Fluid + Electrolytes Flashcards
What senses ECF OSMOLALITY and what does it stimulate the release of?
Hypothalamic Osmoreceptors, releases ADH (AVP) if Na concentration is too high or inhibits release if osmolality is too low (assuming euvolemia)
What pathway is the ECF regulated by?
RAAS pathway, ECF is sodium dependent
What receptors upregulate the RAAS system
Low pressure receptors: RA, pulm vasculature
High pressure receptors: Renal afferent arterioles sense decrease renal perfusion
What are compensating mechanisms for low ECF volume
autonomic nervous system - regulates vascular tone
Posterior pituitary releases AVP
what is the RAAS antagonist system for excessive ECF volume? and what does it cause
ANP release from high pressure baroreceptors in Left Atrium, Carotid Sinus, Aorta. ANP causes naturesis without loss of potassium
What is the response to increased serum osmolality (>290-295 mOsm)?
- increased thirst
- AVP release from posterior pituitary
- negative feedback = decreased serum osmolality, atrial receptor stretch
* *volume reduction OVERRIDES osmolality considerations
What is the action of ADH (AVP)?
- increased H20 reabsorption (cAMP, PKA insert aquaporins)
- increased reabsorption of UREA
- peripheral vasoconstriction
- stimulate NKCC2 and K+ channels in TAL
What is the role of Aquaporin I and where is it located?
NO response to AVP
Proximale tubule, Thin descending limb of Henle
produces countercurrent multiplier system to concentrate urine
What is the role of Aquaporin II and where is it located
Expression regulated by AVP!!!!!
Collecting duct in apical region of principal cells
What is the role of Aquaporins III, IV?
allows water to exit from principal cell to interstitium
How does AVP affect Urea?
induces upregulation of Urea channel proteins (UT-A1, UT-A3) in collecting duct = greater water absorption
Describe Gitelman’s syndrome (where, what channel, associated drug)
loss of fxn of Thiazide sensitive NaCl transporter in DCT
hypokalemic metabolic alkalosis, hypocalcemia, hypomagnesemia
hypovolemia
Describe Bartter’s syndrome (where, what channel, associated drug)
loss of fxn of Bumetanide sensitive NKCC transport in TAL
HYPOKALEMIC alkalosis, hypovolemia
What does ADH deficiency cause? what are the two causes of ADH deficiency?
Diabetes Insipidus
nephrogenic or pituitary causes
What are causes of pituitary Diabetes Insipidus (ADH deficiency), what are Sx
Sheehan syndrome = post delivery pituitary hemorrhage
pituitary hemorrhage - from TB, Malaria, tumors, trauma
Sx: hypernatreima, severe diuresis, volume contraction
What are causes of nephrogenic Diabetes Insipidus (ADH deficiency)
Congenital: abnormal receptors
placental prod of vasopressinase/oxytocinase (3rd trimester) - blocks AVP, Oxytocin, transient
Inflammatory: sarcoid, lupus, scleroderma
Metabolic: hypercalcemia/calciuria, hypokalemia
Diagnostic Lab findings of Diabetes Insipidus
increased serum sodium increased serum osmolality hypotension urine volume high urine osmolality <250 mOsm
Diabetes insipidus vs Polydipsia
check serum sodium + response to water deprivation
Polydipsia = lowered serum sodium, high urine osmolality, fluid deprivation - urine osmolality increases
DI = high urine volume, water deprivation = urine osmolality stays low, CNS issues
How do you treat Pituitary Diabetes Insipidus
AVP analogue
How do you treat Nephrogenic Diabetes Insipidus
thiazides, low sodium diet, indomethacin
Sx of SIADH?
Hyponatremia
hypervolemic
euvolemic (hospital patients)
Treatment of SIADH
firstline - FLUID RESTRICTION
change IV fluids to isotonic saline
Best method for following a IN PATIENT volume?
monitoring daily body weight
How and where does aldosterone affect Volume expansion
increase sodium reabsorption via principal cells in CD
How does Angiotensin II affect Volume Expansion
upregulation of NHE3 (PCT, TAL, CD)
How does the sympathetic nervous system affect volume expansion
Reduces GFR (increasing renin release) catecholamines upregulate apical NHE3, Na-K
How does ADH affect volume expansion
Upregulates NKCC2 and K+ channel in TAL
increase reabsorption of UREA
peripheral vasoconstriction
Where is sodium stored in the body
plasma, bone, cartilage, skin, bound to proteoglycans
what drug can cause osteopenia, osteoporosis
thiazides can cause chronic hyponatremia, increase serum Ca2+
What are the Sx of Hypernatremia
seizures, coma, intracerebral hemorrhage, hypertonia, Cerebral demyelination
Pt shows up with hypernatremia. What is the first question you ask?
What is the volume status of the Pt
What is Anasarca and what does it suggest?
generalized peripheral edema, shows severe volume overload
can also be caused by low oncotic pressure (cirrhosis, nephrotic syndrome)
What are the 3 resuscitation fluids of choice?
normal saline, lactated ringers, isotonic balanced (normosol)
What two ways can you gauge volume correction
Blood pressure and pulse rate
What can happen if hyponatremia correction is too rapid
osmotic demyelination syndrome: biphasic
1) initial Sx reduction
2) grandual onset of new neuro problems (central pontine myenolysis)
What chemicals in the body are active after a high potassium meal?
Insulin + epinephrine = Potassium pushed intracellular
insulin release is blocked by somatostatin
What happens in the distal nephron in response to a large dietary K load
ROMK
BK expressed - can secrete large K+ amounts
What is the effect of Cortisol on the distal Nephron
circadian rhythm related to potassium excretion
high cortisol = high K+ loss
What is the effect of Aldosterone on the distal Nephron
Increase K+ excretion
UNLESS volume depletion (RAAS stimulated) or existing hypokalema (reduces aldosterone)
What are the Sx of Hyperkalemia
Hyperactive DTR’s
Weakness/paralysis
Confusion
Cardiac Asystole
What are the EKG findings of Hyperkalemia (>5)
peaked T wave
Widended QRS
loss of P wave
severe: Sine wave, Asystole = VFIB!!!!!
what effect does licorice have on renal fxn
licorice can imitate aldosteronism = hypokalemia (<3.6)
What is Liddle syndrome (where, which cell type)
principal cells in CCD - hyperactive Na channel
What is Familial Hyperkalemia Hypertension (Where, what channel)
WNK1&4 mutation in DCT
sensitive to thiazides
What are the symptoms of Hypokalemia
TETANY
Muscle weakness, cramps
ORTHOSTATIC HYPOTENSION
UWAVES on EKG
What are the three chemicals involved with Calcium homeostasis and what do they do?
PTH - increases serum Ca2+, inc bone resorption, increase renal resorption
Calcitriol (Vit D) - increased GI, renal absorption
FGF23 - inhibits Vit D activation (kidney) and decreased GI calcium absorption
What two areas are calcium able to be mobilized from in the body?
- periosteum (short term response)
2. Osteoclasts (slower response) - PTH/calcitonin
what does Calcitonin do and where does it come from?
comes from thyroid C cells, decreases serum Ca2+ (inhibits osteoclasts from reabsorbing bone)
What does calcitriol do and where does it come from/where it is processed
skin synthesis -> liver D1 -> renal D2
increase Ca2+ reabsorption (renal + GI)
paradoxically increases Ca release from bone
What are causes of hypercalcemia
- Thiazide diuretics (upregulation of Calbindin)
- Pagets
- Vit A intoxication
- Hyper PTH, too much Vit D
- malignancy
What are the symptoms of Hypercalcemia
Bones, Stones, Moans, groans
osteitis fibrosa, renal calculi, constipation, confusion
What are the physical findings of Hypercalcemia
Hyporeflexia, seizures, confusion, shortened QT interval, METABOLIC ALKALOSIS
What is acute treatment of hypercalcemia
isotonic saline
then try saline diuresis
then furosemide
What are the 2 causes of Hypocalcemia. What is the most common cause?
- low albumin
2. hypomagnesemia (most common) - also causes hypokalemia
What are the symptoms of hypocalcemia
Acral parethesias, lethargy, ab pain/cramps, increased DTR, TETANY, prolong QT interval
Tetany = CHVOSTEK’S SIGN
What are the causes of hyperphosphatemia
Vit D excess
Laxative abuse
Granulomatous disease (Sarcoidosis)
Most common causes: renal disease, endocrinopathies, sickle cell disease
What are the signs/symptoms of Hyperphosphatemia
Tetany-cramps-hyperreflexia
What are the causes of Hypophosphatemia
Vit D deficiency
ALCOHOL abuse
FGF23 producing tumor
What is the treatment for SEVERE hyponatremia
3% saline (513meq NaCl/L)
infuse 1ml/kg/hr
STOP 3% once Na+ = 125meg/L
What is the management for Hyperkalemia (Acute and Slow)
acute: calcium chloride IV push (protect heart)
bicarb
D5W
Beta agonists
Slow correction - loop diuretics, dialysis, enema
