COPY OF Renal MEDI High Yield (katie)
Terms in this set (96)
What is a cause of non-anion/normal/increased chloride gap acidosis?
Na=140, Cl=96, CO2= 8
Is there an anion gap?
No, it's normal 12 mEq/L
Conditions resulting in an increased anion gap
Urinary indices of dehydration
BUN:Cr >20, Na=<20
UOsM > 500, FENa < 1%
High urine specific gravity
Tx for hypovolemic/shock pt that is hypernatremia/shock patient that is hypernatremic
0.9% nl saline
Goal is to correct BP 1st and then approach w/ 0.45 and then D5W
What if you gave a lot of free water/D5W instead of saline?
Tx for acute hyponatremia (happened fast)
@ risk for cerebral edema if uncorrected
3% saline at 1-2 mmol/L/hr/kg body weight
Use loop diuretic to enhance free water excretion
Tx for chronic hyponatremia (compensated, pt on thiazides for years)
@ risk for osmotic demyelination if you corrected too rapidly, if it happened over time then there's no need to correct rapidly
Tx for a pt that's euvolemic, asx (normal BP) and has a low Na
Tx for chronic symptomatic hyponatremia
rapid correction at first and then back off (increase Na by 10% and then 1- 1.5 mmol/L/hr)
Dx of SIADH
do TSH first to r/o hypothyroidism (pt presents euvolemic, asx, slight fluid overload but NO edema- dilutional hypoNa)
dx of exclusion, high UNa and osmolality
Tx of SIADH
Acute SIADH tx is water restriction and chronic treat w/demeclocycline 300-600mg BID and needs 2 weeks for full effect
Sx that warrant emergency medical care (renal stones)
Severe pain w/no comfort and any position, pain accompanied by nausea and vomiting, fever and chills
Imaging of choice for renal stones
CT w/stone protocol
CT of abdomen and pelvis w/o oral or IV contrast
Meds used to prevent struvite stones
long term use of low dose prophylactic antibiotics
Secondary prevention of all stones
hydration, reduce oxalate rich foods, eat a diet low in salt and animal products, eat calcium rich food by no high dose Ca supplementation
Immediate tx for hyperkalemia (>7)
goal= antagonize effects of K+;
**IV Ca gluconate to stabilize cardiac membrane (does nothing to K level)
Immediate tx for hyperkalemia
goal: shift K into cells
insulin (+glucose if needed to protect from hypogylcemia in a pt w/ normal glucose
NaHCO3 (very effective if acidic)
albuterol (nebulizer B agonist)
Delayed onset tx for hyperkalemia
goal: remove K from blood
hemodialysis in absent of renal fxn (fastest and most effective)
Kayexalate in normal renal function (2-4 hrs, works on colon, gives diarrhea)
What else if probably depleted in hypokalemia finding?
it HAS to be corrected along w/K
(K won't correct unless Mg corrected)
IV rate of replacement of K shouldn't exceed
What's the next step if you find hyper/hypocalemia
you must get albumin level to correct for albumin
for every increase in albumin (nl=4) of 1g/dl -->Ca (nl = 10) will increase by 0.8-1mg/dl
What is the equation to correct for albumin
Corrected Ca= Ca + 0.8 (4-Albumin)
More commonly= false hypocalcemia
Pt 1 has an albumin of 3 and total Ca of 10, Dx??
don't need to treat b/c it's only down because albumin is down
Pt 2 has an albumin of 3 and total Ca of 7, Dx??
true hypocalcemia d/t a change in the free Ca
Pt 3 has an albumin of 5 and total Ca of 10.8 Dx?
Pt 4 has an albumin of 5 and total Ca of 12, Dx?
Tx order for hypercalcemic pt?
#1: rehydrate 0.9% nl saline
#2 @ hydration give a loop diuretic, biphosphonates (slow onset) and steroids (Helpful for myeloma and lymphoma)
emergent tx includes: rehydration, loops, calcitonin
What is "re-feeding phenomena" and what causes it?
A patient who hasn't been eating for whatever reason and is re-introduced to food, they start proliferating cells and the cells use phosphate and one of the most common causes of hypophosphatemia
Treatment for hypophospatemia
- Severe and/or Moderate on a ventilator = 0.08-0.16 mmol IV over 2-6 hours
- Moderate not on a ventilator and/or Mild = oral phosphate with 1,000 mg/day
Spurious causes of hyperphosphatemia that effect it at the lab level
heparin, hyperbilirubin, high lipids, alteplase (Ex: cirrhotic patient with high bili and labs return showing hyperphosphatemia)
Treatment of hypermagnesemia
Calcium gluconate (emergent tx) over 5-10 minutes and
Hypomagnesemia (pt in ICU on diuretics or an alcoholic/malnutritioned)
Associated with hypokalemia (↓PTH), can be caused by PPI's-priolosec, impairs GI absorption of Mg2+
Treatment for chloride-responsive alkalosis due to NG suction
replace with NaCl solutions,
replace K+ stores, HCl losses can be reduced by adding a PPI (omeprazole)
Treatment for chloride-responsive alkalosis due to diuretics
replace with KCl and add a K+ sparing diuretic
How do you determine the anion gap
Na+ - [(Cl-+ TCO3 or HCO3)]; where normal is 12 or 3x's
the albumin, you must correct for albumin levels that aren't normal
*Patient 1 with albumin = 4, their normal anion gap is 12 which is normal
*Patient 2 in the ICU for a couple of months not eating well with an albumin = 2, their nl anion gap=6
Normal/Hyperchloremic Anion Gap
Acid has chloride
High anion gap
Acid has no chloride
What are the causes of anion gap acidosis (no chloride)
*MCC is metabolic acidosis (overproduction or decreased excretion of acid)
*Lactic acidosis (type A and B)
*Methanol, Starvation ketosis, DKA, Ethylene glycol, tolulene, aspirin
What are the most common causes if the anion gap is >30?
lactic acidosis or ketoacidosis due to DKA or starvation
Most common causes of a normal anion gap (high chloride) acidosis
renal tubular acidosis where you don't excrete acids
What is type A lactic acidosis due to?
hypoxic, low perfusion states (COPD, cardiac failure)
What is type B lactic acidosis due to?
liver and renal failure, metformin - DO NOT USE in renal failure patients (stop if GFR<50),
Propofol (sedative agent for vent pts) and zyvox.
Chronic acidosis causes
Bone loss because they're constantly trying to buffer the acid by breaking down their bones
MCC of acute renal failure
#1 septic shock, #2 major surgery, #3 hypovolemia
Every time you double Creatinine you lose what % of GFR/kidney function?
Ex: Pt's Creatinine goes from 1 to 2 = 50% kidney function lost (HUGE loss) and changes at a higher levels make minuscule changes
Pre-renal Acute renal failure
Due to ↓effective blood volume and reduction in glomerular perfusion, think the "volume depleted pt" who is holding onto water and salt (therefore they are losing LITTLE amounts of Na+
*LABS: BUN:Cr >20:1, ↑urine osm, FE Na+ < 1% -excreting little sodium
*Exception dry with a BUN:Cr < 5-10 in reduced urea production/severe liver disease
*Tx: stop NSAID/ACE/ARB, NaCl to replace fluid loss and tx the underlying cause of ARF
*normal kidney size on renal ultrasound
*auto-regulation via afferent dilation and efferent constriction (AngII) to ↑GFR
Renal/ATN Acute renal failure
Due to nephro-toxins, ischemia and/or anything causing
tubular loss (can recover to an extent), the pt can't absorb salt so you lose tons of salt in your urine (vs. pre-renal causes in which you lose little salt)
*LABS: ↓urine osm, ↑urine Na+
*Initial phase = exposed to toxin
*Maintenance phase = injury established, GFR stabilized, urine output @ its lowest
*Recovery phase = gradual rise in urine output and decrease in creatinine, may have
Polyuric phase with ↑urine volume due to ↑BUN (urea is a diuretic), FE Na+ > 1% -leaking out a lot of sodium
Post-renal Acute renal failure
Due to obstruction at the lower urinary tract level (men - think prostate cancer, females - think ovarian cancer), laying on their back too long
*Imaging of choice is a renal ultrasound
*Tx: stop meds and possible dialysis
Indications for dialysis
Symptomatic uremia, hyperkalemia, fluid overload (things that even after treatment are unresolved and dialysis is the only way)
Hepatorenal syndrome pathogenesis
Severe renal vasoconstriction with NORMAL kidneys,
resembles prerenal ARF. Impaired Na+ and water handling leads to fluid retention, ascites and edema. It only improves with a liver transplant because the underlying cause is liver disease.
Type 1 worse prognosis than Type 2. Get rid of triggers (NSAIDs, diuretics, diarrhea, hypovolemia, infection).
Diagnostic factors of hepatorenal syndrome
Chronic or active liver disease, Creatinine > 1.5 (very little muscle mass) OR GFR <40, no shock/fluid loss, no improvement with fluids or albumin, no proteinuria (<500mg/day), oliguria, dilutional hyponatremia
Pharmacologic treatment of hepatorenal syndrome
Combo of Midodrine, octreotide and albumin
Which electrolyte abnormalities are assoc with rhabdomyolysis
*HYPER - Phosphatemia, kalemia, uricemia
*HYPO - natremia, calcemia
*Very high numbers due to cell injury, lab get worse when perfused
What does the urine look like in rhabdomyolysis
reddish-brown color without hematuria,
stains + for blood but hardly any there, should be 4+ on a urine dipstick (due to myoglobin) and micro shows no blood
IV drug user passed out and laying in one position on the floor for several days (similar to a crush injury, what are his lab findings?
↑CPK, urine dipstick = 4+ RBC's and Micro = 2-5 RBC's
Based on the above, what electrolyte abnormality IS NOT associated with rhabdomyolysis
Medications that can cause rhabdomyolysis
HMG-CoA reductase inhibitors (statins), gemfibrozil, fibrates (accumulate)
Treatment of rhabdomyolysis
IV bicarb and mannitol diuretic (Loop would prevent bicarb in the urine) - stop both if the patient isn't making urine to avoid alkalosis and hyperosm via tx
Factors that decrease renal perfusion
NSAIDS, ACE inhibitors, ARB's and diuretics,
diabetics ↑ risk (stop these meds 48 hrs before procedure s kidney can autoregulate if needed)
Prevention of contrast nephrotoxicity
1 - Identifying the patient at risk is most important
2 - Saline bolus to hydrate (hydration is the best preventative measure)
3 - N-Acetylcysteine = antioxidant & vasodilatory effects, mixed data but he uses it
What IV contrast is used for MRI's and what problem(s) does it cause?
Gladolinium; usually rapidly cleared in healthy adults but in renal and liver failure pts it can cause
Nephrogenic Systemic Fibrosis and causes tissue deposits
*catastrophic complication - starts distally and moves proximally, swelling, thickening and hardening of the skin leading to irreversible flexure contractures
*Absolute Contraindication if GFR<30
*Caution if GFR 30-60
How does renal function change with increasing age?
"atherosclerosis of the kidneys",
↓GFR (decreasing 1% per year starting at 40 y/o), creatinine does not change due to aging,
more vulnerable to drug toxicity and microalbuminuria is normal and may indicate CV morbidity
Elderly, 40kg woman, serum Creatinine of 1.4
Normal lab values do not reflect patient size and muscle mass.
Serum Creatinine and subsequently GFR depend on muscle mass (because some creatinine is also cleared into the urine via tubular secretion). You MUST look at GFR.
alone can cause kidney disease (CKD and ESRD)
patients usually do not have nephrotic syndrome (>3 protein) and this is even in pts without HTN or hyperglycemia/DM.
Isolated proteinuria pt
normal BP and creatinine, 1+ urine protein. Due to glomerular dysfunction where the basement membrane acts like a sieve and proteins leak out into urine.
LMW proteins first and then HMW proteins (more severe), unless the patient has symptoms
Mild isolated proteinuria
<1gm/day, due to "stressful situations" - exercise, fever, CHF,
wait to do a 24 hr urine collection until they are well, if completely well patient (no health problems) then observe
1-2gm/day, MC in adolescents
*rare in > 30 y/o and if asymptomatic and no other illnesses do a split 24 hr urine to find out if all of the protein is during the day when up and active
Proteinuria >3 gm/day
BIOPSY (exception diabetics bc proteinuria is normal for them)
Persistent fixed proteinuria
Reassess in 6-12 months and if GFR or BP is abnormal, if proteinuria ↑ then you need to do a renal biopsy. If normal at the 6-12 month assessment then reassess yearly.
blood WITHOUT protein, send to a urologist, because if it is a renal problem then proteinuria would most likely also be present
proteinuria >2gm/day and hematuria, MCC IgA nephropathy and thin basement membrane nephropathy
Nephrotic syndrome characteristics
protein is 3.5gm/day with edema, hyperlipidemia and
MCC membranous nephropathy and focal segmental glomerulosclerosis, leaking out EVERYTHING (immunoglobins, albumin, anti-thrombin 3, T4, Vit D, Ca2+) and become hyper-coag with ↑risk of thromboembolic disease
What are the causes of hyperlipidemia in nephrotic syndrome pts?
*↑cholesterol due to overproduction of liver due to ↓ oncotic pressure
*↑LDL due to acquired LDL receptor defect resulting in little clearance
*↑triglycerides due to ↓ catabolism
*RBC casts due to hematuria, ↑BP, JVD, ↓ serum albumin, abrupt onset ↑creatinine
*MCC crescenteric/rapidly progressive glomerulonephritis, IgA nephropathy
MC HIV-associated nephropathy presentation
African American male with nephritic range protein (>3.5 g), renal dysfunction, normal BP,
large kidney noted on ultrasound, no significant HTN or edema, false auto-antibodies, poorly controlled HIV and usually presents late in the disease
Treatment goals in diabetic nephropathy (in all diabetics)
120/70, LDL <70 and HgbA1c <7
Treatment for proteinuria found in diabetic nephropathy
give ACE-Inhibitor(-pril's) or ARB (-sartan's) AND watch for Hyperkalemia, rhabdomyolysis
Common clinical findings of tubulointerstitial nephritis (TIN)
*sterile pyuria & WBC casts because it's inflammatory (not hematuria & RBC casts)
*Triad of fever, rash and eosinophilia (almost a definitive dx)
*polyuria and nocturia (concentration defect)
*Labs: no significant proteinuria and hypoalbuminemia
What is considered "classical TIN"?
occurs 10-20 days after onset of drug therapy, NSAID association
Treatment of "classical TIN"
remove the offending drug, renal biopsy AND treat with a
corticosteroid (if early and severe) OR use cyclophosphamide if steroids fail
How does minimal change disease appear on electronmicroscopy (EM)
effacement of visceral foot processes
Clinical findings of focal segmental glomerulosclerosis
varying degree of proteinuria, hematuria, HTN and renal failure (worse prognosis = higher creatinine levels at dx, ↑proteinuria and males)
What's the most common cause of nephritic syndrome in adults and how do they present?
MC is male in his 40-50's with edema, nephrotic syndrome,
possible association with carcinoma, hypercoag state, and proteinuria
Presentation of Type 1 membranoproliferative glomerulonephritis
associated with Hep C, children 8-16 y/o, hypocomplementemia (in both types),
tx underlying disease
Presentation of Type 2 membranoproliferative glomerulonephritis
dense deposit disease, poor prognosis, hypocomplementemia (in both types), no good tx
Clinical findings of Rapidly progressive glomerulonephritis aka "crescentic GN"
nephritic syndrome, hematuria/RBC casts, rapid loss of renal function
Pt presents with microhematuria, no edema, no HTN, 24 hr urine collection shows 1.4gm protein, what's your dx
IgA nephropathy aka "Bergers disease",
MCC GN worldwide, 20-30's males,
asymptomatic hematuria progresses to hematuria and then crescentic GN, TX with ACE-
Inhibitor or ARB (anyone with proteinuria should be on ACEI/ARB)
cANCA most prominent in Wegner's and is specific for PR3
pANCA most prominent in renal limited pauci-immune crescentic GMN and is specific for MPO
IgG antibodies to a specific component of GBM, associated with crescentic GMN (linear IgA deposits), alveolar hemorrhage, 30-60's, white male, present with a lung hemorrhage
What is the primary cause of chronic renal failure/dialysis
diabetes (#1-HTN, #2 DM)
Kidney damage stages
*Stage 1 - normal GFR (> 90ml/min) + kidney damage
*Stage 4 - severe ↓ in GFR (15-29 ml/min)
*Stage 5 - < 15ml/min, not on dialysis
***Stage 6 - < 15 ml/min and ON DIALYSIS
What is uremia and how do you TX
*Advanced stage of CKD when multi-organ system derangements become clinically manifest;
*renal osteodystrophy, VitD deficiency and secondary hyperPTH
*TX- dietary phosphate restriction, phosphate binders/PhosLo, Vit D supplement,restrict Na+
*NO USE OF salt substitute, NSAIDS, aldo inhibitors, oral hypoglycemics , K+ and water intake, watch ACE's and ARB's
How do you DX and TX a coagulopathy?
*DX - prolonged bleeding time, normal PT, PPT, & Platelet count
*TX - Erythropoietin (EPO) takes 7 days to work, Cryoprecipitate for acute bleeds, Desmopressin, estrogens and dialysis
Dialysis emergencies include
acute uremia, acute hyperK+, fluid overload/pulmonary edema, severe metabolic acidosis
YOU MIGHT ALSO LIKE...
ASCP MLT/MLS Certification Exam (BOC) Preparation
PDCI: Renal Failure
Internal Med MKSAP nephrology
Acute renal Failure: pre renal and post renal
OTHER SETS BY THIS CREATOR
Boards - COMLEX Pharm Q's
PALS AHA 2015 written Test
AHA ACLS Written Test
AHA ACLS Written Test
THIS SET IS OFTEN IN FOLDERS WITH...
Physiology Renal Block 1A
Path Renal Block
Physio Renal Block 1B
Pharm Renal Block