w/ the test for creatinine and may falsely elevate results

A
  • acetone

- cefoxitin

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29
Q

indicates either PRERENAL AZOTEMIA (low flow and increased absorption), or increased protein breakdown

A

elevated (> 20:1) BUN:Cr ratio

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30
Q

is a nonglycosylated protein that better reflects GFR than sCr

A

cystatin C

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31
Q

a measure of overall renal function

A

glomerular filtration rate (GFR)

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32
Q

what is used to estimate GFR?

A

creatinine clearance

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33
Q

formula to calculate GFR

A

GFR = U(Cr)V/P(Cr)

= (total urine creatinine/24H)/sCr

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34
Q

name the 2 main creatinine-based GFR formulas used to calculate GFR in pts w/ IMPAIRED renal function

A
  1. modification of diet in renal disease (MDRD)

2. Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)

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35
Q

what is required to calculate the MDRD?

A
  • sCr
  • race
  • sex
  • age
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36
Q

is MORE accurate than MDRD at NEAR-normal kidney function (eGFR > 60mL/min/1.73m2)

A

CKD-EPI

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37
Q

is another acceptable way to estimate GFR

A

Cockcroft-Gault formula

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38
Q

the equation of choice in the general population, especially at higher levels of GFR

A

CKD-EPI

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39
Q

when should you not calculate GFR?

A

during AKI

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40
Q

when will estimates of GFR be inaccurate?

A
  • extreme age
  • extreme weight
  • pts w/ amputations
  • cirrhosis
  • pregnancy
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41
Q

how do you calculate GFR in pts w/ extreme age, extreme weight, pts w/ amputations, cirrhosis, pregnancy?

A
  • 24H urine

- measure serum cystatin C

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42
Q

the fractional excretion of sodium (FeNa+) is the ratio of?

A

excreted Na+:total filtered load of Na+

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43
Q

when is calculating the FeNa+ most useful?

A

evaluating oliguric AKI to differentiate PRERENAL AZOTEMIA from acute tubular necrosis (ATN)

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44
Q

FeNa+ for prerenal azotemia

A

less than 1%

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45
Q

FeNa+ for acute tubular necrosis (ATN)

A

more than 2%

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46
Q

other causes of AKI w/ FeNa+ less than 1% (6)

A
  • contrast-induced ATN
  • cardiorenal syndrome
  • hepatorenal syndrome
  • nonoliguric ATN
  • pigment nephropathy (hemoglobinuria, myoglobinuria)
  • acute glomerulonephritis
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47
Q

formula to calculate FeNa+(%)

A

(sCr x uNa)/(sNa x uCr) x 100

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48
Q

since diuretics may increase FeNa+, what can be used instead?

A

FeUrea

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49
Q

the fractional excretion of urea (FeUrea) is the ratio of?

A

excreted urea:total filtered load of urea

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50
Q

formula to calculate FeUrea

A

(sCr x U(urea))/(BUN x U(Cr)) x 100

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51
Q

what FeUrea is suggestive of prerenal state?

A

less than 35%

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52
Q
  • is used to diagnose unexplained causes of AKI, nephrotic syndrome, and GN
  • routinely utilized to evaluate increases in sCr to distinguish between medication toxicity, ATN, viral infections, and acute rejection
A

renal biopsy

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53
Q

primary acid-base disorders are either what or what in origin?

A

respiratory or metabolic

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54
Q

primary respiratory disorders:

  • change in what?
  • compensated how?
A
  • PaCO2

- kidney SLOWLY dumping/holding on to HCO3- in the OPPOSITE direction

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55
Q

primary metabolic disorders:

  • change in what?
  • compensated how?
A
  • HCO3-

- respiratory rate IMMEDIATELY increases or decreases

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56
Q
  • Henderson-Hasselbalch equation

- and its easier derivation of

A
  • pH = pK + log(HCO3- / [0.03 x PaCO2])

- H+ = 24 x (PaCO2 / HCO3-)

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57
Q

Henderson-Hasselbalch equation tells us the body only has 2 ways to control serum pH, which are?

A
  1. regulate RR and TV, thus control PaCO2

2. regulate kidney’s absorption of HCO3-

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58
Q

what determines pH?

A

the RATIO of PaCO2 to HCO3-, NOT the absolute values

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59
Q

significant alkalemia of any etiology can cause what?

A

diffuse paresthesias/numbness and muscle spasms, usually associated w/ acute hyperventilation (acute resp. alkalosis)

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60
Q

diffuse paresthesias/numbness and muscle spasms are usually associated w/ acute hyperventilation (acute resp. alkalosis), but can also be caused by?

A
  • rapid overload w/ IV HCO3-

- citrate (massive blood transfusion)

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61
Q

why are pts with metabolic acidosis and hypocalcemia protected from the hypocalcemia?

A

since acidosis decreases the fraction of BOUND Ca2+ and INCREASES the IONIZED Ca2+

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62
Q

correction of acidosis prior to correction of hypocalcemia can cause what?

A

removes protective effect of acidosis, and precipitate seizures

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63
Q

serum anion gap (AG) equation

A

AG = (Na+ - HCO3-) - Cl-

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64
Q

AG is a determination of?

A

unmeasured anions

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65
Q

name the anions in the blood

A
  • HCO3-
  • Cl-
  • phosphate (phos)
  • sulfate
  • albumin
  • organic acids
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66
Q

name the cations in the blood

A
  • Na+
  • K+
  • Ca++
  • Mg++
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67
Q

remember that any increase in unmeasured anions always is 1:1 w/ the increase of

A

H+

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68
Q

HIGH AG ALWAYS INDICATES

A

METABOLIC ACIDOSIS

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69
Q

under NORMAL conditions, what anion is the main contributor to the AG?

A

albumin

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70
Q

what is the correction for hypoalbuminemia to calculate AG?

A

about 2.5 mEq/L for each 1G/dL decrease in albumin

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71
Q

does ethanol itself cause elevated AG?

A

no, but alcoholic ketoacidosis does

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72
Q

when is the urine anion gap (UAG) used?

A

to evaluate the etiology of NAGMA to differentiate between GI loss of HCO3- and RTA

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73
Q

formula for UAG

A

UAG = Na+ + K+ - Cl-

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74
Q

normal value of UAG

A

close to 0

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75
Q

positive UAG value suggests

A

low urinary NH4+ (e.g. RTA TYPE 4)

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76
Q

neGUTive UAG value suggests

A

HIGH urinary NH4+ (e.g. DIARRHEA)

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77
Q

in the setting of metabolic acidosis d/t EXTRA-renal HCO3- losses, why is the urinary NH4+ high?

A

renal H+ is excreted in the form of NH4+

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78
Q

serum osmolality is mainly determined by concentrations of?

A

Na+, glucose, and urea

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79
Q

osmolal gap (OG) helps determine what?

A

whether unmeasured osmotically active substances (osmoles) are circulating in the blood (possibly causing acidosis)

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80
Q

formula for Osm(calc)

A

Osm(calc) = 2[Na+] + (BUN/2.8) + (glucose/18)

simplified equation: Osm(calc) = 2[Na+] + (BUN/3) + (glucose/20)

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81
Q

formula for OG

A

OG = Osm(meas) - Osm(calc)

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82
Q

what is the normal OG?

A

less than 10

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83
Q

important causes of high OG

A
  • METHANOL
  • ETHYLENE GLYCOL
  • PROPYLENE GLYCOL
  • CKD (d/t retention of small solutes)
  • lactic acidosis and ketoacidosis (ALSO d/t retention of small solutes and not from the actual lactic acid or ketoacids themselves)
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84
Q

is NOT associated with acidosis (AG is normal), but osmolal gap is increased

A

ISOPROPYL alcohol

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85
Q

nontoxic causes of increased OG and normal AG (3)

A
  1. mannitol
  2. sorbitol
  3. glycerol
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86
Q

what is the main use of OG?

A

w/u of pt w/ possible acid alcohol ingestion (e.g. ethylene glycol, methanol, or propylene glycol)

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87
Q

when should possible acid alcohol ingestion especially be considered?

A

if OG is more than 25 mOsm/kg

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88
Q

ethylene glycol is a common primary ingredient in?

A

ANTIFREEZE

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89
Q

methanol is a common ingredient in?

A
  • PAINT THINNERS

- DEICING solutions (e.g. windshield washer fluids)

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90
Q

rarely, an inadvertent contaminant of “MOONSHINE;” a by-product of grain fermentation

A

methanol

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91
Q

propylene glycol is a SOLVENT used in?

A

IV lorazepam

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92
Q

what quickly happens w/ ethylene glycol, methanol, and propylene glycol, and what is the effect on the OG and AG?

A

initial substrates cause high OG and HAGMA, but are quickly converted to their TOXIC metabolites, which do not cause OG, but cause HAGMA

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93
Q

ethanol, ISOPROPYL ALCOHOL, or ACETONE ingestion will give what OG and AG?

A
  • HIGH OG withOUT acidosis
  • normal chemistry
  • normal AG
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94
Q

toxic metabolites of ethylene glycol

A

mainly glycolic acid and oxalic acid

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95
Q

toxic metabolite of methanol

A

formic acid

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96
Q

toxic metabolites of propylene glycol

A
  • pyruvic acid (normal)
  • lactic acid (normal)
  • acetic acid
  • propionaldehyde
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97
Q

metabolite of isopropyl alcohol

A

acetone (less toxic)

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98
Q

signs of possible acid alcohol ingestions

A
  • stupor
  • coma
  • hypotension
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99
Q

AG and OG in the obtunded patient:

  • methanol and ethylene glycol
  • ketoacidosis and lactic acidosis
  • chronic kidney disease
A
  • high AG

- very high OG

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100
Q

AG and OG in the obtunded patient:

  • ketoacidosis and lactic acidosis
  • chronic kidney disease
A
  • high AG

- high OG

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101
Q

AG and OG in the obtunded patient:

  • salicylate poisoning
  • methanol or ethylene glycol ingestion after substrates have been converted to acid metabolites
A
  • high AG

- normal OG

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102
Q

AG and OG in the obtunded patient:

  • isopropyl alcohol, acetone, or ethanol ingestion
A
  • normal AG

- high OG

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103
Q

AG and OG in the obtunded patient:

  • think carbon monoxide poisoning; BEFORE lactic acidosis develops
A
  • normal AG

- normal OG

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104
Q
  • commensurate increase in Cl- w/ the decrease in HCO3-

- also called “hyperchloremic” acidosis

A

NAGMA

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105
Q

why is the Cl- retained in NAGMA?

A

to maintain electrical neutrality

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106
Q

3 main causes of NAGMA

A
  1. usual: LOSS of HCO3- d/t DIARRHEA or PROXIMAL RTA
  2. increased organic acids (NH4+, e.g. pts on TPN)
  3. inability of kidney to excrete endogenous acids (renal failure or DISTAL RTA)
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107
Q

NAGMA plus HYPERkalemia, think of?

A

RTA type 4 (hypOaldosteronism)

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108
Q

NAGMA plus HYPOkalemia is caused by

A
  • GI loss (sometimes)

- RTA types 1 (distal) and 2 (proximal)

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109
Q

is a common solvent in glues and paints and can cause NAGMA

A

toluene

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110
Q

treat NAGMA with?

A

sodium bicarbonate replacement

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111
Q

in HAGMA, is there an equivalent increase in Cl-?

A

no

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112
Q

net charge in the serum is always?

A

neutral

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113
Q

because the net charge in the serum is always neutral, in HAGMA there must be what?

A

increase in UNmeasured anions

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114
Q

what tests should immediately be performed in a pt w/ unexplained HAGMA?

A
  • fundoscopic exam
  • toxicology screen
  • serum glucose; urine and serum ketones
  • lactic acid level
  • serum osm w/ calculation of OG
  • UA to assess for calcium oxalate crystals
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115
Q

common causes of HAGMA

A
  • severe CKD: decreased acid (especially NH4) excretion (MCC)
  • uremia: sulfate, phosphate, urate
  • diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketoacidosis
  • lactic acidosis: drugs, toxins, circulatory compromise
  • poisonings: salicylates, methanol, ethylene glycol, propylene glycol
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116
Q

common causes of NAGMA

A
  • renal tubular acidosis
  • diarrhea
  • carbonic anhydrase inhibitors
  • hyperalimentation w/ TPN
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117
Q

check for what in ketosis?

A
  • B-hydroxybutyrate

- urine ketones

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118
Q

treatment for DKA

A
  • insulin
  • IVF
  • electrolyte replacement
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119
Q

classic findings of AKA (alcoholic ketoacidosis)

A
  • HAGMA
  • hypophosphatemia
  • hypoglycemia
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120
Q

treatment for AKA

A

dextrose

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121
Q

how does uremia cause HAGMA?

A

causes an accumulation of anions: SULFATE, PHOSPHATE, URATE

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122
Q

what is lactic acidosis type A?

A

d/t muscle hypOperfusion during shock, cardiac failure, or sepsis

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123
Q

what is lactic acidosis type B?

A
  • findings of systemic hypoperfusion are lacking
  • DRUG-induced mitochondrial dysfunction (zidovudine, metformin, propofol)
  • tumor-induced LA
  • alcoholism
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124
Q
  • high doses of propofol for more than 48 hours
  • renal failure
  • rhabdomyolysis
  • hyperlipidemia
  • J-point elevation on EKG
  • various arrhythmias
A

propofol-related infusion syndrome (type B lactic acidosis)

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125
Q
  • can occur in pts w/ short bowel syndrome

- present w/ typical neurologic sxs (from slurred speech to obtundation)

A

D-lactic acidosis

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126
Q
  • key clue is MIXED RESPIRATORY ALKALOSIS and HAGMA
  • initially causes respiratory alkalosis, THEN additionally the HAGMA
  • suspect in elderly pts taking pain meds for arthritis
A

salicylate overdose

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127
Q
  • key clue is CALCIUM OXALATE crystals in urine

- metabolizes to glycolic acid and oxalic acid resulting in HAGMA

A

ethylene glycol

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128
Q
  • key clue is visual sxs described as “walking through a sandstorm”
  • metabolizes to formaldehyde and formic acid resulting in HAGMA
  • nausea, vomiting, abdominal pain
A

methanol

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129
Q

standard of care for ethylene glycol poisoning and methanol poisoning

A

fomepizole and dialysis

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130
Q
  • is used as a solvent for IV LORAZEPAM
  • caused by continuous infusion or large IV doses of lorazepam
  • HAGMA w/ OG
A

propylene glycol

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131
Q

treatment for HAGMA

A

treat underlying cause

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132
Q

treatment for propofol-related infusion syndrome

A
  • d/c propofol

- if AKI and severe acidosis; HD

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133
Q

treatment for salicylate poisoning

A

aggressive sodium bicarbonate therapy (protects CNS)

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134
Q

when should DKA be treated with bicarbonate?

A

pH less than 7.0

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135
Q

when should lactic acidosis be treated with bicarbonate?

A

pH less than 7.1

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136
Q

pyroglutamic acidosis is caused by?

A

chronic acetaminophen use

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137
Q

commonly results from VOLUME CONTRACTION caused by diuretics or vomiting/gastric suctioning

A

metabolic alkalosis

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138
Q

metabolic alkalosis always involves what 2 phases?

A
  • generation phase = initial H+ loss or HCO3- gain)

- maintenance phase = failure of kidney to excrete HCO3- to correct the alkalosis

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139
Q

vomiting and NG suction leads to

A

HCl loss via GASTRIC secretions

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140
Q

primary hyperaldosteronism leads to

A

RENAL acid loss

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141
Q

diuretic-induced “contraction” alkalosis leads to

A

RENAL loss of bicarb-free FLUID –> reduction in ECF volume around fixed quantity of EC bicarbonate

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142
Q

metabolic alkalosis is MAINTAINED by

A

volume depletion, which leads to decreased distal Cl- delivery and high aldosterone levels

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143
Q

aldosterone enhances distal sodium reabsorption by activating what?

A

distal tubular Na+/H+ and Na+/K+ pumps

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144
Q

what is the expected urine pH in the setting of metabolic alkalosis?

A

LOW; “paradoxical aciduria”

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145
Q

what happens to K+ levels in metabolic alkalosis?

A

K+ shifts from extracellular space to intracellular space in exchange for H+

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146
Q

what are the 2 types of metabolic alkalosis?

A
  • chloride responsive

- chloride resistant

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147
Q

what is elevated in metabolic alkalosis even though there is volume depletion and why?

A
  • U(Na+) and FeNa+

- bc bicarbonaturia takes Na+ as accompanying cation

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148
Q

what is the expected urine Cl- in metabolic alkalosis in the setting of volume depletion and why?

A
  • U(Cl-) less than 10 meq/L

- bc NaCl is desperately reabsorbed to maintain intravascular volume

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149
Q

if urine Cl- is greater than 10 meq/L think of (8)

A
  • Cushing syndrome
  • Bartter syndrome
  • Gitelman syndrome
  • primary hyperaldosteronism
  • Liddle syndrome
  • licorice ingestion
  • severe hypokalemia
  • increased intake of HCO3- (i.e. milk-alkali syndrome)
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150
Q

treatment for chloride-responsive alkalosis (urinary Cl- < 10 meq/L)

A

RESTORATION OF VOLUME and POTASSIUM CORRECTION

both interrupt aldosterone production, which is causing H+ and K+ in the distal tubule

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151
Q

treatment for SEVERE metabolic alkalosis (> 7.55)

A

HCl through central venous catheter in ICU

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152
Q

chloride resistant WITH HTN

A
  • exogenous steroids
  • endogenous steroids
    (- primary hyperaldosteronism)
    (- Cushing syndrome)
    (- 11-OH deficiency)
    (- Liddle syndrome)
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153
Q

chloride resistant withOUT HTN

A
  • Bartter syndrome
  • Gitelman syndrome
  • surreptitious syndrome
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154
Q

list the 4 steps to interpreting acid-base disorders

A
  1. pH: determine is acidemic or alkalemic
  2. calculate AG
    3a. calculate expected HCO3-
    3b. expected HCO3- - measured HCO3-
    4a. calculate expected pCO2
    4b. compare expected pCO2 to actual pCO2 from the blood gas
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155
Q

what is the body’s main extracellular buffer?

A

bicarb

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156
Q

what happens to HCO3- as anions go up?

A

go down proportionally: about 1:1 ratio, but sometimes 1.6:1

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157
Q

if the MEASURED BICARBONATE is LESS, then what is expected?

A

NAGMA

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158
Q

if the MEASURED BICARBONATE is MORE, then what is expected?

A

METABOLIC ALKALOSIS

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159
Q

if the AG is elevated, then the expected bicarb =

A

[25 - (change in AG)]

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160
Q

in metabolic acidosis, the expected pCO2 =

A

15 + actual HCO3- from the chemistry

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161
Q

in metabolic alkalosis, the expected pCO2 increases by

A

0.7 mmHg for every 1 meq/L increase in HCO3-

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162
Q

if pCO2 is HIGHER than expected, then

A

respiratory ACIDOSIS

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163
Q

if pCO2 is LOWER than expected, then

A

respiratory ALKALOSIS

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164
Q

if HCO3- is less than 9, or greater than 40, then what happens to expected pCO2?

A

may be unreliable

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165
Q

in chronic respiratory acidosis, the serum bicarb does NOT increase above what?

A

38 meq/L

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166
Q

pCO2 greater than 55 usually suggests what?

A

an additional primary respiratory acidosis

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167
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

acute hyperventilation episode

A
  • acute respiratory alkalosis

- 7.56/20/90/22

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168
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

acute asthma/PE/chest trauma

A
  • acute respiratory alkalosis d/t hypoxia

- 7.56/20/50/24

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169
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

CNS problem, chronic hyperventilation

A
  • chronic respiratory alkalosis w/ metabolic compensation

- 7.44/25/90/16

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170
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

COPD w/ chronic bronchitis

A
  • chronic respiratory alkalosis w/ metabolic compensation w/ hypoxia
  • 7.43/30/60/20
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171
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

pt in transition to respiratory failure

A
  • normal except hypoxia

- 7.40/40/50/24

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172
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

sedative overdose

A
  • acute respiratory acidosis

- 7.24/60/80/26

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173
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

respiratory failure from hypoxia

A
  • acute respiratory acidosis w/ hypoxia

- 7.16/70/50/25

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174
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

emphysematous COPD

A
  • respiratory acidosis w/ metabolic compensation

- 7.37/60/60/34

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175
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

bicarbonate overdose

A
  • metabolic alkalosis w/ respiratory compensation

- 7.44/60/90/39

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176
Q

expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)

sepsis, ASA overdose, renal failure

A
  • metabolic acidosis w/ respiratory compensation

- 7.36/28/90/15

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177
Q

what is normal serum osmolality?

A

282 +/- 2 mOsm/kg H2O

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178
Q

what is the common term for arginine vasopressin (AVP)?

A

antidiuretic hormone (ADH)

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179
Q

what are the most important mechanisms that regulate ADH levels?

A
  1. osmoreceptors in the hypothalamus

2. volume (stretch) receptors in the LA

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180
Q

what is the STRONGEST stimulant for ADH release?

A

significant VOLUME LOSS resulting in hypotension

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181
Q

what is CRITICAL in determining treatment for a pt w/ a sodium abnormality?

A

volume status

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182
Q

in general, if a pt is EDEMATOUS, what is the volume status?

A

volume OVERLOAD

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183
Q

if the pt has clinical signs of VOLUME LOSS, what is the volume status?

A

volume DEFICIT

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184
Q

if the pt is neither edematous, nor showing signs of volume loss, what is the volume status?

A

euvolemic

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185
Q

what are the clinical clues to hypovolemia?

A
  • tachycardia
  • narrowed pulse pressure
  • orthostatic hypotension
  • resting tachycardia w/ hypotension
  • low central venous pressure
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186
Q

what is the MC electrolyte abnormality?

A

hyponatremia

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187
Q

how is hyponatremia further classified?

A
  • ISOOSMOLAR
  • HYPEROSMOLAR
  • HYPOOSMOLAR
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188
Q

what is the 1st step after discovering hyponatremia?

A

determine serum osmolality

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189
Q

artifactual decrease in serum Na+ associated w/ older lab instruments

A

isoosmolar hyponatremia

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190
Q

both GLUCOSE and MANNITOL cause an osmotic shift of water OUT of cells, which dilutes plasma Na+

A

hyperosmolar hyponatremia

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191
Q

by far, the largest low-Na+ subgroup

A

hypoosmolar hyponatremia

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192
Q

low osmolality causes water movement into cells, leading to

A

INTRACELLULAR SWELLING

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193
Q

what can occur when Na+ falls ACUTELY (usually < 120)?

A
  • neuromuscular excitability
  • seizures
  • coma
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194
Q

how is the hypoosmolar subgroup of hyponatremia further subdivided?

A

VOLUME status: low, high, and normal

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195
Q

serum sodium concentration is a ratio of total body sodium to water, which means the pt has more water relative to total body sodium; what are the 3 ways this can happen?

A
  1. loss of sodium
  2. true water excess
  3. total body sodium excess exceeded by water excess
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196
Q

what is the FIRST thing to do in a pt w/ hypotonic hyponatremia?

A

assess volume status (done clinically)

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197
Q

in a pt w/ hypotonic hyponatremia, what does volume status essentially reflect?

A

total body sodium content

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198
Q

why do LOW-VOLUME pts have hypotonic hyponatremia?

A

lose both water and Na+, but more Na+ than water

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199
Q

what are causes of hypotonic hypovolemic hyponatremia?

A
  • diuretics
  • GI losses (vomiting and diarrhea)
  • third spacing of fluid
  • adrenal insufficiency (Addison disease)
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200
Q

how does primary adrenal insufficiency cause hypotonic hypovolemic hyponatremia?

A
  • cortisol and aldosterone deficiency
  • low aldosterone = renal Na+ wasting, decreased K+ and H+ excretion resulting in hypovolemia (sometimes w/ hypotension), hyperkalemia, and metabolic acidosis
  • low cortisol = stimulates ADH production
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201
Q

why do HIGH-VOLUME pts (w/ dependent EDEMA and JVD) have hypotonic hyponatremia?

A

retain water and Na+, but more water than Na+

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202
Q

what are causes of hypotonic hypervolemic hyponatremia?

A
  • heart failure
  • cirrhosis
  • nephrotic syndrome
  • kidney failure: acute or chronic
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203
Q

treatment for hypotonic hypervolemic hyponatremia

A

WATER and Na+ restriction

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204
Q

treatment for hypotonic hypervolemic hyponatremia if water and Na+ restriction are not enough

A

LITHIUM or DEMECLOCYCLINE = induce tubular resistance to ADH

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205
Q

what can worsen hypotonic hypervolemic hyponatremia by impairing urinary-diluting ability?

A

THIAZIDE diuretics

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206
Q

what type of diuretic can be very effective in the treatment of high-volume hyponatremia?

A

loop diuretics

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207
Q

what high-volume pt has a low GFR even w/ a normal creatinine and rapid diuresis can easily precipitate AKI?

A

cirrhotic pt

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208
Q

what are causes of hypotonic euvolemic hyponatremia?

A
  • SIADH
  • drugs that mimic ADH or release ADH
  • psychogenic polydipsia
  • hypothyroidism
  • isolated glucocorticoid deficiency
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209
Q

causes of SIADH

A
  • CNS disease (e.g. meningitis)
  • lung disease (e.g. pneumonia)
  • neoplasms (especially small cell lung cancer)
  • drugs
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210
Q

MC drugs associated w/ SIADH

A
  • NSAIDs
  • SSRIs
  • carbamazepine and oxcarbazepine
  • psychotropic drugs: haloperidol, amitriptyline
  • IV cyclophosphamide
  • vincristine/vinblastine
  • cisplatin
  • chlorpropamide (now rarely used)
  • ecstasy (methylenedioxymethamphetamine)
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211
Q

diagnosis for SIADH

A

compare urine and serum osmolalities (serum osm will be low, urine osm inappropriately high (> 250 mOsm/L))

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212
Q

serum and urine osms in psychogenic polydipsia

A
  • serum osm = low

- urine osm = low (kidney is excreting free water by making dilute urine)

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213
Q

what is the mechanism for ADH release in moderate-to-severe hypothyroidism?

A

decreased cardiac output –> stimulates carotid baroreceptors

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214
Q

what should be r/o in all pts w/ hyponatremia before making a dx of SIADH, and why?

A
  • hypothyroidism
  • glucocorticoid deficiency
  • both can cause low serum osmolalities and high urine osmolalities
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215
Q

what drug class can cause euvolemic low osmolality hyponatremia via ADH-related and non-ADH-related mechanisms?

A

thiazides

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216
Q

how can cause euvolemic low osmolality hyponatremia?

A
  • inducing mild volume depletion –> stimulates ADH release

- impairs urinary dilution in early DISTAL tubule

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217
Q

what pt population is highly susceptible to thiazides impairing urinary dilution?

A

elderly pts

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218
Q

how is ASYMPTOMATIC hyponatremia treated?

A

based on etiology

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219
Q

treatment for normal serum osmolality hyponatremia

A

artifact, no treatment required

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220
Q

treatment for high serum osmolality hyponatremia

A

treat underlying cause (e.g. DKA)

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221
Q

treatment for low serum osmolality HYPOvolemic hyponatremia

A

normal saline to replenish deficit (watch for over-rapid correction!)

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222
Q

treatment for low serum osmolality HYPERvolemic hyponatremia

A

fluid restriction (about 800 cc/day) +/- loop diuretics

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223
Q

treatment for low serum osmolality euvolemic hyponatremia

A

treat SIADH w/ fluid restriction (about 800 cc/day)

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224
Q

treatment for refractory SIADH

A

ADH receptor antagonist (-vaptan; conivaptan, tolvaptan)

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225
Q

when are conivaptan, or tolvaptan used to treat SIADH?

A

severe, chronic hyponatremia (Na+ < 120 mg/dL)

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226
Q

what are the SEVERE symptoms of hyponatremia?

A
  • lethargy
  • confusion
  • coma
  • seizures
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227
Q

what is the treatment of hyponatremia if symptoms are SEVERE, and when should it be used?

A
  • 100mL bolus of 3% saline (to quickly raise Na+ by 2-3 meq/L)
  • if the pt is NOT hypovolemic
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228
Q

what correction rate should NEVER be exceeded when correcting for hyponatremia, and why?

A
  • 9 MEQ/L OVER 24 HOURS

- risk of osmotic demyelination syndrome

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229
Q

treatment for severe symptoms of hyponatremia if symptoms persist after the initial bolus

A

2 more boluses of 3% saline in 10-minute intervals

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230
Q

treatment for MODERATE symptoms (confusion, lethargy) of hyponatremia and suspected SIADH

A

3% saline at initial rate of 0.5-1 mL/kg lean body weight/hour

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231
Q

in what pt is osmotic demyelination syndrome more likely to occur in?

A

pt w/ chronic, severe hyponatremia (Na+ < 115 meq/L for > 2 days) whose sodium is corrected rapidly (> 10 meq/L over 24 hours)

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232
Q

what are the symptoms of osmotic demyelination syndrome?

A
  • speech and swallowing difficulties
  • weakness, or paralysis
  • cognitive deficits
  • coma
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233
Q
  • can cause severe and sometimes symptomatic hyponatremia

- reported in marathon runners

A

exercise-induced hyponatremia

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234
Q

severe hypernatremia is fairly rare but ALWAYS represents what?

A

WATER DEFICIT

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235
Q

unlike hyponatremia, hypernatremic pts are ALWAYS

A

HYPEROSMOLAR

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236
Q

what is the 1st step in a pt w/ hypernatremia?

A

determining volume status

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237
Q

treatment for severe hypovolemic hypernatremia

A

NORMAL SALINE first to correct volume deficit, then hypotonic fluids to further replace the water deficit

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238
Q

calculation for free water deficit

A

Vol(water) = total body water x ([Na+(serum) - 140]/140)

Vol(water) = 0.6 x body weight x ([Na+(serum) - 140]/140)

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239
Q

correction rate for hypernatremia

A

0.5 meq/L/hr or 10-12 meq/L/day

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240
Q

what can occur from too rapid a correction of any severe hyperosmolar state, such as hypernatremia, nonketotic hyperglycemic coma, and severe uremia?

A

cellular swelling

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241
Q

what can cellular swelling cause?

A
  • cerebral edema
  • seizures
  • coma
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242
Q

causes of high-volume hypernatremia

A
  • salt water drowning

- large amounts of sodium bicarbonate or hypertonic saline during ACLS

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243
Q

treatment for high-volume hypernatremia

A

loop diuretics and free water

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244
Q

causes of normal-volume hypernatremia

A
  • diabetes insipidus (DI)

- reduced access to water (become hypernatremic) before developing volume depletion

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245
Q

what’s the Na+ level of a typical DI pt?

A

NORMAL or BORDERLINE-HIGH (bc they’re constantly drinking water)

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246
Q

primary complaint of a DI pt

A

polyuria and polydipsia

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247
Q
  • pt w/ high Na+ and high urine volume

- h/o recent neurosurgery, head trauma, brain cancer/metastases

A

central DI

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248
Q

causes of nephrogenic DI

A
  • can be hereditary (mutations in vasopressin 2 receptor or aquaporin 2 genes)
  • hypercalcemia (serum Ca2+ > 11 mg/dL)
  • chronic hypokalemia ( serum K+ < 3 meq/L)
  • intrinsic renal disease (especially SJOGREN syndrome)
  • drugs (especially LITHIUM)
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249
Q

what test not only diagnoses DI, but also differentiates between central and nephrogenic types?

A

water restriction test

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250
Q

in CENTRAL DI, even w/ water restriction, what happens to the ADH level and urine osmolality?

A
  • ADH stays LOW

- urine is dilute

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251
Q

in a normal pt, what happens to the ADH level and urine concentration when the plasma osmolality increases to 295?

A
  • ADH level is high

- urine is maximally concentrated (> 700 mOsm/L)

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252
Q

treatment for MILD cases of central DI

A

thiazides and salt restriction

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253
Q

treatment for PARTIAL central DI when desmopressin might be too potent or limited in supply

A
  • chlorpropamide

- carbamazepine

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254
Q

treatment for resistant central DI

A

oral or intranasal desmopressin (synthetic vasopressin analog)

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255
Q

in NEPHROGENIC DI, what happens to the ADH level and urine osmolality w/ water restriction?

A
  • ADH is appropriately high

- urine is DILUTE

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256
Q

treatment for nephrogenic DI

A

thiazide diuretics or amiloride

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257
Q

treatment for hereditary forms of nephrogenic DI

A

NSAIDs

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258
Q

URINE OSMOLALITY range

A

50-1,200 mOsm/L

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259
Q

what must be known in order to make sense of the urine osmolality?

A

URINE OUTPUT (L/d)

multiply osmolality by output (1 kg = 1 L)

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260
Q

what is a normal urine osmolality?

A

about 500

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261
Q

after glomerular filtration, the filtrate flows through which sections of tubules?

A
  • proximal tubule
  • loop of Henle
    (- thin descending segment)
    (- thin ascending segment)
    (- thick ascending segment)
  • early distal tubule
  • late distal tubule and cortical collecting duct
  • medullary collecting duct
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262
Q

what is filtered in the proximal tubule?

A

65% of filtered Na+, Cl-, and water is reabsorbed

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263
Q

is water permeable in the proximal tubule?

A

yes, very permeable; is reabsorbed in 1:1 fashion w/ Na+ (filtrate volume is reduced along tubule)

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264
Q

name the transport channels in the proximal tubule

A
  • counter-transport of Na+ (into interstitium) and H+ (into filtrate); via secondary active transport
  • counter-transport of Na+ (into interstitium) and K+ (into filtrate); via ATPase active transport
  • cotransport of Na+, Cl-, K+, glucose, amino acids (into interstitium)
  • paracellular absorption of Ca2+, and other solutes
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265
Q

how is the Na+/H+ counter-transport channel in the PT stimulated and what drugs inhibit it?

A
  • stimulated by angiotensin II

- CARBONIC ANHYDRASE INHIBITORS and THIAZIDES (slightly)

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266
Q

how much HCO3- is reabsorbed in PT?

A

90% of filtered HCO3- is reabsorbed indirectly by Na+/H+ counter-transport pump

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267
Q

for each H+ secreted, what is reabsorbed in the PT and how?

A
  • one Na+ and one HCO3-
  • H+ is counter-transported into filtrate –> combines w/ filtered HCO3- to form H2CO3 (carbonic acid) –> CA converts H2CO3 to H2O and CO2 –> CO2 is absorbed into tubular cells –> gets converted back to HCO3- –> HCO3- reabsorbed into interstitium
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268
Q

what also affects Na+/H+ counter-transporter?

A

POTASSIUM CONCENTRATION

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269
Q

how does hypOkalemia affect serum acid-base level?

A

stimulates H+ secretion –> stimulates bicarb reabsorption –> alkalosis

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270
Q

how does hypERkalemia affect serum acid-base level?

A

inibhits H+ secretion –> inhibits bicarb reabsorption –> acidosis

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271
Q

what are the clinical effects of proximal tubule damage?

A
  • failure to REABSORB water
  • failure to SECRETE ACID and REABSORB BICARBONATE = proximal (type 2) NAGMA
  • failure to reabsorb solutes (Na+, Cl-, K+, glucose, aa) = Fanconi syndrome +/- hypokalemia
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272
Q

in the THIN descending segment, how much H2O moves from the filtrate into the interstitium? and, where is the maximum concentration of fluid?

A
  • 20%

- base of the loop

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273
Q

WHY is the renal medulla very hypERtonic?

A
  • in THIN ascending segment NaCl passively diffuses into interstitium
  • in THICK ascending segment solutes ACTIVELY transported into interstitium
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274
Q

cotransport of Na+, 2 Cl-, and K+ (into interstitium) is INHIBITED by

A

LOOP diuretics

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275
Q

name the 4 loop diuretics

A
  1. furosemide
  2. bumetanide
  3. torsemide
  4. ethacrynic acid
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276
Q

at what GFR do loop diuretics REMAIN EFFECTIVE?

A

low GFR = CrCl < 20 (just have to increase dose and/or give IV)

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277
Q

which 2 loop diuretics are associated w/ permanent ototoxicity at high IV bolus doses?

A
  • furosemide

- ethacrynic acid

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278
Q

what are the 2 mechanisms in which loop diuretics cause diuresis?

A
  1. prevent Na+ reabsorption in THICK ascending segment

2. prevent development of interstitial osmotic gradient in the THIN descending segment

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279
Q

when are LOOP DIURETICS used to treat hypercalcemia?

A

use is considered QUESTIONABLE, UNLESS becomes VOLUME OVERLOAD

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280
Q

cotransport of Na+ and Cl- (into interstitium) in the EARLY distal tubule is inhibited by

A

thiazide diuretics

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281
Q

name the 4 thiazide diuretics

A
  1. chlorothiazide
  2. hydrochlorothiazide
  3. chlorthalidone
  4. metolazone
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282
Q

why are thiazide diuretics less effective at an extremely low GFR?

A

have to be secreted INTO filtrate

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283
Q

how do thiazides cause hypOkalemia?

A

slightly inhibit carbonic anhydrase in proximal tubule –> increased delivery of Na+ to early distal tubule –> upregulation of Na/K ATPase counter-transport channel

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284
Q

which diuretics INCREASE CALCIUM REABSORPTION?

A

thiazides

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285
Q

can help in reducing urinary calcium in pts w/ kidney stones

A

thiazides

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286
Q

allow for further solute and water reabsorption and are controlled by ALDOSTERONE and ADH

A

LATE DISTAL tubule and CORTICAL COLLECTING DUCT

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287
Q

2 cell types in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT that reabsorb solutes

A
  1. principal cells

2. intercalated cells

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288
Q

what gets counter-transported in the principal cells?

A

Na+ (into interstitium) and K+ (into filtrate)

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289
Q

what stimulates principal cells in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT?

A
  • aldosterone

- hyperkalemia

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290
Q

what inhibits principal cells in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT?

A

potassium-sparing diuretics (amiloride, triamterene, spironolactone, eplerenone)

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291
Q

what gets secreted in the intercalated cells?

A

H+ (into filtrate)

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292
Q

what controls water reabsorption in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT?

A

ADH which stimulates AQUAPORINS

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293
Q

name 2 diseases that affect the last distal tubules and cortical collecting ducts

A
  • distal (type 1 RTA)

- distal (type 4 RTA)

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294
Q
  • impairment of H+-ATPase active transport pump in intercalated cells –> inability to secrete acid (and reabsorb bicarb)
  • urine pH is always > 5.3
A

distal (type 1 RTA) NAGMA

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295
Q
  • tubular aldosterone resistance –> impairment of Na+/K+ ATPase counter-transporter
  • HYPERKALEMIA
  • can also occur in DM
A

distal (type 4 RTA) NAGMA

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296
Q

where is the remaining 10% of Na+ and water absorbed?

A

medullary collecting duct

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297
Q

in the absence of ADH, which segments of the nephron are relatively impermeable to water?

A

LATE DISTAL tubule and CORTICAL COLLECTING DUCT

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298
Q
  • name 2 ADH-receptor antagonists

- sometimes used to treat hypOnatremia

A
  • conivaptan (IV only)

- tolvaptan (PO)

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299
Q
  • problem in H+-ATPase
  • failure to acidify urine
  • HYPOkalemia
  • hypercalciuria +/- nephrocalcinosis
A

distal (type 1) RTA

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300
Q

MCC of distal (type 1) RTA

A
  • genetic (presents in childhood)
  • autoimmune (Sjogren’s, SLE, RA)
  • hereditary hypercalciuria
  • drugs (amphotericin B, lithium)
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301
Q

treatment for distal (type 1) RTA

A
  • NaHCO3
  • K+ replacement
  • tx underlying cause
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302
Q
  • problem w/ cells in PROXIMAL tubule –> BICARBONATE WASTING
  • also, problems w/ cotransport of Na+ w/ glucose, aa, Cl-, and K+
A

proximal (type 2) RTA

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303
Q

MCC of proximal (type 2) RTA

A
  • monoclonal gammopathies (MM) w/ buildup of light chains that damage tubule cells
  • CA inhibitors
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304
Q

treatment for proximal (type 2) RTA

A
  • bicarbonate (very large doses)
  • K+ replacement
  • vitamin D supplementation
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305
Q
  • HYPORENINEMIC HYPOALDOSTERONISM (or ALDOSTERONE RESISTANCE) in the principal cells of the late distal tubule and cortical collecting duct
  • nonfunctioning Na+/K+ ATPase counter-transport
  • associated w/ HYPERkalemia
A

type 4 (distal) RTA

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306
Q

causes of hyporeninemic hypoaldosteronism (3)

A
  1. diabetic nephropathy
  2. obstructive uropathy
  3. chronic interstitial nephritis
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307
Q

common drugs that can lead to hyperkalemic metabolic acidosis SIMILAR to type 4 (distal) RTA

A
  • spironolactone
  • ACEIs/ARBs
  • NSAIDs (exacerbates a concurrent hyporeninemic state)
308
Q

treatment for type 4 (distal) RTA

A
  • dietary potassium restriction
  • or bicarbonate administration
  • furosemide if 1st 2 don’t work
309
Q
  • HYPERCALCIURIA
  • +/- NEPHROCALCINOSIS
  • high urine pH
  • HYPOKALEMIA
A

type 1 (distal) RTA

310
Q
  • BICARBONATE WASTING
  • FANCONI’S
  • urine pH and serum K+ are variable
  • think MYELOMA
A

type 2 (proximal) RTA

311
Q
  • ALDOSTERONE DEFICIENCY or RESISTANCE
  • mild acidosis
  • HYPERkalemia
  • think causes of hyporeninemic hypoaldosteronism (interstitial disease, diabetes, NSAIDs, ACEIs)
A

type 4 (distal) RTA

312
Q

which chemistry profile is associated w/ the following clinical scenario?

  • DKA

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

A

D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100

313
Q

which chemistry profile is associated w/ the following clinical scenario?

  • pt w/ DM and CKD

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

A

B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100

314
Q

which chemistry profile is associated w/ the following clinical scenario?

  • pt w/ myeloma

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

A

C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100

315
Q

which chemistry profile is associated w/ the following clinical scenario?

  • woman w/ nephrolithiasis

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

A

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100

316
Q

which chemistry profile is associated w/ the following clinical scenario?

  • pt w/ heavy metal poisoning

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

A

C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100

317
Q

which chemistry profile is associated w/ the following clinical scenario?

  • pt w/ chronic diarrhea

A) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

A

E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10

318
Q

any situation that causes aldosterone to be released (or mimics aldosterone), will have what effect on K+?

A

LOWERS it

319
Q

situations that cause aldosterone release (4)

A
  1. increased renin d/t decreased effective arterial blood volume
    - volume depletion (GI losses, diuretics)
    - decreased renal perfusion (HF, renovascular dz, NSAIDs)
  2. increased renin d/t inappropriate release
    - renin-secreting renal tumors
  3. increased aldosterone d/t inappropriate release
    - B/L adrenal hyperplasia
    - aldosterone-secreting adrenal adenoma
  4. increased excretion of hormone w/ aldosterone-like effects
    - Cushing syndrome
320
Q

any situation that INHIBITS aldosterone release or action, will have what effect on K+?

A

INCREASES it

321
Q

situations that cause aldosterone release (4)

A
  1. K+-sparing diuretics (spironolactone blocks aldosterone receptor; amiloride blocks the channel its action depends on)
  2. dysfunctional kidneys that do not release renin (chronic interstitial nephritis, DM, exacerbated by NSAIDs)
  3. ACEIs, ARBs, renin inhibition
  4. only primary adrenal disease (Addison’s) [NOT secondary adrenal insufficiency]
  5. heparins (both UFH and LMWH) (directly toxic to zona glomerulosa)
322
Q

what increase K+ uptake causing hypOkalemia?

A
  • alkalosis
  • beta-agonists
  • insulin
323
Q

what decrease K+ uptake causing hypERkalemia?

A
  • acidosis

- alpha-agonists

324
Q

what electrolyte abnormality can cause alkalosis?

A

hypOkalemia

325
Q

what electrolyte abnormality can cause acidosis?

A

hypERkalemia

326
Q

conditions leading to increased cell turnover associated w/ hypERkalemia (3)

A
  1. tumor lysis syndrome
  2. rhabdomyolysis
  3. acute leukemia
327
Q

medication that interferes w/ K+ secretion in principal cells (late distal tubule and cortical collecting duct) causing hypERkalemia

A

trimethoprim in TMP/SMX

328
Q

RTA associated w/ hypOkalemia for unclear reasons

A

type 1 (distal) RTA

329
Q

block absorption of solutes and water causing hypOkalemia

A

loop and thiazide diuretics

330
Q

drugs associated w/ renal K+ wasting causing hypOkalemia

A
  • cisplatin

- penicillins

331
Q

genetic syndromes associated w/ hypOkalemia (3)

A
  1. Liddle’s
  2. Barter’s
  3. Gitelman’s
332
Q

presentation of hypERkalemia (signs/symptoms)

A
  • significant weakness or paralysis
  • conduction abnormalities
  • arrhythmias
333
Q

if a pt is weak d/t hypERkalemia, will there be EKG changes?

A

yes, but the opposite is not necessarily true

334
Q

name the sequence of EKG changes w/ progressive hypERkalemia

A
  • peaked T wave and short QT interval, then
  • progressive lengthening of PR and QRS intervals, then
  • loss of P wave, and QRS widening into sine wave, then
  • ventricular fibrillation or cardiac standstill
335
Q

treatment for acute hypERkalemia w/ EKG changes

A
  • IV calcium gluconate (or CaCl if pt has central line)
  • insulin w/ glucose
  • NaHCO3 (if acidosis is present)
  • albuterol nebulization/injection
  • loop diuretics (in pts who make urine)
  • dialysis
336
Q

when calcium gluconate not be given for the treatment of hypERkalemia?

A

pts on digoxin

337
Q

sodium polystyrene sulfonate (SPS; Kayexalate) in sorbitol (MC preparation) has been associated w/?

A

colon necrosis

especially w/i a week after surgery and pts w/ ileus

338
Q

when should hypERkalemia be treatment even w/o symptoms or EKG changes?

A

6.5 or more

339
Q

what hypERkalemia treatment can cause edema and may precipitate cardiac decompensation?

A

NaHCO3

340
Q

signs and symptoms of severe hypOkalemia

A
  • U waves
  • decreased tendon reflexes
  • rhabdomyolysis
341
Q

at what net loss of K+ will serum K+ decrease?

A

200-300 meq

342
Q

what comorbid electrolyte deficiency can cause renal K+ wasting?

A

magnesium

343
Q

caused by disease in the adrenal gland

A

primary hyperaldosteronism

344
Q

caused by disease in the kidneys or a restricted blood flow in the renal arteries

A

secondary hyperaldosteronism

345
Q

mechanism of secondary hyperaldosteronism

A

decreased renal blood flow –> increased renin –> increased angiotensin II –> increased aldosterone

346
Q

what should be considered in a pt w/ hypokalemia w/o an obvious cause, HTN, and metabolic alkalosis?

A

hyperaldosteronism

347
Q
  • HTN
  • hypOkalemic metabolic alkalosis
  • primary Na+ retention
  • rare genetic mutation activating the epithelial Na+ channel in principal cells of the late distal tubule and cortical collecting duct
  • decreased renin and aldosterone levels
A

Liddle syndrome

348
Q

name 2 syndromes that are d/t rare genetic or sporadic defects that cause abnormal solute transport in the THICK ASCENDING segment and EARLY DISTAL TUBULE

A
  1. Bartter syndrome

2. Gitelman syndrome

349
Q
  • 4 types
  • typically AR
  • clinically, pts look like they’re taking a loop diuretic
  • onset = infants/children
  • type 4 is associated w/ deafness
  • HYPERcalciuria/nephrocalcinosis
  • hypOkalemic, METABOLIC ALKALOSIS
A

Bartter syndrome

350
Q
  • defect in Na+/Cl- cotransporter in early distal tubule
  • clinically, pts look like they’re taking a thiazide diuretic
  • some pts have SEVERE MAGNESIUM WASTING
  • onset = early adults
  • present w/ sxs of muscle weakness, cramps, and spasms d/t hypomagnesemia
  • HYPOcalciuria
  • hypOkalemic, METABOLIC ALKALOSIS
A

Gitelman syndrome

351
Q

clinical approach to hypOkalemia

A
  • hypokalemia and NAGMA WITHOUT HTN
  • hypokalemia and metabolic alkalosis AND HTN
  • hypokalemia and metabolic alkalosis WITHOUT HTN
352
Q

causes of hypokalemia and NAGMA WITHOUT HTN (3)

A
  • diarrhea
  • type 1 (distal) RTA
  • type 2 (proximal) RTA
353
Q

causes of hypokalemia and metabolic alkalosis AND HTN (5)

A
  • diuretics (MC)
  • hyperaldosteronism (primary or secondary)
  • Cushing syndrome
  • Liddle syndrome
  • adrenal hydroxylase deficiencies
354
Q

causes of hypokalemia and metabolic alkalosis WITHOUT HTN (2)

A
  • Bartter syndrome

- Gitelman syndrome

355
Q

hypERcalcemia found incidentally in an asymptomatic pt is usually d/t

A
  • THIAZIDE diuretics or

- PRIMARY HYPERPARATHYROIDISM (especially if h/o NECK IRRADIATION)

356
Q

most common causes of hypOcalcemia (5)

A
  1. vitamin D deficiency
  2. CKD
  3. severe pancreatitis
  4. rhabdomyolysis
  5. hypermagnesemia
357
Q

less common causes of hypOcalcemia (4)

A
  1. hungry bone syndrome following parathyroidectomy
  2. hypoparathyroidism
  3. pseudohypoparathyroidism
  4. citrate
358
Q

both increased and decreased magnesium can cause

A

hypOcalcemia

359
Q

how does increased calcium affect magnesium?

A

hypOmagnesemia

360
Q

hypOmagnesemia has what effect on K+?

A

hypOkalemia

361
Q

causes of hypOmagnesemia (VERY COMMON electrolyte abnormality) (9)

A
  • GI disease
  • kidney losses (especially tubular disease)
  • medications that affect the tubules
  • PPIs
  • hungry bone syndrome
  • alcohol abuse
  • post-surgical state
  • foscarnet (d/t chelation)
  • hypERcalcemia
362
Q

clinical manifestations of hypOmagnesemia

A
  • muscle weakness, spasms, tetany
  • wide QRS
  • peaked T waves
363
Q

depleted magnesium STORES, even w/ a NORMAL serum LEVEL are associated w/ what?

A

REFRACTORY cardiac arrhythmias

364
Q

how many meq of Mg++ are in 1G?

A

8.12 meq

365
Q

causes of hypERmagnesemia (RARE)

A
  • Mg-containing laxatives, antacids, enemas in pts w/ renal failure (CONTRAINDICATED)
  • over-infusion during eclampsia tx
  • less common: TLS, milk-alkali syndrome, lithium overdose, Epsom salts ingestion
366
Q

when do sxs from hypERmagnesemia occur?

A

> 4-6 meq/L

367
Q

clinical manifestations of hypERmagnesemia

A

nausea initially –> sedation –> muscle WEAKNESS –> loss of DTRs –> paralysis (including heart/respiratory mm)

368
Q

treatment for hypERmagnesemia

A
  • IVF and Ca2+

- HD in renal failure

369
Q

ACUTE increases of phosphate causing hypERphosphatemia (3)

A
  • ATN (especially if d/t rhabdo)
  • IV solutions
  • rapid cell turnover (tumor lysis or acute leukemia)
370
Q

CHRONIC increases of phosphate causing hypERphosphatemia (2)

A
  • CKD

- hypOparathyroidism

371
Q

causes of hypOphosphatemia

A
  • think ALCOHOLISM and ALCOHOLIC KETOACIDOSIS

- REFEEDING syndrome

372
Q

clinical manifestations of severe hypOphosphatemia (if PO4 < 1 mg/dL)

A
  • rhabdomyolysis
  • cardiomyopathy
  • respiratory insufficiency (diaphragm function failure)
  • irritability and hyperventilation –> profound muscle weakness –> seizures –> coma –> death
373
Q

volume contraction: vomiting
choose the correct answer

a. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 10 urine calc osm 700
b. Na+ low-NL Cl- 115 HCO3- 15 urine Cl- 10 urine calc osm 700
c. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 100 urine calc osm 700
d. Na+ low-NL Cl- NL HCO3- NL urine Cl- 100 urine calc osm 300 (but high volume)

A

a. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 10 urine calc osm 700

374
Q

volume contraction: diarrhea
choose the correct answer

a. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 10 urine calc osm 700
b. Na+ low-NL Cl- 115 HCO3- 15 urine Cl- 10 urine calc osm 700
c. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 100 urine calc osm 700
d. Na+ low-NL Cl- NL HCO3- NL urine Cl- 100 urine calc osm 300 (but high volume)

A

b. Na+ low-NL Cl- 115 HCO3- 15 urine Cl- 10 urine calc osm 700

375
Q

volume contraction: thiazides
choose the correct answer

a. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 10 urine calc osm 700
b. Na+ low-NL Cl- 115 HCO3- 15 urine Cl- 10 urine calc osm 700
c. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 100 urine calc osm 700
d. Na+ low-NL Cl- NL HCO3- NL urine Cl- 100 urine calc osm 300 (but high volume)

A

c. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 100 urine calc osm 700

376
Q

volume contraction: osmotic diuretics
choose the correct answer

a. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 10 urine calc osm 700
b. Na+ low-NL Cl- 115 HCO3- 15 urine Cl- 10 urine calc osm 700
c. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 100 urine calc osm 700
d. Na+ low-NL Cl- NL HCO3- NL urine Cl- 100 urine calc osm 300 (but high volume)

A

d. Na+ low-NL Cl- NL HCO3- NL urine Cl- 100 urine calc osm 300 (but high volume)

377
Q

volume contraction

VOMITING causes metabolic ALKALOSIS and:

A
  • low serum Cl-

- hypOkalemia d/t aldosterone

378
Q

volume contraction

DIARRHEA causes metabolic ACIDOSIS (NAGMA) and:

A
  • appropriately high serum Cl-

- Cl- is reabsorbed to make up for HCO3- loss

379
Q

THIAZIDE diuretics also cause metabolic ALKALOSIS w/ low serum Cl-, but has what effect on urinary Cl-?

A

HIGH

380
Q

when do DIABETES INSIPIDUS pts become hypERnatremic?

A

only pts who are unable to drink

usually have a NORMAL intravascular volume and Na+ concentration

381
Q

how is HTN diagnosed?

A

2 or more readings taken on 2 or more visits

382
Q

what is stage ONE HTN?

A

SBP 140-159, or DBP 90-99

383
Q

what is stage TWO HTN?

A

SBP 160 or more, or DBP 100 or more

384
Q

in any stage of HTN, which sex and race has a higher morbidity and mortality?

A
  • MEN

- BLACKS

385
Q

when should you f/u or w/u?

  • DBP < 85
A

recheck in 2-3 years

386
Q

when should you f/u or w/u?

  • 85-90
A

recheck in 1 year

387
Q

when should you f/u or w/u?

  • 90-104
A

recheck w/i 2 months

388
Q

when should you f/u or w/u?

  • 105-114
A

w/u w/i 2 weeks

389
Q

when should you f/u or w/u?

  • > 115
A

w/u immediately

390
Q

standard evaluation for newly diagnosed HTN

A
  • major cardiovascular disease risk factors

- IDENTIFIABLE CAUSES of HTN

391
Q

list the IDENTIFIABLE CAUSES of HTN (8)

A
  • pheochromocytoma
  • renovascular HTN
  • coarctation of aorta
  • polycystic kidneys
  • renal parenchymal disease
  • hyperparathyroidism
  • granulomatous disease
  • hyperaldosteronism
392
Q
  • labile HTN
  • medullary thyroid cancer
  • primary hyperparathyroidism (MEN2)
A

pheochromocytoma

393
Q
  • HTN

- continuous abdominal bruit

A

renovascular HTN (renal artery stenosis or fibromuscular dysplasia)

394
Q
  • HTN

- decreased BP in LEs or absent/delayed femoral pulses

A

coarctation of aorta

395
Q
  • HTN

- abdominal or flank masses

A

polycystic kidneys

396
Q
  • HTN

- elevated creatinine or abnormal UA

A

renal parenchymal disease

397
Q
  • HTN

- hypercalcemia

A
  • hyperparathyroidism

- granulomatous disease

398
Q
  • HTN

- hypokalemia

A

hyperaldosteronism

399
Q

what are the indications for evaluation of secondary HTN?

A
  • abnormal initial lab tests (hypERcalcemia/hypOkalemia)
  • abrupt onset
  • onset at age < 30 yoa or > 55 yoa
  • malignant HTN
  • refractory HTN (BP > target despite 3 meds, one being a diuretic)
400
Q

MCC of secondary HTN

A

renovascular HTN (renal artery stenosis or fibromuscular dysplasia)

401
Q
  • treatment for HTN w/

- edema w/ HF or CKD

A

loop diuretic

402
Q
  • treatment for HTN w/

- systolic dysfunction and low EF or problems w/ hypokalemia

A

spironolactone

403
Q

what dose of HCTZ provides the greatest antihypertensive effect?

A

12.5 mg

404
Q

which antihypertensive medication can cause severe hypOnatremia in pts w/ poor solute intake; especially the elderly?

A

thiazide diuretics

405
Q

how does angiotensin II increase BP?

A
  • DIRECT VASOCONSTRICTION
  • potentiation of the SYMPATHETIC NERVOUS SYSTEM
  • increasing Na+ reabsorption in the proximal tubule
  • stimulation of ALDOSTERONE PRODUCTION by the ADRENAL GLAND
406
Q

name the 10 ACEIs

A
  1. captopril
  2. enalapril
  3. benazepril
  4. fosinopril
  5. lisinopril
  6. quinapril
  7. moexipril
  8. ramipril
  9. perindopril
  10. trandolapril
407
Q

MOA of ACEIs

A

inhibit angiotensin-converting enzyme

408
Q

MOA of ARBs

A

block angiotensin receptors, which blocks angiotensin II effect

409
Q

what effect do ACEIs/ARBs have on the glomerulus?

A

DILATION OF EFFERENT arteriole –> decreased glomerular capillary pressure

410
Q

what decreases progression of both DIABETIC and HYPERTENSIVE nephropathies, and other types of CKD?

A

decreased glomerular pressure

411
Q

name the 7 ARBs

A
  1. candesartan
  2. eprosartan
  3. irbesartan
  4. losartan
  5. olmesartan
  6. telmisartan
  7. valsartan
412
Q

what are the absolute INDICATIONS for ACEIs/ARBs? (4)

A
  • systolic dysfunction
  • h/o STEMI
  • anterior NSTEMI
  • CKD (especially w/ proteinuria)
413
Q

complications of ACEIs

A
  • increase in serum K+ by 0.5 meq/L

- renal function decline

414
Q

when do you stop ACEI or ARB?

A
  • creatinine increases to > 30% over baseline

- and/or serum K+ is uncontrollable

415
Q

ACEIs + what combination is particularly noteworthy for complications?

A

HF and sudden initiation of NSAIDs

416
Q

up to 20% of pts have to stop ACEIs because of

A

COUGH

417
Q

what is a possible FATAL adverse effect of ACEIs?

A

angioedema

418
Q

ACEIs/ARBs are absolutely CI in _____ bc they are?

A
  • pregnancy

- TERATOGENIC

419
Q

ACEIs/ARBs should be avoided in which pts?

A

hyperkalemic pts

420
Q

ACEIs/ARBs should be used w/ caution in which pts?

A
  • B/L RAS
  • HF
  • ADPKD
  • hypertensive nephrosclerosis
421
Q

what is ALISKIREN?

A

renin inhibitor; acts similarly to ACEIs/ARBs

422
Q

aliskiren plus an ACEI or ARB in type 2 diabetics showed an increased risk in?

A
  • stroke
  • hyperkalemia
  • low BP
  • renal insufficiency
423
Q

what are the 2 types of CCBs?

A
  • dihydropyridines

- non-dihydropyridines

424
Q

name the dihydropyridine CCBs (6)

A
  • amlodipine
  • clevidipine
  • felodipine
  • isradipine
  • nicardipine
  • nisoldipine
425
Q

name the non-dihydropyridine CCBs (2)

A
  • verapamil

- diltiazem

426
Q

CCBs are used to treat what?

A
  • HTN
  • angina
  • arrhythmias
427
Q

what are the complications of CCBs?

A

significant EDEMA (especially w/ dihydropyridines), and CONSTIPATION (especially w/ non-dihydropyridines)

428
Q

several studies have shown adverse associations (e.g. increased risk of death post-MI) w/?

A

short-acting CCBs (but not long-acting ones)

429
Q

may increase proteinuria in pts w/ DM and CKD

A

dihydropyridines (but not verapamil or diltiazem)

430
Q

are NOT recommended as 1st line treatment for HTN

A

BBs

431
Q

some indications for BBs

A
  • post-MI
  • stable HF
  • AF (rate control)
  • angina
432
Q

try to AVOID BBs in pts w/

A
  • reactive airway disease
  • frequent hypoglycemic episodes
  • hyperlipidemia
  • PVD
433
Q

HTN treatment:

  • general NONblack population
  • +/- DM
A
  • THIAZIDE
  • CCB
  • ACEI/ARB
434
Q

HTN treatment:

  • BLACK population
  • +/- DM
A
  • THIAZIDE

- CCB

435
Q

in HEART FAILURE, treat HTN w/

A
  • thiazide-type diuretic
436
Q

bottom line for HTN treatment

A
  • use any drug or drug combination w/ fewest side effects to get BP < 140/90 (< 150/90 if > 60 yoa)
437
Q

which antihypertensive is NOT recommended as monotherapy d/t increased risk of STROKE and HEART DISEASE?

A

BB

438
Q

monotherapy w/ a thiazide, ACEI/ARB, or long-acting CCB is fine for pts w/?

A

MILD HTN

439
Q

blacks do better w/ which antihypertensives?

A

thiazide or long-acting CCB

440
Q

young pts do best w/ which antihypertensives?

A

ACEI

441
Q

pts who are NOT controlled w/ monotherapy usually do better w/?

A

LOW-DOSE 2nd DRUG

442
Q

when should pts INITIALLY be treated w/ 2 drugs?

A

BP > 160/100

443
Q

what are the lifestyle guidelines for preventing and controlling HTN?

A
  • smoking cessation
  • lose weight/DASH diet
  • regular aerobic activity
  • moderate alcohol and Na+ intake
  • sufficient K+, Mg++, and Ca++ intake
  • reduce saturated and cholesterol intake
444
Q

JNC 8 goals of treatment are based on

A
  • AGE
  • DM
  • CKD
445
Q

BP goals of treatment

  • general population < 60 yoa
A

< 140/90

446
Q

BP goals of treatment

  • general population > 60 yoa
A

< 150/90

447
Q

BP goals of treatment

  • all ages, NO CKD, diabetes
A

< 140/90

448
Q

BP goals of treatment

  • all ages, CKD, with/without DM
A

< 140/90

449
Q

elderly persons generally have what type of HTN?

A

ISOLATED SYSTOLIC

450
Q

should pts > 80 yoa w/ isolated systolic HTN be treated?

A

YES

451
Q

if pharmacologic treatment for high BP in pts > 60 yoa leads to BP < 140 and is well tolerated, does it need to be adjusted?

A

no

452
Q

what is malignant HTN?

A

HTN w/:

  • papilledema, retinal hemorrhages, exudates
  • nephrosclerosis (AKI, proteinuria, hematuria)
453
Q

what is hypertensive encephalopathy?

A

severe HTN w/ signs of cerebral edema

presents as HA, N/V, confusion, coma, and/or seizures

454
Q

treatment goal for hypertensive crisis

A

decrease DBP to 100-105 mmHg w/i 2-6 hours w/o dropping BP by > 25%

455
Q

when treating a hypertensive crisis, TOO RAPID of drop in BP can result in

A
  • ischemic stroke

- MI

456
Q

MCC of secondary HTN

A

renovascular disease causing secondary hyperaldosteronism

457
Q

2 main causes of renovascular HTN

A
  1. atherosclerotic RAS (often BILATERAL, mainly MEN > 50, especially diabetics)
  2. fibromuscular dysplasia (also often BILATERAL, mainly WOMEN < 40)
458
Q

strongly suggestive of renovascular HTN (especially w/ other risk factors; > 55 yoa, diabetic)

A
  • continuous abdominal bruit

- hypOkalemia

459
Q

which pts should be worked up for renovascular HTN?

A
  • have a moderate-to-high risk for disease

- are candidates for intervention (surgery, or angioplasty w/ stent placement)

460
Q

if POTASSIUM levels are NORMAL, screen pts for secondary HTN w/?

A
  • imaging studies
  • CTA
  • MRA
  • duplex Doppler US
461
Q

which pts w/ secondary HTN d/t renovascular disease are almost always candidates for intervention?

A

FIBROMUSCULAR DYSPLASIA, bc they can frequently be CURED

462
Q

when atherosclerotic renal artery stenosis be considered for intervention?

A

ONLY if ONE of the following criteria is met:

  1. uncontrolled BP despite 3 or more meds
  2. recurrent “flash” pulmonary edema
  3. renal salvage (progressive decline in renal function)
463
Q

should elderly pts be screened for secondary HTN?

A

definitely DO NOT SCREEN if mild HTN and normal serum K+

464
Q

pts w/ possible secondary HTN, if the serum K+ is:

NORMAL, what is the next step?

A

go straight to imaging:

  • CTA
  • MRA
  • duplex Doppler US
465
Q

pts w/ possible secondary HTN, if the serum K+ is:

LOW, what is the next step?

A

screen for primary hyperaldosteronism:

  • PAC:PRA (plasma aldosterone concentration to plasma renin activity) ratio
466
Q

pts w/ possible secondary HTN, who are NOT candidates for intervention:

what is the next step?

A

do NOT screen

467
Q

what is the GOLD STANDARD for renovascular HTN?

A

ARTERIOGRAPHY

468
Q

pt not on diuretics, hypOkalemia of unknown etiology, and HTN, suspect?

A

primary or secondary hyperaldosteronism

469
Q

what are the 2 main causes of primary hyperaldosteronism?

A
  1. adrenal adenomas (70%; Conn syndrome)

2. idiopathic B/L adrenal hyperplasia (25%)

470
Q

screening and diagnosis of primary hyperaldosteronism

A

PAC:PRA (plasma aldosterone concentration to plasma renin activity) ratio

471
Q

next step after diagnosing primary hyperaldosteronism w/ PAC:PRA ratio

A

CT scan of adrenals to characterize the gland

472
Q

PAC:PRA ratio indicating primary hyperaldosteronism

A

> 20

473
Q

in a suspected primary hyperaldosteronism pt, how can you assess whether you can suppress aldosterone?

A

recheck aldosterone level after either fluid or salt loading

474
Q

initial treatment of primary hyperaldosteronism

A
  • salt and water restriction
  • K+ sparing diuretics (spironolactone, triamterene, amiloride)
  • +/- thiazide diuretic
475
Q
  • cause of secondary HTN
  • VERY RARE
  • 90% occur in adrenal MEDULLA
  • 90% U/L
  • 90% BENIGN
  • 90% SPORADIC
A

pheochromocytoma

476
Q

paroxysmal signs and symptoms of pheochromocytoma

A
  • palpitations
  • dizziness
  • HTN
477
Q

how many pts w/ pheochromocytoma have SUSTAINED HTN?

A

1/2-2/3

478
Q

diagnosis of pheochromocytoma if low-pretest probability

A

24-hour urine for fractionated metanephrines and catecholamines

479
Q

diagnosis of pheochromocytoma in higher risk pts (family h/o pheo, MEN2, NF)

A

screen w/ fractionated metanephrines on RANDOM PLASMA sample

480
Q

next step in diagnosis for pheochromocytoma if biochemical tests are suggestive

A

CT or MRI w/ contrast

481
Q

test to diagnose pheochromocytoma if imaging is negative and you still suspect pheo

A

metaiodobenzylguanidine scintigraphy (norepinephrine analog that concentrates in adrenal pheo)

482
Q

what should BP always be in pregnancy?

A

< 120/80

483
Q

what are the 4 categories of HTN in pregnancy?

A
  1. chronic HTN
  2. preeclampsia
  3. gestational HTN
  4. chronic HTN w/ superimposed preeclampsia
484
Q

define chronic HTN in pregnancy

A

preexisting HTN or HTN BEFORE 20th WEEK of gestation

485
Q

define preeclampsia in pregnancy

A

HTN + proteinuria AFTER 20th WEEK of gestation in woman w/o h/o HTN

486
Q

define gestational HTN in pregnancy

A

HTN AFTER 20th WEEK of gestation WITHOUT proteinuria in woman w/o h/o HTN

487
Q

define chronic HTN w/ superimposed preeclampsia in pregnancy

A

worsening HTN + NEW ONSET proteinuria AFTER 20th WEEK of gestation WITH h/o controlled, chronic HTN

488
Q

define eclampsia

A

grand mal seizures in a woman w/ preeclampsia or gestational HTN

489
Q

what are the defining features of preeclampsia?

A

proteinuria and HTN, not symptoms

490
Q

what an indication of preeclampsia severity?

A

signs and symptoms

491
Q

what are the signs and symptoms of preeclampsia?

A
  • HA
  • vision changes
  • seizures
  • low platelets
  • stroke
  • intracerebral hemorrhage
  • pulmonary edema
  • hepatic and/or renal failure
  • placental abruption
492
Q

what is HELLP syndrome?

A

severe form of preeclampsia

  • Hemolytic anemia
  • Elevated Liver enzymes
  • Low Platelets
493
Q

what are the risk factors for preeclampsia?

A
  • DM
  • chronic HTN
  • multiple gestations (twins, triplets)
  • h/o preeclampsia
494
Q

what medication should be given in pregnant women w/ moderate-to-high risk for preeclampsia?

  • reduces preeclampsia risk by 24%
  • reduces premature birth risk by 14%
  • reduces intrauterine growth restriction risk by 20%
A

aspirin 81mg PO daily

495
Q

BP goal for SEVERE HTN in pregnancy regardless of category

A

< 160/110

496
Q

recommendations to start BP treatment for preeclampsia

A
  1. if symptoms are present

2. asymptomatic w/ SBP 150 or more, or DBP 95 or more

497
Q

target BP in preeclampsia

A

130-150/80-100

498
Q

what BP medications need to be d/c’d for chronic hypertensives thinking about getting pregnant

A
  • ACEIs/ARBs

- thiazides

499
Q

BP meds of choice in pregnancy

A
  • a-methyldopa
  • labetalol
  • nifedipine
500
Q

parenteral antihypertensives of choice in malignant HTN in pregnancy

A
  • labetalol (preferred)
  • hydralazine
  • nicardipine (2nd line)
501
Q

antihypertensives C/I in pregnancy

A
  • ACEIs/ARBs
  • renin inhibitors
  • nitroprusside (cyanide poisoning in the baby)
502
Q

what are the 1ST LINE PO agents used to treat:

  • CHRONIC, asymptomatic preeclampsia
  • GESTATIONAL HTN
  • and CHRONIC HTN in pregnancy
A
  • LABETALOL
  • A-METHYLDOPA
  • XR-NIFEDIPINE
503
Q

what are the 2ND LINE PO agents used to treat:

  • CHRONIC, asymptomatic preeclampsia
  • GESTATIONAL HTN
  • and CHRONIC HTN in pregnancy
A
  • DILTIAZEM
  • VERAPAMIL
  • THIAZIDES (watch for s/s of volume contraction; including oligohydramnios)
504
Q

other important secondary causes of HTN that must be excluded

A
  • OCPs
  • coarctation of the aorta
  • treatment of obesity
  • decreasing alcohol intake to 2 drinks or less/day
  • correcting CALCIUM or POTASSIUM deficiency
505
Q

AKI can be

A
  • non-oliguric
  • oliguric
  • anuric
506
Q

definition of AKI

A
  • increase in serum Cr by 0.3 mg/dL
  • 1.5-fold over baseline w/i 48 hours
  • or oliguria (UO < 0.5 mL/kg/hour) for at least 6 hours
507
Q

define ANURIA

A

UO < 50 mL/DAY

508
Q

PRErenal AKI is caused by

A

UNDERPERFUSION, either from:

  • true volume loss
  • or decreased effective arterial blood volume
509
Q

POSTrenal AKI is caused by

A

OBSTRUCTION w/i urinary system

510
Q

INTRINSIC AKI is caused by

A

problem w/:

  • glomeruli
  • tubules
  • interstitium
511
Q

prerenal AKI is ALWAYS d/t a real or “effective”

A

DECREASE in renal BLOOD FLOW:

  • severe intravascular volume loss from volume depletion, blood loss, hypOtension, or diuretics
  • RAS or FMD
  • systolic dysfunction (CRS)
  • NSAIDs or posttransplant immunosuppression drugs
  • hepatorenal syndrome
  • abdominal compartment syndrome
512
Q

NSAIDs can cause AKI by causing CONSTRICTION of the

A

AFFERENT arteriole decreasing GFR

513
Q

evidence of portal HTN (ascites, esophageal varices, splenomegaly, leukopenia, thrombocytopenia, anemia) and jaundice w/ AKI, think

A

hepatorenal syndrome

514
Q

what are the diagnostic criteria to diagnose hepatorenal syndrome?

A
  • cirrhosis w/ ascites and evidence of portal HTN
  • serum Cr > 1.5 mg/dL progressing over days/weeks
  • lack of improvement in renal function after w/d of diuretics and volume expansion w/ albumin for at least 2 days
  • no evidence of parenchymal kidney disease
  • no other apparent cause of AKI
515
Q

organ dysfunction caused by intraabdominal HTN that can cause AKI

A

abdominal compartment syndrome

516
Q

how do you calculate abdominal perfusion pressure (APP)?

A

MAP - IAP = AAP

mean arterial pressure - intraabdominal pressure = abdominal perfusion pressure

517
Q

prerenal AKI: labs

  • BUN:Cr ratio
A

typically > 20

518
Q

prerenal AKI: labs

  • urine osmolality
A

> 400, and often > 700

519
Q

prerenal AKI: labs

  • URINE Na+
A

< 20 (indicating normal tubular function and avid reabsorption of Na+ to increase glomerular pressure)

520
Q

prerenal AKI: labs

  • urine sediment
A

usually normal; can show granular or hyaline casts

521
Q

prerenal AKI: labs

  • FeNa+
A

< 1%

522
Q

what is more accurate than FeNa+ if pt is on diuretics?

A

FeUrea or FeUric Acid

523
Q

postrenal AKI results from

A

either EXTERNAL COMPRESSION or intraluminal/intratubular OBSTRUCTION

524
Q

causes of intratubular OBSTRUCTION

A
  • uric acid precipitation
  • oxalate depositions
  • hypercalcemia w/ intrarenal deposits
  • MM w/ light chains
  • certain drugs that crystallize in the urine (METHOTREXATE, INDINAVIR, ACYCLOVIR, GANCICLOVIR, and SULFA ABX)
525
Q

usual causes of postrenal AKI

A
  • prostatic hypertrophy

- stones

526
Q

in postrenal AKI, does knowing the amount of urine produced give an indication about the degree of obstruction?

A

NO

527
Q

anuria almost never occurs with urinary obstruction unless it is?
which is commonly associated w/?

A
  • complete

- shock

528
Q

postrenal AKI: labs

  • UA
A

typically “bland” (no abnormalities)

529
Q

PAPILLARY NECROSIS occurs in (3)

A
  • pyogenic kidneys w/ postrenal obstruction
  • chronic analgesic abuse
  • SCD
530
Q

if you suspect stones, diagnosis for urinary obstruction

A

US or CT scan

531
Q

3 main categories of intrinsic renal AKI

A
  1. acute tubular necrosis (ATN)
  2. interstitial disease
  3. glomerular disease
532
Q

MCC of intrinsic renal AKI

A

acute tubular necrosis (ATN)

533
Q

acute tubular necrosis (ATN) causes

A
  • ISCHEMIA

- NEPHROTOXIN

534
Q

what are the 2 causes of nephrotoxic ATN?

A
  • ENDOgenous

- EXOgenous

535
Q

what are the causes of ENDOgenous nephrotoxic ATN?

A
  • free myoglobin (rhabdomyolysis)

- free hemoglobin (intravascular hemolysis)

536
Q

what are the causes of EXOgenous nephrotoxic ATN?

A
  • contrast-related
  • drugs
  • osmotic nephropathy
  • acute phosphate nephropathy
  • use of bowel purgatives containing sodium phosphate
537
Q

what is acute phosphate nephropathy?

A

AKI occurring after the use of bowel purgatives containing SODIUM PHOSPHATE

538
Q

CLUE leading to diagnosis of acute phosphate nephropathy

A

hyperphosphatemia out of proportion to degree of kidney injury

539
Q

what are the 2 renal problems caused by contrast-related AKI?

A
  • immediate contrast-induced ATN (improves and has no skin findings)
  • cholesterol atheroemboli
540
Q

contrast-related AKI occurring days after procedure

A

cholesterol atheroembolic kidney disease

541
Q
  • blue toes
  • livedo reticularis
  • stepwise progression
  • eosinophilia
  • eosinophiluria
  • low complements
A

cholesterol atheroembolic kidney disease

542
Q

“STEPWISE PROGRESSION” of renal failure

A

cholesterol atheroembolic kidney disease

543
Q

cholesterol emboli in retinal arterioles that appear as orange-white dots interrupting circulation

A

Hollenhorst plaques

544
Q

treatment for AKI d/t cholesterol emboli

A

SUPPORTIVE only

545
Q

ATN: labs

  • BUN:Cr ratio
A

10-15:1

546
Q

ATN: labs

  • urine osmolality
A

< 350 (tubules cannot concentrate urine)

547
Q

ATN: labs

  • URINE Na+
A

> 40 (but, can be dilute if water reabsorption is significantly affected)

548
Q

ATN: labs

  • FeNa+
A

> 2%

can be LOW in CONTRAST-induced nephropathy

549
Q

ATN: labs

  • urine sediment
A
  • MUDDY BROWN, “DIRTY” GRANULAR CASTS (nonspecific, but very sensitive)
  • epithelial cell casts
550
Q

initial management of ATN

A
  • treat precipitating cause

- treat any hypERkalemia

551
Q

OLIGURIC ATN usually resolves in

A

1-4 weeks

552
Q

is oliguria required for the diagnosis of ATN?

A

NO

553
Q

if oliguric, pts w/ ATN are more prone to?

A

becoming hypERkalemic, and volume-overloaded

554
Q

causes of rhabdomyolysis

A
  • crush injuries (compartment syndromes)
  • coma
  • traumatic immobilization
  • prolonged surgeries
  • strenuous exercise
  • generalized seizures
  • heat stroke
  • severe volume contraction
  • drugs
  • infections (usually viral, esp influenza A and B)
  • endocrinopathies (DKA, hypothyroidism, hyperthyroidism, pheochromocytoma)
  • electrolyte abnormalities (severe hypOkalemia, hypOphosphatemia)
555
Q

lab abnormalities in rhabdomyolysis

A
  • INCREASED CPK (> 100,000 IU/L)
  • nonspecific increases in AST and ALT
  • elevated Cr
  • hypERkalemia
  • hypERphosphatemia
  • increased UA
  • hypOcalcemia
556
Q

UA shows what in rhabdomyolysis

A
  • MUDDY BROWN CASTS
  • POSITIVE BLOOD
  • NO RBCs
557
Q

2 mechanisms causing hypOcalcemia in rhabdomyolysis

A
  1. decreased production of 1,25-(OH)2-D d/t renal injury

2. hypERphosphatemia d/t renal injury and tissue breakdown

558
Q

what electrolyte can become significantly increased during recovery?

A

CALCIUM

559
Q

what electrolyte abnormality, in ATN d/t rhabdomyolysis, should only be treated if severe or pt is symptomatic?

A

hypOcalcemia

560
Q

treatment for rhabdomyolysis

A
  • isotonic fluid resuscitation, or

- forced diuresis w/ ALKALINIZATION OF URINE

561
Q

how does hemoglobinuria d/t severe intravascular hemolysis cause ATN?

A

Hb causing mechanical obstruction of tubules

562
Q

interstitial kidney disease is caused by

A

inflammation and/or fibrosis of interstitium

563
Q

acute interstitial nephritis (AIN) is caused by

A

drugs

564
Q

proteinuria in tubular and interstitial diseases

A

low-grade (< 1-1.5 g/day)

565
Q

acute (or allergic) interstitial nephritis (AIN) is most often a _____

A

drug-induced HYPERSENSITIVITY reaction

566
Q

acute (or allergic) interstitial nephritis (AIN) can present w/

A
  • fever
  • eosinophilia
  • rash

(only 10% present w all 3)

567
Q

MC drugs that cause acute (or allergic) interstitial nephritis (AIN)

A
  • NSAIDs
  • abx
  • PPIs
  • cimetidine
  • thiazides
  • allopurinol
568
Q

MC abx causing acute (or allergic) interstitial nephritis (AIN)

A
  • beta-lactams
  • TMP/SMX
  • rifampin
  • ciprofloxacin
569
Q

now identified as a MAJOR cause of interstitial nephritis

A

PPIs

570
Q
  • typically ingested for MONTHS before symptoms occur

- rash, fever, and eosinophilia are frequently absent

A

NSAID-induced AIN

571
Q

NSAID-induced AIN typically causes what range proteinuria?

A

NEPHROTIC-RANGE PROTEINURIA

572
Q

NSAID-induced AIN results in glomerular changes consistent w/?

A

MINIMAL CHANGE DISEASE

573
Q

what are other causes, besides drugs, of acute (or allergic) interstitial nephritis AIN?

A
  • sarcoidosis
  • SLE
  • Sjogren’s
  • transplant rejection
  • infection
574
Q

acute (or allergic) interstitial nephritis: labs

  • urine sediment
A
  • few red cells
  • white cells +/- WBC casts
  • mild protein (< 1 g/day)
  • urinary eosinophils w/ Hansel stain
575
Q

acute (or allergic) interstitial nephritis: labs

  • FeNa+
A

usually > 1%

576
Q

treatment for acute (or allergic) interstitial nephritis

A

discontinuing offending drug and observing

577
Q

causes of chronic interstitial nephritis

A
  • drugs
  • HTN
  • heavy metals (esp lead and cadmium)
  • obstruction
  • infections
  • sarcoidosis
  • Sjogren’s disease
  • SCD
  • MM
578
Q

what drug combination can lead to chronic interstitial nephritis?

A

acetaminophen + ASA, esp if further combined w/ caffeine or codeine

579
Q
  • pt w/ h/o frequent pain
  • low urine SG
  • minimal proteinuria
  • sterile pyuria
  • elevated Cr
A

analgesic-abuse nephropathy (chronic interstitial nephritis)

580
Q

in analgesic-abuse nephropathy (chronic interstitial nephritis), a noncontrast CT of the kidneys may show what?

A

papillary necrosis

581
Q

possible sources of lead poisoning leading to chronic interstitial nephritis

A
  • OCCUPATIONAL exposure
  • drinking “MOONSHINE”
  • HERBAL MEDICATIONS
  • LEAD-GLAZED PLATES or COOKWARE
  • smoking MARIJUANA
582
Q
  • nephropathy develops after YEARS
  • presents as azotemia
  • tiny bit of proteinuria
  • hyperuricemia
  • bland urine sediment
  • may have crystalline arthropathy (“SATURNINE GOUT”)
A

chronic interstitial nephritis 2/2 LEAD poisoning

583
Q

what ingredient found in Chinese herbs for weight-loss can cause an unusual kind of renal interstitial fibrosis?

A

ARISTOLOCHIC ACID

584
Q

what 2 patterns are glomerular diseases divided into?

A
  1. nephritic

2. nephrotic

585
Q
  • acute, subacute, or chronic
  • potentially reversible
  • INFLAMMATORY process
  • presents w/ hematuria, proteinuria (usually < 2 g/day), +/- RBC casts
A

nephrItic glomerular disease

586
Q

nephrItic glomerular disease can be further subdivided into 2 categories

A
  • focal and mild
    (active sediment w/o HTN or edema)
  • diffuse and severe
    (active sediment w/ heavy proteinuria, renal failure, HTN, and edema)
587
Q
  • noninflammatory process
  • presents w/ proteinuria and edema, +/- urine oval fat bodies
  • often WITHOUT red cells and casts in urine sediment
A

nephrOtic glomerular disease

588
Q

3 classic features of nephrOtic syndrome

A
  1. HYPERCHOLESTEROLEMIA
  2. HTN
  3. HYPOALBUMINEMIA
589
Q

either nephritic or nephrotic glomerular disease can occur in which 2 diseases?

A
  • SLE

- MPGN (membranoproliferative glomerulonephritis)

590
Q

what are the pulmonary-renal syndromes (AGN)?

A
  • Goodpasture’s
  • granulomatosis w/ polyangiitis
  • microscopic polyangiitis
  • Churg-Strauss
  • Henoch-Schonlein purpura
  • cryoglobulinemia
591
Q

what are the basement membrane syndromes (AGN)?

A
  • anti-GBM disease (Goodpasture’s)
  • Alport’s
  • thin basement membrane disease
592
Q

what are the infectious disease syndromes (AGN)?

A
  • post-infectious GN
  • endocarditis
  • HIV
  • HBV
  • HCV
  • syphilis
  • malaria
593
Q

definitive diagnosis of AGN (except for diabetic nephropathy) is made w/

A

renal biopsy

594
Q

what differentiates microscopic hematuria coming from the kidney vs lower urinary tract?

A

lower urinary tract = ISOLATED microscopic hematuria

glomerular origin = hematuria WITH proteinuria, dysmorphic red cells, and/or RBC casts

595
Q

urine sediment finding DEFINITIVE for GN

A

RED CELL CASTS

596
Q
  • VARIABLE PROTEINURIA

- “ACTIVE” urine sediment (proteinuria, red cells > 10/hpf, white cells, red cell/white cell/granular casts

A

nephritic GN

597
Q

casts ALWAYS originate in tubules

  • very specific finding
  • seen ONLY in GN
A

red cell casts

598
Q

casts ALWAYS originate in tubules

  • typically seen in pyelonephritis, or AIN
A

white cell casts

599
Q

casts ALWAYS originate in tubules

  • can be nonspecific
  • characteristic of ATN
A

granular casts

600
Q

casts ALWAYS originate in tubules

  • indicate advanced renal disease
A

waxy casts

601
Q

casts ALWAYS originate in tubules

  • in pts w/ a lot of proteinuria
  • characterized by “Maltese crosses” under polarized light
  • can suspend in urine as droplets
A

fatty casts (or oval fat bodies)

602
Q

casts ALWAYS originate in tubules

  • do not indicate disease; seen w/ CONCENTRATED urine
A

hyaline casts

603
Q
  • typically heavy proteinuria
  • urine fat visible as OVAL fat bodies
  • fatty/waxy casts
  • renal tubular cells w/ lipid droplets
  • urine sediment usually normal besides the fat
A

nephrotic GN

604
Q

what is nephrotic-range proteinuria?

A

> 3.5 g/d (or 40-50 mg/kg/d)

605
Q
  • HYPOALBUMINEMIA (w/ secondary EDEMA)
  • HYPOGAMMAGLOBULINEMIA (w/ risk of infections w/ encapsulated organisms)
  • loss of ANTITHROMBIN III (hypercoagulable state; at risk for PULMONARY EMBOLISM and RENAL VEIN thrombosis)
  • HYPERLIPIDEMIA
  • severe PERIPHERAL EDEMA
  • PLEURAL EFFUSIONS
  • ASCITES
A

nephrotic syndrome

606
Q

strategy to classify the glomerular diseases (3 steps)

A
  • is the urine NEPHRITIC or NEPHROTIC?
  • if nephritic, are the complements LOW or NORMAL?
  • does the pt present w/ a SYSTEMIC d/o by H&P, or is the presentation primarily a KIDNEY d/o?
607
Q

name the GN’s

  • nephrOtic
  • presentation: kidney ONLY
A
  • minimal change disease
  • FSGS
  • membranous
608
Q

name the GN’s

  • nephrOtic
  • presentation: systemic
A
  • DM
  • AL amyloidosis
  • AA amyloidosis
609
Q

name the GN’s

  • nephrItic
  • NORMAL complement
  • presentation: kidney ONLY
A
  • IgA

- Alport

610
Q

name the GN’s

  • nephrItic
  • NORMAL complement
  • presentation: systemic
A
  • Goodpasture’s
  • vasculitides
  • TTP/HUS
611
Q

name the GN’s

  • nephrItic
  • LOW complement
  • presentation: kidney ONLY
A
  • PIGN

- MPGN

612
Q

name the GN’s

  • nephrItic
  • LOW complement
  • presentation: systemic
A
  • SLE
  • endocarditis
  • cryoglobulinemia
613
Q

name the GN

  • any nephrItic GN can become _____
  • complement: VARIABLE
  • presentation: VARIABLE
A
  • RPGN
614
Q

C3 is ALWAYS low for how long in PIGN?

A

6-8 weeks

615
Q

FIRST test to order for a NEPHRITIC picture

A

COMPLEMENT levels

616
Q

PIGN is usually caused by

A
  • group A beta-hemolytic streptococcal infections

- also associated w/ staph

617
Q
  • gross hematuria
  • and/or edema
  • sxs occur 1-6 WEEKS after initial illness (average; throat infection = 10 days, skin infection = 2-4 weeks)
A

PIGN

618
Q

what is the diagnostic key in differentiating between PIGN from IgA nephropathy?

A

“LATENCY PERIOD”

619
Q

what are the ANTISTREPTOCOCCAL ANTIBODIES that aid in dx?

A
  • antistreptolysin O (ASO) titer
  • antideoxyribonuclease B (anti-DNase B) titer
  • antihyaluronidase titer
620
Q

how long does antistreptolysin O (ASO) titer stay elevated?

A

SEVERAL WEEKS

621
Q

how long does antideoxyribonuclease B (anti-DNase B) titer stay elevated?

A

several months

622
Q

how long do complement levels remain LOW in PIGN?

A

6-8 weeks

623
Q

PIGN renal biopsy shows what

A

immune deposits (IgG, IgM, complement) in subendothelial and subepithelial regions (“HUMPS”), and neutrophil invasion of glomerulus

624
Q

treatment for PIGN

A
  • abx for underlying infection

- supportive care

625
Q

diagnosis for MPGN

A

biopsy diagnosis

626
Q
  • can be idiopathic w/ isolated kidney disease, but more commonly associated w/ SYSTEMIC diseases
  • 50% of time LOW complement levels
  • usually nephrItic, but nephrOtic is not uncommon
A

MPGN

627
Q

LOW C3 and C4 are more common in which form of MPGN?

A

immune complex-mediated MPGN

628
Q
  • chronic hepatitis C or B w/ or w/o cryoglobulinemia, shunt nephritis, abscess
  • AI disease (SLE, Sjogren’s)
  • monoclonal gammopathy
A

immune complex-mediated MPGN

629
Q
  • d/t dysregulation of alternative complement pathway
  • d/t mutation in complement factors H, I, and B, or
  • Abs against factors H, I, and B
A

complement-mediated MPGN

630
Q

LOW C3 and NORMAL C4 is more common in which form of MPGN?

A

complement-mediated MPGN

631
Q

LOW C3 in PIGN returns to normal after how long?

A

2-3 months

632
Q

C3 remains low in MPGN for how long?

A

INDEFINITELY

633
Q

if you initially suspected PIGN, but C3 stays low > 3 months, what should you suspect instead and what should be done?

A
  • MPGN

- renal biopsy!

634
Q

treatment for MPGN

A

treat underlying cause

635
Q

name the 6 classes of lupus nephritis

A 
class I: normal/minimal mesangial
class II: mesangial
class III: focal proliferative
class IV: diffuse proliferative
class V: membranous
class VI: end-stage/sclerosis
636
Q

which lupus pts are candidates for renal bx?

A

ALL lupus pts w/ active urine sediment REGARDLESS of GFR

637
Q

treatment for lupus nephritis

A
  • mycophenolate mofetil, or

- cyclophosphamide

638
Q
  • WORLDWIDE, MC GN

- more common in Asians and males

A

IgA nephropathy, aka Berger disease

“mesangial proliferative GN”

639
Q

what are the 4 different ways IgA nephropathy can present?

A
  • gross hematuria coincident w/ or immediately following a URI
  • microscopic hematuria w/ proteinuria and progressive disease
  • nephrotic syndrome
  • RPGN
640
Q

when does the hematuria seen in IgA nephropathy occur?

A

either during viral illness, or just after exercise

641
Q

what is an important distinguishing feature between IgA nephropathy and PIGN?

A

NO LATENT PERIOD

642
Q

serum complement levels in IgA nephropathy

A

usually normal

643
Q

renal bx and immunofluorescence staining findings in IgA nephropathy

A
  • bx shows IgA and complement deposits in the mesangium
  • immunofluorescence staining shows IgA and complement deposits in the glomerular capillaries

(- light microscopy shows isolated proliferation in mesangium (w/ CRESCENT formation if dz is severe))

644
Q

what is “secondary IgA nephropathy?”

A

when other illnesses cause IgA deposition in the mesangium, but aren’t actually IgA nephropathy

645
Q

what are the determining factors for the prognosis of IgA nephropathy?

A
  • serum Cr
  • BP
  • amount of proteinuria
646
Q

treatment for IgA nephropathy, if:

normal renal function

A

observe

647
Q

treatment for IgA nephropathy, if:

proteinuria (> 0.5 g/d) and progressive disease

A

ACEI/ARB

648
Q

treatment for IgA nephropathy, if:

persistent proteinuria (> 1 g/d) despite ACEI/ARB x 6 mos

A

corticosteroids

649
Q
  • hereditary (usually X-linked) syndrome
  • chronic GN +/- NERVE DEAFNESS
  • congenital EYE PROBLEMS
A

Alport’s

650
Q

hallmark finding on EM for Alport’s

A

split lamina densa (part of GBM)

651
Q

acute GN w/ evidence of anti-GBM Abs WITH PULMONARY HEMORRHAGE (70% of pts)

A

GOODPASTURE’S

652
Q

Goodpasture’s presentation

A
  • active urine sediment
  • hemoptysis
  • dyspnea
653
Q

diagnosis for anti-GBM disease

A

anti-GBM Abs, or renal bx if serum Abs are negative

654
Q

renal bx finding for anti-GBM disease

A

anti-GBM IgG deposits in LINEAR fashion along GBM

655
Q

treatment for Goodpasture’s

A
  • plasmapheresis (to remove Abs)

- immunomodulation (steroids + cyclophosphamide)

656
Q

what are the main vasculitides that commonly involve an acute GN?

A
  • granulomatosis w/ polyangiitis
  • microscopic polyangiitis
  • eosinophilic granulomatosis w/ polyangiitis (Churg-Strauss)
  • Henoch-Schonlein purpura (HSP)
657
Q

kidney or skin findings in HSP

A

identical to IgA nephropathy

658
Q
  • most aggressive syndrome of AGN
  • refers to any form of AGN that progresses RAPIDLY (DAYS to WEEKS)
  • hallmark histopathologic finding of glomerular CRESCENTS (EXTRACAPILLARY PROLIFERATION) inside Bowman’s capsule
A

rapidly progressive GN

659
Q

RPGN should always be considered, when?

A

severe and progressive renal failure of recent onset w/ NEPHRITIC urine

660
Q

urine sediment findings in RPGN

A
  • PROTEIN
  • RED CELLS
  • sometimes RBC CASTS
661
Q

3 major pathogenic causes of RPGN

A

type 1 = anti-GBM Abs (Goodpasture’s)
type 2 = immune complex deposition
(IgA deposits = IgA nephropathy; ANA = lupus; cryoglobulins = cryoglobulinemia; Abs against infection = eg streptococci)
type 3 = no evidence of immune deposits (“PAUCI-IMMUNE”)

662
Q

evaluation of RPGN

A
  • RAPID HISTOPATHOLOGIC DIAGNOSIS

- measure ANCA titers

663
Q
  • pulmonary hemorrhage
  • LINEAR staining of IgG along GBM on renal bx
  • high titer of serum anti-GBM Abs
A

GOODPASTURE SYNDROME

664
Q
  • ENT manifestations (sinusitis, epistaxis)
  • pulmonary infiltrates/hemoptysis
  • negative immunofluorescence on kidney bx
  • positive c-ANCA
A

GRANULOMATOSIS W/ POLYANGIITIS

665
Q
  • pt w/ h/o ASTHMA/ATOPY w/ peripheral eosinophilia

- positive p-ANCA

A

eosinophilic granulomatosis w/ polyangiitis

666
Q
  • no systemic features
  • negative immunofluorescence on kidney bx
  • positive ANCA
A

PAUCI-IMMUNE GN (aka renal limited-ANCA vasculitis)

667
Q

empiric treatment for RPGN

A

high-dose methylprednisolone, then prednisone + cyclophosphamide +/- plasmapheresis (if pulmonary hemorrhage)

668
Q

treatment for RPGN once renal bx results are available

A

treat underlying cause

669
Q

MCC of primary nephrotic syndrome

A

minimal change disease

670
Q

MCD is most commonly idiopathic, but has been associated w/

A
  • drugs (NSAIDs, rarely others)

- lymphoma (both Hodgkin’s and NHL)

671
Q

presentation of MCD

A

ANASARCA, or severe peripheral EDEMA (develops over weeks), and WITHOUT HTN

672
Q

MCD renal bx findings

A
  • LM shows NO CHANGE

- EM shows FUSION OF EPITHELIAL FOOT PROCESSES (but can be seen in any nephrotic syndrome)

673
Q

initial treatment for MCD

A

steroids

674
Q

treatment for MCD if steroid-resistant

A
  • cyclophosphamide

- cyclosporine

675
Q
  • MCC of idiopathic nephrotic syndrome in blacks
  • MC glomerular process causing ESRD in the US
  • consider if there’s a h/o HIV/AIDS, HEROIN use, obesity, SCD, chronic vesicoureteral reflux
A

focal segmental glomerulosclerosis (FSGS)

676
Q
  • diffuse FOOT PROCESS FUSION
  • additional sclerosis limited to SEGMENTS of the glomeruli
  • hypertensive on presentation
  • 50% have reduced renal function at dx
A

focal segmental glomerulosclerosis (FSGS)

677
Q
  • have slowly progressive renal failure

- those NOT responding to tx REQUIRE DIALYSIS w/i about 5-10 years

A

focal segmental glomerulosclerosis (FSGS)

678
Q

initial treatment for focal segmental glomerulosclerosis (FSGS)

A

ACEIs/ARBs and high-dose steroids

679
Q

secondary causes of membranous nephropathy (MN)

A
  • chronic INFECTIONS (esp. chronic HBV)
  • several DRUGS (NSAIDs, penicillamine, and gold)
  • underlying SOLID TUMORS
  • AI thyroiditis and SLE (consider in young female)
680
Q
  • gradually worsening nephrotic syndrome
  • 50% of pts have red cells in urinary sediment (w/o RBC casts)
  • most have normal BP and renal function at dx
A

membranous nephropathy (MN)

681
Q

renal biopsy results in membranous nephropathy (MN)

A
  • immunofluorescence shows GBM subepithelial IgG and C3 deposits
  • EM shows shows GBM subepithelial deposits w/ loss of overlying foot processes
682
Q

test to distinguish between idiopathic and secondary membranous nephropathy (MN)

A

Abs to M-type phospholipase A2 receptor (anti-PLA2R)

positive in primary

683
Q

treatment for secondary membranous nephropathy (MN)

A
  • discontinue offending drugs

- treat underlying disease

684
Q

when do you aggressively treat membranous nephropathy (MN)?

A

persistent high-grade proteinuria (> 4 g/d) despite at least 6 months w/ an ACEI/ARB and HTN control

685
Q

has the highest prevalence of renal vein thrombosis compared w/ other causes of nephrotic syndrome

A

membranous nephropathy (MN)

686
Q

pt w/ known membranous nephropathy (MN) has flank pain, hematuria, high LDH, think of

A

RENAL INFARCTION 2/2 renal vein thrombosis

687
Q

MC systemic cause of nephrotic syndrome in adults

A

diabetic nephropathy

688
Q

diabetic nephropathy may be associated w/

A

hyporeninemic hypoaldosteronism and type 4 RTA

689
Q

in diabetic nephropathy, what PRECEDES NEPHROPATHY?

A

RETINOPATHY

690
Q

renal biopsy results in diabetic nephropathy

A
  • expansion of mesangium
  • thickening of GBM
  • sclerosis of glomeruli (KIMMELSTIEL-WILSON lesion)
691
Q

how many phases does diabetic nephropathy occur in, and what are they?

A
  • 2
  • phase 1 = silent or preclinical phase
  • phase 2 = clinical phase
692
Q

what is the 1st measurable change in renal function in phase 1 of diabetic nephropathy?

A

MICROALBUMINURIA (30-300 mg/24H)

693
Q

next step in diabetics tested yearly for albuminuria

A

treat w/ ACEI/ARB EVEN IF NORMOTENSIVE

694
Q

clinical phase of diabetic nephropathy is associated w/

A
  • proteinuria (> 300 mg/d, and often nephrotic range)
  • HTN
  • progressive loss of kidney function
695
Q

what slows progression of diabetic nephropathy?

A
  • BP control < 140/90 w/ ACEI/ARB

- and glycemia control (HbA1c < 7)

696
Q

in what 2 scenarios should a pt with DM undergo a renal bx to exclude other possible causes of nephrotic syndrome?

A
  • NO eye disease

- dysmorphic red cells on urine sediment

697
Q

as renal function decreases, insulin requirements

A

decrease (2/2 decreased metabolism by kidneys)

698
Q

MM can cause which of the following problems w/ renal involvement?

A
  • cast nephropathy (myeloma kidney)
  • hypercalcemia
  • primary “AL” amyloidosis
  • monoclonal Ig deposition disease (MIDD)
  • secondary “AA” amyloidosis
699
Q

MC form of renal involvement d/t MM

A

cast nephropathy (myeloma kidney)

700
Q
  • immunoglobulins (Bence Jones proteins) precipitate in tubules leading to acute renal failure
  • NEGATIVE DIPSTICK protein, but POSITIVE PROTEINURIA
A

cast nephropathy (myeloma kidney)

701
Q

electrolyte imbalance in MM that can acute renal failure

A

hypercalcemia

702
Q
  • multisystem disease
  • nephrotic syndrome and renal failure
  • (Congo-red stain shows deposits w/ apple-green birefringence)
A

primary “AL” amyloidosis associated w/ MM

703
Q
  • monoclonal immunoglobulin light chains or heavy chains are deposited in GBM
  • can resemble diabetic nephropathy w/ nodular glomerulosclerosis
A

monoclonal Ig deposition disease (MIDD)

704
Q
  • seen in chronic inflammatory states (RA and familial Mediterranean fever (FMF))
  • also caused by recurrent skin/soft tissue infections
  • carpal tunnel syndrome
  • new-onset HF assoc. w/ nephrotic syndrome
A

secondary “AA” amyloidosis

705
Q

controlling what is vital in ANY glomerular disease

A

glomerular pressure

706
Q

best in decreasing intraglomerular pressure

A

ACEIs or ARBs

707
Q

treatments used in MOST nephrotic syndromes, EXCEPT those caused by AMYLOID and DIABETES

A

glucocorticoids +/- cytotoxics

708
Q

hypocomplementemia NEVER occurs in

A

the nephrotic syndromes (MCD, FSGS, MG, diabetic nephropathy, amyloid nephropathy)

709
Q

RBC casts are NOT seen in

A

the nephrotic syndromes (MCD, FSGS, MG, diabetic nephropathy, amyloid nephropathy)

710
Q

urine sediment in renal disease:

bland UA; occasionally granular and/or hyaline casts

A

prerenal failure

711
Q

urine sediment in renal disease:

frequently bland, may have blood; WBC casts if d/t infection; sterile pyuria if d/t papillary necrosis; NEVER red cells casts

A

postrenal failure

712
Q

urine sediment in renal disease:

dirty brown granular casts

A

intrinsic renal: ATN

713
Q

DILATION of AFFERENT arteriole and maintenance of glomerular perfusion pressure require

A

prostaglandins (PG)

714
Q

mechanism of NSAIDs causing hyperkalemia

A

block PG-mediated renin release from JGA –> low aldosterone –> decreased renal K+ excretion

715
Q

what types of kidney problems are chronic injection drug users at risk for?

A
  • acute bacterial endocarditis –> progressive GN by IMMUNE COMPLEX DEPOSITION
  • septic EMBOLI (renal infarction and hematuria)
  • chronically progressive FOCAL SCLEROSIS
  • HIV-associated nephropathy caused by FSGS
716
Q

possible reasons for AKI in cancer

A
  • direct infiltration
  • obstruction
  • glomerular disease
  • chemotherapy drug toxicity
  • hypercalcemia
717
Q

possible reasons for AKI in cancer:

  • direct infiltration causes
A
  • lymphoma
  • leukemia
  • myeloma
718
Q

possible reasons for AKI in cancer:

  • obstruction
A
  • pelvic/abdominal tumors
  • intratubular uric acid obstruction d/t TLS
  • methotrexate crystallization
719
Q

possible reasons for AKI in cancer:

  • glomerular disease
A
  • MCD = Hodgkin disease
  • secondary MGN = solid tumors
  • amyloidosis = MM
720
Q

possible reasons for AKI in cancer:

  • chemotherapy drug toxicity
A
  • mitomycin C-induced HEMOLYTIC UREMIC SYNDROME
  • cisplatin-induced tubular injury
  • bevacizumab-induced thrombotic microangiopathy
  • ifosfamide causing ATN
721
Q

electrolyte abnormality causing AKI in cancer

A

hypercalcemia

722
Q

prophylactic treatment for TLS (acute urate nephropathy)

A
  • aggressive IV hydration (hypotonic or isotonic saline)

- ALLOPURINOL, or RASBURICASE

723
Q

rasburicase is CI in which pts?

A

G6PD deficiency

724
Q

definition of CKD

A
  • kidney damage > 3 mos, w/ or w/o decreased GFR, w/ either pathological abnormalities or markers of kidney damage
  • GFR < 60 mL/min/1.73m2 > 3 mos, w/ or w/o kidney damage
725
Q

CKD stages

A
  • stage 1 = normal GFR
  • stage 2 = 60-89 mL/min/1.73m2 body surface area
  • stage 3 = 30-59
  • stage 4 = 15-29
  • stage 5 = < 15 or on dialysis
726
Q

pts w/ CKD have an increased risk of

A

heart disease

727
Q

1 cause of death in pts w/ CKD

A

heart disease

728
Q

serum phosphorus levels remain normal until what stage?

A

about CKD stage 3

729
Q

mechanism of chronic kidney disease-mineral bone disorders (CKD-MBD)

A
  • phosphorus retention –> stimulates PTH release
  • hypocalcemia-induced PTH release
    1. calcium-phosphorus complex deposits in vasculature and tissues
    2. decreased active vitamin D production
730
Q

is associated w/ increased risk of death and heart disease, even in pts w/o CKD; but especially in those w/ CKD stages 3-5

A

hyperphosphatemia

731
Q

what are the 2 types of phosphate binders?

A
  • CALCIUM-BASED (CaCO3; Ca acetate)

- NONCALCIUM-BASED (sevelamer; lanthanum)

732
Q

CKD stage 3 or more causes what?

A
  • increased PO4
  • normal/low-normal Ca2++
  • increased iPTH
  • low 1,25-(OH)2-D
733
Q

ideal management to control PO4 in CKD

A

diet and binder

734
Q

controlling PO4 in CKD leads to what?

A
  • normalization of PO4
  • increased Ca2++
  • decreased iPTH
735
Q

if PTH is not adequately corrected with diet and PO4 binder, next step?

A

add 1,25-(OH)2-D (calcitriol)

736
Q

pts w/ CKD can have what 3 types of bone d/o’s?

A
  1. osteitis fibrosa cystica
  2. adynamic bone disease
  3. osteomalacia
737
Q

secondary hyperparathyroidism labs

A
  • high PO4
  • low 1,25-(OH)2-D
  • very high iPTH
  • normal/low-normal Ca2++
738
Q

treatment for secondary hyperparathyroidism 2/2 CKD

A
  • follow iPTH
  • phosphate binder
  • 1,25-(OH)2-D, or paricalcitol/doxercalciferol
  • +/- cinacalcet
739
Q

how do you choose which phosphate binder to use?

A

based on serum Ca++ level

740
Q

what is the goal when using phosphate binders?

A

normalize phosphorus WITHOUT creating adynamic bone

741
Q

adynamic bone disease labs

A
  • high/normal PO4
  • low 1,25-(OH)2-D
  • LOW iPTH
  • normal/high Ca2++
742
Q

cause for adynamic bone disease

A

oversuppression of PTH by phosphate binders and concomitant use of vitamin D analogs

743
Q
  • associated w/ GFR < 15 mL/min
  • anorexia
  • N/V
  • pericardial and pleural effusions
  • hemorrhagic pericarditis
  • platelet dysfunction and bleeding
  • pruritis
  • sensory neuropathies
  • central nervous system dysfunction (confusion, difficulty concentrating, encephalopathy, coma)
A

uremia

744
Q

what endocrine problems can be caused in CKD?

A
  • decreased glucose intolerance
  • decreased gonadal hormone production (w/ impotence or amenorrhea/infertility)
  • low T3 w/ normal TSH
745
Q

anemia of chronic kidney disease is a diagnosis of

A

exclusion

746
Q

first r/o iron deficiency; responds dramatically to recombinant erythropoietin

A

NORMOCHROMIC-NORMOCYTIC ANEMIA in CKD

747
Q

what should be checked before starting ESAs?

A

iron stores:

  • Fe sat > 20%
  • ferritin > 100
748
Q

target Hb when treating w/ ESAs

A
  • no specific target

- NO IMPROVEMENT in outcome and INCREASED MORBIDITY and MORTALITY if Hb is CORRECTED TO NORMAL (> 13)

749
Q

progression of CKD is slowed by which meds?

A

ACEIs or ARBs

750
Q

progression of CKD is also slowed down by management of which comorbidities?

A
  • metabolic acidosis
  • hyperlipidemia
  • stop smoking
751
Q

AVOID NEPHROTOXINS in CKD, especially

A
  • contrast dye
  • NSAIDs
  • aminoglycosides
752
Q

treatment for gout in CKD

A

colchicine or NSAIDs +/- allopurinol

753
Q

CONTRAINDICATED in treatment for gout in CKD

A

probenecid

754
Q

when do you start dialysis?

A

when CKD pt has ADVANCING UREMIA: ANY uremic sxs in pt w/ CrCl < 15 mL/min

755
Q

MCC of DEATH in dialysis pts

A
  • CARDIOVASCULAR disease

- next is infection

756
Q

one of the key factors in reducing morbidity and mortality in dialysis pts

A

maintaining ADEQUATE NUTRITION

757
Q

what is the main complication for CAPD?

A

PERITONITIS

758
Q

peritonitis in CAPD is usually caused by which bugs?

A

gram-positive skin flora (S. epidermidis or S aureus), followed by gram-negative organisms

759
Q

can be completely removed during dialysis, and therefore need to be re-dosed after treatment

A

AMINOGLYCOSIDES

760
Q

which abx have some clearance during dialysis and need to be re-dosed afterwards and may require supplemental doses?

A
  • most beta-lactams
  • daptomycin
  • metronidazole
  • ciprofloxacin
  • levofloxacin
761
Q

in CKD STAGES 4 AND 5, which contrast type should be AVOIDED?

A

GADOLINIUM

762
Q

GADOLINIUM can cause this this in pts w/ advanced CKD (all forms, regardless of whether on dialysis or what type of dialysis)

A

NEPHROGENIC SYSTEMIC FIBROSIS (NSF)

763
Q
  • presents as a thickening of skin w/ symmetrical plaques, papules, or nodules
  • STARTS DISTALLY
  • disease course is progressive, sometimes fulminant
A

NEPHROGENIC SYSTEMIC FIBROSIS (NSF)

764
Q

is NOT associated w/ nephrogenic systemic fibrosis (NSF)

A

livedo reticularis

765
Q

diagnosis for nephrogenic systemic fibrosis (NSF)

A

deep punch bx of involved skin

ABIM (9 decks)

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