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Nephrology Flashcards

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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
rhabdomyolysis labs: - CPK level - potassium level - calcium level - serum bicarbonate level
- ELEVATED CPK - hypERkalemia - hypOcalcemia - decreased bicarb
26
MOST ACCURATE test for rhabdomyolysis
urine myoglobin
27
mechanism of hypOcalcemia in rhabdomyolysis
damaged sarcolemma outside of SER can bind as much Ca2+ as it wants
28
treatment for rhabdomyolysis
1. NS bolus 2. mannitol (decrease contact time of myoglobin with the tubules) 3. alkalinization of urine (decreases precipitation of myoglobin in the tubules)
29
suicide by antifreeze ingestion (ethylene glycol) HAGMA
oxalate crystals
30
best INITIAL test for ethylene glycol poisoning
UA (envelope-shaped oxalate crystals)
31
best INITIAL treatment for ethylene glycol poisoning
- ethanol or fomepizole | - with IMMEDIATE dialysis
32
tumor lysis syndrome
uric acid crystals
33
treatment for tumor lysis syndrome
1. hydration 2. allopurinol 3. rasburicase
34
rasburicase MOA
breaks down uric acid
35
what to do in a patient who MUST have a radiologic procedure with contrast and renal insufficiency
hydrate with NS, and give bicarbonate and N-acetylcysteine
36
diagnostic clues for AIN
- medication ingestion - fever and rash - UA shows white cells (can't discern between neutrophils and eosinophils)
37
MOST ACCURATE test for eosinophils in UA
Wright stain or Hansel's stain
38
treatment for AIN
no specific therapy, resolves on its own
39
ALL forms of glomerulonephritis (GN) can have the following: | 5 findings
- RBCs in urine - red cell casts in urine - mild proteinuria (less than 2G/24H) - may lead to nephrOtic - edema
40
MOST ACCURATE test for GN (but not always necessary)
kidney biopsy
41
diagnostic clues for Goodpasture syndrome
- COUGH - HEMOPTYSIS - SOB - lung findings (e.g. diffuse infiltrates)
42
best INITIAL test for Goodpasture syndrome
anti-basement membrane Abs
43
MOST ACCURATE test for Goodpasture syndrome
kidney biopsy = LINEAR DEPOSITS
44
treatment for Goodpasture syndrome
plasmapheresis and steroids
45
diagnostic clues for Churg-Strauss syndrome
- ASTHMA - COUGH - EOSINOPHILIA
46
best INITIAL test for Churg-Strauss syndrome
CBC (check eosinophil count)
47
MOST ACCURATE test for Churg-Strauss syndrome
kidney biopsy
48
best INITIAL treatment for Churg-Strauss syndrome
glucocorticoids (e.g. prednisone)
49
what do you do for Churg-Strauss syndrome if NO response to prednisone?
ADD cyclophosphamide
50
diagnostic clues for Wegener granulomatosis (now known as, granulomatosis with polyangiitis)
- SINUSITIS, or OTITIS (biggest clues to diagnosis, and main distinguishing factor between Goodpasture syndrome) - lung findings (e.g. nodules)
51
best INITIAL test for granulomatosis with polyangiitis
c-ANCA (antineutrophil cytoplasmic Abs)
52
MOST ACCURATE test for granulomatosis with polyangiitis
kidney biopsy
53
best INITIAL treatment for granulomatosis with polyangiitis
cyclophosphamide and steroids
54
diagnostic clues for polyarteritis nodosa (PAN)
- systemic vasculitis with involvement of every organ EXCEPT the lungs - MULTIPLE MOTOR DEFICITS - SENSORY NEUROPATHY WITH PAIN (are key to diagnosis)
55
best INITIAL test for PAN
ESR
56
MOST ACCURATE test for PAN
SURAL nerve biopsy, or kidney biopsy
57
what should be tested for in PAN?
hepatitis B and C (30% association)
58
what test for PAN can spare the need for biopsy?
angiography showing "beading"
59
best INITIAL treatment for PAN
steroids and cyclophosphamide
60
diagnostic clues for IgA nephropathy (Berger's disease)
- PAINLESS RECURRENT HEMATURIA - Asian - recent viral respiratory tract infection
61
best INITIAL test for IgA nephropathy
NO specific test (IgA may be elevated...) | complement levels are normal
62
MOST ACCURATE test for IgA nephropathy
kidney biopsy is ESSENTIAL
63
treatment for IgA nephropathy
NO proven effective therapy - steroids: for sudden worsening of proteinuria - ACEIs: used for all patients with proteinuria
64
diagnostic clues for Henoch-Schonlein purpura
- child or adolescent - RAISED, NONTENDER, PURPURIC SKIN LESIONS (especially on buttocks and LE's) - abdominal pain - possible bleeding - joint pain
65
best INITIAL test for Henoch-Schonlein purpura
clinical
66
MOST ACCURATE test for Henoch-Schonlein purpura
kidney biopsy = IgA deposition | not necessary though
67
treatment for Henoch-Schonlein purpura
NO specific therapy; RESOLVES SPONTANEOUSLY
68
diagnostic clues for post-streptococcal glomerulonephritis (PSGN)
- dark, "tea," or "cola" colored urine - PERIORBITAL EDEMA - HTN - can occur after throat and skin infections
69
best INITIAL test for PSGN
- antistreptolysin O (ASLO) - anti-DNase - antihyaluronidase - LOW complement levels
70
MOST ACCURATE test for PSGN
kidney biopsy = SUBepithelial IgG and C3 deposits but should NOT always be done; blood test are usually enough
71
treatment for PSGN
- PCN or other antibiotics for infection | - diuretics for HTN and edema
72
diagnostic clues for cryoglobulinemia
- h/o hepatitis C with renal involvement - joint pain - purpuric skin lesions
73
best INITIAL test for cryoglobulinemia
- serum cryoglobulin component levels | - LOW complement levels (especially C4)
74
MOST ACCURATE test for cryoglobulinemia
kidney biopsy
75
treatment for cryoglobulinemia
- hepatitis C genotype 1: ledipasvir and sofosbuvir - for treatment-experienced pts: add ribavirin - for other genotypes: sofosbuvir and ribavirin
76
diagnostic clues for lupus nephritis
- h/o SLE
77
what does drug-induced lupus spare?
kidney and brain
78
best INITIAL test for lupus nephritis
- ANA and anti-dsDNA Ab
79
MOST ACCURATE test for lupus nephritis
kidney biopsy | very important; not for diagnosis, used to determine extent of disease, which determines therapy
80
treatment for lupus nephritis: sclerosis ONLY
NO treatment
81
treatment for lupus nephritis: mild disease, early stage, nonproliferative
steroids
82
treatment for lupus nephritis: severe disease, advanced, proliferative
mycophenolate mofetil AND steroids
83
diagnostic clues for Alport syndrome
- congenital - eye and ear problems (deafness) - renal failure in second/third decade of life
84
treatment for Alport syndrome
- NO specific treatment
85
HUS triad (think about the name)
1. intravascular hemolysis 2. elevated creatinine 3. thrombocytopenia (h/o E. coli O157:H7)
86
TTP findings (again, think about the name)
1. intravascular hemolysis 2. elevated creatinine 3. thrombocytopenia PLUS 4. fever 5. neurological abnormalities
87
treatment for HUS
supportive; do NOT treat with antibiotics
88
treatment for TTP
plasmapheresis in SEVERE cases; do NOT treat with platelets
89
ANY of the glomerulonephritides can lead to?
nephrOtic syndrome
90
nephrOtic syndrome has the following:
1. hypERproteinuria (more than 3.5G/day) 2. hypOproteinemia 3. hypERlipidemia 4. edema 5. HTN 6. thrombosis
91
best INITIAL test for nephrOtic syndrome
UA; shows markedly elevated protein level
92
NEXT best test for nephrOtic syndrome
spot urine for protein:creatinine ratio; more than 3.5:1 | equal in efficacy to 24H urine protein collection
93
MOST ACCURATE test for nephrOtic syndrome
kidney biopsy
94
primary renal d/o with NO specific PE findings (only associations): MC in children
minimal change disease
95
primary renal d/o with NO specific PE findings (only associations): seen in adults with cancer such as lymphoma
membranous
96
primary renal d/o with NO specific PE findings (only associations): hepatitis C
membranoproliferative
97
primary renal d/o with NO specific PE findings (only associations): HIV/heroin use
focal segmental
98
primary renal d/o with NO specific PE findings (only associations): unclear
mesangial
99
best INITIAL test for primary renal d/o with NO specific PE findings (only associations)
UA, then spot urine
100
MOST ACCURATE test for primary renal d/o with NO specific PE findings (only associations)
kidney biopsy
101
best INITIAL treatment for ALL primary renal d/o with NO specific PE findings (only associations)
steroids
102
if NO response to steroids AFTER 12 WEEKS for primary renal d/o with NO specific PE findings (only associations), then next in treatment
cyclophosphamide
103
first step when patient presents with mild proteinuria | can occur in 2-10% of population at any given time
REPEAT UA
104
if proteinuria persists on repeat UA, what are 4 possibilities that need to be ruled out?
1. CHF 2. fever 3. exercise 4. infection
105
if there is no apparent reason for proteinuria, what is the next possibility?
ORTHOSTATIC proteinuria | h/o patient standing all day; waiter/teacher/security guard
106
first step to CONFIRM orthostatic proteinuria
SPLIT THE URINE: morning urine AND afternoon urine
107
what result indicates a patient has orthostatic proteinuria?
protein in AFTERNOON urine ONLY, and NOT in the morning
108
treatment for orthostatic proteinuria
none; does not need to be treated
109
if proteinuria is PERSISTENT and not orthostatic, next step is
24H urine, OR spot protein:creatinine ratio
110
when evaluating for persistent proteinuria, if 24H urine, OR spot protein:creatinine ratio is elevated next step is
kidney biopsy
111
absolute indications for dialysis (3)
1. uremic pericarditis 2. uremic pleuritis 3. uremic encephalopathy
112
common indications for dialysis (8)
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
phosphate binders
- sevelamer - lanthanum - calcium acetate - calcium carbonate
114
manifestation of uremia and treatment: hyperphosphatemia
- calcium acetate | - calcium carbonate
115
manifestation of uremia and treatment: hypermagnesemia
dietary magnesium restriction
116
manifestation of uremia and treatment: anemia
erythropoietin replacement
117
manifestation of uremia and treatment: hypocalcemia
vitamin D replacement
118
hypERnatremia always implies
free water deficit
119
treatment for dehydration, even in hypERnatremia
normal saline
120
possible causes of hypERnatremia, aside from dehydration
- poor oral intake - fever - pneumonia - other insensible losses
121
the other main cause of hypERnatremia
diabetes insipidus (DI)
122
what are the 2 types of DI?
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
hypERnatremia leads to
NEUROLOGICAL ABNORMALITIES: - confusion - disorientation - seizures - COMA
124
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?
- LOW urine osmolality - LOW urine sodium - INCREASED urine volume - NO change in urine osmolality with water deprivation
125
what happens in CENTRAL DI to urine volume, and urine osmolality when you give DDAVP/vasopressin?
- DECREASE in urine volume | - INCREASE in urine osmolality
126
what happens in NEPHROGENIC DI to urine volume, and urine osmolality when you give DDAVP/vasopressin?
- NO CHANGE in urine volume | - NO CHANGE in urine osmolality
127
what is the difference between vasopressin and DDAVP?
- vasopressin aka ADH = natural de novo hormone | - DDAVP is the trade name for desmopressin = synthetic ADH replacement
128
treatment for central DI
desmopressin or vasopressin
129
treatment for nephrogenic DI
correct underlying cause
130
hypOnatremia presents with
NEUROLOGICAL ABNORMALITIES: - CONFUSION - DISORIENTATION - SEIZURES - COMA
131
FIRST STEP in management of hypOnatremia
ASSESS VOLUME STATUS
132
hypERvolemic hypOnatremia causes (3)
1. CHF 2. nephrotic syndrome 3. cirrhosis
133
treatment for hypERvolemic hypOnatremia
correct/manage underlying cause
134
hypOvolemic hypOnatremia causes (3)
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
treatment for hypOvolemic hypOnatremia
correct underlying cause, and replace with NORMAL (ISOTONIC) SALINE
136
EUvolemic hypOnatremia causes (4)
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
reason Addison's disease (primary adrenal insufficiency) causes hypOnatremia
insufficient ALDOSTERONE production
138
key to diagnosis of Addison's disease (primary adrenal insufficiency)
hypOnatremia with hypERkalemia, and mild metabolic acidosis
139
treatment for Addison's disease (primary adrenal insufficiency)
fludrocortisone
140
causes of SIADH
- any CNS abnormalities - any lung disease - medications (sulfonylureas, SSRIs, carbamazepine) - cancer
141
findings for SIADH
- 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
treatment for SIADH: mild hypOnatremia (no symptoms)
fluid restriction
143
treatment for SIADH: moderate to severe hypOnatremia (confusion, seizures)
- SALINE INFUSION with loop diuretics - HYPERTONIC (3%) saline - check serum Na+ frequently - ADH blockers (conivaptan, tolvaptan)
144
at what rate should you correct hypOnatremia?
- 4-6 meq/L in the FIRST 24 HOURS | - SHOULD NOT BE RAISED MORE THAN 9 meq/L within 24H
145
what can happen if you correct hypOnatremia too rapidly?
CENTRAL PONTINE MYELINOLYSIS
146
treatment for CHRONIC SIADH (from malignancy)
- demeclocycline (blocks ADH at kidney) | - conivaptan/tolvaptan (inhibit ADH at V2 receptor of collecting duct)
147
hypERkalemia causes
(predominantly caused by release from tissues) - muscles = rhabdomyolysis, or crush injury - RBCs = hemolysis - dietary K+ ONLY in renal insufficiency
148
other causes of hypERkalemia
- 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
pseudohypERkalemia
- hemolysis of RBCs | - prolonged tourniquet placement
150
hypERkalemia can lead to
cardiac arrhythmia
151
potassium disorders are NOT associated with
seizures, or neurological disorders
152
sodium disorders are NOT associated with
cardiac arrhythmias
153
EKG changes from hypERkalemia in order
1. peaked T waves 2. prolonged P waves 3. widening of QRS complexes
154
hyperlipidemia mechanism in nephrOtic syndrome
LDL and VLDL are removed from serum by lipoproteins; lipoproteins are lost in urine
155
mechanism of hypERkalemia with beta blockers
block Na+/K+ ATPase channels
156
treatment for moderate hypERkalemia (NO EKG abnormalities)
1. IV insulin and glucose 2. bicarbonate 3. kayexalate
157
treatment for severe hypERkalemia (EKG abnormalities, such as peaked T waves)
1. IV calcium gluconate/calcium chloride 2. IV insulin and glucose 3. kayexalate
158
mechanism of how bicarbonate lower potassium
bicarbonate pulls H+ CATIONS out of cells so K+ goes IN
159
hypOkalemia causes
dietary insufficiency
160
other causes of hypOkalemia
- 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
hypOkalemia can lead to
- cardiac rhythm disturbance | - muscle weakness
162
EKG changes in hypOkalemia
U waves (Purkinje fiber repolarization)
163
treatment for hypOkalemia
- 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
hypERmagnesemia causes
- magnesium-containing laxative abuse | - iatrogenic administration
165
hypERmagnesemia leads to
- muscle weakness | - loss of deep tendon reflexes
166
treatment for hypERmagnesemia
- restrict intake - saline administration (provoke diuresis) - maybe dialysis
167
hypOmagnesemia causes
- loop diuretics - alcohol withdrawal/starvation - gentamicin/amphotericin/diuretics - cisplatin - parathyroid surgery - pancreatitis
168
hypOmagnesemia presents with
hypOcalcemia and cardiac arrhythmias
169
which hormone needs magnesium to function
PTH (parathyroid hormone)
170
metabolic acidosis with increased anion gap (HAGMA) causes
MUDPILES ``` Methanol Uremia DKA Propylene glycol Isoniazid Lactic acidosis Ethylene glycol Salicylates ```
171
metabolic acidosis with normal anion gap (NAGMA) causes
- diarrhea (bicarbonate loss) | - RTA
172
cause of lactic acidosis
any form of hypoperfusion resulting in anaerobic metabolism
173
aspirin overdose mechanism of metabolic acidosis
- respiratory alkalosis from hyperventilation | - metabolic acidosis (loss of aerobic metabolism from mitochondrial poisoning leading to lactic acidosis)
174
treatment for aspirin overdose
bicarbonate
175
what is methanol metabolized into?
formaldehyde than formic acid
176
adverse effect of methanol poisoning
visual disturbance
177
treatment for methanol poisoning
fomepizole or ethanol
178
what 3 substances lead to an increased anion gap in DKA?
1. acetone 2. acetoacetate 3. beta hydroxybutyric acid
179
what will you see in the urine in ethylene glycol poisoning?
oxalate crystals
180
treatment for ethylene glycol poisoning
fomepizole or ethanol
181
distal RTA (type 1)
inability to EXCRETE acid of hydrogen ions in DISTAL tubule
182
diagnostic clues for distal RTA (type 1)
- LOW serum K+ (since body can't excrete H+) - LOW serum bicarbonate - metabolic acidosis - alkaline urine
183
test for distal RTA (type 1)
administer IV acid (AlCl; should lower urine pH secondary to increased H+ formation) urine will stay abnormally basic
184
treatment for distal RTA (type 1)
bicarbonate
185
proximal RTA (type 2)
inability to REABSORB bicarbonate in PROXIMAL tubule
186
adverse effect of distal RTA (type 1)
alkaline urine = kidney stones
187
diagnostic clues for proximal RTA (type 2)
- initially urine pH is elevated, bc of bicarbonate loss, but then becomes acidic
188
test for proximal RTA (type 2)
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
treatment for proximal RTA (type 2)
- thiazide diuretic (causes volume contraction which concentrates serum bicarbonate) - large quantities of bicarbonate
190
hypOreninemic hypOaldosteronism (type 4)
- decreased aldosterone production - diabetic patient with NAGMA - ELEVATED K+
191
treatment for hypOreninemic hypOaldosteronism (type 4)
fludrocortisone
192
distal RTA (type 1) - urine pH - serum K+ - stones? - test - treatment
- HIGH urine pH - LOW K+ - YES - give acid (aluminum chloride) - bicarbonate
193
proximal RTA (type 2) - urine pH - serum K+ - stones? - test - treatment
- LOW urine pH - LOW K+ - NO - give bicarbonate - thiazide diuretic and high dose bicarbonate
194
hypOreninemic hypOaldosteronism (type 4) - urine pH - serum K+ - stones? - test - treatment
- LOW urine pH - HIGH K+ - NO - urine Na+ loss - fludrocortisone
195
how do you distinguish between diarrhea and RTA?
URINE ANION GAP
196
how do you calculate the urine anion gap (UAG)?
UAG = urine Na+ - urine Cl-
197
what is the UAG in diarrhea?
NEGATIVE, bc kidneys are working (able to excrete acid)
198
what is the UAG in RTA?
POSITIVE, bc kidneys CANNOT excrete acid (urine Cl- decreases)
199
how is acid excreted from the kidneys?
NH4Cl
200
causes of metabolic alkalosis (6)
1. volume contraction 2. Conn syndrome 3. Cushing syndrome 4. hypOkalemia 5. milk-alkali syndrome (too much liquid antacid) 6. vomiting
201
how does volume contraction cause metabolic alkalosis?
secondary hypERaldosteronism, causes increased urinary acid loss
202
how do Conn syndrome and Cushing syndrome cause metabolic alkalosis?
primary hypERaldosteronism, causes increased urinary acid loss
203
how does hypokalemia cause metabolic alkalosis?
K+ shifts OUT of cells to correct hypOkalemia; H+ shift INTO cells
204
how does vomiting cause metabolic alkalosis?
(acid loss from stomach, AND volume contraction leading to secondary hypERaldosteronism
205
- recurrent hematuria - stones - infections - CYSTS THROUGHOUT THE BODY (liver, ovaries, circle of Willis) - MVP - diverticulosis
autosomal dominant polycystic kidney disease (ADPKD)
206
MCC of death in ADPKD
ESRD
207
treatment for ADPKD
NO specific treatment
208
urge incontinence - presentation - testing - treatment
- PAIN followed by urge to urinate - urodynamic pressure monitoring - behavior modification/anticholinergic medications
209
stress incontinence - presentation - testing - treatment
- NO pain - COUGHING, and LAUGHING - observe leakage with coughing - Kegel exercise/exercise cream
210
next step in management in a patient presenting with HTN
repeat BP measurement
211
what routine tests should be done in a pt with HTN?
- UA - EKG - eye exam (retinopathy) - cardiac exam (murmur/S4 gallop)
212
initial treatment for HTN
lifestyle modifications: - Na+ restriction - weight loss - dietary modification - exercise - relaxation techniques
213
what is the MOST effective lifestyle modification for HTN?
WEIGHT LOSS
214
when do you initiate medical therapy for HTN?
3-6 months if lifestyle modifications don't work
215
treatment for HTN, AND: CAD
BB
216
treatment for HTN, AND: CHF
BB, or ACEI/ARB
217
treatment for HTN, AND: migraine
BB, or CCB
218
treatment for HTN, AND: hyperthyroidism
BB
219
treatment for HTN, AND: osteoporosis
thiazide
220
treatment for HTN, AND: depression
AVOID BB
221
treatment for HTN, AND: asthma
AVOID BB
222
treatment for HTN, AND: pregnancy
a-methyldopa, or labetalol
223
treatment for HTN, AND: BPH
a-blocker
224
treatment for HTN, AND: DM
ACEI/ARB
225
check for secondary HTN, when?
- less than 30 yoa, or more than 60 yoa - uncontrolled HTN with 3 medications - specific findings on history and PE
226
finding in RAS
bruit
227
finding in pheochromocytoma
EPISODIC HTN
228
finding in Conn syndrome (primary hypERaldosteronism)
hypOkalemia
229
finding in Cushing syndrome
- buffalo hump - truncal obesity - striae
230
finding in coarctation of aorta
upper extremity pressure greater than lower extremity pressure
231
finding in congenital adrenal hyperplasia (CAH)
hirsutism
232
best INITIAL test for RAS
renal US with DOPPLER
233
best NEXT test if SMALL kidney is seen in patient suspected to have RAS
- MRA - duplex ultrasonogram - nuclear renogram
234
MOST ACCURATE test for RAS
renal angiogram
235
best INITIAL treatment for RAS
renal artery angioplasty and stenting
236
how does radius affect flow?
flow increases as radius increases | to the fourth power
237
causes of secondary HTN based on age: children and adolescents (birth to age 18)
- renal parenchymal disease | - coarctation of aorta
238
causes of secondary HTN based on age: young adults (ages 19-39)
- thyroid dysfunction - fibromuscular dysplasia - renal parenchymal disease
239
causes of secondary HTN based on age: middle-aged adults (ages 40-69)
- aldosteronism - thyroid dysfunction - obstructive sleep apnea - Cushing syndrome - pheochromocytoma
240
causes of secondary HTN based on age: older adults (age greater than 65)
- atherosclerotic renal artery stenosis | - renal failure
241
2 medications should be started if baseline BP is >?
160/100
Project - USMLE Step 3
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