Electrolyte Imbalances (Exam 2) Flashcards
Primary Functions of Kidneys (7)
regulating blood volume and blood pressure
regulating extracellular fluid, osmolarity, electrolyte concentrations and acid base balance
stabilizing pH of the blood
conserving nutrients
maintain body temperature
detoxify poisons
transport of wastes
like the liver, the kidneys can
detoxify poisons
other functions of kidneys (4)
removes wastes
secretes renin
produce erythropoietin for RBC production
converts vitamin d to active form
acidosis
arterial blood pH less than 7.35
respiratory or metabolic
alkalosis
arterial blood pH greater than 7.45
respiratory or metabolic
how is carbonic acid regulated?
lungs excrete CO2
how is bicarbonate regulated?
kidneys make or waste bicarbonate
normal range of albumin
3.4-5.4 g/dL
normal range of serum globulin
2.0-3.5g/dL
normal range of BUN
10-20mg/dL
normal range of BUN to creatinine ratio
5-18mg/dL
normal range of Calcium
8.5-10.5 mg/dL
normal range of phosphorus
1-1.5 mEq/L
normal range of sodium
135-147mEq/L
normal range of potassium
3.5 - 5 mmol/L
normal range of chloride
96 - 106 mEq/L
normal range of Creatinine
men - 0.9 to 1.5 mg/dL
women - 0.6 - 1.1 mg/dL
normal range of estimated GFR
90 - 120 mL/minute
normal range of glucose
<140 mg/dL
what is glucose levels for a diabetic?
over 200 mg/dL
normal range for carbon dioxide
less than 2.3%
smokers: 2.1% to 4.2%
renal blood flow
blood flowing through kidney/minute
renal plasma flow
plasma flowing through kidneys per minute
filtration fraction
% of plasma removed as filtrate by the Bowman’s capsule
Glomerular filtration rate
amount of filtrate formed by kidneys per minute times plasma flowing through Bowman’s capsule
what does GFR require in order to be measured?
inulin - a polysaccharide substance that is not secreted or reabsorbed at all
how is GFR measured?
inulin is injected
measure the rate of urine output, the concentration of inulin in the urine and in the blood
GFR is most often estimated from
creatinine excretion
creatinine renal clearance (range)
140 ml/min
creatinine clearance test
compares the creatinine level in a 24 hour urine sample with the creatinine level in the blood
what is one of the most important causes of slow by progressive kidney injury
electrolyte imbalances
glomerulus
extremely high water permeability
no transporters
proximal convoluted tubule
very high water permeability
Na/H, carbonic anhydrase (transporter and drug target)
proximal tubule, straight segments
very high water permeability
Acid (uric acid) and base transporters
thin descending limb of Henle’s loop
high water permeability
aquaporins
thick descending limb of Henle’s loop
very low water permeability
distal convoluted tubule
very low water permeability
Na/Cl (NCC)
cortical collecting tubule
variable water permeability
Na+ channels, K channels, H+ transporter, aquaporins
medullary collecting duct
variable water permeability
aquaporins
body’s fluid distribution
2/3 - intracellular
1/3 - extracellular
electrolyte disorders can result from
AKI, chronic renal failure, or from drugs used to modify renal function
major electrolyte imbalances are all caused by
endocrine, vascular, GI tract and kidneys
hypokalemia
K+ < 3.5 mmol/L
hypokalemia drug and non drug causes
drug - loop and thiazide diuretics, corticosteroid
non drug - diarrhea/vomiting
hypokalemia treatment
under 3.0 mmol/L
IV or oral K+ supplementation
hyperkalemia
K+ > 5.0 mmol/L
hyperkalemia causes
kidney does not excrete K+
hyperkalemia treatment
loop diuretic
IV or oral sodium polystyrene sulfonate
imbalance in potassium can also affect
the heart
Acidemia can cause
inhibition of reabsorption of K+ which reduces K+ excretion in the urine –> hyperkalemia
insulin stimulates
the reuptake of K+ resulting in hypokalemia
hyponatremia
Na+ < 135 mEq/L
commonest electrolyte abnormality
most common cause of hyponatremia
hypotonic plasma - excess of extracellular water (usually from secretion of vasopressin)
treatment of hyponatremia
slow IV 3% saline
Bolus 150-150ml
diuretic induced - demeclocycline
AVP receptor antagonist - conivaptan
hypernatremia
Na > 145 mEq/L
can be hypervolemic or euvolemic
common with fluid losses
common non drug causes of hypernatremia
most common - water deprivation
2nd common - hyperglycemic osmotic diuresis in diabetic patients
most common drug induced cause of hypernatremia
corticosteroids (inhibit ADH release)
treatment of hypernatremia
IV 5% dextrose / half normal saline depending on patient condition
loop diuretic and 5% dextrose
hypernatremia accompanied with high plasma osmolarity in the brain leads to
seizure, coma and death
fractional excretion of sodium (FENa)
% of Na filtered by the kidney which is excreted in the urine
measure of renal clearance in the context of low urine output
low fractional excretion indicates
sodium retention by kidney
high fractional excretion indicates
sodium wasting due to acute tubular necrosis
FENa =
(urine Na x serum Cr) divided by (serum Na x urine Cr)
hypocalcemia
Ca < 8.5 mg/dL
uncommon overall
hypocalcemia is most commonly observed in
elderly, malnourished patients, those with sepsis or alkalosis
symptoms of hypocalcemia
musculo-skeletal cramping
tetany
hypercalcemia
Ca > 10.5 mg/dL
less common than sodium imbalances
hypercalcemia is most commonly observed with
malignancies, myeloma, benign tumors of the parathyroid gland, chronic granulomatous disease, etc.
primary hyperPTH
over secretion of PTH due to adenoma, hyperplasia or carcinoma of PT glands
high PTH, serum calcium, LOW phosphates
secondary HyperPTH
production of PTH due to hypocalcemia
occurs in Vit D deficiency, chronic renal failure
HIGH phosphates
tertiary hyperPTH
long term secondary hyperPTH which leads to hyperplasia of PT glands
loss of response to serum calcium levels
seen in CKD
High PTH and serum calcium
hypocalcemia meds
calcium citrate
calcium carbonate
hypercalcemia meds
calcitonin (miacalcin)
calcimimetics
bisphosphonates
denosumab (prolia, Xgeva)
prednisone
calcimimetics
control overreactive PT glands
cinacalcet (Sensipar)
risks of bisphosphonates
osteonecrosis of the jaw
certain types of jaw fractures
calcitonin
salmon derived hormone
helps calcium levels in the blood
bisphosphonates
IV osteoporosis drugs
quickly lower calcium levels
treat hypercalcemia due to cancer
denosumab
treat people with cancer-caused hypercalcemia
or those who don’t respond well to bisphosphonates
in high level of vitamin D,
short term use of prednisone is usually helpful
magnesium is related to
calcium metabolism
hypomagnesemia may cause
nausea, vomiting, sleepiness, weakness, personality changes, muscle spasms, tremors and loss of apetite
severe hypomagnesemia
can cause seizures especially in children
hypermagnesemia
uncommon
develops only when people with kidney failure are given Mg salts or take drugs that contain Mg
Hypermagnesemia can cause
muscle weakness
low blood pressure
impaired breathing
severe - heart stops beating
treatment for hypermagnesemia
calcium gluconate
diuretics
Magnesium is necessary for the
formation of bone and teeth
normal nerve and muscle function
Hypophosphatemia
PO4 < 1.0 mg/dL
Hypophosphatemia is most commonly observed with
chronic alcoholism, chronic ingestion of Mg/Al antacids and IV hyperalimentation without adequate phsophate
symptoms of hypophosphatemia
myalgia
weakness
decreased myocardial contractility
neurologic confusion
symptoms of hypophosphatemia relate to
low ATP stores and tissue hypoxia
treatment for hypophosphatemia
IV phosphate in saline
oral potassium
sodium phosphate - mild cases
ergocalciferol, Vit D
Hyperphosphatemia
PO4 > 4.5 mg/dL
hyperphosphatemia is most commonly observed in
renal failure patients
treatment of hyperphosphatemia
calcium salt infusion
oral phosphate binding calcium carbonate/acetate
primary adverse effect of hyperphosphatemia is
constipation
hypophosphatemia is associated with
high PTH, high serum calcium and LOW phosphates
in hyperphophartemia, low GFR leads to inadequate phosphate excretion, causing
plasma phosphorus complexing with CA2+ and precipitating in soft tissues (joints, BV, heart and kidneys)
