Nephrology Flashcards
(765 cards)
1
Q
what is a normal 24-hour urine protein?
A
less than 150 mg
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)
3
Q
how much protein w/i 24 hours indicates significant INTERSTITIAL pathology?
A
less than 1 g/day
4
Q
the only exceptions in which there can be pathology and a NORMAL URINE SEDIMENT with MINIMAL proteinuria (2)
A
- medullary cystic disease
2. obstructive uropathy
5
Q
will urinary light chains in myeloma be picked up on a urine dipstick?
A
NO
6
Q
causes of false-positive urine albumin on urine dipstick: (6)
A
- very alkaline urine with a pH > 8
- fever
- heart failure (HF)
- urinary tract infection (UTI)
- hematuria
- very concentrated urine
7
Q
common in people during a febrile illness, after strenuous exercise, and in pts w/ HF and COPD
A
transient proteinuria
8
Q
first step in a pt w/ transient proteinuria
A
recheck UA (if negative; benign)
9
Q
proteinuria reverts to near-normal when pt is SUPINE
A
BENIGN ORTHOSTATIC PROTEINURIA
10
Q
what equates to 24-hour urinary protein?
A
spot protein:creatinine ratio
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)
12
Q
EARLIEST indicator of diabetic and hypertensive nephropathy
A
microalbuminuria
13
Q
indicate probable glomerulonephritis/nephritic syndrome
A
RBC casts, or “dysmorphic” RBCs
14
Q
FEW RBCs on microscopic analysis, BUT urine dipstick is POSITIVE for blood
A
HEMOglobinuria or MYOglobinuria (rhabdomyolysis)
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
16
Q
MCC of ISOLATED GLOMERULAR HEMATURIA (normal renal function, NO proteinuria)
A
- IgA nephropathy
- thin basement membrane disease
- early Alport syndrome
17
Q
can cause transient hematuria
A
strenuous exercise
18
Q
pts w/ sickle cell TRAIT may also have
A
hematuria
19
Q
isolated microscopic or gross hematuria is more likely what in origin?
A
urologic
20
Q
in older pts, complete GU imaging must be done to exclude what?
A
renal cell or GU tract carcinomas
21
Q
what GU imaging must be done to r/o renal cell or GU tract carcinomas?
A
US, MRI, or CT
22
Q
w/ EOSINOPHILURIA, think of
A
drug-induced interstitial nephritis
23
Q
w/ COARSE GRANULAR casts, or “MUDDY BROWN” casts, think
A
acute tubular injury
24
Q
w/ OVAL FAT BODIES (“maltese crosses” under polarized light) may be seen in
A
nephrotic syndrome
25
what suggests rhabdomyolysis-induced renal failure?
unusually rapid rise in serum creatinine (more than 1.5 mg/dL over 24H)
26
in the elderly, what will be normal despite reduced renal function?
creatinine
27
serum creatinine (sCr) is artificially INCREASED by these medications (4)
1. cimetidine
2. probenecid
3. tenofovir
4. trimethoprim
28
interfere w/ the test for creatinine and may falsely elevate results
- acetone
| - cefoxitin
29
indicates either PRERENAL AZOTEMIA (low flow and increased absorption), or increased protein breakdown
elevated (> 20:1) BUN:Cr ratio
30
is a nonglycosylated protein that better reflects GFR than sCr
cystatin C
31
a measure of overall renal function
glomerular filtration rate (GFR)
32
what is used to estimate GFR?
creatinine clearance
33
formula to calculate GFR
GFR = U(Cr)V/P(Cr)
= (total urine creatinine/24H)/sCr
34
name the 2 main creatinine-based GFR formulas used to calculate GFR in pts w/ IMPAIRED renal function
1. modification of diet in renal disease (MDRD)
| 2. Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)
35
what is required to calculate the MDRD?
- sCr
- race
- sex
- age
36
is MORE accurate than MDRD at NEAR-normal kidney function (eGFR > 60mL/min/1.73m2)
CKD-EPI
37
is another acceptable way to estimate GFR
Cockcroft-Gault formula
38
the equation of choice in the general population, especially at higher levels of GFR
CKD-EPI
39
when should you not calculate GFR?
during AKI
40
when will estimates of GFR be inaccurate?
- extreme age
- extreme weight
- pts w/ amputations
- cirrhosis
- pregnancy
41
how do you calculate GFR in pts w/ extreme age, extreme weight, pts w/ amputations, cirrhosis, pregnancy?
- 24H urine
| - measure serum cystatin C
42
the fractional excretion of sodium (FeNa+) is the ratio of?
excreted Na+:total filtered load of Na+
43
when is calculating the FeNa+ most useful?
evaluating oliguric AKI to differentiate PRERENAL AZOTEMIA from acute tubular necrosis (ATN)
44
FeNa+ for prerenal azotemia
less than 1%
45
FeNa+ for acute tubular necrosis (ATN)
more than 2%
46
other causes of AKI w/ FeNa+ less than 1% (6)
- contrast-induced ATN
- cardiorenal syndrome
- hepatorenal syndrome
- nonoliguric ATN
- pigment nephropathy (hemoglobinuria, myoglobinuria)
- acute glomerulonephritis
47
formula to calculate FeNa+(%)
(sCr x uNa)/(sNa x uCr) x 100
48
since diuretics may increase FeNa+, what can be used instead?
FeUrea
49
the fractional excretion of urea (FeUrea) is the ratio of?
excreted urea:total filtered load of urea
50
formula to calculate FeUrea
(sCr x U(urea))/(BUN x U(Cr)) x 100
51
what FeUrea is suggestive of prerenal state?
less than 35%
52
- 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
renal biopsy
53
primary acid-base disorders are either what or what in origin?
respiratory or metabolic
54
primary respiratory disorders:
- change in what?
- compensated how?
- PaCO2
| - kidney SLOWLY dumping/holding on to HCO3- in the OPPOSITE direction
55
primary metabolic disorders:
- change in what?
- compensated how?
- HCO3-
| - respiratory rate IMMEDIATELY increases or decreases
56
- Henderson-Hasselbalch equation
| - and its easier derivation of
- pH = pK + log(HCO3- / [0.03 x PaCO2])
| - H+ = 24 x (PaCO2 / HCO3-)
57
Henderson-Hasselbalch equation tells us the body only has 2 ways to control serum pH, which are?
1. regulate RR and TV, thus control PaCO2
| 2. regulate kidney's absorption of HCO3-
58
what determines pH?
the RATIO of PaCO2 to HCO3-, NOT the absolute values
59
significant alkalemia of any etiology can cause what?
diffuse paresthesias/numbness and muscle spasms, usually associated w/ acute hyperventilation (acute resp. alkalosis)
60
diffuse paresthesias/numbness and muscle spasms are usually associated w/ acute hyperventilation (acute resp. alkalosis), but can also be caused by?
- rapid overload w/ IV HCO3-
| - citrate (massive blood transfusion)
61
why are pts with metabolic acidosis and hypocalcemia protected from the hypocalcemia?
since acidosis decreases the fraction of BOUND Ca2+ and INCREASES the IONIZED Ca2+
62
correction of acidosis prior to correction of hypocalcemia can cause what?
removes protective effect of acidosis, and precipitate seizures
63
serum anion gap (AG) equation
AG = (Na+ - HCO3-) - Cl-
64
AG is a determination of?
unmeasured anions
65
name the anions in the blood
- HCO3-
- Cl-
- phosphate (phos)
- sulfate
- albumin
- organic acids
66
name the cations in the blood
- Na+
- K+
- Ca++
- Mg++
67
remember that any increase in unmeasured anions always is 1:1 w/ the increase of
H+
68
HIGH AG ALWAYS INDICATES
METABOLIC ACIDOSIS
69
under NORMAL conditions, what anion is the main contributor to the AG?
albumin
70
what is the correction for hypoalbuminemia to calculate AG?
about 2.5 mEq/L for each 1G/dL decrease in albumin
71
does ethanol itself cause elevated AG?
no, but alcoholic ketoacidosis does
72
when is the urine anion gap (UAG) used?
to evaluate the etiology of NAGMA to differentiate between GI loss of HCO3- and RTA
73
formula for UAG
UAG = Na+ + K+ - Cl-
74
normal value of UAG
close to 0
75
positive UAG value suggests
low urinary NH4+ (e.g. RTA TYPE 4)
76
neGUTive UAG value suggests
HIGH urinary NH4+ (e.g. DIARRHEA)
77
in the setting of metabolic acidosis d/t EXTRA-renal HCO3- losses, why is the urinary NH4+ high?
renal H+ is excreted in the form of NH4+
78
serum osmolality is mainly determined by concentrations of?
Na+, glucose, and urea
79
osmolal gap (OG) helps determine what?
whether unmeasured osmotically active substances (osmoles) are circulating in the blood (possibly causing acidosis)
80
formula for Osm(calc)
Osm(calc) = 2[Na+] + (BUN/2.8) + (glucose/18)
simplified equation: Osm(calc) = 2[Na+] + (BUN/3) + (glucose/20)
81
formula for OG
OG = Osm(meas) - Osm(calc)
82
what is the normal OG?
less than 10
83
important causes of high OG
- 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)
84
is NOT associated with acidosis (AG is normal), but osmolal gap is increased
ISOPROPYL alcohol
85
nontoxic causes of increased OG and normal AG (3)
1. mannitol
2. sorbitol
3. glycerol
86
what is the main use of OG?
w/u of pt w/ possible acid alcohol ingestion (e.g. ethylene glycol, methanol, or propylene glycol)
87
when should possible acid alcohol ingestion especially be considered?
if OG is more than 25 mOsm/kg
88
ethylene glycol is a common primary ingredient in?
ANTIFREEZE
89
methanol is a common ingredient in?
- PAINT THINNERS
| - DEICING solutions (e.g. windshield washer fluids)
90
rarely, an inadvertent contaminant of "MOONSHINE;" a by-product of grain fermentation
methanol
91
propylene glycol is a SOLVENT used in?
IV lorazepam
92
what quickly happens w/ ethylene glycol, methanol, and propylene glycol, and what is the effect on the OG and AG?
initial substrates cause high OG and HAGMA, but are quickly converted to their TOXIC metabolites, which do not cause OG, but cause HAGMA
93
ethanol, ISOPROPYL ALCOHOL, or ACETONE ingestion will give what OG and AG?
- HIGH OG withOUT acidosis
- normal chemistry
- normal AG
94
toxic metabolites of ethylene glycol
mainly glycolic acid and oxalic acid
95
toxic metabolite of methanol
formic acid
96
toxic metabolites of propylene glycol
- pyruvic acid (normal)
- lactic acid (normal)
- acetic acid
- propionaldehyde
97
metabolite of isopropyl alcohol
acetone (less toxic)
98
signs of possible acid alcohol ingestions
- stupor
- coma
- hypotension
99
AG and OG in the obtunded patient:
- methanol and ethylene glycol
- ketoacidosis and lactic acidosis
- chronic kidney disease
- high AG
| - very high OG
100
AG and OG in the obtunded patient:
- ketoacidosis and lactic acidosis
- chronic kidney disease
- high AG
| - high OG
101
AG and OG in the obtunded patient:
- salicylate poisoning
- methanol or ethylene glycol ingestion after substrates have been converted to acid metabolites
- high AG
| - normal OG
102
AG and OG in the obtunded patient:
- isopropyl alcohol, acetone, or ethanol ingestion
- normal AG
| - high OG
103
AG and OG in the obtunded patient:
- think carbon monoxide poisoning; BEFORE lactic acidosis develops
- normal AG
| - normal OG
104
- commensurate increase in Cl- w/ the decrease in HCO3-
| - also called "hyperchloremic" acidosis
NAGMA
105
why is the Cl- retained in NAGMA?
to maintain electrical neutrality
106
3 main causes of NAGMA
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)
107
NAGMA plus HYPERkalemia, think of?
RTA type 4 (hypOaldosteronism)
108
NAGMA plus HYPOkalemia is caused by
- GI loss (sometimes)
| - RTA types 1 (distal) and 2 (proximal)
109
is a common solvent in glues and paints and can cause NAGMA
toluene
110
treat NAGMA with?
sodium bicarbonate replacement
111
in HAGMA, is there an equivalent increase in Cl-?
no
112
net charge in the serum is always?
neutral
113
because the net charge in the serum is always neutral, in HAGMA there must be what?
increase in UNmeasured anions
114
what tests should immediately be performed in a pt w/ unexplained HAGMA?
- 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
115
common causes of HAGMA
- 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
116
common causes of NAGMA
- renal tubular acidosis
- diarrhea
- carbonic anhydrase inhibitors
- hyperalimentation w/ TPN
117
check for what in ketosis?
- B-hydroxybutyrate
| - urine ketones
118
treatment for DKA
- insulin
- IVF
- electrolyte replacement
119
classic findings of AKA (alcoholic ketoacidosis)
- HAGMA
- hypophosphatemia
- hypoglycemia
120
treatment for AKA
dextrose
121
how does uremia cause HAGMA?
causes an accumulation of anions: SULFATE, PHOSPHATE, URATE
122
what is lactic acidosis type A?
d/t muscle hypOperfusion during shock, cardiac failure, or sepsis
123
what is lactic acidosis type B?
- findings of systemic hypoperfusion are lacking
- DRUG-induced mitochondrial dysfunction (zidovudine, metformin, propofol)
- tumor-induced LA
- alcoholism
124
- high doses of propofol for more than 48 hours
- renal failure
- rhabdomyolysis
- hyperlipidemia
- J-point elevation on EKG
- various arrhythmias
propofol-related infusion syndrome (type B lactic acidosis)
125
- can occur in pts w/ short bowel syndrome
| - present w/ typical neurologic sxs (from slurred speech to obtundation)
D-lactic acidosis
126
- 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
salicylate overdose
127
- key clue is CALCIUM OXALATE crystals in urine
| - metabolizes to glycolic acid and oxalic acid resulting in HAGMA
ethylene glycol
128
- key clue is visual sxs described as "walking through a sandstorm"
- metabolizes to formaldehyde and formic acid resulting in HAGMA
- nausea, vomiting, abdominal pain
methanol
129
standard of care for ethylene glycol poisoning and methanol poisoning
fomepizole and dialysis
130
- is used as a solvent for IV LORAZEPAM
- caused by continuous infusion or large IV doses of lorazepam
- HAGMA w/ OG
propylene glycol
131
treatment for HAGMA
treat underlying cause
132
treatment for propofol-related infusion syndrome
- d/c propofol
| - if AKI and severe acidosis; HD
133
treatment for salicylate poisoning
aggressive sodium bicarbonate therapy (protects CNS)
134
when should DKA be treated with bicarbonate?
pH less than 7.0
135
when should lactic acidosis be treated with bicarbonate?
pH less than 7.1
136
pyroglutamic acidosis is caused by?
chronic acetaminophen use
137
commonly results from VOLUME CONTRACTION caused by diuretics or vomiting/gastric suctioning
metabolic alkalosis
138
metabolic alkalosis always involves what 2 phases?
- generation phase = initial H+ loss or HCO3- gain)
| - maintenance phase = failure of kidney to excrete HCO3- to correct the alkalosis
139
vomiting and NG suction leads to
HCl loss via GASTRIC secretions
140
primary hyperaldosteronism leads to
RENAL acid loss
141
diuretic-induced "contraction" alkalosis leads to
RENAL loss of bicarb-free FLUID --> reduction in ECF volume around fixed quantity of EC bicarbonate
142
metabolic alkalosis is MAINTAINED by
volume depletion, which leads to decreased distal Cl- delivery and high aldosterone levels
143
aldosterone enhances distal sodium reabsorption by activating what?
distal tubular Na+/H+ and Na+/K+ pumps
144
what is the expected urine pH in the setting of metabolic alkalosis?
LOW; "paradoxical aciduria"
145
what happens to K+ levels in metabolic alkalosis?
K+ shifts from extracellular space to intracellular space in exchange for H+
146
what are the 2 types of metabolic alkalosis?
- chloride responsive
| - chloride resistant
147
what is elevated in metabolic alkalosis even though there is volume depletion and why?
- U(Na+) and FeNa+
| - bc bicarbonaturia takes Na+ as accompanying cation
148
what is the expected urine Cl- in metabolic alkalosis in the setting of volume depletion and why?
- U(Cl-) less than 10 meq/L
| - bc NaCl is desperately reabsorbed to maintain intravascular volume
149
if urine Cl- is greater than 10 meq/L think of (8)
- Cushing syndrome
- Bartter syndrome
- Gitelman syndrome
- primary hyperaldosteronism
- Liddle syndrome
- licorice ingestion
- severe hypokalemia
- increased intake of HCO3- (i.e. milk-alkali syndrome)
150
treatment for chloride-responsive alkalosis (urinary Cl- < 10 meq/L)
RESTORATION OF VOLUME and POTASSIUM CORRECTION
| both interrupt aldosterone production, which is causing H+ and K+ in the distal tubule
151
treatment for SEVERE metabolic alkalosis (> 7.55)
HCl through central venous catheter in ICU
152
chloride resistant WITH HTN
- exogenous steroids
- endogenous steroids
(- primary hyperaldosteronism)
(- Cushing syndrome)
(- 11-OH deficiency)
(- Liddle syndrome)
153
chloride resistant withOUT HTN
- Bartter syndrome
- Gitelman syndrome
- surreptitious syndrome
154
list the 4 steps to interpreting acid-base disorders
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
155
what is the body's main extracellular buffer?
bicarb
156
what happens to HCO3- as anions go up?
go down proportionally: about 1:1 ratio, but sometimes 1.6:1
157
if the MEASURED BICARBONATE is LESS, then what is expected?
NAGMA
158
if the MEASURED BICARBONATE is MORE, then what is expected?
METABOLIC ALKALOSIS
159
if the AG is elevated, then the expected bicarb =
[25 - (change in AG)]
160
in metabolic acidosis, the expected pCO2 =
15 + actual HCO3- from the chemistry
161
in metabolic alkalosis, the expected pCO2 increases by
0.7 mmHg for every 1 meq/L increase in HCO3-
162
if pCO2 is HIGHER than expected, then
respiratory ACIDOSIS
163
if pCO2 is LOWER than expected, then
respiratory ALKALOSIS
164
if HCO3- is less than 9, or greater than 40, then what happens to expected pCO2?
may be unreliable
165
in chronic respiratory acidosis, the serum bicarb does NOT increase above what?
38 meq/L
166
pCO2 greater than 55 usually suggests what?
an additional primary respiratory acidosis
167
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
acute hyperventilation episode
- acute respiratory alkalosis
| - 7.56/20/90/22
168
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
acute asthma/PE/chest trauma
- acute respiratory alkalosis d/t hypoxia
| - 7.56/20/50/24
169
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
CNS problem, chronic hyperventilation
- chronic respiratory alkalosis w/ metabolic compensation
| - 7.44/25/90/16
170
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
COPD w/ chronic bronchitis
- chronic respiratory alkalosis w/ metabolic compensation w/ hypoxia
- 7.43/30/60/20
171
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
pt in transition to respiratory failure
- normal except hypoxia
| - 7.40/40/50/24
172
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
sedative overdose
- acute respiratory acidosis
| - 7.24/60/80/26
173
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
respiratory failure from hypoxia
- acute respiratory acidosis w/ hypoxia
| - 7.16/70/50/25
174
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
emphysematous COPD
- respiratory acidosis w/ metabolic compensation
| - 7.37/60/60/34
175
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
bicarbonate overdose
- metabolic alkalosis w/ respiratory compensation
| - 7.44/60/90/39
176
expected ABGs with certain conditions:
(assuming consistent HCO3- and Cl-)
sepsis, ASA overdose, renal failure
- metabolic acidosis w/ respiratory compensation
| - 7.36/28/90/15
177
what is normal serum osmolality?
282 +/- 2 mOsm/kg H2O
178
what is the common term for arginine vasopressin (AVP)?
antidiuretic hormone (ADH)
179
what are the most important mechanisms that regulate ADH levels?
1. osmoreceptors in the hypothalamus
| 2. volume (stretch) receptors in the LA
180
what is the STRONGEST stimulant for ADH release?
significant VOLUME LOSS resulting in hypotension
181
what is CRITICAL in determining treatment for a pt w/ a sodium abnormality?
volume status
182
in general, if a pt is EDEMATOUS, what is the volume status?
volume OVERLOAD
183
if the pt has clinical signs of VOLUME LOSS, what is the volume status?
volume DEFICIT
184
if the pt is neither edematous, nor showing signs of volume loss, what is the volume status?
euvolemic
185
what are the clinical clues to hypovolemia?
- tachycardia
- narrowed pulse pressure
- orthostatic hypotension
- resting tachycardia w/ hypotension
- low central venous pressure
186
what is the MC electrolyte abnormality?
hyponatremia
187
how is hyponatremia further classified?
- ISOOSMOLAR
- HYPEROSMOLAR
- HYPOOSMOLAR
188
what is the 1st step after discovering hyponatremia?
determine serum osmolality
189
artifactual decrease in serum Na+ associated w/ older lab instruments
isoosmolar hyponatremia
190
both GLUCOSE and MANNITOL cause an osmotic shift of water OUT of cells, which dilutes plasma Na+
hyperosmolar hyponatremia
191
by far, the largest low-Na+ subgroup
hypoosmolar hyponatremia
192
low osmolality causes water movement into cells, leading to
INTRACELLULAR SWELLING
193
what can occur when Na+ falls ACUTELY (usually < 120)?
- neuromuscular excitability
- seizures
- coma
194
how is the hypoosmolar subgroup of hyponatremia further subdivided?
VOLUME status: low, high, and normal
195
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?
1. loss of sodium
2. true water excess
3. total body sodium excess exceeded by water excess
196
what is the FIRST thing to do in a pt w/ hypotonic hyponatremia?
assess volume status (done clinically)
197
in a pt w/ hypotonic hyponatremia, what does volume status essentially reflect?
total body sodium content
198
why do LOW-VOLUME pts have hypotonic hyponatremia?
lose both water and Na+, but more Na+ than water
199
what are causes of hypotonic hypovolemic hyponatremia?
- diuretics
- GI losses (vomiting and diarrhea)
- third spacing of fluid
- adrenal insufficiency (Addison disease)
200
how does primary adrenal insufficiency cause hypotonic hypovolemic hyponatremia?
- 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
201
why do HIGH-VOLUME pts (w/ dependent EDEMA and JVD) have hypotonic hyponatremia?
retain water and Na+, but more water than Na+
202
what are causes of hypotonic hypervolemic hyponatremia?
- heart failure
- cirrhosis
- nephrotic syndrome
- kidney failure: acute or chronic
203
treatment for hypotonic hypervolemic hyponatremia
WATER and Na+ restriction
204
treatment for hypotonic hypervolemic hyponatremia if water and Na+ restriction are not enough
LITHIUM or DEMECLOCYCLINE = induce tubular resistance to ADH
205
what can worsen hypotonic hypervolemic hyponatremia by impairing urinary-diluting ability?
THIAZIDE diuretics
206
what type of diuretic can be very effective in the treatment of high-volume hyponatremia?
loop diuretics
207
what high-volume pt has a low GFR even w/ a normal creatinine and rapid diuresis can easily precipitate AKI?
cirrhotic pt
208
what are causes of hypotonic euvolemic hyponatremia?
- SIADH
- drugs that mimic ADH or release ADH
- psychogenic polydipsia
- hypothyroidism
- isolated glucocorticoid deficiency
209
causes of SIADH
- CNS disease (e.g. meningitis)
- lung disease (e.g. pneumonia)
- neoplasms (especially small cell lung cancer)
- drugs
210
MC drugs associated w/ SIADH
- NSAIDs
- SSRIs
- carbamazepine and oxcarbazepine
- psychotropic drugs: haloperidol, amitriptyline
- IV cyclophosphamide
- vincristine/vinblastine
- cisplatin
- chlorpropamide (now rarely used)
- ecstasy (methylenedioxymethamphetamine)
211
diagnosis for SIADH
compare urine and serum osmolalities (serum osm will be low, urine osm inappropriately high (> 250 mOsm/L))
212
serum and urine osms in psychogenic polydipsia
- serum osm = low
| - urine osm = low (kidney is excreting free water by making dilute urine)
213
what is the mechanism for ADH release in moderate-to-severe hypothyroidism?
decreased cardiac output --> stimulates carotid baroreceptors
214
what should be r/o in all pts w/ hyponatremia before making a dx of SIADH, and why?
- hypothyroidism
- glucocorticoid deficiency
- both can cause low serum osmolalities and high urine osmolalities
215
what drug class can cause euvolemic low osmolality hyponatremia via ADH-related and non-ADH-related mechanisms?
thiazides
216
how can cause euvolemic low osmolality hyponatremia?
- inducing mild volume depletion --> stimulates ADH release
| - impairs urinary dilution in early DISTAL tubule
217
what pt population is highly susceptible to thiazides impairing urinary dilution?
elderly pts
218
how is ASYMPTOMATIC hyponatremia treated?
based on etiology
219
treatment for normal serum osmolality hyponatremia
artifact, no treatment required
220
treatment for high serum osmolality hyponatremia
treat underlying cause (e.g. DKA)
221
treatment for low serum osmolality HYPOvolemic hyponatremia
normal saline to replenish deficit (watch for over-rapid correction!)
222
treatment for low serum osmolality HYPERvolemic hyponatremia
fluid restriction (about 800 cc/day) +/- loop diuretics
223
treatment for low serum osmolality euvolemic hyponatremia
treat SIADH w/ fluid restriction (about 800 cc/day)
224
treatment for refractory SIADH
ADH receptor antagonist (-vaptan; conivaptan, tolvaptan)
225
when are conivaptan, or tolvaptan used to treat SIADH?
severe, chronic hyponatremia (Na+ < 120 mg/dL)
226
what are the SEVERE symptoms of hyponatremia?
- lethargy
- confusion
- coma
- seizures
227
what is the treatment of hyponatremia if symptoms are SEVERE, and when should it be used?
- 100mL bolus of 3% saline (to quickly raise Na+ by 2-3 meq/L)
- if the pt is NOT hypovolemic
228
what correction rate should NEVER be exceeded when correcting for hyponatremia, and why?
- 9 MEQ/L OVER 24 HOURS
| - risk of osmotic demyelination syndrome
229
treatment for severe symptoms of hyponatremia if symptoms persist after the initial bolus
2 more boluses of 3% saline in 10-minute intervals
230
treatment for MODERATE symptoms (confusion, lethargy) of hyponatremia and suspected SIADH
3% saline at initial rate of 0.5-1 mL/kg lean body weight/hour
231
in what pt is osmotic demyelination syndrome more likely to occur in?
pt w/ chronic, severe hyponatremia (Na+ < 115 meq/L for > 2 days) whose sodium is corrected rapidly (> 10 meq/L over 24 hours)
232
what are the symptoms of osmotic demyelination syndrome?
- speech and swallowing difficulties
- weakness, or paralysis
- cognitive deficits
- coma
233
- can cause severe and sometimes symptomatic hyponatremia
| - reported in marathon runners
exercise-induced hyponatremia
234
severe hypernatremia is fairly rare but ALWAYS represents what?
WATER DEFICIT
235
unlike hyponatremia, hypernatremic pts are ALWAYS
HYPEROSMOLAR
236
what is the 1st step in a pt w/ hypernatremia?
determining volume status
237
treatment for severe hypovolemic hypernatremia
NORMAL SALINE first to correct volume deficit, then hypotonic fluids to further replace the water deficit
238
calculation for free water deficit
Vol(water) = total body water x ([Na+(serum) - 140]/140)
Vol(water) = 0.6 x body weight x ([Na+(serum) - 140]/140)
239
correction rate for hypernatremia
0.5 meq/L/hr or 10-12 meq/L/day
240
what can occur from too rapid a correction of any severe hyperosmolar state, such as hypernatremia, nonketotic hyperglycemic coma, and severe uremia?
cellular swelling
241
what can cellular swelling cause?
- cerebral edema
- seizures
- coma
242
causes of high-volume hypernatremia
- salt water drowning
| - large amounts of sodium bicarbonate or hypertonic saline during ACLS
243
treatment for high-volume hypernatremia
loop diuretics and free water
244
causes of normal-volume hypernatremia
- diabetes insipidus (DI)
| - reduced access to water (become hypernatremic) before developing volume depletion
245
what's the Na+ level of a typical DI pt?
NORMAL or BORDERLINE-HIGH (bc they're constantly drinking water)
246
primary complaint of a DI pt
polyuria and polydipsia
247
- pt w/ high Na+ and high urine volume
| - h/o recent neurosurgery, head trauma, brain cancer/metastases
central DI
248
causes of nephrogenic DI
- 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)
249
what test not only diagnoses DI, but also differentiates between central and nephrogenic types?
water restriction test
250
in CENTRAL DI, even w/ water restriction, what happens to the ADH level and urine osmolality?
- ADH stays LOW
| - urine is dilute
251
in a normal pt, what happens to the ADH level and urine concentration when the plasma osmolality increases to 295?
- ADH level is high
| - urine is maximally concentrated (> 700 mOsm/L)
252
treatment for MILD cases of central DI
thiazides and salt restriction
253
treatment for PARTIAL central DI when desmopressin might be too potent or limited in supply
- chlorpropamide
| - carbamazepine
254
treatment for resistant central DI
oral or intranasal desmopressin (synthetic vasopressin analog)
255
in NEPHROGENIC DI, what happens to the ADH level and urine osmolality w/ water restriction?
- ADH is appropriately high
| - urine is DILUTE
256
treatment for nephrogenic DI
thiazide diuretics or amiloride
257
treatment for hereditary forms of nephrogenic DI
NSAIDs
258
URINE OSMOLALITY range
50-1,200 mOsm/L
259
what must be known in order to make sense of the urine osmolality?
URINE OUTPUT (L/d)
multiply osmolality by output (1 kg = 1 L)
260
what is a normal urine osmolality?
about 500
261
after glomerular filtration, the filtrate flows through which sections of tubules?
- 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
262
what is filtered in the proximal tubule?
65% of filtered Na+, Cl-, and water is reabsorbed
263
is water permeable in the proximal tubule?
yes, very permeable; is reabsorbed in 1:1 fashion w/ Na+ (filtrate volume is reduced along tubule)
264
name the transport channels in the proximal tubule
- 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
265
how is the Na+/H+ counter-transport channel in the PT stimulated and what drugs inhibit it?
- stimulated by angiotensin II
| - CARBONIC ANHYDRASE INHIBITORS and THIAZIDES (slightly)
266
how much HCO3- is reabsorbed in PT?
90% of filtered HCO3- is reabsorbed indirectly by Na+/H+ counter-transport pump
267
for each H+ secreted, what is reabsorbed in the PT and how?
- 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
268
what also affects Na+/H+ counter-transporter?
POTASSIUM CONCENTRATION
269
how does hypOkalemia affect serum acid-base level?
stimulates H+ secretion --> stimulates bicarb reabsorption --> alkalosis
270
how does hypERkalemia affect serum acid-base level?
inibhits H+ secretion --> inhibits bicarb reabsorption --> acidosis
271
what are the clinical effects of proximal tubule damage?
- 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
272
in the THIN descending segment, how much H2O moves from the filtrate into the interstitium? and, where is the maximum concentration of fluid?
- 20%
| - base of the loop
273
WHY is the renal medulla very hypERtonic?
- in THIN ascending segment NaCl passively diffuses into interstitium
- in THICK ascending segment solutes ACTIVELY transported into interstitium
274
cotransport of Na+, 2 Cl-, and K+ (into interstitium) is INHIBITED by
LOOP diuretics
275
name the 4 loop diuretics
1. furosemide
2. bumetanide
3. torsemide
4. ethacrynic acid
276
at what GFR do loop diuretics REMAIN EFFECTIVE?
low GFR = CrCl < 20 (just have to increase dose and/or give IV)
277
which 2 loop diuretics are associated w/ permanent ototoxicity at high IV bolus doses?
- furosemide
| - ethacrynic acid
278
what are the 2 mechanisms in which loop diuretics cause diuresis?
1. prevent Na+ reabsorption in THICK ascending segment
| 2. prevent development of interstitial osmotic gradient in the THIN descending segment
279
when are LOOP DIURETICS used to treat hypercalcemia?
use is considered QUESTIONABLE, UNLESS becomes VOLUME OVERLOAD
280
cotransport of Na+ and Cl- (into interstitium) in the EARLY distal tubule is inhibited by
thiazide diuretics
281
name the 4 thiazide diuretics
1. chlorothiazide
2. hydrochlorothiazide
3. chlorthalidone
4. metolazone
282
why are thiazide diuretics less effective at an extremely low GFR?
have to be secreted INTO filtrate
283
how do thiazides cause hypOkalemia?
slightly inhibit carbonic anhydrase in proximal tubule --> increased delivery of Na+ to early distal tubule --> upregulation of Na/K ATPase counter-transport channel
284
which diuretics INCREASE CALCIUM REABSORPTION?
thiazides
285
can help in reducing urinary calcium in pts w/ kidney stones
thiazides
286
allow for further solute and water reabsorption and are controlled by ALDOSTERONE and ADH
LATE DISTAL tubule and CORTICAL COLLECTING DUCT
287
2 cell types in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT that reabsorb solutes
1. principal cells
| 2. intercalated cells
288
what gets counter-transported in the principal cells?
Na+ (into interstitium) and K+ (into filtrate)
289
what stimulates principal cells in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT?
- aldosterone
| - hyperkalemia
290
what inhibits principal cells in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT?
potassium-sparing diuretics (amiloride, triamterene, spironolactone, eplerenone)
291
what gets secreted in the intercalated cells?
H+ (into filtrate)
292
what controls water reabsorption in the LATE DISTAL tubule and CORTICAL COLLECTING DUCT?
ADH which stimulates AQUAPORINS
293
name 2 diseases that affect the last distal tubules and cortical collecting ducts
- distal (type 1 RTA)
| - distal (type 4 RTA)
294
- impairment of H+-ATPase active transport pump in intercalated cells --> inability to secrete acid (and reabsorb bicarb)
- urine pH is always > 5.3
distal (type 1 RTA) NAGMA
295
- tubular aldosterone resistance --> impairment of Na+/K+ ATPase counter-transporter
- HYPERKALEMIA
- can also occur in DM
distal (type 4 RTA) NAGMA
296
where is the remaining 10% of Na+ and water absorbed?
medullary collecting duct
297
in the absence of ADH, which segments of the nephron are relatively impermeable to water?
LATE DISTAL tubule and CORTICAL COLLECTING DUCT
298
- name 2 ADH-receptor antagonists
| - sometimes used to treat hypOnatremia
- conivaptan (IV only)
| - tolvaptan (PO)
299
- problem in H+-ATPase
- failure to acidify urine
- HYPOkalemia
- hypercalciuria +/- nephrocalcinosis
distal (type 1) RTA
300
MCC of distal (type 1) RTA
- genetic (presents in childhood)
- autoimmune (Sjogren's, SLE, RA)
- hereditary hypercalciuria
- drugs (amphotericin B, lithium)
301
treatment for distal (type 1) RTA
- NaHCO3
- K+ replacement
- tx underlying cause
302
- problem w/ cells in PROXIMAL tubule --> BICARBONATE WASTING
- also, problems w/ cotransport of Na+ w/ glucose, aa, Cl-, and K+
proximal (type 2) RTA
303
MCC of proximal (type 2) RTA
- monoclonal gammopathies (MM) w/ buildup of light chains that damage tubule cells
- CA inhibitors
304
treatment for proximal (type 2) RTA
- bicarbonate (very large doses)
- K+ replacement
- vitamin D supplementation
305
- 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
type 4 (distal) RTA
306
causes of hyporeninemic hypoaldosteronism (3)
1. diabetic nephropathy
2. obstructive uropathy
3. chronic interstitial nephritis
307
common drugs that can lead to hyperkalemic metabolic acidosis SIMILAR to type 4 (distal) RTA
- spironolactone
- ACEIs/ARBs
- NSAIDs (exacerbates a concurrent hyporeninemic state)
308
treatment for type 4 (distal) RTA
- dietary potassium restriction
- or bicarbonate administration
- furosemide if 1st 2 don't work
309
- HYPERCALCIURIA
- +/- NEPHROCALCINOSIS
- high urine pH
- HYPOKALEMIA
type 1 (distal) RTA
310
- BICARBONATE WASTING
- FANCONI'S
- urine pH and serum K+ are variable
- think MYELOMA
type 2 (proximal) RTA
311
- ALDOSTERONE DEFICIENCY or RESISTANCE
- mild acidosis
- HYPERkalemia
- think causes of hyporeninemic hypoaldosteronism (interstitial disease, diabetes, NSAIDs, ACEIs)
type 4 (distal) RTA
312
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
D) Na+ 140 K+ 4 Cl- 105 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
313
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
B) Na+ 140 K+ 5.5 Cl- 117 HCO3- 13 urine pH 6 urine K+ 50 urine Na+ 100
314
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
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
315
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) Na+ 140 K+ 2.6 Cl- 113 HCO3- 17 urine pH 7.9 urine K+ 50 urine Na+ 100
316
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
C) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 50 urine Na+ 100
317
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
E) Na+ 140 K+ 4 Cl- 115 HCO3- 15 urine pH 6 urine K+ 10 urine Na+ 10
318
any situation that causes aldosterone to be released (or mimics aldosterone), will have what effect on K+?
LOWERS it
319
situations that cause aldosterone release (4)
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
any situation that INHIBITS aldosterone release or action, will have what effect on K+?
INCREASES it
321
situations that cause aldosterone release (4)
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
what increase K+ uptake causing hypOkalemia?
- alkalosis
- beta-agonists
- insulin
323
what decrease K+ uptake causing hypERkalemia?
- acidosis
| - alpha-agonists
324
what electrolyte abnormality can cause alkalosis?
hypOkalemia
325
what electrolyte abnormality can cause acidosis?
hypERkalemia
326
conditions leading to increased cell turnover associated w/ hypERkalemia (3)
1. tumor lysis syndrome
2. rhabdomyolysis
3. acute leukemia
327
medication that interferes w/ K+ secretion in principal cells (late distal tubule and cortical collecting duct) causing hypERkalemia
trimethoprim in TMP/SMX
328
RTA associated w/ hypOkalemia for unclear reasons
type 1 (distal) RTA
329
block absorption of solutes and water causing hypOkalemia
loop and thiazide diuretics
330
drugs associated w/ renal K+ wasting causing hypOkalemia
- cisplatin
| - penicillins
331
genetic syndromes associated w/ hypOkalemia (3)
1. Liddle's
2. Barter's
3. Gitelman's
332
presentation of hypERkalemia (signs/symptoms)
- significant weakness or paralysis
- conduction abnormalities
- arrhythmias
333
if a pt is weak d/t hypERkalemia, will there be EKG changes?
yes, but the opposite is not necessarily true
334
name the sequence of EKG changes w/ progressive hypERkalemia
- 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
treatment for acute hypERkalemia w/ EKG changes
- 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
when calcium gluconate not be given for the treatment of hypERkalemia?
pts on digoxin
337
sodium polystyrene sulfonate (SPS; Kayexalate) in sorbitol (MC preparation) has been associated w/?
colon necrosis
| especially w/i a week after surgery and pts w/ ileus
338
when should hypERkalemia be treatment even w/o symptoms or EKG changes?
6.5 or more
339
what hypERkalemia treatment can cause edema and may precipitate cardiac decompensation?
NaHCO3
340
signs and symptoms of severe hypOkalemia
- U waves
- decreased tendon reflexes
- rhabdomyolysis
341
at what net loss of K+ will serum K+ decrease?
200-300 meq
342
what comorbid electrolyte deficiency can cause renal K+ wasting?
magnesium
343
caused by disease in the adrenal gland
primary hyperaldosteronism
344
caused by disease in the kidneys or a restricted blood flow in the renal arteries
secondary hyperaldosteronism
345
mechanism of secondary hyperaldosteronism
decreased renal blood flow --> increased renin --> increased angiotensin II --> increased aldosterone
346
what should be considered in a pt w/ hypokalemia w/o an obvious cause, HTN, and metabolic alkalosis?
hyperaldosteronism
347
- 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
Liddle syndrome
348
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
1. Bartter syndrome
| 2. Gitelman syndrome
349
- 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
Bartter syndrome
350
- 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
Gitelman syndrome
351
clinical approach to hypOkalemia
- hypokalemia and NAGMA WITHOUT HTN
- hypokalemia and metabolic alkalosis AND HTN
- hypokalemia and metabolic alkalosis WITHOUT HTN
352
causes of hypokalemia and NAGMA WITHOUT HTN (3)
- diarrhea
- type 1 (distal) RTA
- type 2 (proximal) RTA
353
causes of hypokalemia and metabolic alkalosis AND HTN (5)
- diuretics (MC)
- hyperaldosteronism (primary or secondary)
- Cushing syndrome
- Liddle syndrome
- adrenal hydroxylase deficiencies
354
causes of hypokalemia and metabolic alkalosis WITHOUT HTN (2)
- Bartter syndrome
| - Gitelman syndrome
355
hypERcalcemia found incidentally in an asymptomatic pt is usually d/t
- THIAZIDE diuretics or
| - PRIMARY HYPERPARATHYROIDISM (especially if h/o NECK IRRADIATION)
356
most common causes of hypOcalcemia (5)
1. vitamin D deficiency
2. CKD
3. severe pancreatitis
4. rhabdomyolysis
5. hypermagnesemia
357
less common causes of hypOcalcemia (4)
1. hungry bone syndrome following parathyroidectomy
2. hypoparathyroidism
3. pseudohypoparathyroidism
4. citrate
358
both increased and decreased magnesium can cause
hypOcalcemia
359
how does increased calcium affect magnesium?
hypOmagnesemia
360
hypOmagnesemia has what effect on K+?
hypOkalemia
361
causes of hypOmagnesemia (VERY COMMON electrolyte abnormality) (9)
- 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
clinical manifestations of hypOmagnesemia
- muscle weakness, spasms, tetany
- wide QRS
- peaked T waves
363
depleted magnesium STORES, even w/ a NORMAL serum LEVEL are associated w/ what?
REFRACTORY cardiac arrhythmias
364
how many meq of Mg++ are in 1G?
8.12 meq
365
causes of hypERmagnesemia (RARE)
- 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
when do sxs from hypERmagnesemia occur?
> 4-6 meq/L
367
clinical manifestations of hypERmagnesemia
nausea initially --> sedation --> muscle WEAKNESS --> loss of DTRs --> paralysis (including heart/respiratory mm)
368
treatment for hypERmagnesemia
- IVF and Ca2+
| - HD in renal failure
369
ACUTE increases of phosphate causing hypERphosphatemia (3)
- ATN (especially if d/t rhabdo)
- IV solutions
- rapid cell turnover (tumor lysis or acute leukemia)
370
CHRONIC increases of phosphate causing hypERphosphatemia (2)
- CKD
| - hypOparathyroidism
371
causes of hypOphosphatemia
- think ALCOHOLISM and ALCOHOLIC KETOACIDOSIS
| - REFEEDING syndrome
372
clinical manifestations of severe hypOphosphatemia (if PO4 < 1 mg/dL)
- rhabdomyolysis
- cardiomyopathy
- respiratory insufficiency (diaphragm function failure)
- irritability and hyperventilation --> profound muscle weakness --> seizures --> coma --> death
373
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. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 10 urine calc osm 700
374
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)
b. Na+ low-NL Cl- 115 HCO3- 15 urine Cl- 10 urine calc osm 700
375
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)
c. Na+ low-NL Cl- 95 HCO3- 35 urine Cl- 100 urine calc osm 700
376
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)
d. Na+ low-NL Cl- NL HCO3- NL urine Cl- 100 urine calc osm 300 (but high volume)
377
volume contraction
VOMITING causes metabolic ALKALOSIS and:
- low serum Cl-
| - hypOkalemia d/t aldosterone
378
volume contraction
DIARRHEA causes metabolic ACIDOSIS (NAGMA) and:
- appropriately high serum Cl-
| - Cl- is reabsorbed to make up for HCO3- loss
379
THIAZIDE diuretics also cause metabolic ALKALOSIS w/ low serum Cl-, but has what effect on urinary Cl-?
HIGH
380
when do DIABETES INSIPIDUS pts become hypERnatremic?
only pts who are unable to drink
| usually have a NORMAL intravascular volume and Na+ concentration
381
how is HTN diagnosed?
2 or more readings taken on 2 or more visits
382
what is stage ONE HTN?
SBP 140-159, or DBP 90-99
383
what is stage TWO HTN?
SBP 160 or more, or DBP 100 or more
384
in any stage of HTN, which sex and race has a higher morbidity and mortality?
- MEN
| - BLACKS
385
when should you f/u or w/u?
- DBP < 85
recheck in 2-3 years
386
when should you f/u or w/u?
- 85-90
recheck in 1 year
387
when should you f/u or w/u?
- 90-104
recheck w/i 2 months
388
when should you f/u or w/u?
- 105-114
w/u w/i 2 weeks
389
when should you f/u or w/u?
- > 115
w/u immediately
390
standard evaluation for newly diagnosed HTN
- major cardiovascular disease risk factors
| - IDENTIFIABLE CAUSES of HTN
391
list the IDENTIFIABLE CAUSES of HTN (8)
- pheochromocytoma
- renovascular HTN
- coarctation of aorta
- polycystic kidneys
- renal parenchymal disease
- hyperparathyroidism
- granulomatous disease
- hyperaldosteronism
392
- labile HTN
- medullary thyroid cancer
- primary hyperparathyroidism (MEN2)
pheochromocytoma
393
- HTN
| - continuous abdominal bruit
renovascular HTN (renal artery stenosis or fibromuscular dysplasia)
394
- HTN
| - decreased BP in LEs or absent/delayed femoral pulses
coarctation of aorta
395
- HTN
| - abdominal or flank masses
polycystic kidneys
396
- HTN
| - elevated creatinine or abnormal UA
renal parenchymal disease
397
- HTN
| - hypercalcemia
- hyperparathyroidism
| - granulomatous disease
398
- HTN
| - hypokalemia
hyperaldosteronism
399
what are the indications for evaluation of secondary HTN?
- 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
MCC of secondary HTN
renovascular HTN (renal artery stenosis or fibromuscular dysplasia)
401
- treatment for HTN w/
| - edema w/ HF or CKD
loop diuretic
402
- treatment for HTN w/
| - systolic dysfunction and low EF or problems w/ hypokalemia
spironolactone
403
what dose of HCTZ provides the greatest antihypertensive effect?
12.5 mg
404
which antihypertensive medication can cause severe hypOnatremia in pts w/ poor solute intake; especially the elderly?
thiazide diuretics
405
how does angiotensin II increase BP?
- DIRECT VASOCONSTRICTION
- potentiation of the SYMPATHETIC NERVOUS SYSTEM
- increasing Na+ reabsorption in the proximal tubule
- stimulation of ALDOSTERONE PRODUCTION by the ADRENAL GLAND
406
name the 10 ACEIs
1. captopril
2. enalapril
3. benazepril
4. fosinopril
5. lisinopril
6. quinapril
7. moexipril
8. ramipril
9. perindopril
10. trandolapril
407
MOA of ACEIs
inhibit angiotensin-converting enzyme
408
MOA of ARBs
block angiotensin receptors, which blocks angiotensin II effect
409
what effect do ACEIs/ARBs have on the glomerulus?
DILATION OF EFFERENT arteriole --> decreased glomerular capillary pressure
410
what decreases progression of both DIABETIC and HYPERTENSIVE nephropathies, and other types of CKD?
decreased glomerular pressure
411
name the 7 ARBs
1. candesartan
2. eprosartan
3. irbesartan
4. losartan
5. olmesartan
6. telmisartan
7. valsartan
412
what are the absolute INDICATIONS for ACEIs/ARBs? (4)
- systolic dysfunction
- h/o STEMI
- anterior NSTEMI
- CKD (especially w/ proteinuria)
413
complications of ACEIs
- increase in serum K+ by 0.5 meq/L
| - renal function decline
414
when do you stop ACEI or ARB?
- creatinine increases to > 30% over baseline
| - and/or serum K+ is uncontrollable
415
ACEIs + what combination is particularly noteworthy for complications?
HF and sudden initiation of NSAIDs
416
up to 20% of pts have to stop ACEIs because of
COUGH
417
what is a possible FATAL adverse effect of ACEIs?
angioedema
418
ACEIs/ARBs are absolutely CI in _____ bc they are?
- pregnancy
| - TERATOGENIC
419
ACEIs/ARBs should be avoided in which pts?
hyperkalemic pts
420
ACEIs/ARBs should be used w/ caution in which pts?
- B/L RAS
- HF
- ADPKD
- hypertensive nephrosclerosis
421
what is ALISKIREN?
renin inhibitor; acts similarly to ACEIs/ARBs
422
aliskiren plus an ACEI or ARB in type 2 diabetics showed an increased risk in?
- stroke
- hyperkalemia
- low BP
- renal insufficiency
423
what are the 2 types of CCBs?
- dihydropyridines
| - non-dihydropyridines
424
name the dihydropyridine CCBs (6)
- amlodipine
- clevidipine
- felodipine
- isradipine
- nicardipine
- nisoldipine
425
name the non-dihydropyridine CCBs (2)
- verapamil
| - diltiazem
426
CCBs are used to treat what?
- HTN
- angina
- arrhythmias
427
what are the complications of CCBs?
significant EDEMA (especially w/ dihydropyridines), and CONSTIPATION (especially w/ non-dihydropyridines)
428
several studies have shown adverse associations (e.g. increased risk of death post-MI) w/?
short-acting CCBs (but not long-acting ones)
429
may increase proteinuria in pts w/ DM and CKD
dihydropyridines (but not verapamil or diltiazem)
430
are NOT recommended as 1st line treatment for HTN
BBs
431
some indications for BBs
- post-MI
- stable HF
- AF (rate control)
- angina
432
try to AVOID BBs in pts w/
- reactive airway disease
- frequent hypoglycemic episodes
- hyperlipidemia
- PVD
433
HTN treatment:
- general NONblack population
- +/- DM
- THIAZIDE
- CCB
- ACEI/ARB
434
HTN treatment:
- BLACK population
- +/- DM
- THIAZIDE
| - CCB
435
in HEART FAILURE, treat HTN w/
- thiazide-type diuretic
436
bottom line for HTN treatment
- use any drug or drug combination w/ fewest side effects to get BP < 140/90 (< 150/90 if > 60 yoa)
437
which antihypertensive is NOT recommended as monotherapy d/t increased risk of STROKE and HEART DISEASE?
BB
438
monotherapy w/ a thiazide, ACEI/ARB, or long-acting CCB is fine for pts w/?
MILD HTN
439
blacks do better w/ which antihypertensives?
thiazide or long-acting CCB
440
young pts do best w/ which antihypertensives?
ACEI
441
pts who are NOT controlled w/ monotherapy usually do better w/?
LOW-DOSE 2nd DRUG
442
when should pts INITIALLY be treated w/ 2 drugs?
BP > 160/100
443
what are the lifestyle guidelines for preventing and controlling HTN?
- 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
JNC 8 goals of treatment are based on
- AGE
- DM
- CKD
445
BP goals of treatment
- general population < 60 yoa
< 140/90
446
BP goals of treatment
- general population > 60 yoa
< 150/90
447
BP goals of treatment
- all ages, NO CKD, diabetes
< 140/90
448
BP goals of treatment
- all ages, CKD, with/without DM
< 140/90
449
elderly persons generally have what type of HTN?
ISOLATED SYSTOLIC
450
should pts > 80 yoa w/ isolated systolic HTN be treated?
YES
451
if pharmacologic treatment for high BP in pts > 60 yoa leads to BP < 140 and is well tolerated, does it need to be adjusted?
no
452
what is malignant HTN?
HTN w/:
- papilledema, retinal hemorrhages, exudates
- nephrosclerosis (AKI, proteinuria, hematuria)
453
what is hypertensive encephalopathy?
severe HTN w/ signs of cerebral edema
| presents as HA, N/V, confusion, coma, and/or seizures
454
treatment goal for hypertensive crisis
decrease DBP to 100-105 mmHg w/i 2-6 hours w/o dropping BP by > 25%
455
when treating a hypertensive crisis, TOO RAPID of drop in BP can result in
- ischemic stroke
| - MI
456
MCC of secondary HTN
renovascular disease causing secondary hyperaldosteronism
457
2 main causes of renovascular HTN
1. atherosclerotic RAS (often BILATERAL, mainly MEN > 50, especially diabetics)
2. fibromuscular dysplasia (also often BILATERAL, mainly WOMEN < 40)
458
strongly suggestive of renovascular HTN (especially w/ other risk factors; > 55 yoa, diabetic)
- continuous abdominal bruit
| - hypOkalemia
459
which pts should be worked up for renovascular HTN?
- have a moderate-to-high risk for disease
| - are candidates for intervention (surgery, or angioplasty w/ stent placement)
460
if POTASSIUM levels are NORMAL, screen pts for secondary HTN w/?
- imaging studies
- CTA
- MRA
- duplex Doppler US
461
which pts w/ secondary HTN d/t renovascular disease are almost always candidates for intervention?
FIBROMUSCULAR DYSPLASIA, bc they can frequently be CURED
462
when atherosclerotic renal artery stenosis be considered for intervention?
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
should elderly pts be screened for secondary HTN?
definitely DO NOT SCREEN if mild HTN and normal serum K+
464
pts w/ possible secondary HTN, if the serum K+ is:
NORMAL, what is the next step?
go straight to imaging:
- CTA
- MRA
- duplex Doppler US
465
pts w/ possible secondary HTN, if the serum K+ is:
LOW, what is the next step?
screen for primary hyperaldosteronism:
- PAC:PRA (plasma aldosterone concentration to plasma renin activity) ratio
466
pts w/ possible secondary HTN, who are NOT candidates for intervention:
what is the next step?
do NOT screen
467
what is the GOLD STANDARD for renovascular HTN?
ARTERIOGRAPHY
468
pt not on diuretics, hypOkalemia of unknown etiology, and HTN, suspect?
primary or secondary hyperaldosteronism
469
what are the 2 main causes of primary hyperaldosteronism?
1. adrenal adenomas (70%; Conn syndrome)
| 2. idiopathic B/L adrenal hyperplasia (25%)
470
screening and diagnosis of primary hyperaldosteronism
PAC:PRA (plasma aldosterone concentration to plasma renin activity) ratio
471
next step after diagnosing primary hyperaldosteronism w/ PAC:PRA ratio
CT scan of adrenals to characterize the gland
472
PAC:PRA ratio indicating primary hyperaldosteronism
> 20
473
in a suspected primary hyperaldosteronism pt, how can you assess whether you can suppress aldosterone?
recheck aldosterone level after either fluid or salt loading
474
initial treatment of primary hyperaldosteronism
- salt and water restriction
- K+ sparing diuretics (spironolactone, triamterene, amiloride)
- +/- thiazide diuretic
475
- cause of secondary HTN
- VERY RARE
- 90% occur in adrenal MEDULLA
- 90% U/L
- 90% BENIGN
- 90% SPORADIC
pheochromocytoma
476
paroxysmal signs and symptoms of pheochromocytoma
- palpitations
- dizziness
- HTN
477
how many pts w/ pheochromocytoma have SUSTAINED HTN?
1/2-2/3
478
diagnosis of pheochromocytoma if low-pretest probability
24-hour urine for fractionated metanephrines and catecholamines
479
diagnosis of pheochromocytoma in higher risk pts (family h/o pheo, MEN2, NF)
screen w/ fractionated metanephrines on RANDOM PLASMA sample
480
next step in diagnosis for pheochromocytoma if biochemical tests are suggestive
CT or MRI w/ contrast
481
test to diagnose pheochromocytoma if imaging is negative and you still suspect pheo
metaiodobenzylguanidine scintigraphy (norepinephrine analog that concentrates in adrenal pheo)
482
what should BP always be in pregnancy?
< 120/80
483
what are the 4 categories of HTN in pregnancy?
1. chronic HTN
2. preeclampsia
3. gestational HTN
4. chronic HTN w/ superimposed preeclampsia
484
define chronic HTN in pregnancy
preexisting HTN or HTN BEFORE 20th WEEK of gestation
485
define preeclampsia in pregnancy
HTN + proteinuria AFTER 20th WEEK of gestation in woman w/o h/o HTN
486
define gestational HTN in pregnancy
HTN AFTER 20th WEEK of gestation WITHOUT proteinuria in woman w/o h/o HTN
487
define chronic HTN w/ superimposed preeclampsia in pregnancy
worsening HTN + NEW ONSET proteinuria AFTER 20th WEEK of gestation WITH h/o controlled, chronic HTN
488
define eclampsia
grand mal seizures in a woman w/ preeclampsia or gestational HTN
489
what are the defining features of preeclampsia?
proteinuria and HTN, not symptoms
490
what an indication of preeclampsia severity?
signs and symptoms
491
what are the signs and symptoms of preeclampsia?
- HA
- vision changes
- seizures
- low platelets
- stroke
- intracerebral hemorrhage
- pulmonary edema
- hepatic and/or renal failure
- placental abruption
492
what is HELLP syndrome?
severe form of preeclampsia
- Hemolytic anemia
- Elevated Liver enzymes
- Low Platelets
493
what are the risk factors for preeclampsia?
- DM
- chronic HTN
- multiple gestations (twins, triplets)
- h/o preeclampsia
494
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%
aspirin 81mg PO daily
495
BP goal for SEVERE HTN in pregnancy regardless of category
< 160/110
496
recommendations to start BP treatment for preeclampsia
1. if symptoms are present
| 2. asymptomatic w/ SBP 150 or more, or DBP 95 or more
497
target BP in preeclampsia
130-150/80-100
498
what BP medications need to be d/c'd for chronic hypertensives thinking about getting pregnant
- ACEIs/ARBs
| - thiazides
499
BP meds of choice in pregnancy
- a-methyldopa
- labetalol
- nifedipine
500
parenteral antihypertensives of choice in malignant HTN in pregnancy
- labetalol (preferred)
- hydralazine
- nicardipine (2nd line)
501
antihypertensives C/I in pregnancy
- ACEIs/ARBs
- renin inhibitors
- nitroprusside (cyanide poisoning in the baby)
502
what are the 1ST LINE PO agents used to treat:
- CHRONIC, asymptomatic preeclampsia
- GESTATIONAL HTN
- and CHRONIC HTN in pregnancy
- LABETALOL
- A-METHYLDOPA
- XR-NIFEDIPINE
503
what are the 2ND LINE PO agents used to treat:
- CHRONIC, asymptomatic preeclampsia
- GESTATIONAL HTN
- and CHRONIC HTN in pregnancy
- DILTIAZEM
- VERAPAMIL
- THIAZIDES (watch for s/s of volume contraction; including oligohydramnios)
504
other important secondary causes of HTN that must be excluded
- OCPs
- coarctation of the aorta
- treatment of obesity
- decreasing alcohol intake to 2 drinks or less/day
- correcting CALCIUM or POTASSIUM deficiency
505
AKI can be
- non-oliguric
- oliguric
- anuric
506
definition of AKI
- 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
define ANURIA
UO < 50 mL/DAY
508
PRErenal AKI is caused by
UNDERPERFUSION, either from:
- true volume loss
- or decreased effective arterial blood volume
509
POSTrenal AKI is caused by
OBSTRUCTION w/i urinary system
510
INTRINSIC AKI is caused by
problem w/:
- glomeruli
- tubules
- interstitium
511
prerenal AKI is ALWAYS d/t a real or "effective"
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
NSAIDs can cause AKI by causing CONSTRICTION of the
AFFERENT arteriole decreasing GFR
513
evidence of portal HTN (ascites, esophageal varices, splenomegaly, leukopenia, thrombocytopenia, anemia) and jaundice w/ AKI, think
hepatorenal syndrome
514
what are the diagnostic criteria to diagnose hepatorenal syndrome?
- 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
organ dysfunction caused by intraabdominal HTN that can cause AKI
abdominal compartment syndrome
516
how do you calculate abdominal perfusion pressure (APP)?
MAP - IAP = AAP
mean arterial pressure - intraabdominal pressure = abdominal perfusion pressure
517
prerenal AKI: labs
- BUN:Cr ratio
typically > 20
518
prerenal AKI: labs
- urine osmolality
> 400, and often > 700
519
prerenal AKI: labs
- URINE Na+
< 20 (indicating normal tubular function and avid reabsorption of Na+ to increase glomerular pressure)
520
prerenal AKI: labs
- urine sediment
usually normal; can show granular or hyaline casts
521
prerenal AKI: labs
- FeNa+
< 1%
522
what is more accurate than FeNa+ if pt is on diuretics?
FeUrea or FeUric Acid
523
postrenal AKI results from
either EXTERNAL COMPRESSION or intraluminal/intratubular OBSTRUCTION
524
causes of intratubular OBSTRUCTION
- 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
usual causes of postrenal AKI
- prostatic hypertrophy
| - stones
526
in postrenal AKI, does knowing the amount of urine produced give an indication about the degree of obstruction?
NO
527
anuria almost never occurs with urinary obstruction unless it is?
which is commonly associated w/?
- complete
| - shock
528
postrenal AKI: labs
- UA
typically "bland" (no abnormalities)
529
PAPILLARY NECROSIS occurs in (3)
- pyogenic kidneys w/ postrenal obstruction
- chronic analgesic abuse
- SCD
530
if you suspect stones, diagnosis for urinary obstruction
US or CT scan
531
3 main categories of intrinsic renal AKI
1. acute tubular necrosis (ATN)
2. interstitial disease
3. glomerular disease
532
MCC of intrinsic renal AKI
acute tubular necrosis (ATN)
533
acute tubular necrosis (ATN) causes
- ISCHEMIA
| - NEPHROTOXIN
534
what are the 2 causes of nephrotoxic ATN?
- ENDOgenous
| - EXOgenous
535
what are the causes of ENDOgenous nephrotoxic ATN?
- free myoglobin (rhabdomyolysis)
| - free hemoglobin (intravascular hemolysis)
536
what are the causes of EXOgenous nephrotoxic ATN?
- contrast-related
- drugs
- osmotic nephropathy
- acute phosphate nephropathy
- use of bowel purgatives containing sodium phosphate
537
what is acute phosphate nephropathy?
AKI occurring after the use of bowel purgatives containing SODIUM PHOSPHATE
538
CLUE leading to diagnosis of acute phosphate nephropathy
hyperphosphatemia out of proportion to degree of kidney injury
539
what are the 2 renal problems caused by contrast-related AKI?
- immediate contrast-induced ATN (improves and has no skin findings)
- cholesterol atheroemboli
540
contrast-related AKI occurring days after procedure
cholesterol atheroembolic kidney disease
541
- blue toes
- livedo reticularis
- stepwise progression
- eosinophilia
- eosinophiluria
- low complements
cholesterol atheroembolic kidney disease
542
"STEPWISE PROGRESSION" of renal failure
cholesterol atheroembolic kidney disease
543
cholesterol emboli in retinal arterioles that appear as orange-white dots interrupting circulation
Hollenhorst plaques
544
treatment for AKI d/t cholesterol emboli
SUPPORTIVE only
545
ATN: labs
- BUN:Cr ratio
10-15:1
546
ATN: labs
- urine osmolality
< 350 (tubules cannot concentrate urine)
547
ATN: labs
- URINE Na+
> 40 (but, can be dilute if water reabsorption is significantly affected)
548
ATN: labs
- FeNa+
> 2%
| can be LOW in CONTRAST-induced nephropathy
549
ATN: labs
- urine sediment
- MUDDY BROWN, "DIRTY" GRANULAR CASTS (nonspecific, but very sensitive)
- epithelial cell casts
550
initial management of ATN
- treat precipitating cause
| - treat any hypERkalemia
551
OLIGURIC ATN usually resolves in
1-4 weeks
552
is oliguria required for the diagnosis of ATN?
NO
553
if oliguric, pts w/ ATN are more prone to?
becoming hypERkalemic, and volume-overloaded
554
causes of rhabdomyolysis
- 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
lab abnormalities in rhabdomyolysis
- INCREASED CPK (> 100,000 IU/L)
- nonspecific increases in AST and ALT
- elevated Cr
- hypERkalemia
- hypERphosphatemia
- increased UA
- hypOcalcemia
556
UA shows what in rhabdomyolysis
- MUDDY BROWN CASTS
- POSITIVE BLOOD
- NO RBCs
557
2 mechanisms causing hypOcalcemia in rhabdomyolysis
1. decreased production of 1,25-(OH)2-D d/t renal injury
| 2. hypERphosphatemia d/t renal injury and tissue breakdown
558
what electrolyte can become significantly increased during recovery?
CALCIUM
559
what electrolyte abnormality, in ATN d/t rhabdomyolysis, should only be treated if severe or pt is symptomatic?
hypOcalcemia
560
treatment for rhabdomyolysis
- isotonic fluid resuscitation, or
| - forced diuresis w/ ALKALINIZATION OF URINE
561
how does hemoglobinuria d/t severe intravascular hemolysis cause ATN?
Hb causing mechanical obstruction of tubules
562
interstitial kidney disease is caused by
inflammation and/or fibrosis of interstitium
563
acute interstitial nephritis (AIN) is caused by
drugs
564
proteinuria in tubular and interstitial diseases
low-grade (< 1-1.5 g/day)
565
acute (or allergic) interstitial nephritis (AIN) is most often a _____
drug-induced HYPERSENSITIVITY reaction
566
acute (or allergic) interstitial nephritis (AIN) can present w/
- fever
- eosinophilia
- rash
(only 10% present w all 3)
567
MC drugs that cause acute (or allergic) interstitial nephritis (AIN)
- NSAIDs
- abx
- PPIs
- cimetidine
- thiazides
- allopurinol
568
MC abx causing acute (or allergic) interstitial nephritis (AIN)
- beta-lactams
- TMP/SMX
- rifampin
- ciprofloxacin
569
now identified as a MAJOR cause of interstitial nephritis
PPIs
570
- typically ingested for MONTHS before symptoms occur
| - rash, fever, and eosinophilia are frequently absent
NSAID-induced AIN
571
NSAID-induced AIN typically causes what range proteinuria?
NEPHROTIC-RANGE PROTEINURIA
572
NSAID-induced AIN results in glomerular changes consistent w/?
MINIMAL CHANGE DISEASE
573
what are other causes, besides drugs, of acute (or allergic) interstitial nephritis AIN?
- sarcoidosis
- SLE
- Sjogren's
- transplant rejection
- infection
574
acute (or allergic) interstitial nephritis: labs
- urine sediment
- few red cells
- white cells +/- WBC casts
- mild protein (< 1 g/day)
- urinary eosinophils w/ Hansel stain
575
acute (or allergic) interstitial nephritis: labs
- FeNa+
usually > 1%
576
treatment for acute (or allergic) interstitial nephritis
discontinuing offending drug and observing
577
causes of chronic interstitial nephritis
- drugs
- HTN
- heavy metals (esp lead and cadmium)
- obstruction
- infections
- sarcoidosis
- Sjogren's disease
- SCD
- MM
578
what drug combination can lead to chronic interstitial nephritis?
acetaminophen + ASA, esp if further combined w/ caffeine or codeine
579
- pt w/ h/o frequent pain
- low urine SG
- minimal proteinuria
- sterile pyuria
- elevated Cr
analgesic-abuse nephropathy (chronic interstitial nephritis)
580
in analgesic-abuse nephropathy (chronic interstitial nephritis), a noncontrast CT of the kidneys may show what?
papillary necrosis
581
possible sources of lead poisoning leading to chronic interstitial nephritis
- OCCUPATIONAL exposure
- drinking "MOONSHINE"
- HERBAL MEDICATIONS
- LEAD-GLAZED PLATES or COOKWARE
- smoking MARIJUANA
582
- nephropathy develops after YEARS
- presents as azotemia
- tiny bit of proteinuria
- hyperuricemia
- bland urine sediment
- may have crystalline arthropathy ("SATURNINE GOUT")
chronic interstitial nephritis 2/2 LEAD poisoning
583
what ingredient found in Chinese herbs for weight-loss can cause an unusual kind of renal interstitial fibrosis?
ARISTOLOCHIC ACID
584
what 2 patterns are glomerular diseases divided into?
1. nephritic
| 2. nephrotic
585
- acute, subacute, or chronic
- potentially reversible
- INFLAMMATORY process
- presents w/ hematuria, proteinuria (usually < 2 g/day), +/- RBC casts
nephrItic glomerular disease
586
nephrItic glomerular disease can be further subdivided into 2 categories
- focal and mild
(active sediment w/o HTN or edema)
- diffuse and severe
(active sediment w/ heavy proteinuria, renal failure, HTN, and edema)
587
- noninflammatory process
- presents w/ proteinuria and edema, +/- urine oval fat bodies
- often WITHOUT red cells and casts in urine sediment
nephrOtic glomerular disease
588
3 classic features of nephrOtic syndrome
1. HYPERCHOLESTEROLEMIA
2. HTN
3. HYPOALBUMINEMIA
589
either nephritic or nephrotic glomerular disease can occur in which 2 diseases?
- SLE
| - MPGN (membranoproliferative glomerulonephritis)
590
what are the pulmonary-renal syndromes (AGN)?
- Goodpasture's
- granulomatosis w/ polyangiitis
- microscopic polyangiitis
- Churg-Strauss
- Henoch-Schonlein purpura
- cryoglobulinemia
591
what are the basement membrane syndromes (AGN)?
- anti-GBM disease (Goodpasture's)
- Alport's
- thin basement membrane disease
592
what are the infectious disease syndromes (AGN)?
- post-infectious GN
- endocarditis
- HIV
- HBV
- HCV
- syphilis
- malaria
593
definitive diagnosis of AGN (except for diabetic nephropathy) is made w/
renal biopsy
594
what differentiates microscopic hematuria coming from the kidney vs lower urinary tract?
lower urinary tract = ISOLATED microscopic hematuria
glomerular origin = hematuria WITH proteinuria, dysmorphic red cells, and/or RBC casts
595
urine sediment finding DEFINITIVE for GN
RED CELL CASTS
596
- VARIABLE PROTEINURIA
| - "ACTIVE" urine sediment (proteinuria, red cells > 10/hpf, white cells, red cell/white cell/granular casts
nephritic GN
597
casts ALWAYS originate in tubules
- very specific finding
- seen ONLY in GN
red cell casts
598
casts ALWAYS originate in tubules
- typically seen in pyelonephritis, or AIN
white cell casts
599
casts ALWAYS originate in tubules
- can be nonspecific
- characteristic of ATN
granular casts
600
casts ALWAYS originate in tubules
- indicate advanced renal disease
waxy casts
601
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
fatty casts (or oval fat bodies)
602
casts ALWAYS originate in tubules
- do not indicate disease; seen w/ CONCENTRATED urine
hyaline casts
603
- 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
nephrotic GN
604
what is nephrotic-range proteinuria?
> 3.5 g/d (or 40-50 mg/kg/d)
605
- 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
nephrotic syndrome
606
strategy to classify the glomerular diseases (3 steps)
- 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
name the GN's
- nephrOtic
- presentation: kidney ONLY
- minimal change disease
- FSGS
- membranous
608
name the GN's
- nephrOtic
- presentation: systemic
- DM
- AL amyloidosis
- AA amyloidosis
609
name the GN's
- nephrItic
- NORMAL complement
- presentation: kidney ONLY
- IgA
| - Alport
610
name the GN's
- nephrItic
- NORMAL complement
- presentation: systemic
- Goodpasture's
- vasculitides
- TTP/HUS
611
name the GN's
- nephrItic
- LOW complement
- presentation: kidney ONLY
- PIGN
| - MPGN
612
name the GN's
- nephrItic
- LOW complement
- presentation: systemic
- SLE
- endocarditis
- cryoglobulinemia
613
name the GN
- any nephrItic GN can become _____
- complement: VARIABLE
- presentation: VARIABLE
- RPGN
614
C3 is ALWAYS low for how long in PIGN?
6-8 weeks
615
FIRST test to order for a NEPHRITIC picture
COMPLEMENT levels
616
PIGN is usually caused by
- group A beta-hemolytic streptococcal infections
| - also associated w/ staph
617
- gross hematuria
- and/or edema
- sxs occur 1-6 WEEKS after initial illness (average; throat infection = 10 days, skin infection = 2-4 weeks)
PIGN
618
what is the diagnostic key in differentiating between PIGN from IgA nephropathy?
"LATENCY PERIOD"
619
what are the ANTISTREPTOCOCCAL ANTIBODIES that aid in dx?
- antistreptolysin O (ASO) titer
- antideoxyribonuclease B (anti-DNase B) titer
- antihyaluronidase titer
620
how long does antistreptolysin O (ASO) titer stay elevated?
SEVERAL WEEKS
621
how long does antideoxyribonuclease B (anti-DNase B) titer stay elevated?
several months
622
how long do complement levels remain LOW in PIGN?
6-8 weeks
623
PIGN renal biopsy shows what
immune deposits (IgG, IgM, complement) in subendothelial and subepithelial regions ("HUMPS"), and neutrophil invasion of glomerulus
624
treatment for PIGN
- abx for underlying infection
| - supportive care
625
diagnosis for MPGN
biopsy diagnosis
626
- 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
MPGN
627
LOW C3 and C4 are more common in which form of MPGN?
immune complex-mediated MPGN
628
- chronic hepatitis C or B w/ or w/o cryoglobulinemia, shunt nephritis, abscess
- AI disease (SLE, Sjogren's)
- monoclonal gammopathy
immune complex-mediated MPGN
629
- 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
complement-mediated MPGN
630
LOW C3 and NORMAL C4 is more common in which form of MPGN?
complement-mediated MPGN
631
LOW C3 in PIGN returns to normal after how long?
2-3 months
632
C3 remains low in MPGN for how long?
INDEFINITELY
633
if you initially suspected PIGN, but C3 stays low > 3 months, what should you suspect instead and what should be done?
- MPGN
| - renal biopsy!
634
treatment for MPGN
treat underlying cause
635
name the 6 classes of lupus nephritis
```
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
which lupus pts are candidates for renal bx?
ALL lupus pts w/ active urine sediment REGARDLESS of GFR
637
treatment for lupus nephritis
- mycophenolate mofetil, or
| - cyclophosphamide
638
- WORLDWIDE, MC GN
| - more common in Asians and males
IgA nephropathy, aka Berger disease
| "mesangial proliferative GN"
639
what are the 4 different ways IgA nephropathy can present?
- gross hematuria coincident w/ or immediately following a URI
- microscopic hematuria w/ proteinuria and progressive disease
- nephrotic syndrome
- RPGN
640
when does the hematuria seen in IgA nephropathy occur?
either during viral illness, or just after exercise
641
what is an important distinguishing feature between IgA nephropathy and PIGN?
NO LATENT PERIOD
642
serum complement levels in IgA nephropathy
usually normal
643
renal bx and immunofluorescence staining findings in IgA nephropathy
- 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
what is "secondary IgA nephropathy?"
when other illnesses cause IgA deposition in the mesangium, but aren't actually IgA nephropathy
645
what are the determining factors for the prognosis of IgA nephropathy?
- serum Cr
- BP
- amount of proteinuria
646
treatment for IgA nephropathy, if:
normal renal function
observe
647
treatment for IgA nephropathy, if:
proteinuria (> 0.5 g/d) and progressive disease
ACEI/ARB
648
treatment for IgA nephropathy, if:
persistent proteinuria (> 1 g/d) despite ACEI/ARB x 6 mos
corticosteroids
649
- hereditary (usually X-linked) syndrome
- chronic GN +/- NERVE DEAFNESS
- congenital EYE PROBLEMS
Alport's
650
hallmark finding on EM for Alport's
split lamina densa (part of GBM)
651
acute GN w/ evidence of anti-GBM Abs WITH PULMONARY HEMORRHAGE (70% of pts)
GOODPASTURE'S
652
Goodpasture's presentation
- active urine sediment
- hemoptysis
- dyspnea
653
diagnosis for anti-GBM disease
anti-GBM Abs, or renal bx if serum Abs are negative
654
renal bx finding for anti-GBM disease
anti-GBM IgG deposits in LINEAR fashion along GBM
655
treatment for Goodpasture's
- plasmapheresis (to remove Abs)
| - immunomodulation (steroids + cyclophosphamide)
656
what are the main vasculitides that commonly involve an acute GN?
- granulomatosis w/ polyangiitis
- microscopic polyangiitis
- eosinophilic granulomatosis w/ polyangiitis (Churg-Strauss)
- Henoch-Schonlein purpura (HSP)
657
kidney or skin findings in HSP
identical to IgA nephropathy
658
- 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
rapidly progressive GN
659
RPGN should always be considered, when?
severe and progressive renal failure of recent onset w/ NEPHRITIC urine
660
urine sediment findings in RPGN
- PROTEIN
- RED CELLS
- sometimes RBC CASTS
661
3 major pathogenic causes of RPGN
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
evaluation of RPGN
- RAPID HISTOPATHOLOGIC DIAGNOSIS
| - measure ANCA titers
663
- pulmonary hemorrhage
- LINEAR staining of IgG along GBM on renal bx
- high titer of serum anti-GBM Abs
GOODPASTURE SYNDROME
664
- ENT manifestations (sinusitis, epistaxis)
- pulmonary infiltrates/hemoptysis
- negative immunofluorescence on kidney bx
- positive c-ANCA
GRANULOMATOSIS W/ POLYANGIITIS
665
- pt w/ h/o ASTHMA/ATOPY w/ peripheral eosinophilia
| - positive p-ANCA
eosinophilic granulomatosis w/ polyangiitis
666
- no systemic features
- negative immunofluorescence on kidney bx
- positive ANCA
PAUCI-IMMUNE GN (aka renal limited-ANCA vasculitis)
667
empiric treatment for RPGN
high-dose methylprednisolone, then prednisone + cyclophosphamide +/- plasmapheresis (if pulmonary hemorrhage)
668
treatment for RPGN once renal bx results are available
treat underlying cause
669
MCC of primary nephrotic syndrome
minimal change disease
670
MCD is most commonly idiopathic, but has been associated w/
- drugs (NSAIDs, rarely others)
| - lymphoma (both Hodgkin's and NHL)
671
presentation of MCD
ANASARCA, or severe peripheral EDEMA (develops over weeks), and WITHOUT HTN
672
MCD renal bx findings
- LM shows NO CHANGE
| - EM shows FUSION OF EPITHELIAL FOOT PROCESSES (but can be seen in any nephrotic syndrome)
673
initial treatment for MCD
steroids
674
treatment for MCD if steroid-resistant
- cyclophosphamide
| - cyclosporine
675
- 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
focal segmental glomerulosclerosis (FSGS)
676
- diffuse FOOT PROCESS FUSION
- additional sclerosis limited to SEGMENTS of the glomeruli
- hypertensive on presentation
- 50% have reduced renal function at dx
focal segmental glomerulosclerosis (FSGS)
677
- have slowly progressive renal failure
| - those NOT responding to tx REQUIRE DIALYSIS w/i about 5-10 years
focal segmental glomerulosclerosis (FSGS)
678
initial treatment for focal segmental glomerulosclerosis (FSGS)
ACEIs/ARBs and high-dose steroids
679
secondary causes of membranous nephropathy (MN)
- chronic INFECTIONS (esp. chronic HBV)
- several DRUGS (NSAIDs, penicillamine, and gold)
- underlying SOLID TUMORS
- AI thyroiditis and SLE (consider in young female)
680
- 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
membranous nephropathy (MN)
681
renal biopsy results in membranous nephropathy (MN)
- immunofluorescence shows GBM subepithelial IgG and C3 deposits
- EM shows shows GBM subepithelial deposits w/ loss of overlying foot processes
682
test to distinguish between idiopathic and secondary membranous nephropathy (MN)
Abs to M-type phospholipase A2 receptor (anti-PLA2R)
| positive in primary
683
treatment for secondary membranous nephropathy (MN)
- discontinue offending drugs
| - treat underlying disease
684
when do you aggressively treat membranous nephropathy (MN)?
persistent high-grade proteinuria (> 4 g/d) despite at least 6 months w/ an ACEI/ARB and HTN control
685
has the highest prevalence of renal vein thrombosis compared w/ other causes of nephrotic syndrome
membranous nephropathy (MN)
686
pt w/ known membranous nephropathy (MN) has flank pain, hematuria, high LDH, think of
RENAL INFARCTION 2/2 renal vein thrombosis
687
MC systemic cause of nephrotic syndrome in adults
diabetic nephropathy
688
diabetic nephropathy may be associated w/
hyporeninemic hypoaldosteronism and type 4 RTA
689
in diabetic nephropathy, what PRECEDES NEPHROPATHY?
RETINOPATHY
690
renal biopsy results in diabetic nephropathy
- expansion of mesangium
- thickening of GBM
- sclerosis of glomeruli (KIMMELSTIEL-WILSON lesion)
691
how many phases does diabetic nephropathy occur in, and what are they?
- 2
- phase 1 = silent or preclinical phase
- phase 2 = clinical phase
692
what is the 1st measurable change in renal function in phase 1 of diabetic nephropathy?
MICROALBUMINURIA (30-300 mg/24H)
693
next step in diabetics tested yearly for albuminuria
treat w/ ACEI/ARB EVEN IF NORMOTENSIVE
694
clinical phase of diabetic nephropathy is associated w/
- proteinuria (> 300 mg/d, and often nephrotic range)
- HTN
- progressive loss of kidney function
695
what slows progression of diabetic nephropathy?
- BP control < 140/90 w/ ACEI/ARB
| - and glycemia control (HbA1c < 7)
696
in what 2 scenarios should a pt with DM undergo a renal bx to exclude other possible causes of nephrotic syndrome?
- NO eye disease
| - dysmorphic red cells on urine sediment
697
as renal function decreases, insulin requirements
decrease (2/2 decreased metabolism by kidneys)
698
MM can cause which of the following problems w/ renal involvement?
- cast nephropathy (myeloma kidney)
- hypercalcemia
- primary "AL" amyloidosis
- monoclonal Ig deposition disease (MIDD)
- secondary "AA" amyloidosis
699
MC form of renal involvement d/t MM
cast nephropathy (myeloma kidney)
700
- immunoglobulins (Bence Jones proteins) precipitate in tubules leading to acute renal failure
- NEGATIVE DIPSTICK protein, but POSITIVE PROTEINURIA
cast nephropathy (myeloma kidney)
701
electrolyte imbalance in MM that can acute renal failure
hypercalcemia
702
- multisystem disease
- nephrotic syndrome and renal failure
- (Congo-red stain shows deposits w/ apple-green birefringence)
primary "AL" amyloidosis associated w/ MM
703
- monoclonal immunoglobulin light chains or heavy chains are deposited in GBM
- can resemble diabetic nephropathy w/ nodular glomerulosclerosis
monoclonal Ig deposition disease (MIDD)
704
- 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
secondary "AA" amyloidosis
705
controlling what is vital in ANY glomerular disease
glomerular pressure
706
best in decreasing intraglomerular pressure
ACEIs or ARBs
707
treatments used in MOST nephrotic syndromes, EXCEPT those caused by AMYLOID and DIABETES
glucocorticoids +/- cytotoxics
708
hypocomplementemia NEVER occurs in
the nephrotic syndromes (MCD, FSGS, MG, diabetic nephropathy, amyloid nephropathy)
709
RBC casts are NOT seen in
the nephrotic syndromes (MCD, FSGS, MG, diabetic nephropathy, amyloid nephropathy)
710
urine sediment in renal disease:
bland UA; occasionally granular and/or hyaline casts
prerenal failure
711
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
postrenal failure
712
urine sediment in renal disease:
dirty brown granular casts
intrinsic renal: ATN
713
DILATION of AFFERENT arteriole and maintenance of glomerular perfusion pressure require
prostaglandins (PG)
714
mechanism of NSAIDs causing hyperkalemia
block PG-mediated renin release from JGA --> low aldosterone --> decreased renal K+ excretion
715
what types of kidney problems are chronic injection drug users at risk for?
- 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
possible reasons for AKI in cancer
- direct infiltration
- obstruction
- glomerular disease
- chemotherapy drug toxicity
- hypercalcemia
717
possible reasons for AKI in cancer:
- direct infiltration causes
- lymphoma
- leukemia
- myeloma
718
possible reasons for AKI in cancer:
- obstruction
- pelvic/abdominal tumors
- intratubular uric acid obstruction d/t TLS
- methotrexate crystallization
719
possible reasons for AKI in cancer:
- glomerular disease
- MCD = Hodgkin disease
- secondary MGN = solid tumors
- amyloidosis = MM
720
possible reasons for AKI in cancer:
- chemotherapy drug toxicity
- mitomycin C-induced HEMOLYTIC UREMIC SYNDROME
- cisplatin-induced tubular injury
- bevacizumab-induced thrombotic microangiopathy
- ifosfamide causing ATN
721
electrolyte abnormality causing AKI in cancer
hypercalcemia
722
prophylactic treatment for TLS (acute urate nephropathy)
- aggressive IV hydration (hypotonic or isotonic saline)
| - ALLOPURINOL, or RASBURICASE
723
rasburicase is CI in which pts?
G6PD deficiency
724
definition of CKD
- 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
CKD stages
- 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
pts w/ CKD have an increased risk of
heart disease
727
1 cause of death in pts w/ CKD
heart disease
728
serum phosphorus levels remain normal until what stage?
about CKD stage 3
729
mechanism of chronic kidney disease-mineral bone disorders (CKD-MBD)
- 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
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
hyperphosphatemia
731
what are the 2 types of phosphate binders?
- CALCIUM-BASED (CaCO3; Ca acetate)
| - NONCALCIUM-BASED (sevelamer; lanthanum)
732
CKD stage 3 or more causes what?
- increased PO4
- normal/low-normal Ca2++
- increased iPTH
- low 1,25-(OH)2-D
733
ideal management to control PO4 in CKD
diet and binder
734
controlling PO4 in CKD leads to what?
- normalization of PO4
- increased Ca2++
- decreased iPTH
735
if PTH is not adequately corrected with diet and PO4 binder, next step?
add 1,25-(OH)2-D (calcitriol)
736
pts w/ CKD can have what 3 types of bone d/o's?
1. osteitis fibrosa cystica
2. adynamic bone disease
3. osteomalacia
737
secondary hyperparathyroidism labs
- high PO4
- low 1,25-(OH)2-D
- very high iPTH
- normal/low-normal Ca2++
738
treatment for secondary hyperparathyroidism 2/2 CKD
- follow iPTH
- phosphate binder
- 1,25-(OH)2-D, or paricalcitol/doxercalciferol
- +/- cinacalcet
739
how do you choose which phosphate binder to use?
based on serum Ca++ level
740
what is the goal when using phosphate binders?
normalize phosphorus WITHOUT creating adynamic bone
741
adynamic bone disease labs
- high/normal PO4
- low 1,25-(OH)2-D
- LOW iPTH
- normal/high Ca2++
742
cause for adynamic bone disease
oversuppression of PTH by phosphate binders and concomitant use of vitamin D analogs
743
- 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)
uremia
744
what endocrine problems can be caused in CKD?
- decreased glucose intolerance
- decreased gonadal hormone production (w/ impotence or amenorrhea/infertility)
- low T3 w/ normal TSH
745
anemia of chronic kidney disease is a diagnosis of
exclusion
746
first r/o iron deficiency; responds dramatically to recombinant erythropoietin
NORMOCHROMIC-NORMOCYTIC ANEMIA in CKD
747
what should be checked before starting ESAs?
iron stores:
- Fe sat > 20%
- ferritin > 100
748
target Hb when treating w/ ESAs
- no specific target
| - NO IMPROVEMENT in outcome and INCREASED MORBIDITY and MORTALITY if Hb is CORRECTED TO NORMAL (> 13)
749
progression of CKD is slowed by which meds?
ACEIs or ARBs
750
progression of CKD is also slowed down by management of which comorbidities?
- metabolic acidosis
- hyperlipidemia
- stop smoking
751
AVOID NEPHROTOXINS in CKD, especially
- contrast dye
- NSAIDs
- aminoglycosides
752
treatment for gout in CKD
colchicine or NSAIDs +/- allopurinol
753
CONTRAINDICATED in treatment for gout in CKD
probenecid
754
when do you start dialysis?
when CKD pt has ADVANCING UREMIA: ANY uremic sxs in pt w/ CrCl < 15 mL/min
755
MCC of DEATH in dialysis pts
- CARDIOVASCULAR disease
| - next is infection
756
one of the key factors in reducing morbidity and mortality in dialysis pts
maintaining ADEQUATE NUTRITION
757
what is the main complication for CAPD?
PERITONITIS
758
peritonitis in CAPD is usually caused by which bugs?
gram-positive skin flora (S. epidermidis or S aureus), followed by gram-negative organisms
759
can be completely removed during dialysis, and therefore need to be re-dosed after treatment
AMINOGLYCOSIDES
760
which abx have some clearance during dialysis and need to be re-dosed afterwards and may require supplemental doses?
- most beta-lactams
- daptomycin
- metronidazole
- ciprofloxacin
- levofloxacin
761
in CKD STAGES 4 AND 5, which contrast type should be AVOIDED?
GADOLINIUM
762
GADOLINIUM can cause this this in pts w/ advanced CKD (all forms, regardless of whether on dialysis or what type of dialysis)
NEPHROGENIC SYSTEMIC FIBROSIS (NSF)
763
- presents as a thickening of skin w/ symmetrical plaques, papules, or nodules
- STARTS DISTALLY
- disease course is progressive, sometimes fulminant
NEPHROGENIC SYSTEMIC FIBROSIS (NSF)
764
is NOT associated w/ nephrogenic systemic fibrosis (NSF)
livedo reticularis
765
diagnosis for nephrogenic systemic fibrosis (NSF)
deep punch bx of involved skin
