Firecracker - Electrolytes Flashcards
hyponatremia - value
<135
SIADH - explanation
inapproriate secretion of ADH –> water retention, hyponatremia
Causes of SIADH
Organic CNS disease: Meningitis, encephalitis, cerebrovascular accident, head trauma
Acute Psychosis
Tumors, especially small cell lung cancer (paraneoplastic)
Other pulmonary diseases (pneumonia, acute respiratory failure)
Meds that cause SIADH
Antidepressants (SSRIs) and Antipsychotics
Narcotics and NSAIDs
Chlorpropamide
hyponatremia (big picture) =
increase in intracellular osmolality relative to extracellular osmolality.
As result, water shifts into cells,
and in the CNS can cause brain edema.
hyperglycemia & hyponatremia
Glucose is osmotically active, and it draws water into the extracellular space. Increased vascular volume increases diuresis, leading to hyponatremia.
Corrected Serum Sodium
Measured serum sodium + 0.016 * (Serum glucose – 100)
symptoms of hyponatremia
nausea and malaise. Symptoms can progress to lethargy, and confusion.
Na <115
seizures + coma
plasma osmolality in hyponatremia
Plasma osmolality is normally low in hyponatremia. The exception is in the case of osmotically active solutes, such as glucose, sorbitol, and mannitol.
urine in hyponatremia
kidneys should secrete a dilute urine (< 100 mOsm/L) in response to hyponatremia. If the urine is not diluted, it is suggestive of SIADH.
sodium correction
sodium correction should not exceed 12 meq in 24 hour
raise the serum sodium level by 1 meq per hour the first few hours to a level of 120 meq/L.
treatment of euvolemic hyponatremia
fluid restriction, loop diuretics ( to lower the urine osmolality), and/or salt tablets. The use of tolvaptan (Samsca) can also be prescribed in cases of refractory hyponatremia
Samsca
refractory hyponatremia. It causes a free water diuresis through its action on the aquaporin receptor.
hyperkalemia value
> 5
hypokalemic transcellular shift (cause hyperkalemia)
insul def, acidosis
b blockers
massive cell destruction - tumor lysis syndrome
drugs that cause hyperkalemia through transcellular shift
digitalis, succinylcholine
Nsaids
ACEIs, ARBs, K sparring diuretcis
symptoms of hyperkalemia
palpitations, syncope, sudden cardiac death
excitability of skeletal muscles –> weakness, flaccid paralysis, hypoventilation
TTKG
trans-tubular potassium gradient
evaluate renal K+ loss
TTKG>10
increase in renal excretion
TTKG <7
def of aldosterosone/decreased response
hypercalcemia values
total serum calcium >10.3
ionized calcium >5.2
majority of causes of hypercalcemia
primary hyperparathyroidism
malignancy
primary hyperparathyroidism
elevated Ca, decreased Po4
benign adenoma, hyperplasia, carcinoma
hypercalcemia - malignacy
osteoclast stimulation by tumor cells
PTHrP from tumor cells
calcitriol from tumor cells
malignacies associated with hypercalcemia
small cell lung cancer
multiple myeloma
leukemias
lymphomas
chronic granulomatous inflamm
increased calcitriol –> increased calcium
tuberculosis, sarcoidosis
pharmacological causes of hypercalcemia
milk-alkali syndrome
vit d intox
thiazide dirutetics
lithium
rare causes of hypercalcemia
adrenal insuff
paget’s disease
hyperthyroidism
when do symptoms of hypercalcemia appear
> 12
hypercalcemia due to what bone cell
increased osteoclast
can lead to osteopenia, fractures, osteitis fibrosa cystica
EKG findings of hypercalcemia
shorted QT interval
severe - AV block
corrected calcium
ca + .8 x 4-albumin
etiology of hypercalcemia - stepwise approach
1) serum pth
2) PTHrp if normal PTH
3) vit d
4) phosphorus
phosphorus and hypercalcemia
decreased in hyperparathyroidism
increased in paget’s, vit d excess
treatment of hypercalcemia
1) correct hypovolemia with 0.9% saline
2) loop diuretics
3) bisphosphonates
4) calcitonin
5) glucocorticoids
6) gallium nitrate
7) dialysis
bisphosphonates
inhibit osteoclast
gallium nitrate
inhibit osteoclasts
nephrotoxic
