Fluid + Electrolytes Flashcards by John Fang

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)

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What pathway is the ECF regulated by?

RAAS pathway, ECF is sodium dependent

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What receptors upregulate the RAAS system

Low pressure receptors: RA, pulm vasculature

High pressure receptors: Renal afferent arterioles sense decrease renal perfusion

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What are compensating mechanisms for low ECF volume

autonomic nervous system - regulates vascular tone

Posterior pituitary releases AVP

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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

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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

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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

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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

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What is the role of Aquaporin II and where is it located

Expression regulated by AVP!!!!!

Collecting duct in apical region of principal cells

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What is the role of Aquaporins III, IV?

allows water to exit from principal cell to interstitium

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How does AVP affect Urea?

induces upregulation of Urea channel proteins (UT-A1, UT-A3) in collecting duct = greater water absorption

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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

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Describe Bartter’s syndrome (where, what channel, associated drug)

loss of fxn of Bumetanide sensitive NKCC transport in TAL

HYPOKALEMIC alkalosis, hypovolemia

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What does ADH deficiency cause? what are the two causes of ADH deficiency?

Diabetes Insipidus

nephrogenic or pituitary causes

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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

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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

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Diagnostic Lab findings of Diabetes Insipidus

increased serum sodium
increased serum osmolality
hypotension
urine volume high
urine osmolality <250 mOsm

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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

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How do you treat Pituitary Diabetes Insipidus

AVP analogue

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How do you treat Nephrogenic Diabetes Insipidus

thiazides, low sodium diet, indomethacin

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Sx of SIADH?

Hyponatremia
hypervolemic
euvolemic (hospital patients)

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Treatment of SIADH

firstline - FLUID RESTRICTION

change IV fluids to isotonic saline

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Best method for following a IN PATIENT volume?

monitoring daily body weight

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How and where does aldosterone affect Volume expansion

increase sodium reabsorption via principal cells in CD

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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?

1. 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

1. Thiazide diuretics (upregulation of Calbindin) 2. Pagets 3. Vit A intoxication 4. Hyper PTH, too much Vit D 5. 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?

1. 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