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453 Cards in this Set
- Front
- Back
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6 functions of the kidney
|
electrolyte balance
water handling BP control secretion of toxins acid/base regulation hormone production |
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|
what percentage of plasma volume entering the nephron is filtered?
|
80%
|
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what percentage of plasma volume entering the nephron is secreted?
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20%
|
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what percentage of plasma volume entering the nephron is reabsorbed?
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19%
|
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what percentage of plasma volume entering the nephron is excreted?
|
1%
|
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|
define Stage 1 CKD
|
kidney damage with normal or increased GFR
GFR > 90 |
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define Stage 2 CKD
|
kidney damage with mild decrease in GFR
GFR 60-89 |
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define Stage 3 CKD
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moderate decrease in GFR
30-59 |
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define Stage 4 CKD
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severe decrease in GFR
15 - 29 |
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define Stage 5 CKD
|
kidney failure
<15 or dialysis |
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rank odds ratios for ESRD by ethnicity
|
black
native americans asian white especially in the "stroke belt" SE US |
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CV mortality in general population and dialysis patients by race
|
35x higher in dialysis patients, regardless of race or age
|
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describe cardiorenal syndrome
|
increased SCr increases mortality
|
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strongest indicator of obese adolescents
|
low household income level
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most frequent diagnosis for patients who start dialysis
|
50% DM
27% HTN 13% glomerulonephritis |
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incidence of ESRD in African Americans with
DM? HTN? |
432M DM
338M HTN |
|
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incidence of ESRD in Native Americans with
DM? HTN? |
558M DM
93M HTN |
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how does dialysis treatment correlate with age?
|
increases with age
|
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2 other names for renal failure
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azotemia
acute kidney injury |
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2 categories of renal failure
|
pre-renal
intrarenal post-renal |
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|
describe pre-renal failure
|
pre-renal azotemia
-reduced renal perfusion -volume depletion -hypotension -CV -hemodynamic -hepatorenal syndrome |
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in pre-renal azotemia, what are 2 examples of volume depletion?
|
renal loss
extrarenal loss |
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in pre-renal azotemia, what are 2 examples of CV causes?
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HF
cardiogenic shock |
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in pre-renal azotemia, what are 2 examples of hemodynamic causes?
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intense intrarenal vasoconstriction
7 meds -NSAID -ACEI -amphotericin B -radiocontrast -cyclosporine -tacrolimus |
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4 intrarenal sites of renal failure
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vascular
glomerular tubular interstitial |
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3 causes of tubular intrarenal failure
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ischemia
toxins pigments |
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describe acute tubular necrosis (ATN)
|
renal insults such as
-renal ischemia (hypoperfusion) -exposure to exogenous or endogenous nephrotoxins (oliguria) rapid decline in renal fxn that may require dialysis before spontaneous resolution debris and necrotic cells cause obstruction (acute renal failure - ARF) |
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Tx of ATN
|
hydration, blood transfusions
caution not to induce HF |
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in ATN, cause of renal ischemia, urine output?
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severe prerenal disease from any cause
anuria |
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in ATN, examples of nephrotoxins, urine output?
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amphotericin B
aminoglycosides heme/myo pigments NSAIDs oliguria "stupid urine", only water leaves |
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2 major histological changes that take place in ATN
|
-tubular necrosis with sloughing of the epithelial cells
-occlusion of the tubular lumina by casts and cellular debris |
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1 example cause of acute tubular necrosis
|
abdominal aortic aneurysm
causes renal ischemia because blood is forced into the abdominal area (cause of severe back pain) |
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3 types of postrenal failure
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prostate hypertrophy
intraureteral obstruction extraureteral obstruction |
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4 examples of intraureteral obstruction
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crystal
stone (urolithiasis) clots tumor |
|
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2 examples of extraureteral obstruction
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cervical tumor
prostate tumor |
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4 sites of pathology in intrinsic/intrarenal azotemia
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vascular
glomerular tubular interstitium |
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5 examples of intrarenal azotemia involving the vasculature
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renal infarction
renal artery stenosis renal vein thrombosis malignant HTN atheroemboli |
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3 examples of intrarenal azotemia involving the glomerulus
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acute glomerulonephritis
vasculitis thrombotic microangiopathy ---hemolytic-uremic syndrome ---Thrombotic thrombocytopenic purpura |
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2 examples of intrarenal azotemia involving the tubule
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ischemia
nephrotoxic |
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2 things that can cause tubular ischemia
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prolonged prerenal ischemia
sepsis |
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2 tubular nephrotoxins
|
aminoglycosides
rhabdomyolysis |
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2 examples of intrarenal azotemia involving the interstitium
|
medications
tumor infiltration |
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3 classes of medications that are interstitial nephrotoxins
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penicillins
PPIs cephalosporins |
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describe the filtration barrier in the kidney
|
filtration through the flomerular capillary wall occurs along an *extracellular pathway* in which no cell membranes are interposed
|
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3 components of the filtration barrier
|
endothelial pores
glomerular basement membrane slit diaphragms of podocytes |
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3 major insults to the glomerulus in glomerulonephritis
|
immune attack
metabolic stress (DM) mechanical stress (high pressure) |
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typical urine volume
|
750-2000 mL/day
1-1.5 mL/kg/h |
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oliguria urine volume
|
<400 mL/day
|
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auria urine volume
|
<100 mL/day
|
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polyuria urine volume
|
>3000 mL/day
|
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questions to ask regarding urine volume
|
have you been gaining weight?
have you been urinating? how much have you been urinating? |
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relationship between plasma creatinine and GFR
|
increases in creatinine concentration relate to a decrease in GFR
|
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relationship between plasma creatinine and renal damage
|
NOT proportional to renal damage
|
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plasma creatinine depends on...
|
input/output
muscle mass/age/sex/weight |
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what is one way to identify the progression of chronic renal disease?
|
plot reciprocal of SCr to time
can predict when dialysis will be required |
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|
advantages of BUN msrmt
|
-quick, simple msrmt
-sensitive -useful in prerenal disease, rises faster than SCr |
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disadvantages of BUN msrmt
|
-consider input, output, patient's fluid volume
-wide reference range -not specific index of illness |
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6 things that cause increases in BUN
|
-GI bleed
-trauma -renal hypoperfusion/decreased RBF/decreased ECFV -acute renal impairment -chronic renal disease -post-renal obstruction |
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2 methods of estimating creatinine clearance
|
-CG equation
-MDRD equation |
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describe Cockcroft Gault equation
|
variables: age, weight, gender, SCr
Gold standard for drug dosing |
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describe MDRM equation
|
variables: age, race, gender, SCr
more accurate than CG |
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2 drugs that affect the tubular secretion of creatinine
|
cimetidine
TMP/(SMZ) drugs will cause a rise in SCr and a decline in creatinine clearance |
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|
describe cystatin C
|
-protein produced by all cells at a constant rate
-freely filtered -reabsorbed and catabolized by the kidney -doesn't appear in the urine |
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advantages of cystatin C over SCr
|
not dependent on age, weight, muscle
experimental use v. clinical |
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3 charactistics to consider in urinalysis
|
appearance
specific gravity pH |
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3 characteristics of urine appearance
|
blood
color turbidity |
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urine color can indicate presence of
|
hemoglobin
myoglobin |
|
|
urine turbidity can indicate the presence of
|
infection
nephrotic syndrome proteinuria |
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specific gravity of the urine only measures
|
ionic species
(i.e., not glucose) |
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normal urine pH
|
acidic, except after eating
|
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|
examples of urine sediments
|
fat droplets
red cell casts white cell casts bacteruria polymorphs |
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pylonephritis might be indicated by
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white cell casts
polymorphs bacteruria |
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lower UTI might be indicated by
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polymoprhs, no casts
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acute GN might be indicated by
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hematuria
cells casts |
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chronic GN might be indicated by
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less sediment
|
|
|
cell casts generally indicate
|
glomerular injury
-cell casts are formed within the nephron -can be made up of protein, lipid, cells, or mixed |
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|
whole blood cells generally indicate
|
infection
|
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crystalluria tends to indicate
|
high concentration or altered solubility
|
|
|
WBC/RBC in urine can indicate
|
UTI
GN pylonephirtis |
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|
epithelial casts in urine can indicate
|
tubular damage
ARF ATN |
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WBC casts in the urine can indicate
|
acute interstitial nephritis
pyelonephritis |
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waxy casts in the urine can indicate
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ATN
pre-renal azotemia |
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urine oxalate crystals in the urine can be caused by which drugs
|
acyclovir
SMX/TMP methotrexate ethylene glycol radiocontrast agents due to solubility of the drug do not necessarily grow into a stone but do block up the nephron |
|
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eosinophiluria can indicate
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acute allergic interstitial nephritis
atheroembolism |
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granular casts can indicate
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ATN
GN interstitial nephritis |
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leukocytosis can be common in
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ARF
(infection, sepsis, inflammation) |
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leukopenia and thrombocytopenia can indicate
|
SLE
TTP |
|
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CPK elevations can indicate
|
rhabdomyolysis
MI |
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elevations in liver transaminases can indicate
|
rapidly progressive liver failure and hepatorenal syndrome
|
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2 common complications of ARF
|
hypocalcemia
hyperkalemia |
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3 medications that frequently cause hyperkalemia
|
spironolactone
ACEI septra |
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in pre-renal ARF, urine tends to be....
|
concentrated
pt is usually anuric |
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in ATN, urine tends to be
|
dilute
|
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what is FeNa?
|
fractional excretion of sodium
(urine Na/plasma Na) ---------------------------------------------- (urine creatinine/plasma creatinine) |
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FeNa in prerenal ARF?
|
<1%
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FeNa in ATN?
|
FeNa > 1% in ATN
|
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FeNa in intrinsic renal failure?
|
FeNa > 2%
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in urinalysis, increased blood glucose indicates
|
low renal threshold for Glu
or other tubular disorders |
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normal amount of protein in urine / 24 hours
|
<200 mg protein / 24 hours
|
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|
urine sticks detect proteinuria at what level
|
>300 mg/L
|
|
|
causes of proteinuria
|
overflow (raised plasma, Low MW proteins, myoglobin)
glomerular leak protein renal origin exercise |
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proteinuria is defined as how much protein in urine per day
|
>150 mg/day
|
|
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how much of normal protein excreted should be albumin?
|
15-20 mg albumin
|
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|
microalbuminuria is defined as
|
30-300 mg/day albumin, but this is not detectable by urine dipstick
|
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since urine dipstick doesn't detect microalbuminuria, how can you detect it?
|
-24 hour timed urine collection
(30-300 mg/day or 20-200 mcg/min) -urine albumin/creatinine ration (>30 mcg/mg creatinine) -spot microalbumin tests (detects >2 mcg/mL) |
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|
macroalbuminuria is defined as
|
300-3500 mg/day
urine dipsticks detect >15 mg/dL |
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nephrotic syndrome is defined as
|
urine protein excretion > 3.5 g / day
urine dipsticks detect >300 mg/dL (with hypoalbuminemia, edema, and hyperlipidemia) |
|
|
normal protein values for office urine dipstick
trace 1+ 2+ 3+ 4+ |
Trace 15 mg/dL
1+ 30 mg/dL 2+ 100 mg/dL 3+ 300 mg/dL 4+ 2000 mg/dL DOESN'T DETECT MICROALBUMINURIA |
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|
changes in plasma composition due in CKD when
CrCL is 60-120 mL/min |
no changes in plasma
|
|
|
changes in plasma composition due in CKD when
CrCL is 30-60 mL/min |
increased creatinine
increased urea |
|
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changes in plasma composition due in CKD when
CrCL is 20-30 mL/min |
increased potassium
decreased bicarbonate |
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|
changes in plasma composition due in CKD when
CrCL is 10-20 mL/min |
increased phosphate
increased uric acid |
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|
inciting factors of
prerenal azotemia v. ATN |
prerenal azotemia
---low volume ATN ---toxins ---ischemia ---medications |
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|
BUN/creatinine
prerenal azotemia v. ATN |
prerenal azotemia
--- >20/1 ATN --- <20/1 |
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|
urinary Na
prerenal azotemia v. ATN |
prerenal azotemia
--- <20 mEq ATN --- >40 mEq |
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FeNa
prerenal azotemia v. ATN |
prerenal azotemia
--- <1 ATN --- >2 |
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|
urine osmolality
prerenal azotemia v. ATN |
prerenal azotemia
--- >500 ATN --- <350 |
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urine cells and casts
prerenal azotemia v. ATN |
prerenal azotemia
--- bland ATN --- lots of cells, muddy, granular, dirty brown casts |
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summarize advantages of GFR
|
impractical
|
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summarize advantages of CrCl
|
unreliable
|
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summarize advantages of SCr
|
specific, but insensitive
|
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summarize advantages of plasma urea
|
subject to problems
|
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summarize advantages of urine volume
|
helpful, but often forgotten
|
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when should DM1's be screened for kidney disease
|
after 5 years, then annually
|
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when should DM2's be screened for kidney disease
|
at diagnosis, then annually
|
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how should diabetics be screened for kidney disease?
|
albumin-to-creatinine ratio in random urine
---microalbuminuria = 30-300 mg/g ---macroproteinuria estimate GFR from SCr retinopathy |
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|
clinical definition of diabetic nephropathy
|
-clinical diagnosis by Hx, exam, and urine albumin/creatinine
-longstanding Hx of DM +/- retinopathy -macroalbuminuria (aka overt nephropathy) defined as urine albumin/creatnine >300 mg/g -HTN (>90%) |
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natural history of diabetic nephropathy
|
-albuminuria
-HTN -declining GFR -INCREASED CV DEATH RISK |
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development of _____ heralds rapid decline in GFR in DM2
|
macroalbuminuria
|
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rather than progress to ESRD, diabetics with nephropathy are more likely to ____
|
die
|
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what do diabetics with nephropathy die from?
|
stroke
MI HF sudden death |
|
|
improving outcomes in diabetic nephropathy aids in the ___
|
prevention of CV events
prevention of ESRD |
|
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which albuminuria is detected by a dipstick?
|
macroalbuminuria (nephropathy)
|
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|
urine albumin/Cr in
microalbuminuria macroalbuminuria |
microalbuminuria 30-300 mg/g
macroalbuminuria >300 mg/g |
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|
renal risk in diabetics with
microalbuminuria macroalbuminuria |
microalbuminuria - marker of future nephropathy in some
macroalbuminuria - marker of progressive renal disease |
|
|
CV risk in diabetics with
microalbuminuria macroalbuminuria |
increased in both
micro/macroalbuminuria Why? unknown |
|
|
diabetic nephropathy affects which renal compartments
|
ALL
mesangial arterial glomerular capillaries tubulointerstitium |
|
|
how many stages of kidney disease are there?
|
5
|
|
|
define stage 1 of kidney disease
|
HYPERFILTRATION
-increase in GFR -kidneys increase in size -due to glucose induced osmotic diuresis |
|
|
define stage 2 of kidney disease
|
BASEMENT MEMBRANE THICKENING AND RETINOPATHY
-glomeruli begin to show damage and microalbuminurea occurs |
|
|
define stage 3 of kidney disease
|
-mesangial expansion
-albumin excretion rate (AER) exceeds 200 micrograms/minute, and blood levels of creatinine and urea-nitrogen rise -blood pressure may rise |
|
|
define stage 4 of kidney disease
|
-nodular glomerulosclerosis
-GFR decreases to less than 75 mL/min -large amounts of protein pass into the urine, and HTN almost always occurs -levels of creatinine and urea-nitrogen in the blood rise further |
|
|
define stage 5 of kidney disease
|
KIDNEY FAILURE or ESRD
-GFR <10 mL/min |
|
|
what is the average length of time to progress from Stage 1 CKD to Stage 4
|
DM1 - 17 years
|
|
|
what is the average length of time to progress from Stage 1 CKD to Stage 5
|
DM1 - 23 years
|
|
|
normal people lose how much GFR?
|
1 mL/min/year
|
|
|
people with CKD lose how much GFR?
|
1 mL/min/month
|
|
|
what is the difference between dippers and non-dippers in those with DM and CKD?
|
non-dippers have a major risk factor for CV death
|
|
|
what is the pathogenesis of kidney disease in diabetics?
|
-advanced glycosylation end products
-non-enzymatic glycosylation of proteins (e.g. hemoglobin) -glycosylation of BM proteins (mesangial expansion) -stimulation of adhesion molecule expression |
|
|
nephropathy prevention strategies in DM
|
***normalize blood pressure
-Goal 125/75 -ACEIs are particularly beneficial dietary protein restriction -0.6-0.8 g/kg/d w/ established macroalbuminuria or falling GFR glycemic control regular monitoring for nephropathy avoid nephrotoxins (NSAIDs, Abx) |
|
|
what are the components of the renal injury triad?
|
angiotensin II
HTN proteinuria |
|
|
effect of ACEIs and ARBs on diabetic nephropathy
|
-slows increases in SCr
-decreases ESRD, death -slows microalbuminuria -slows decline in GFR |
|
|
each hypertensive drug tends to decreases BP by how much
|
10 / 5-7
|
|
|
most HTN patients require how many medications?
|
3-4
|
|
|
in diabetics, proteinuria predicts
|
CHD events and stroke
|
|
|
in diabetics, is it appropriate to give them ARBs and ACEIs?
|
yes
antiproteinuric effect (COOPERATE STUDY) |
|
|
aliskerin
|
novel, orally available renin inhibitor
-highly soluble in water and biological fluids -nonpeptide drug suitable for oral administration -very expensive -PO F = 0.04 |
|
|
results of AVOID study
|
after 6 months on aliskiren
-UACR dec 20% -UAER dec 18% -no changes in eGFR -nonsig dec in mBP |
|
|
since, ACEI + ARB in DM are not enough to stop nephropathy, what else must be considered?
|
blockade of RAAS
|
|
|
in DM nephropathy, CV risk reduction is better with
tight BP control or tight Glu control? |
tight BP control
|
|
|
7 modifiable risk factors for progression of renal disease
|
HTN
albuminuria/proteinuria dyslipidemia HbA1C smoking anemia/nephrotoxins CaPO4 |
|
|
3 nonmodifiable RF progression of renal disease
|
age
ethnicity gender |
|
|
what is the risk of ischemic heart disease in diabetics related to?
|
high SBP
microalbuminuria |
|
|
what are the benefits of lowering BP?
|
In Stage 1 HTN + add'l RF's
-achieving a sustained 12 mmHg-reduction in SBP over 10 years will prevent 1 death for every 11 patients treated |
|
|
how is mean BP calculated?
|
BP = cardiac output x total systemic vascular resistance
|
|
|
mechanisms of renal damage in HTN
|
-glomerular HTN
-hyperfiltration -glomerular barrier dysfxn -proteinuria -mesangial hyperplasia -intrarenal inflammatory processor -endothelial dysfxn -VSMC proliferation |
|
|
describe the pathogenesis of fibrosis and loss of nephron units
|
TGF-beta plays a key role in extracellular matrix formation in mesangium and interstitium that leads to fibrosis and loss of nephron units
|
|
|
JNC7 suggests 1' medication is....
but Ali thinks... |
thiazides
ACEI |
|
|
at the proximal tubule, the carrier or channel inhibited is...?
FeNa? |
various?
60-65% |
|
|
at the loop of Henle, the carrier or channel inhibited is...?
FeNa? |
Na-K-2Cl carrier
up to 25% |
|
|
at the distal tubule and connecting segment, the carrier or channel inhibited is...?
FeNa? |
Na-Cl carrier
up to 3-5% |
|
|
at the cortical collecting tubule, the carrier or channel inhibited is...?
FeNa? |
Na channel
up to 1-2% |
|
|
MOA of loop diuretics
|
act directly on teh ascending limb of the loop of Henle to inhibit Na and Cl resorption
increase renal PGs, resulting int eh dilation of blood vessels and reduced peripheral vascular resistance |
|
|
4 loop diuretics
|
bumetanide
-short half life, TID dosing ethacrynic acid -use with sulfa allergy, but most ototoxic furosemide -not absorbed if edematous GI tissue torsemide -expensive |
|
|
3 thiazide diuretics
|
HCTZ
chlorthiazide trichlormethiazide |
|
|
2 thiazide-like diuretics
|
chlorthalidone
metolazone |
|
|
chlorthalidone v. HCTZ
|
chlorthalidone decreases SBP better
|
|
|
MOA of K-sparing diuretics
|
-work in collecting ducts and DCTs
-interfere with Na-K exchange -competitively bind to aldosterone receptors -block the resorption of Na and water usually induced by aldosterone |
|
|
4 K-sparing diuretics
|
amiloride
spironolactone -most common, probably better than eplerenone triamterene eplerenone -$$$, use if gynecomastia -improved aldosterone receptor selectivity |
|
|
therapeutic uses of K-sparing diuretics
|
-decrease proteinuria
-hyperaldosteronism -HTN -reverse the K loss caused by K-wasting drugs -ascites |
|
|
interaction between ACEI and K-sparing diuretics
|
increased hyperkalemia
cardiac problems (monitor K closely) |
|
|
interaction between aminoglycosides and loop diuretics
|
ototoxicity and nephrotoxicity
(monitor hearing and SCr closely) |
|
|
interaction between digoxin and
thiazides, loops |
hypokalemia
increased digoxin binding and toxicity (monitor K and cardiac function) |
|
|
interaction between beta blockers and thiazide diuretics
|
hyperglycemia
hyperlipidemia hyperuricemia |
|
|
interaction between steroids and
thiazides and loops |
increased risk of hypokalemia
|
|
|
interaction between
carbamazepine/chlorpropamide and thiazide diuretics |
increased risk of hyponatremia
|
|
|
2 causes of non-proliferative glomerulopathy
|
-damage by antibodies
-damage mediated by complements (as in SLE) |
|
|
1 cause of proliferative glomerulonephropathy
|
-damage by circulating proinflammatory cells (especiallu neutrophils and macrophages)
|
|
|
3 types of glomerulonephritis
|
diffuse
focal segmental |
|
|
define diffuse GN
|
when all glomeruli of the kidney are involved in the disease process
(whole glomerulus collapsed, very little urine) |
|
|
define focal GN
|
when some glomeruli of the kidney are involved in the disease process
|
|
|
define segemntal GN
|
when part of a glomerulus is involved in the disease process
|
|
|
describe proliferative GN
|
when there are increased numbers of cells in the glomeruli, which may die to infiltration of PMNs (polymorphonuclear leukocytes)
|
|
|
consequences of proliferative GN
|
-inflammation of GN
-decreased urinary space -decreased ultrafiltrate and urine -increased SCr, edema, BP |
|
|
describe membranous GN
|
thickened basement membrane
-hematuria -often in malaria (leading cause of GN in the rest of the world) |
|
|
acute nephritic syndrome is characterized by:
|
-hematuria
-oliguria (in severe) -edema (periorbital) -HTN -reduced GFR -proteinuria -fluid overload |
|
|
etiology of nephritic syndrome
|
-most common cause is acute post infectious GN
-streptococci -IgA disease -henoch-schonlein purpura -crescentic GN -SLE |
|
|
features of nephrotic syndrome
|
-edema
-proteinuria >3.5 g/24h -serum albumin <30 g/L -HLD -hypercaogulable state -HTN, DM |
|
|
5 types of GN that have heavy proteinuria
|
-minimal change disease
-focal sclerosis -membranous -DM -amyloidosis |
|
|
4 types of GN that have both proteinuria and hematuria
|
-lupus nephritis
-membranoproliferative -endocarditis -Henoch-Schonlein purpura |
|
|
3 types of GN that predominantly have hematuria
|
-IgA
-post strep -crescentic (RPGN - rapid progressive GN) -hemolytic uremic syndrome |
|
|
the type of GN that has the worst outcome
|
RPGN
|
|
|
5 ways to manage nephritic syndrome
|
-appropriate diagnostics (swabs, strep, complement, urea, createnine electrolytes, urinalysis, CXR)
-BP, urine output and daily weight -fluid and diet mgmt -treat HTN and fluid overload -treat Infxn |
|
|
acute GN can be divided into which two types?
|
-acute post-streptococcal GN (more common, esp in children)
-nonstreptococcal causes |
|
|
poststreptococcal GN commonly presents when?'
in which population? |
2-3 week post URTI
10 d p pharyngitis 14 d p skin infection men and children |
|
|
presentation of post strep GN
|
-mild
-nephritic and oliguric ARF -gross hematuria, HA, HTN, hypervolemia, edema |
|
|
progression of post strep GN
|
-99% reversible
-quick resolution -SCr returns in 3-4 w -hematuria resolves in 3-6m -proteinuria resolves slower |
|
|
Tx of poststrep GN
|
-Abx to treat strep
-supportive therapy -diuretics and antiHTNs to control BP and extracellular volume |
|
|
IgA nephropathy is aka...
|
Berger's disease
|
|
|
IgA is the most common cause of GN, especially in
|
Asians
|
|
|
etiology of IgA nephropathy
|
-exaggerated mucosal IgA response
-trapped in glomeruli -mesangial cell proliferation |
|
|
presentation of IgA nephropathy
|
-gross hematuria with URI
-microscopic hematuria and (RBC) proteinuria) common |
|
|
prognosis of IgA nephropathy
|
good unless proteinuria >2 g/d
|
|
|
Tx of IgA nephropathy
|
-ACEI
-steroids -cyclophosphamide -fish oil |
|
|
minimal change disease
nephrotic or nephritic? |
nephrotic
|
|
|
minimal change disease most common in
|
children 2-6
|
|
|
minimal change disease
type of proteinuria |
selective albuminuria
-due to loss of normal charge barrier of GBM |
|
|
etiology of minimal change disease
|
lymphokine production by T cells/B cells/cytokines that destroy foot processes
this collapses the epithelial cell |
|
|
membranous nephropathy
nephrotic or nephritic? |
nephrotic
|
|
|
membranous nephropathy most common in...
|
adults
|
|
|
etiology of membranous nephropathy
|
-idiopathic or genetic
-drugs: penicillamine, lithium -SLE, DM -adenocarcinoma of the lung and colon |
|
|
clinical features of membranous nephropathy
|
-HTN, hematuria
-variable and indolent course -40% progress to renal failure in 2-20 years -no effect with steroids |
|
|
describe presentation of Wegener's Granulomatosis in the nose
|
-nasal crusting
-frequent nosebleeds -erosion and perforation of the nasal septum |
|
|
**describe presentation of Wegener's Granulomatosis in the kidney
|
-GN w/ ass'd hematuria and proteinuria
-can lead to renal failure if not treated aggressively -active urine sediment: RBC casts |
|
|
Tx of Wegener's granulomatosis
|
high dose cyclophosphamide
pulmonary presentation causes death more than the kidney |
|
|
Diagnostic Criteria of SLE
|
4/11
SOAP BRAIN MD -blood disorders: dec RBC, PLT, WCC -renal: P + H +/- casts -ANA titer > 1:160 |
|
|
Tx of SLE
|
-depends on severity (WHO class I-V)
-corticosteroids -Class IV usually get corticosteroids and cyclophosphamide |
|
|
Tx to slow progression of renal disease
|
-BP control
-ACEI -nonDHP CCBs (or DHPs with ACEIs) -diuretics -diet - Na, protein restriction -smoking cessation -Tx of HLD |
|
|
renal biopsy is frequently necessary, esp in:
|
RPGN
nephrotic syndromes |
|
|
describe autosomal dominant polycystic kidney disease
|
-leads to renal failure 50% of the time
-cysts also on liver and pancreas -sometimes sacular cerebral aneurysms -get MRI or CT if FH indicates subarachnoid hemorrhage -complications include: HTN, pyelonephritis, abdominal pain, hematuria, renal stones |
|
|
Tx of ADPKD
|
-diligent BP control
-ACEI and ARB not advantageous over other BP agents -extended UTI Tx |
|
|
most common cause of AIN
|
drugs 71%
Abx 1/3 of that |
|
|
common drugs that cause AIN
|
penicillins
allopurinol omeprazole |
|
|
bacterial cuases of AIN
|
C. diphtheriae
legionella staphylocci streptococci yersinia |
|
|
viral causes of AIN
|
CMV
EBV HIV HCV HSV hanta mumps polyoma |
|
|
other infectious causes of AIN
|
leptospira
mycobacterium mycoplasma rickettsia syphillis toxoplasmosis |
|
|
clinical presentation of AIN of any cause
|
N/V/malaise
|
|
|
clinical presentation of drug-induced AIN
|
-rash
-fever -eosinophilia -eosinouria sometimes aSxatic |
|
|
laboratory manifestations of AIN
|
-acute rise in SCr
-eosinophilia, eosinophiluria -urine sediments: WBC and casts, RBC -proteinnuria (<1 g /d) -signs of tubulointerstitial damage |
|
|
8 causes of rhabdomyolysis
|
-alcohol abuse
-massive muscle compression from immobilization in drug induced coma -drugs (statins, quinone) -seizures -occlusive peripheral vascular disease -combination therapy with itraconazole, simvastatin, and cyclosporine -conversion from one fibric acid to another, or from one statin-fibrate combo to another -detergent ingestion |
|
|
2 classic causes of pre-renal AKI
|
hypovolemia
hypotension |
|
|
2 classic causes of intrinsic AKI
|
ATN
toxic injury |
|
|
1 classic cause of post-renal AKI
|
renal outflow tract obstruction
|
|
|
50% of AKI cases are caused by
|
sepsis
|
|
|
3 combinatorial factors of sepsis
|
immunological
toxic inflammatory |
|
|
sepsis affects
|
renal microvasculature and
tubular cells |
|
|
4 causes of prerenal AKI
|
-intravascular volume depletion
-altered intrarenal hemodynamics (ACEI + HF) -decreased effective arterial blood volume -abdominal compartment syndrome (belly full of cytokines, inflamed belly, get rid of necrotic tissue) |
|
|
urine sediment in prerenal AKI
|
-usually normal, without cellular elements or abnormal casts, unless CKD is present)
-UNa <15 mEQ/L -U/SCr > 20 -FeNa <1% -UNa/K <1/4 -BUN/SCr > 20 |
|
|
urine output in postrenal AKI can be
|
anuric - if complete
normal, polyuric, or either - if incomplete |
|
|
in AKI, monitor....
|
-fluid balance, urine output
-BP, cardiac function -electrolytes, kidney function |
|
|
in AKI, do no harm by avoiding:
|
-and treating hypotension
-and treating hypovolemia -avoid and treat oliguria -avoid contrast agents -avoid nephrotoxins |
|
|
when is early intervention with CRRT appropriate?
|
HF w/out sepsis
-early fluid overload -cytokine removal in sepsis -toxin removal after contrast administration |
|
|
what is the myth about furosemide in AKI?
|
it should reduce tubular injury by shutting down Na/K/Cl ATPase, reduce oxygen demand, help with fluid balance, but
-no clinical evidence -accumulates in oliguria -nephrotoxic and ototoxic -may actually increase mortality or need for RRT |
|
|
what is the myth about dopamine in AKI?
|
low dose DA is "renal dose"
-but no effect on mortality or need for RRT |
|
|
what is the myth about vasopressors in AKI?
|
-although noradrenaline causes vasoconstriction with renal vascualture,
-no evidence of worsening AKI should be used after adequate volume resuscitation |
|
|
what is the myth about mannitol in AKI?
|
currently no evidence of protective effect
causes an osmotic diuresis which may benefit fluid balance |
|
|
at <5% dehydration, what are the clincal symptoms?
|
-rapid heart rate
-dry mucous membranes -concentration of urine -poor tear production |
|
|
at 5-9% dehydration, what are the clincal symptoms?
|
-increased severity
-decreased skin turgor -sunken eyeballs -oliguria |
|
|
at >10% dehydration, what are the clincal symptoms?
|
-pronounced severity of above signs
-supine hypotension -delayed capillary refill -acidosis (large base deficit) |
|
|
how much fluid should people intake and output per day
|
1-1.5 L
|
|
|
how much water in a person is in the
-intracellular fluid -extracellular fluid |
-intracellular compartment: 27 L (2/3)
-extracellular compartment: 15 L (1/3) |
|
|
the extracellular compartment is divided into....
|
interstitial fluid
intravascular fluid |
|
|
how much water in a person is in the
interstitial fluid intravascular fluid |
interstitial fluid: 11 L (3/4)
intravascular fluid 4 L (1/4) |
|
|
Darrow Yannet equation
|
ECF volume = total body water - new ICF volume
can be shifted by Na intake, but can't quickly increase, so fluid shifts to cerebrum, causing cerebral edema, which has 90% chance of death |
|
|
assuming renal blood flow is fairly constant, what are the 2 main hypothesis of control of GFR?
|
myogenic mechanism
paracrine mechanism |
|
|
describe myogenic mechanism
|
-increased renal arterial pressure
-increased renal blood flow -increased vascular wall tension (vasodilation) -increased transmural pressure and decreased radius of afferent arteriole |
|
|
describe paracrine mechanism
|
-macula densa senses low NaCl
-activates RAAS -increases glomerular hydrostatic pressure -decreased afferent arteriolar resistance decreases hydrostatic pressure |
|
|
during resuscitation, which types of fluids are provided
why |
cyrstalloid
colloid replace acute losses (hemorrhagic, GI, 3rd space) |
|
|
during maintenance, which types of fluids are provided
why |
electrolytes
nutrition -replace normal loss (IWL + urine + fecal) -nutritional support |
|
|
describe hypovolemic shock
|
10% blood loss
|
|
|
how much does 1 unit of blood raise the hematocrit?
|
2-3%
if so, "patient responded appropriately" |
|
|
what is normal HCT?
|
45%
|
|
|
what is the threshold for low HCT?
|
20% normal people
25% unhealthy people |
|
|
function of whole blood
|
volume expander
|
|
|
function of washed RBCs
|
-pts with allergic reactions to plasma proteins
-CA |
|
|
function of packed RBCs
|
-most commonly used
-saves volume anemia + HF ESLD |
|
|
function of leuko-poor RBCs
|
CA
pts with febrile, non-hemolytic reactions to plasma WBCs |
|
|
whole blood v packed RBCs
|
-same increases in HCT
-same amount of RBC -just a different volume |
|
|
what is the danger of having too few platelets?
|
subarachnoid hemorrhage
easy bruising |
|
|
what are the cutoffs for too low platelets?
|
danger: <50k platelets
frank bleeding: <10k platelets |
|
|
each unit of platelets increases count by...
|
10k
6-8 units usually transferred |
|
|
what is the hypotonic IV fluid?
|
1/2 NS
|
|
|
which are the 5 isotonic IV fluids?
|
NS
LR albumin D5 1/2NS |
|
|
what is the hypertonic IV fluid?
|
3% saline
|
|
|
which are the crystalloid IV fluids?
|
NS, LR
|
|
|
which is the colloid IV fluid?
|
albumin
|
|
|
when to use blood v. fluids?
|
use blood if oxygenation is an issue
|
|
|
hypotonic fluids can cause
|
hemolysis
|
|
|
what is the hypothetical benefit of using colloids?
|
-large particles don't fit through vascular pores, so they stay in the circulation
-much smaller amounts can be used for the same volume expansion 250 mL albumin 25% = 4 L NS -but edema tends to stay -albumin can trigger anaphylaxis |
|
|
how to determine replacement fluid therapy
|
use weight differences
1% = 1 pound give over 24-48 hours most use NS because it stays in intravascular area |
|
|
when to use maintence fluid therapy
|
when individual is not expected to eat or drink normally for a longer time
|
|
|
what is the 100:50:20 rule?
|
using IBW
100 ml/kg/d for 1st 10 kg 50 ml/kg/d for 2nd 10 kg 20 ml/kg/d for every kg over 20 |
|
|
what is the 4:2:1 rule?
|
using IBW
4 ml/h x 10 kg = 40 ml/hr 2 ml/h x 10 kg = 20 ml/hr 1 x (weight - 20) ml/hr = weight (kg) + 40 = maintenance VI rate/hr |
|
|
which fluid to start maintenance with?
|
1/2NS + 20 mEq K
add D5W if pt is NPO NTE 120 ml/h adjust Na and K as necessary |
|
|
what is the ideal replacement fluid?
|
NS (stays in intravascular compartment)
|
|
|
what is the ideal maintenance fluid?
|
D5 1/2 NS + 20 mEq
|
|
|
what are repair fluids?
|
NaHC03 8.4% (acidosis)
KCl 25 mEq/25 mL NaCl 3% (dangerous) |
|
|
where do hypotonic infusions go?
|
D5W goes to all compartments
to replace normal loss (IWL + urine) increases ICF > ECF |
|
|
where do isotonic infusions go in normal pts?
|
LR, NS
replaces acute/abnormal loss increases ECF (plasma and interstitial fluid) |
|
|
where do isotonic infusions go in edematous pts?
|
plasma and
especially the interstitial fluid |
|
|
where does 5% albumin go?
|
plasma
good in edematous pts in the first 8-10 hours, esp. w/ furosemide shift fluid into vessels |
|
|
what is the normal range of serum potassium?
|
3.5 - 5.1 mEq/L
mainly an intracellular ion |
|
|
what is the presentation of K <3.0 mEq/L?
|
muscle weakness
cardiac toxicity |
|
|
what does insulin do to K?
|
insulin pushes K into cells
|
|
|
what does acidosis do to K?
|
acidosis pulls K from cells
|
|
|
po forms of K replacement
|
tabs
lquid powder slow release |
|
|
IV forms of K replacement
|
KCl IV 10 mEq/h via peripheral line
KCl IV 15-20 mEq/h via central line |
|
|
6 risk factors for developing hypokalemia***
|
-diarrhea, vomiting
-amphotericin B -diuretics -metabolic alkalosis -insuline -beta2 agonists (terbutaline) |
|
|
why should you never give K IV push?
|
phlebitis
|
|
|
what is the ideal concentration for K
|
<60 mEq/L
|
|
|
what is the ideal rate of administration for K?
|
<10-20 mEq/h
|
|
|
how do you monitor IV K?
|
ECG
serum K urine output >0.5 ml/kg/h |
|
|
how does hypERkalemia affect an ECG?
|
peaked T wave
wide QRS |
|
|
when can K be given PO?
|
asymptomatic pts with K < 3.8 mEq/L
|
|
|
what is the dose for PO K?
|
40-100 mEq/d in 2-4 dd
start with 20-40 mEq/d and titrate |
|
|
what is the dosing interval for PO K
|
q 2 h for a maximum dose of 120 mEq in 6 hours
|
|
|
when PO and IV K is given, what is the maximum total dose?
|
120 mEq/6 hours
|
|
|
when should K levels be monitored?
|
after each replacement dose or in AM lab (unless K is very low - more frequently)
if using K IR, check after at least 2 hours if using K SR, check after at least 4-6 hours monitoring not required for maintenance K doses |
|
|
what is normal Ca range?
|
8.5-10.5 mg/dL
|
|
|
when considering calcium concentrations, also consider...
|
serum albumin
for ever 1 g/dL decrease of SAlb below 4 g/dL, add 0.8 mg/dL to total serum calcium |
|
|
If pt has Ca of 7.5 mg/dL and an albumin of 1.0 g/dL, should Ca be supplemented?
|
Albumin: 4.0 - 1.0 = 3.0
Calcium 3.0 x 0.8 + 7.5 = 9.9 mg/dL Ca is OK, no adjustment necessary |
|
|
correct Ca when concentration is
|
Ca < 8 mg/dL is low
or if there is a high risk of complications secondary to hypocalcemia |
|
|
when to use CaCl v. CaGluconate
|
Calcium Chloride (13.2 mEq or 272 mg elemental) in CENTRAL lines
Calcium gluconate in PERIPHERAL lines (4.7 mEq or 94 mg elemental) |
|
|
for every gram of Calcium gluconate given, how much should the Ca (total) increase?
|
9.5 mg/dL
|
|
|
Sx of hypocalcium
|
tingling lips, face, fingers, arrhythmias
|
|
|
how to infuse calcium
|
over 30-60 minutes
except during a code rapid admin can cause bradycardia, hypotension, vasodilation infiltration can cause tissue necrosis and sloughing |
|
|
PO Ca replacement options
|
CaCO3 (TUMS** most Ca per tab)
CaGluconate CaCitrate CalciumLactation |
|
|
normal magnesium levels
|
1.8-2.5 mg/dL
(intracellular) |
|
|
options for Mg replacement
|
PO, but has low absorption, preferred in asymptomatic patients
IV: 1 g MgSO4 in 100 mL given over 60 minutes |
|
|
normal phosphorous levels
|
2.4 - 4.7 mg/dL
|
|
|
if P and K are low, what do you give?
|
15 mmol K Phosphate (0.25 mmol/kg) in 250 mL LV solution over 4-6 hours
(don't give additional K) |
|
|
if P is low and K is high, what do you give?
|
15 mmol Na Phosphate (0.25 mmol/kg) in 250 mL LV solution over 4-6 hours
|
|
|
why don't you push P?
|
causes Ca to shift from bones
|
|
|
KPhos Neutral
Neutra Phos Neutra Phos K all have how much P? |
250 mg P
but various amounts of K and Na |
|
|
dosing regiment for phosphorous
|
1 tablet/packet TID
|
|
|
MOA of D5W
|
-taken up by cells and metabolized to CO2 and water = "free water"
-net result is delivery of water -distribution to ECF and ICF volumes |
|
|
uses of D5W
|
-correction of hypernatremia
-delivery of IV meds in non-diabetic patiet -to keep vein open (KVO) for delivery of IV meds |
|
|
MOA of isotonic saline solutions (NS, LR)
|
-expanstion of ECF volume
|
|
|
uses of isotonic saline solutions
|
-ECF volume depletion of any cause
-in conjunction w/ blood transfusions (hypotonic solutions may cause lysis of RBCs) -burns |
|
|
MOA of hypotonic saline solutions (1/2 NS)
|
-sodium expands ECF volume and free water corrects hypertonicity
|
|
|
uses of hypotonic saline solutions
|
-ECF volume depletion with hypernatremia
-severe hyperglycemia (use 1/2NS, not D5 1/2NS) |
|
|
-best IV solution for a diabetic patient with chest pain being transferred to the coronary care unit
-VS unstable -Pt is hypotensive with rapid pulse |
NS or LR
because of hypotension |
|
|
best IV solution for a 40 yo patient with septic shock
|
NS
-increase intravascular volume shock = hypoxemia + anaerobic metabolism and increased lactic acid LR worsens shock |
|
|
best IV oslution for a diabetic patient with glucose 1300 mg/dL, Na 150 mEq/L, BP 60/40, pulse 120 bpm
|
NS or LR
hypotensive |
|
|
best IV solution for a diabetic patient with glucose 1300 mg/dL, Na 150 mEq/L, but is now hemodynamically stable
|
1/2 NS
the water portion helps correct hypernatremia |
|
|
how much water is lost in the lungs, skin, and stool each day?
|
500-100 ml/d
|
|
|
how much water is lost in urine output each day?
|
1500 mL/d
|
|
|
what is the daily water requirement?
|
2000-2500 mL/d
higher in patients with fever, undergoing mechanical ventilation, or GI losses (diarrhea) |
|
|
sodium in maintenance IV fluids
|
50-100 mEq/d as NaCl
|
|
|
be careful with sodium replacement in which 3 disease?
|
renal disease
CHF cirrhosis |
|
|
what happens if you give Na without K?
|
-increased distal delivery of Na
-Na-K exchange -increased K loss in the urine |
|
|
potassium in maintenance IVs
|
20-60 mEq/d
|
|
|
careful with potassium replacement in which diseases...
|
arrhythmias
increased concentration in central line |
|
|
describe hypovolemia
|
fluid loss from any source will result in volume contraction if losses are not concurrently replaced
|
|
|
2 types of hypovolemia
|
extrarenal losses
renal losses |
|
|
describe extrarenal losses
|
GI
-vomiting -gastric suction -diarrhea -laxatives skin -severe sweating -burns -severe dermatitis 3rd space - burns volume depletion |
|
|
describe renal losses
|
diuretics
|
|
|
5 clinical findings of decreased volume
|
-flat or absence of neck veins/pulse
-hypotension -tachycardia -decreased skin turgor -+/- low urine output |
|
|
4 clinical findings of volume overload
|
-jugular venous distention
-basilar lung rales -S3 gallop -edema |
|
|
fluid therapy should be tailored to...
|
fluid losses
serum electrolyte status |
|
|
GI fluids are mainly comprised of
|
Na
Cl replace with NS |
|
|
Colon fluids are mainly comprised of
|
Na
Ka Cl HCO3 replace with 1/2NS KCl NaHCO3 |
|
|
skin fluids are mainly comprised of
|
Na
replace with D5W |
|
|
urine is mainly comprised of
|
Na
K Cl 1/2NS, KCl |
|
|
TBW is what proportion of body weight?
|
60%
42 L for 70 kg man |
|
|
2/3 of the total body water is
|
intracellular fluid
27-29 L |
|
|
1/3 of the total body water is
|
extracellular fluid
13 L |
|
|
3/4 of extracellular fluid is
|
interstitial fluid
10-11 L |
|
|
1/4 of extracellular fluid is
|
intravascular fluid
3-4 L |
|
|
3 principles of maintaining body water distribution
|
-no active movement of water between body compartments
-all membranes in the body are freely permeable to water except in the nephron -mvmt of water between body compartments follows osmolar forces |
|
|
what is the most abundant anion or cation that regulates the size of the ECF?
|
Na
|
|
|
definition of osmolality
|
-concentration of solutes or particles in a solution
|
|
|
under normal conditions, how do the osmolality of the ICF and ECF compare?
|
the osmolality of the ICF and ECF are equal
|
|
|
major solutes in the ECF are
|
sodium
|
|
|
minor solutes in the ECF are
|
glucose and urea
|
|
|
effective solute =
|
sodium
|
|
|
addition of sodium =
|
water moves across cell membrane from low osmolality to high osmolality
|
|
|
ineffective solute =
|
urea
|
|
|
addition of ineffective solutes =
|
free diffusion across cell membranes
do not cause net movement of water between intracellular and extracellular spaces |
|
|
how is osmolality calculated
|
Osmolality = 2 x Na +(glucose)/18 + (urea)/2.8
|
|
|
an osmolal gap is created when
|
solutes other than sodium, glucose, or urea are present in abnormal conditions
|
|
|
examples of other effective osmoles that contribute to osmolal gap
|
ethanol
mannitol glyceorl contrast dye ethylene glycol methanol |
|
|
when is an osmolal gap considered abnormal?
|
> 10 mOsm/L
|
|
|
what is normal sodium osmolality?
|
isotonic Na is 280 mOsm/kg
|
|
|
describe isotonic hyponatremia
|
AKA pseudohyponatremia
-rare -severe hyperTG (1000s) -severe hyperproteinemia -----malignancies -accumulation of lipids, proteins in plasma, resulting in low serum Na -artifact -contrast media ----decreased serum Na until pt excretes the contrast |
|
|
effective solute =
|
sodium
|
|
|
addition of sodium =
|
water moves across cell membrane from low osmolality to high osmolality
|
|
|
ineffective solute =
|
urea
|
|
|
addition of ineffective solutes =
|
free diffusion across cell membranes
do not cause net movement of water between intracellular and extracellular spaces |
|
|
how is osmolality calculated
|
Osmolality = 2 x Na +(glucose)/18 + (urea)/2.8
|
|
|
an osmolal gap is created when
|
solutes other than sodium, glucose, or urea are present in abnormal conditions
|
|
|
examples of other effective osmoles that contribute to osmolal gap
|
ethanol
mannitol glyceorl contrast dye ethylene glycol methanol |
|
|
when is an osmolal gap considered abnormal?
|
> 10 mOsm/L
|
|
|
what is normal sodium osmolality?
|
isotonic Na is 280 mOsm/kg
|
|
|
describe isotonic hyponatremia
|
AKA pseudohyponatremia
-rare -severe hyperTG (1000s) -severe hyperproteinemia -----malignancies -accumulation of lipids, proteins in plasma, resulting in low serum Na -artifact -contrast media ----decreased serum Na until pt excretes the contrast |
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management of isotonic hyponatremia
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D/C IV infusions
hyponatremia will usually resolve over the next 24 hours as the solutions are eliminated from the body |
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describe hypertonic hyponatremia
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-presence of excess non Na effective osmoles
--hyperglycemia --administration of hypertonic solutions of glucose, mannitol |
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hypertonic hyponatremia is aka
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tranlocational hyponatremia
--glucose, witohut insulin, is not permeant across cell membranes --in the ECF, glucose causes water movement from cells to the ECF space, causing -cellular dehydration and decreased SNa |
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for every increase of 100 mg/dL in glucose concentration above 100 mg/dL, the sodium concentration falls about
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1.6 mEq/L
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management of hypertonic hyponatremia
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D/C IV infusions
hyponatremia will usually resolve over the next 24 hours as the solutions are eliminated from the body |
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what effect would mannitol have on brain cells?
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mannitol would caus water to move out of cells, thus reducing cerebral edema
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what is the most common form of hyponatremia
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hypovolemic
hypotonic hyponatremia |
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how to differentiate fluid loss source with urine Na
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extra renal loss
U Na<10 renal losses U Na >20 |
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why are UNa so low with extrarenal loss
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kidney responds to volume contraction by avid Na retention
Na is being reabsorbed by the renal tubules, therefore the urinary concentration will be low |
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2 reasons for high UNa in renal losses
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nonreabsorbable solutes obligate renal Na excretion
or decreased aldosterone decreases Na uptake in distal tubules w/ resulstant diuresis |
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management of hypotonic hypovolemic hyponatremia
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NS, LR x 1-2 L
then 1/2NS to avoid abrupt correction of serum electrolytes |
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monitoring of hypotonic hypovolemic hyponatremia
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VS every few hours
labs urine output |
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cause of isovolemic hypotonic hyponatremia
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excess vasopressin (ADH)
-stimulates the release of ADH -increase the kidney's response to ADH |
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what happens with excess vasopressin?
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-collecting tubules become permeable to water
-water reabsorption -concentrated urine -hyponatremia |
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ADH is formed where
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supraoptic and paraventricular nuclei
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where is ADH transported (3)
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-posterior pituitary
-portal capillaries of median eminence -CSF of 3rd ventricle |
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ADH secretion is influenced by
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-extracellular sodium -"effective" osmotic pressure of body fluids
-sodium's effect on ADH is mediated by osmoreceptors in the anterior hypothalamus |
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ADH acts on
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V2 receptors, activating the adenylcyclase pathway
-results in aquaporin water channel expression -water is reabsorbed and retained |
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when is ADH secreted
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-when plasma osmolality increases and plasma Na increases
-increased plasma ADH -reabsorption of water -maximal ANTIdiuresis -increased urine osmolality (>800 mOsm/kg) -decreased urine flow rate |
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what happens to ADH when plasma osmolality/Na decreases
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-decreased ADH to low or undetectable levels
-water diuresis -maximally dilute urine -prevents further dilution of body fluids |
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how is thirst regulated in increased plasma osmolality or Na
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thirst is regulated by osmoreceptors in close proximity but separate from osmoreceptors that regulate ADH
-conserve water -become thirsty -restore osmotic pressure to normal |
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how is thirst regulated in decreased plasma osmolality or Na
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-decreased ADH secretion
-water diuresis -inhbits thirst |
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etiology of SIADH
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-malignant tumors
-CNS disorders -pulmonary -surgery -drugs |
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drugs that can cause SIADH
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-SSRIs
-narcotics -CA chemo -CBZ -chlorpropamide -clofibrate -PPIs |
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clinical presentation of SIADH
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-related to hyponatremia and hypoosmolemia
-confusion, lethargy, muscle cramps, N/V, anorexia -profound or rapidly developing hyponatremia: convulsions, coma, death |
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management of SIADH
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-prevention is key
-eliminate drug-induced causes of increased ADH -avoid admin of inapp. large volumes of fluids -correction of hyponatremia dictated by severity and duration |
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Tx of asymptomatic/moderate SIADH
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-restrict water, negative water balance
-loop diuretics to promote free water excretion |
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Tx of unremitting SIADH (p 1-2 w)
4 options |
demeclocycline
LiCO3 fludrocortisone tolvaptan |
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describe hypervolemic hypotonic hyponatremia
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due to retention of water in excess of sodium
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causes of hypervolemic hypotonic hyponatremia
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cirrhosis/CHF/nephrotic syndrome
-decreased renal perfusion activates RAAS -aldosterone increases Na retention -increased ADH leads to free water retention renal failure |
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if UNa >20 in hypervolemic, hypotonic, hypoNa, what is the likely cause?
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-Acute or CRF
-inability to reabsorb Na |
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if UNa <20 in hypervolemic, hypotonic, hypoNa, what is the likely cause?
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cirrhosis
nephrotic syndrome cardiac failure |
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management of hypervolemic, hypotonic, hypoNa
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-Tx underlying disease
-Na restricted diet (<1 g/d) to minimize Na/water retention -oral water restriction (<1-2 L/d) -diuretics |
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clinical manifestations of Serum Na <130 mEq/L
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lethargy
confusion agitation muscle cramps nausea |
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clinical manifestations of Serum Na <120 mEq/L
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decreased reflexes
Cheyne-Stokes respirations seizures coma |
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clinical manifestations of hyponatremia plus respiratory arrest
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100% mortality
CNS Sx are medullary related |
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describe acute hyponatremia
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-occuring within less than 24-48 hours
-serum Na <120 mmol/L significant decrease in ECF osmolality occurs rapidly -sudden shift of water from eCF to cellular compartment -cellular swelling -cerebral edema |
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describe chronic hyponatremia
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-when hyponatremia evolves more slowly
-extrusion of osmolytes (intracellular solutes) -eliminates osmotic gradient created by fall in extracellular Na can be asymptomatic |
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in chronic hyponatremia, should you rapidly correct ECF osmolality?
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NO, DANGEROUS
-rapid shift of water out of the cells causes osmotic demyelinization syndrome -reverse osmotic gradient |
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describe osmotic demyelinization syndrome
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-AKA central pontine myelinolysis (CPM)
-ass'd with loss of myelin and supporting structures in the pons and other areas of the brain -slow neurologic deterioration (lethargy, confusion,.... coma) |
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patients at risk for ODS
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alcoholism
malnutrition liver disease |
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ODS is diagnosed by
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MRI
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mgmt of acute Sx hyponatremia
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duration <48 hours
increase SNa by 1.5-2 mEq/L/h x 3-4 hours NTE 10-12 mEq/L in 24 h 3% NaCl +/- loop diuretics |
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***mgmt of chronic hyponatremia
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duration >48 hours
slow correction of <12 mEq/L in 24 hours or <18 mEq/L in 18 hours |
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***how is Na deficit calculated?
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0.5L/kg x weight x (target Na - actual Na)
in 60 kg pt with Na 109 0.5 L/kg x 60 kg x (120-109) = 330 mEq |
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describe hypovolemic hypernatremia
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preferential loss of water over Na
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causes of hypovolemic hypernatremia
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diuretics
diarrhea GI loss skin loss glycosuria renal failure |
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insensible losses due to fever
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60-80 mL/24 hours for every degree above normal
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2 main causes for isovolemic hypernatremia
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central diabetes insipidus
nephrogenic diabetes insipidus |
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describe central DI
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decreased release of vasopressin/ADH from the posterior pituitary
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describe nephrogenic DI
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decreased sensitivity of the kidney to ADH
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features of DI
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water diuresis
dilute urine polyuria polydypsia hypernatremia |
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purpose of water deprivation test
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distinguishing between central and nephrogenic DI
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describe water deprivation test
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deprive water
msr Na, Sosm, Uosm -continue until osm reaches plateau |
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normal response to water deprivation test
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normal SNa
normal Sosm decreased urine output increased urine concentration |
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water deprivation test shows DI if....
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cannot concentrate urine
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If DI is suspected, how can you tell if it is central or nephrogenic?
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administer exogenous DI
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exogenous DI increases the osmolality in....
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central DI
not nephrogenic DI |
