Flashcards in LYTES NTR Deck (6):
SIADH causes persistent sodium retention in the kidney leading to electrolyte abnormalities and concentrated urine. Patients with SIADH will remain normovolemic.
Patients with similar findings who are hypovolemic more likely have cerebral salt wasting disease.
Bottom Line: SIADH is associated with normovolemia.
Fat malabsorption secondary to bile acid deficiency in patients with extensive ileal resection is associated with an increased risk
of oxalate kidney stones if the colon is preserved.
long-chain FATTY acids (from steatorrhea) compete with oxalate for available luminal calcium.
larger amount of free oxalate is make it to the colon, where it is absorbed by the colon and ultimately excreted by the kidney.
Therefore, patients with short bowel syndrome who do not have a colon in continuity are not at increased risk.
Treatment of hyperoxaluria consists of
restriction of oxalate
If hyperoxaluria persists,
oral administration of calcium citrate
the extra calcium precipitates dietary oxalate, and the citrate prevents stone growth in the urine.
lyte abnormalities and EKG changes
Hypocalcemia- Prolonged ST and QT intervals
Hypercalcemia- shortened ST segment
- widened T wave
Hypokalemia- ST depression
- shallow, flat, inverted T wave
- Prominent U wave
Hyperkalemia- Tall, peaked T waves
- Flat P waves
- widened QRS complex
- Prolonged PR interval
Hypomagnesemia- Tall T waves
- Depressed ST segment
Hypermagnesemia- Prolonged PR interval
- widened QRS complexes
lyte abnormalities and EKG changes mneumonic
think how it starts and end...so it starts with p followed by q r s t
so let's start from where it begins...
p flat hyperkalemia
pr prolonged hyperkalemia hypermagnesemia
qrs widened hyperkalemia hypermagnesemia
qt prolonged hypocalcemia
st prolonged hypocacemia
st shortened hypercalcemia
st depressed hypokalemia hypomagnesemia
t widened hypercalcemia
t tall hyperkalemia hypomagnesemia
t inverted hypokalemia
u prominent hypokalemia