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1 USMLE Step 3 Main one > Nephrology > Flashcards

Nephrology Flashcards

1
Q

first step in evaluating renal failure

A
  1. PRErenal (perfusion)
  2. RENAL (parenchymal)
  3. POSTrenal (drainage)
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2
Q

clues renal failure is ACUTE

A
  1. normal kidney size
  2. normal hematocrit
  3. normal Ca2+
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3
Q

clues renal failure is CHRONIC

A
  1. smaller kidneys
  2. renal failure of more than 2 weeks will drop Hct (decreased erythropoietin production)
  3. Ca2+ levels drop (decreased vitamin D hydroxylation)
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4
Q

causes of PRErenal azotemia

A
  • ANY cause of hypOperfusion
  • hypOtension (SBP less than 90)
  • hypOvolemia (dehydration or blood loss)
  • low oncotic pressure (low albumin)
  • CHF (heart can’t PUMP)
  • constrictive pericarditis (heart can’t FILL)
  • RAS
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5
Q

characteristic diagnostic tests for PRErenal azotemia

A
  • BUN:Cr ratio of more than 15:1, and often more than 20:1
  • LOW urinary Na+ (less than 20)
  • urine osmolality more than 500
  • may have hyaline casts on UA
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6
Q

treatment for PRErenal azotemia

A

treat UNDERLYING cause

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7
Q

mechanism of BUN elevation in PRErenal azotemia

A

low volume status, increases ADH, and ADH increases urea transporter activity in collecting duct

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8
Q

causes of POSTrenal azotemia (postobstructive uropathy)

A
  • stones
  • strictures
  • cancer
  • neurogenic bladder (MS or DM)
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9
Q

BUN:Cr ratio seen in POSTrenal azotemia

A

also more than 15:1

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10
Q

clues to obstructive uropathy

A
  • distended bladder on exam
  • large volume diuresis after Foley catheter placement
  • B/L hydronephrosis on US
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11
Q

what must be true in order for postobstructive uropathy to cause renal failure?

A

MUST BE BILATERAL

UNIlateral obstructive cannot cause renal failure

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12
Q

INTRArenal causes of renal failure

A
  • ATN (acute tubular necrosis)
  • AGN (acute glomerulonephritis)
  • AIN (acute interstitial nephritis)
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13
Q

causes of ATN (acute tubular necrosis)

A
  • either hypOperfusion or toxic injury
  • surgery
  • severe burns
  • aminoglycosides/amphotericin/contrast/chemotherapy
  • rhabdomyolysis
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14
Q

causes of AGN (acute glomerulonephritis)

name 11

A
  • Goodpasture’s syndrome
  • Churg-Strauss syndrome
  • Wegener’s granulomatosis
  • polyarteritis nodosa
  • IgA nephropathy (Berger’s disease)
  • Henoch-Schonlein purpura
  • poststreptococcal glomerulonephritis
  • cryoglobulinemia
  • lupus nephritis
  • Alport syndrome
  • TTP/HUS
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15
Q

causes of AIN (acute interstitial nephritis)

A
  • antibiotics
  • NSAIDs
  • infection (e.g. Streptococcus, viral, Legionella)
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16
Q

characteristic diagnostic tests for INTRArenal renal failure

A
  • BUN:Cr ratio of 10:1
  • urinary sodium more than 40
  • urine osmolality less than 350
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17
Q

how many days of use does it usually take for aminoglycosides to cause kidney damage?

A

4-5 days

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18
Q

mechanism of rapid onset of renal failure with contrast agent

A
  • directly toxic to kidney tubules
  • also, causes intense vasoconstriction of Afferent arterioles (decreased perfusion)

(hypOperfusion = LOW urine sodium)

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19
Q

what does UA show in ATN?

A

“muddy brown,” or granular casts

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20
Q

treatment for ATN

A

NO specific therapy

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21
Q

adverse effect of cyclophosphamide

A

hemorrhagic cystitis

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22
Q

cause of renal failure from rhabdomyolysis

A

direct TOXIC effect of MYOGLOBIN on kidney tubule

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23
Q

causes of rhabdomyolysis

A
  • crush injury
  • seizure
  • cocaine toxicity
  • prolonged immobility
  • hypOkalemia resulting in muscle necrosis
  • recent initiation of STATIN
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24
Q

best INITIAL test for rhabdomyolysis

A

UA (large blood)

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25
Q

rhabdomyolysis labs:

  • CPK level
  • potassium level
  • calcium level
  • serum bicarbonate level
A
  • ELEVATED CPK
  • hypERkalemia
  • hypOcalcemia
  • decreased bicarb
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26
Q

MOST ACCURATE test for rhabdomyolysis

A

urine myoglobin

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27
Q

mechanism of hypOcalcemia in rhabdomyolysis

A

damaged sarcolemma outside of SER can bind as much Ca2+ as it wants

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28
Q

treatment for rhabdomyolysis

A
  1. NS bolus
  2. mannitol (decrease contact time of myoglobin with the tubules)
  3. alkalinization of urine (decreases precipitation of myoglobin in the tubules)
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29
Q

suicide by antifreeze ingestion (ethylene glycol)

HAGMA

A

oxalate crystals

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30
Q

best INITIAL test for ethylene glycol poisoning

A

UA (envelope-shaped oxalate crystals)

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31
Q

best INITIAL treatment for ethylene glycol poisoning

A
  • ethanol or fomepizole

- with IMMEDIATE dialysis

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32
Q

tumor lysis syndrome

A

uric acid crystals

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33
Q

treatment for tumor lysis syndrome

A
  1. hydration
  2. allopurinol
  3. rasburicase
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34
Q

rasburicase MOA

A

breaks down uric acid

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35
Q

what to do in a patient who MUST have a radiologic procedure with contrast and renal insufficiency

A

hydrate with NS, and give bicarbonate and N-acetylcysteine

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36
Q

diagnostic clues for AIN

A
  • medication ingestion
  • fever and rash
  • UA shows white cells (can’t discern between neutrophils and eosinophils)
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37
Q

MOST ACCURATE test for eosinophils in UA

A

Wright stain or Hansel’s stain

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38
Q

treatment for AIN

A

no specific therapy, resolves on its own

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39
Q

ALL forms of glomerulonephritis (GN) can have the following:

5 findings

A
  • RBCs in urine
  • red cell casts in urine
  • mild proteinuria (less than 2G/24H)
  • may lead to nephrOtic
  • edema
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40
Q

MOST ACCURATE test for GN (but not always necessary)

A

kidney biopsy

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41
Q

diagnostic clues for Goodpasture syndrome

A
  • COUGH
  • HEMOPTYSIS
  • SOB
  • lung findings (e.g. diffuse infiltrates)
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42
Q

best INITIAL test for Goodpasture syndrome

A

anti-basement membrane Abs

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43
Q

MOST ACCURATE test for Goodpasture syndrome

A

kidney biopsy = LINEAR DEPOSITS

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44
Q

treatment for Goodpasture syndrome

A

plasmapheresis and steroids

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45
Q

diagnostic clues for Churg-Strauss syndrome

A
  • ASTHMA
  • COUGH
  • EOSINOPHILIA
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46
Q

best INITIAL test for Churg-Strauss syndrome

A

CBC (check eosinophil count)

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47
Q

MOST ACCURATE test for Churg-Strauss syndrome

A

kidney biopsy

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48
Q

best INITIAL treatment for Churg-Strauss syndrome

A

glucocorticoids (e.g. prednisone)

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49
Q

what do you do for Churg-Strauss syndrome if NO response to prednisone?

A

ADD cyclophosphamide

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50
Q

diagnostic clues for Wegener granulomatosis (now known as, granulomatosis with polyangiitis)

A
  • SINUSITIS, or OTITIS (biggest clues to diagnosis, and main distinguishing factor between Goodpasture syndrome)
  • lung findings (e.g. nodules)
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51
Q

best INITIAL test for granulomatosis with polyangiitis

A

c-ANCA (antineutrophil cytoplasmic Abs)

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52
Q

MOST ACCURATE test for granulomatosis with polyangiitis

A

kidney biopsy

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53
Q

best INITIAL treatment for granulomatosis with polyangiitis

A

cyclophosphamide and steroids

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54
Q

diagnostic clues for polyarteritis nodosa (PAN)

A
  • systemic vasculitis with involvement of every organ EXCEPT the lungs
  • MULTIPLE MOTOR DEFICITS
  • SENSORY NEUROPATHY WITH PAIN
    (are key to diagnosis)
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55
Q

best INITIAL test for PAN

A

ESR

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56
Q

MOST ACCURATE test for PAN

A

SURAL nerve biopsy, or kidney biopsy

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57
Q

what should be tested for in PAN?

A

hepatitis B and C (30% association)

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58
Q

what test for PAN can spare the need for biopsy?

A

angiography showing “beading”

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59
Q

best INITIAL treatment for PAN

A

steroids and cyclophosphamide

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60
Q

diagnostic clues for IgA nephropathy (Berger’s disease)

A
  • PAINLESS RECURRENT HEMATURIA
  • Asian
  • recent viral respiratory tract infection
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61
Q

best INITIAL test for IgA nephropathy

A

NO specific test (IgA may be elevated…)

complement levels are normal

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62
Q

MOST ACCURATE test for IgA nephropathy

A

kidney biopsy is ESSENTIAL

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63
Q

treatment for IgA nephropathy

A

NO proven effective therapy

  • steroids: for sudden worsening of proteinuria
  • ACEIs: used for all patients with proteinuria
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64
Q

diagnostic clues for Henoch-Schonlein purpura

A
  • child or adolescent
  • RAISED, NONTENDER, PURPURIC SKIN LESIONS (especially on buttocks and LE’s)
  • abdominal pain
  • possible bleeding
  • joint pain
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65
Q

best INITIAL test for Henoch-Schonlein purpura

A

clinical

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66
Q

MOST ACCURATE test for Henoch-Schonlein purpura

A

kidney biopsy = IgA deposition

not necessary though

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67
Q

treatment for Henoch-Schonlein purpura

A

NO specific therapy; RESOLVES SPONTANEOUSLY

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68
Q

diagnostic clues for post-streptococcal glomerulonephritis (PSGN)

A
  • dark, “tea,” or “cola” colored urine
  • PERIORBITAL EDEMA
  • HTN
  • can occur after throat and skin infections
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69
Q

best INITIAL test for PSGN

A
  • antistreptolysin O (ASLO)
  • anti-DNase
  • antihyaluronidase
  • LOW complement levels
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70
Q

MOST ACCURATE test for PSGN

A

kidney biopsy = SUBepithelial IgG and C3 deposits

but should NOT always be done; blood test are usually enough

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71
Q

treatment for PSGN

A
  • PCN or other antibiotics for infection

- diuretics for HTN and edema

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72
Q

diagnostic clues for cryoglobulinemia

A
  • h/o hepatitis C with renal involvement
  • joint pain
  • purpuric skin lesions
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73
Q

best INITIAL test for cryoglobulinemia

A
  • serum cryoglobulin component levels

- LOW complement levels (especially C4)

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74
Q

MOST ACCURATE test for cryoglobulinemia

A

kidney biopsy

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75
Q

treatment for cryoglobulinemia

A
  • hepatitis C genotype 1: ledipasvir and sofosbuvir
  • for treatment-experienced pts: add ribavirin
  • for other genotypes: sofosbuvir and ribavirin
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76
Q

diagnostic clues for lupus nephritis

A
  • h/o SLE
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77
Q

what does drug-induced lupus spare?

A

kidney and brain

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78
Q

best INITIAL test for lupus nephritis

A
  • ANA and anti-dsDNA Ab
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79
Q

MOST ACCURATE test for lupus nephritis

A

kidney biopsy

very important; not for diagnosis, used to determine extent of disease, which determines therapy

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80
Q

treatment for lupus nephritis: sclerosis ONLY

A

NO treatment

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81
Q

treatment for lupus nephritis: mild disease, early stage, nonproliferative

A

steroids

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82
Q

treatment for lupus nephritis: severe disease, advanced, proliferative

A

mycophenolate mofetil AND steroids

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83
Q

diagnostic clues for Alport syndrome

A
  • congenital
  • eye and ear problems (deafness)
  • renal failure in second/third decade of life
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84
Q

treatment for Alport syndrome

A
  • NO specific treatment
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85
Q

HUS triad (think about the name)

A
  1. intravascular hemolysis
  2. elevated creatinine
  3. thrombocytopenia

(h/o E. coli O157:H7)

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86
Q

TTP findings (again, think about the name)

A
  1. intravascular hemolysis
  2. elevated creatinine
  3. thrombocytopenia

PLUS

  1. fever
  2. neurological abnormalities
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87
Q

treatment for HUS

A

supportive; do NOT treat with antibiotics

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88
Q

treatment for TTP

A

plasmapheresis in SEVERE cases; do NOT treat with platelets

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89
Q

ANY of the glomerulonephritides can lead to?

A

nephrOtic syndrome

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90
Q

nephrOtic syndrome has the following:

A
  1. hypERproteinuria (more than 3.5G/day)
  2. hypOproteinemia
  3. hypERlipidemia
  4. edema
  5. HTN
  6. thrombosis
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91
Q

best INITIAL test for nephrOtic syndrome

A

UA; shows markedly elevated protein level

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92
Q

NEXT best test for nephrOtic syndrome

A

spot urine for protein:creatinine ratio; more than 3.5:1

equal in efficacy to 24H urine protein collection

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93
Q

MOST ACCURATE test for nephrOtic syndrome

A

kidney biopsy

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94
Q

primary renal d/o with NO specific PE findings (only associations): MC in children

A

minimal change disease

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95
Q

primary renal d/o with NO specific PE findings (only associations): seen in adults with cancer such as lymphoma

A

membranous

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96
Q

primary renal d/o with NO specific PE findings (only associations): hepatitis C

A

membranoproliferative

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97
Q

primary renal d/o with NO specific PE findings (only associations): HIV/heroin use

A

focal segmental

98
Q

primary renal d/o with NO specific PE findings (only associations): unclear

A

mesangial

99
Q

best INITIAL test for primary renal d/o with NO specific PE findings (only associations)

A

UA, then spot urine

100
Q

MOST ACCURATE test for primary renal d/o with NO specific PE findings (only associations)

A

kidney biopsy

101
Q

best INITIAL treatment for ALL primary renal d/o with NO specific PE findings (only associations)

A

steroids

102
Q

if NO response to steroids AFTER 12 WEEKS for primary renal d/o with NO specific PE findings (only associations), then next in treatment

A

cyclophosphamide

103
Q

first step when patient presents with mild proteinuria

can occur in 2-10% of population at any given time

A

REPEAT UA

104
Q

if proteinuria persists on repeat UA, what are 4 possibilities that need to be ruled out?

A
  1. CHF
  2. fever
  3. exercise
  4. infection
105
Q

if there is no apparent reason for proteinuria, what is the next possibility?

A

ORTHOSTATIC proteinuria

h/o patient standing all day; waiter/teacher/security guard

106
Q

first step to CONFIRM orthostatic proteinuria

A

SPLIT THE URINE: morning urine AND afternoon urine

107
Q

what result indicates a patient has orthostatic proteinuria?

A

protein in AFTERNOON urine ONLY, and NOT in the morning

108
Q

treatment for orthostatic proteinuria

A

none; does not need to be treated

109
Q

if proteinuria is PERSISTENT and not orthostatic, next step is

A

24H urine, OR spot protein:creatinine ratio

110
Q

when evaluating for persistent proteinuria, if 24H urine, OR spot protein:creatinine ratio is elevated next step is

A

kidney biopsy

111
Q

absolute indications for dialysis (3)

A
  1. uremic pericarditis
  2. uremic pleuritis
  3. uremic encephalopathy
112
Q

common indications for dialysis (8)

A
  1. declining nutritional status (MC reason to initiate dialysis)
  2. volume overload
  3. fatigue and malaise
  4. mild cognitive impairment
  5. refractory metabolic acidosis
  6. refractory hyperkalemia
  7. refractory hyperphosphatemia
  8. toxicity with dialyzable drug (lithium/ethylene glycol/aspirin)
113
Q

phosphate binders

A
  • sevelamer
  • lanthanum
  • calcium acetate
  • calcium carbonate
114
Q

manifestation of uremia and treatment: hyperphosphatemia

A
  • calcium acetate

- calcium carbonate

115
Q

manifestation of uremia and treatment: hypermagnesemia

A

dietary magnesium restriction

116
Q

manifestation of uremia and treatment: anemia

A

erythropoietin replacement

117
Q

manifestation of uremia and treatment: hypocalcemia

A

vitamin D replacement

118
Q

hypERnatremia always implies

A

free water deficit

119
Q

treatment for dehydration, even in hypERnatremia

A

normal saline

120
Q

possible causes of hypERnatremia, aside from dehydration

A
  • poor oral intake
  • fever
  • pneumonia
  • other insensible losses
121
Q

the other main cause of hypERnatremia

A

diabetes insipidus (DI)

122
Q

what are the 2 types of DI?

A
  1. central = failure to produce antidiuretic hormone (ADH) in the brain
  2. nephrogenic = insensitivity of the kidney to ADH (can result from hypOkalemia, hypERcalcemia, or lithium toxicity)
123
Q

hypERnatremia leads to

A

NEUROLOGICAL ABNORMALITIES:

  • confusion
  • disorientation
  • seizures
  • COMA
124
Q

what will the urine osmolality, urine Na+, and urine volume be in BOTH central and nephrogenic DI, and what will happen to the urine osmolality with water deprivation?

A
  • LOW urine osmolality
  • LOW urine sodium
  • INCREASED urine volume
  • NO change in urine osmolality with water deprivation
125
Q

what happens in CENTRAL DI to urine volume, and urine osmolality when you give DDAVP/vasopressin?

A
  • DECREASE in urine volume

- INCREASE in urine osmolality

126
Q

what happens in NEPHROGENIC DI to urine volume, and urine osmolality when you give DDAVP/vasopressin?

A
  • NO CHANGE in urine volume

- NO CHANGE in urine osmolality

127
Q

what is the difference between vasopressin and DDAVP?

A
  • vasopressin aka ADH = natural de novo hormone

- DDAVP is the trade name for desmopressin = synthetic ADH replacement

128
Q

treatment for central DI

A

desmopressin or vasopressin

129
Q

treatment for nephrogenic DI

A

correct underlying cause

130
Q

hypOnatremia presents with

A

NEUROLOGICAL ABNORMALITIES:

  • CONFUSION
  • DISORIENTATION
  • SEIZURES
  • COMA
131
Q

FIRST STEP in management of hypOnatremia

A

ASSESS VOLUME STATUS

132
Q

hypERvolemic hypOnatremia causes (3)

A
  1. CHF
  2. nephrotic syndrome
  3. cirrhosis
133
Q

treatment for hypERvolemic hypOnatremia

A

correct/manage underlying cause

134
Q

hypOvolemic hypOnatremia causes (3)

A
  1. diuretics (urine Na+ ELEVATED)
  2. GI loss of fluids (vomiting, diarrhea) (urine Na+ LOW)
  3. skin loss of fluids (burns, sweating) (urine Na+ LOW)

lose water and a little salt, but patient replaces free water only

135
Q

treatment for hypOvolemic hypOnatremia

A

correct underlying cause, and replace with NORMAL (ISOTONIC) SALINE

136
Q

EUvolemic hypOnatremia causes (4)

A
  1. syndrome of inappropriate ADH release (SIADH)
  2. hypothyroidism
  3. psychogenic polydipsia
  4. hypERglycemia (Na+ drops by 1.6-2.4 for every 100mg of glucose above normal)
  5. Addison’s disease (primary adrenal insufficiency)
137
Q

reason Addison’s disease (primary adrenal insufficiency) causes hypOnatremia

A

insufficient ALDOSTERONE production

138
Q

key to diagnosis of Addison’s disease (primary adrenal insufficiency)

A

hypOnatremia with hypERkalemia, and mild metabolic acidosis

139
Q

treatment for Addison’s disease (primary adrenal insufficiency)

A

fludrocortisone

140
Q

causes of SIADH

A
  • any CNS abnormalities
  • any lung disease
  • medications (sulfonylureas, SSRIs, carbamazepine)
  • cancer
141
Q

findings for SIADH

A
  • inappropriately HIGH urine Na+ (more than 20meq/L)
  • inappropriately HIGH urine osmolality (more than 100mOsm/kg)
  • LOW serum osmolality (less than 290mOsm/kg)
  • LOW serum uric acid
  • normal BUN, creatinine, and bicarbonate
142
Q

treatment for SIADH: mild hypOnatremia (no symptoms)

A

fluid restriction

143
Q

treatment for SIADH: moderate to severe hypOnatremia (confusion, seizures)

A
  • SALINE INFUSION with loop diuretics
  • HYPERTONIC (3%) saline
  • check serum Na+ frequently
  • ADH blockers (conivaptan, tolvaptan)
144
Q

at what rate should you correct hypOnatremia?

A
  • 4-6 meq/L in the FIRST 24 HOURS

- SHOULD NOT BE RAISED MORE THAN 9 meq/L within 24H

145
Q

what can happen if you correct hypOnatremia too rapidly?

A

CENTRAL PONTINE MYELINOLYSIS

146
Q

treatment for CHRONIC SIADH (from malignancy)

A
  • demeclocycline (blocks ADH at kidney)

- conivaptan/tolvaptan (inhibit ADH at V2 receptor of collecting duct)

147
Q

hypERkalemia causes

A

(predominantly caused by release from tissues)

  • muscles = rhabdomyolysis, or crush injury
  • RBCs = hemolysis
  • dietary K+ ONLY in renal insufficiency
148
Q

other causes of hypERkalemia

A
  • metabolic acidosis (transcellular shift out of cells)
  • adrenal aldosterone deficiency (Addison’s disease)
  • beta blockers
  • digoxin toxicity
  • insulin deficiency (DKA)
  • spironolactone
  • ACEIs/ARBs (inhibit aldosterone)
  • prolonged immobility
  • RTA type 4 (decreased aldosterone effect)
  • renal failure (decreased excretion)
149
Q

pseudohypERkalemia

A
  • hemolysis of RBCs

- prolonged tourniquet placement

150
Q

hypERkalemia can lead to

A

cardiac arrhythmia

151
Q

potassium disorders are NOT associated with

A

seizures, or neurological disorders

152
Q

sodium disorders are NOT associated with

A

cardiac arrhythmias

153
Q

EKG changes from hypERkalemia in order

A
  1. peaked T waves
  2. prolonged P waves
  3. widening of QRS complexes
154
Q

hyperlipidemia mechanism in nephrOtic syndrome

A

LDL and VLDL are removed from serum by lipoproteins; lipoproteins are lost in urine

155
Q

mechanism of hypERkalemia with beta blockers

A

block Na+/K+ ATPase channels

156
Q

treatment for moderate hypERkalemia (NO EKG abnormalities)

A
  1. IV insulin and glucose
  2. bicarbonate
  3. kayexalate
157
Q

treatment for severe hypERkalemia (EKG abnormalities, such as peaked T waves)

A
  1. IV calcium gluconate/calcium chloride
  2. IV insulin and glucose
  3. kayexalate
158
Q

mechanism of how bicarbonate lower potassium

A

bicarbonate pulls H+ CATIONS out of cells so K+ goes IN

159
Q

hypOkalemia causes

A

dietary insufficiency

160
Q

other causes of hypOkalemia

A
  • increased urinary loss caused by diuretics
  • Conn syndrome (high aldosterone)
  • vomiting (leads to metabolic alkalosis; shifts K+ INTO cells [and volume depletion; increases aldosterone])
  • proximal (type 2) and distal (type 1) RTA
  • amphotericin (causes RTA)
  • Bartter syndrome (LOH can’t absorb Na+ or K+; causes secondary hypERaldosteronism)
161
Q

hypOkalemia can lead to

A
  • cardiac rhythm disturbance

- muscle weakness

162
Q

EKG changes in hypOkalemia

A

U waves (Purkinje fiber repolarization)

163
Q

treatment for hypOkalemia

A
  • replace K+
  • avoid glucose-containing fluids (will increase insulin release worsening hypOkalemia)

(NO maximum rate on ORAL K+; bowel will regulate rate of absorption)

164
Q

hypERmagnesemia causes

A
  • magnesium-containing laxative abuse

- iatrogenic administration

165
Q

hypERmagnesemia leads to

A
  • muscle weakness

- loss of deep tendon reflexes

166
Q

treatment for hypERmagnesemia

A
  • restrict intake
  • saline administration (provoke diuresis)
  • maybe dialysis
167
Q

hypOmagnesemia causes

A
  • loop diuretics
  • alcohol withdrawal/starvation
  • gentamicin/amphotericin/diuretics
  • cisplatin
  • parathyroid surgery
  • pancreatitis
168
Q

hypOmagnesemia presents with

A

hypOcalcemia and cardiac arrhythmias

169
Q

which hormone needs magnesium to function

A

PTH (parathyroid hormone)

170
Q

metabolic acidosis with increased anion gap (HAGMA) causes

A

MUDPILES

Methanol
Uremia
DKA
Propylene glycol
Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
171
Q

metabolic acidosis with normal anion gap (NAGMA) causes

A
  • diarrhea (bicarbonate loss)

- RTA

172
Q

cause of lactic acidosis

A

any form of hypoperfusion resulting in anaerobic metabolism

173
Q

aspirin overdose mechanism of metabolic acidosis

A
  • respiratory alkalosis from hyperventilation

- metabolic acidosis (loss of aerobic metabolism from mitochondrial poisoning leading to lactic acidosis)

174
Q

treatment for aspirin overdose

A

bicarbonate

175
Q

what is methanol metabolized into?

A

formaldehyde than formic acid

176
Q

adverse effect of methanol poisoning

A

visual disturbance

177
Q

treatment for methanol poisoning

A

fomepizole or ethanol

178
Q

what 3 substances lead to an increased anion gap in DKA?

A
  1. acetone
  2. acetoacetate
  3. beta hydroxybutyric acid
179
Q

what will you see in the urine in ethylene glycol poisoning?

A

oxalate crystals

180
Q

treatment for ethylene glycol poisoning

A

fomepizole or ethanol

181
Q

distal RTA (type 1)

A

inability to EXCRETE acid of hydrogen ions in DISTAL tubule

182
Q

diagnostic clues for distal RTA (type 1)

A
  • LOW serum K+ (since body can’t excrete H+)
  • LOW serum bicarbonate
  • metabolic acidosis
  • alkaline urine
183
Q

test for distal RTA (type 1)

A

administer IV acid (AlCl; should lower urine pH secondary to increased H+ formation)

urine will stay abnormally basic

184
Q

treatment for distal RTA (type 1)

A

bicarbonate

185
Q

proximal RTA (type 2)

A

inability to REABSORB bicarbonate in PROXIMAL tubule

186
Q

adverse effect of distal RTA (type 1)

A

alkaline urine = kidney stones

187
Q

diagnostic clues for proximal RTA (type 2)

A
  • initially urine pH is elevated, bc of bicarbonate loss, but then becomes acidic
188
Q

test for proximal RTA (type 2)

A

administer bicarbonate

  • normal person with metabolic acidosis = will absorb bicarbonate, and will still have low urine pH
  • proximal RTA patient = cannot absorb bicarbonate, URINE pH WILL RISE
189
Q

treatment for proximal RTA (type 2)

A
  • thiazide diuretic (causes volume contraction which concentrates serum bicarbonate)
  • large quantities of bicarbonate
190
Q

hypOreninemic hypOaldosteronism (type 4)

A
  • decreased aldosterone production
  • diabetic patient with NAGMA
  • ELEVATED K+
191
Q

treatment for hypOreninemic hypOaldosteronism (type 4)

A

fludrocortisone

192
Q

distal RTA (type 1)

  • urine pH
  • serum K+
  • stones?
  • test
  • treatment
A
  • HIGH urine pH
  • LOW K+
  • YES
  • give acid (aluminum chloride)
  • bicarbonate
193
Q

proximal RTA (type 2)

  • urine pH
  • serum K+
  • stones?
  • test
  • treatment
A
  • LOW urine pH
  • LOW K+
  • NO
  • give bicarbonate
  • thiazide diuretic and high dose bicarbonate
194
Q

hypOreninemic hypOaldosteronism (type 4)

  • urine pH
  • serum K+
  • stones?
  • test
  • treatment
A
  • LOW urine pH
  • HIGH K+
  • NO
  • urine Na+ loss
  • fludrocortisone
195
Q

how do you distinguish between diarrhea and RTA?

A

URINE ANION GAP

196
Q

how do you calculate the urine anion gap (UAG)?

A

UAG = urine Na+ - urine Cl-

197
Q

what is the UAG in diarrhea?

A

NEGATIVE, bc kidneys are working (able to excrete acid)

198
Q

what is the UAG in RTA?

A

POSITIVE, bc kidneys CANNOT excrete acid (urine Cl- decreases)

199
Q

how is acid excreted from the kidneys?

A

NH4Cl

200
Q

causes of metabolic alkalosis (6)

A
  1. volume contraction
  2. Conn syndrome
  3. Cushing syndrome
  4. hypOkalemia
  5. milk-alkali syndrome (too much liquid antacid)
  6. vomiting
201
Q

how does volume contraction cause metabolic alkalosis?

A

secondary hypERaldosteronism, causes increased urinary acid loss

202
Q

how do Conn syndrome and Cushing syndrome cause metabolic alkalosis?

A

primary hypERaldosteronism, causes increased urinary acid loss

203
Q

how does hypokalemia cause metabolic alkalosis?

A

K+ shifts OUT of cells to correct hypOkalemia; H+ shift INTO cells

204
Q

how does vomiting cause metabolic alkalosis?

A

(acid loss from stomach, AND volume contraction leading to secondary hypERaldosteronism

205
Q
  • recurrent hematuria
  • stones
  • infections
  • CYSTS THROUGHOUT THE BODY (liver, ovaries, circle of Willis)
  • MVP
  • diverticulosis
A

autosomal dominant polycystic kidney disease (ADPKD)

206
Q

MCC of death in ADPKD

A

ESRD

207
Q

treatment for ADPKD

A

NO specific treatment

208
Q

urge incontinence

  • presentation
  • testing
  • treatment
A
  • PAIN followed by urge to urinate
  • urodynamic pressure monitoring
  • behavior modification/anticholinergic medications
209
Q

stress incontinence

  • presentation
  • testing
  • treatment
A
  • NO pain
  • COUGHING, and LAUGHING
  • observe leakage with coughing
  • Kegel exercise/exercise cream
210
Q

next step in management in a patient presenting with HTN

A

repeat BP measurement

211
Q

what routine tests should be done in a pt with HTN?

A
  • UA
  • EKG
  • eye exam (retinopathy)
  • cardiac exam (murmur/S4 gallop)
212
Q

initial treatment for HTN

A

lifestyle modifications:

  • Na+ restriction
  • weight loss
  • dietary modification
  • exercise
  • relaxation techniques
213
Q

what is the MOST effective lifestyle modification for HTN?

A

WEIGHT LOSS

214
Q

when do you initiate medical therapy for HTN?

A

3-6 months if lifestyle modifications don’t work

215
Q

treatment for HTN, AND: CAD

A

BB

216
Q

treatment for HTN, AND: CHF

A

BB, or ACEI/ARB

217
Q

treatment for HTN, AND: migraine

A

BB, or CCB

218
Q

treatment for HTN, AND: hyperthyroidism

A

BB

219
Q

treatment for HTN, AND: osteoporosis

A

thiazide

220
Q

treatment for HTN, AND: depression

A

AVOID BB

221
Q

treatment for HTN, AND: asthma

A

AVOID BB

222
Q

treatment for HTN, AND: pregnancy

A

a-methyldopa, or labetalol

223
Q

treatment for HTN, AND: BPH

A

a-blocker

224
Q

treatment for HTN, AND: DM

A

ACEI/ARB

225
Q

check for secondary HTN, when?

A
  • less than 30 yoa, or more than 60 yoa
  • uncontrolled HTN with 3 medications
  • specific findings on history and PE
226
Q

finding in RAS

A

bruit

227
Q

finding in pheochromocytoma

A

EPISODIC HTN

228
Q

finding in Conn syndrome (primary hypERaldosteronism)

A

hypOkalemia

229
Q

finding in Cushing syndrome

A
  • buffalo hump
  • truncal obesity
  • striae
230
Q

finding in coarctation of aorta

A

upper extremity pressure greater than lower extremity pressure

231
Q

finding in congenital adrenal hyperplasia (CAH)

A

hirsutism

232
Q

best INITIAL test for RAS

A

renal US with DOPPLER

233
Q

best NEXT test if SMALL kidney is seen in patient suspected to have RAS

A
  • MRA
  • duplex ultrasonogram
  • nuclear renogram
234
Q

MOST ACCURATE test for RAS

A

renal angiogram

235
Q

best INITIAL treatment for RAS

A

renal artery angioplasty and stenting

236
Q

how does radius affect flow?

A

flow increases as radius increases

to the fourth power

237
Q

causes of secondary HTN based on age: children and adolescents (birth to age 18)

A
  • renal parenchymal disease

- coarctation of aorta

238
Q

causes of secondary HTN based on age: young adults (ages 19-39)

A
  • thyroid dysfunction
  • fibromuscular dysplasia
  • renal parenchymal disease
239
Q

causes of secondary HTN based on age: middle-aged adults (ages 40-69)

A
  • aldosteronism
  • thyroid dysfunction
  • obstructive sleep apnea
  • Cushing syndrome
  • pheochromocytoma
240
Q

causes of secondary HTN based on age: older adults (age greater than 65)

A
  • atherosclerotic renal artery stenosis

- renal failure

241
Q

2 medications should be started if baseline BP is >?

A

160/100

1 USMLE Step 3 Main one (37 decks)

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