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Nephrology > Fluid + Electrolytes > Flashcards

Fluid + Electrolytes Flashcards

1
Q

What senses ECF OSMOLALITY and what does it stimulate the release of?

A

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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2
Q

What pathway is the ECF regulated by?

A

RAAS pathway, ECF is sodium dependent

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3
Q

What receptors upregulate the RAAS system

A

Low pressure receptors: RA, pulm vasculature

High pressure receptors: Renal afferent arterioles sense decrease renal perfusion

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4
Q

What are compensating mechanisms for low ECF volume

A

autonomic nervous system - regulates vascular tone

Posterior pituitary releases AVP

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5
Q

what is the RAAS antagonist system for excessive ECF volume? and what does it cause

A

ANP release from high pressure baroreceptors in Left Atrium, Carotid Sinus, Aorta. ANP causes naturesis without loss of potassium

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6
Q

What is the response to increased serum osmolality (>290-295 mOsm)?

A
  1. increased thirst
  2. AVP release from posterior pituitary
  3. negative feedback = decreased serum osmolality, atrial receptor stretch
    * *volume reduction OVERRIDES osmolality considerations
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7
Q

What is the action of ADH (AVP)?

A
  1. increased H20 reabsorption (cAMP, PKA insert aquaporins)
  2. increased reabsorption of UREA
  3. peripheral vasoconstriction
  4. stimulate NKCC2 and K+ channels in TAL
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8
Q

What is the role of Aquaporin I and where is it located?

A

NO response to AVP
Proximale tubule, Thin descending limb of Henle
produces countercurrent multiplier system to concentrate urine

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9
Q

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

A

Expression regulated by AVP!!!!!

Collecting duct in apical region of principal cells

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10
Q

What is the role of Aquaporins III, IV?

A

allows water to exit from principal cell to interstitium

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11
Q

How does AVP affect Urea?

A

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

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12
Q

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

A

loss of fxn of Thiazide sensitive NaCl transporter in DCT
hypokalemic metabolic alkalosis, hypocalcemia, hypomagnesemia
hypovolemia

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13
Q

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

A

loss of fxn of Bumetanide sensitive NKCC transport in TAL

HYPOKALEMIC alkalosis, hypovolemia

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14
Q

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

A

Diabetes Insipidus

nephrogenic or pituitary causes

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15
Q

What are causes of pituitary Diabetes Insipidus (ADH deficiency), what are Sx

A

Sheehan syndrome = post delivery pituitary hemorrhage
pituitary hemorrhage - from TB, Malaria, tumors, trauma
Sx: hypernatreima, severe diuresis, volume contraction

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16
Q

What are causes of nephrogenic Diabetes Insipidus (ADH deficiency)

A

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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17
Q

Diagnostic Lab findings of Diabetes Insipidus

A 
increased serum sodium
increased serum osmolality
hypotension
urine volume high
urine osmolality <250 mOsm
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18
Q

Diabetes insipidus vs Polydipsia

A

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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19
Q

How do you treat Pituitary Diabetes Insipidus

A

AVP analogue

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20
Q

How do you treat Nephrogenic Diabetes Insipidus

A

thiazides, low sodium diet, indomethacin

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21
Q

Sx of SIADH?

A

Hyponatremia
hypervolemic
euvolemic (hospital patients)

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22
Q

Treatment of SIADH

A

firstline - FLUID RESTRICTION

change IV fluids to isotonic saline

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23
Q

Best method for following a IN PATIENT volume?

A

monitoring daily body weight

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24
Q

How and where does aldosterone affect Volume expansion

A

increase sodium reabsorption via principal cells in CD

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25
Q

How does Angiotensin II affect Volume Expansion

A

upregulation of NHE3 (PCT, TAL, CD)

26
Q

How does the sympathetic nervous system affect volume expansion

A 
Reduces GFR (increasing renin release)
catecholamines upregulate apical NHE3, Na-K
27
Q

How does ADH affect volume expansion

A

Upregulates NKCC2 and K+ channel in TAL
increase reabsorption of UREA
peripheral vasoconstriction

28
Q

Where is sodium stored in the body

A

plasma, bone, cartilage, skin, bound to proteoglycans

29
Q

what drug can cause osteopenia, osteoporosis

A

thiazides can cause chronic hyponatremia, increase serum Ca2+

30
Q

What are the Sx of Hypernatremia

A

seizures, coma, intracerebral hemorrhage, hypertonia, Cerebral demyelination

31
Q

Pt shows up with hypernatremia. What is the first question you ask?

A

What is the volume status of the Pt

32
Q

What is Anasarca and what does it suggest?

A

generalized peripheral edema, shows severe volume overload

can also be caused by low oncotic pressure (cirrhosis, nephrotic syndrome)

33
Q

What are the 3 resuscitation fluids of choice?

A

normal saline, lactated ringers, isotonic balanced (normosol)

34
Q

What two ways can you gauge volume correction

A

Blood pressure and pulse rate

35
Q

What can happen if hyponatremia correction is too rapid

A

osmotic demyelination syndrome: biphasic

1) initial Sx reduction
2) grandual onset of new neuro problems (central pontine myenolysis)

36
Q

What chemicals in the body are active after a high potassium meal?

A

Insulin + epinephrine = Potassium pushed intracellular

insulin release is blocked by somatostatin

37
Q

What happens in the distal nephron in response to a large dietary K load

A

ROMK

BK expressed - can secrete large K+ amounts

38
Q

What is the effect of Cortisol on the distal Nephron

A

circadian rhythm related to potassium excretion

high cortisol = high K+ loss

39
Q

What is the effect of Aldosterone on the distal Nephron

A

Increase K+ excretion

UNLESS volume depletion (RAAS stimulated) or existing hypokalema (reduces aldosterone)

40
Q

What are the Sx of Hyperkalemia

A

Hyperactive DTR’s
Weakness/paralysis
Confusion
Cardiac Asystole

41
Q

What are the EKG findings of Hyperkalemia (>5)

A

peaked T wave
Widended QRS
loss of P wave
severe: Sine wave, Asystole = VFIB!!!!!

42
Q

what effect does licorice have on renal fxn

A

licorice can imitate aldosteronism = hypokalemia (<3.6)

43
Q

What is Liddle syndrome (where, which cell type)

A

principal cells in CCD - hyperactive Na channel

44
Q

What is Familial Hyperkalemia Hypertension (Where, what channel)

A

WNK1&4 mutation in DCT

sensitive to thiazides

45
Q

What are the symptoms of Hypokalemia

A

TETANY
Muscle weakness, cramps
ORTHOSTATIC HYPOTENSION
UWAVES on EKG

46
Q

What are the three chemicals involved with Calcium homeostasis and what do they do?

A

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

47
Q

What two areas are calcium able to be mobilized from in the body?

A
  1. periosteum (short term response)

2. Osteoclasts (slower response) - PTH/calcitonin

48
Q

what does Calcitonin do and where does it come from?

A

comes from thyroid C cells, decreases serum Ca2+ (inhibits osteoclasts from reabsorbing bone)

49
Q

What does calcitriol do and where does it come from/where it is processed

A

skin synthesis -> liver D1 -> renal D2
increase Ca2+ reabsorption (renal + GI)
paradoxically increases Ca release from bone

50
Q

What are causes of hypercalcemia

A
  1. Thiazide diuretics (upregulation of Calbindin)
  2. Pagets
  3. Vit A intoxication
  4. Hyper PTH, too much Vit D
  5. malignancy
51
Q

What are the symptoms of Hypercalcemia

A

Bones, Stones, Moans, groans

osteitis fibrosa, renal calculi, constipation, confusion

52
Q

What are the physical findings of Hypercalcemia

A

Hyporeflexia, seizures, confusion, shortened QT interval, METABOLIC ALKALOSIS

53
Q

What is acute treatment of hypercalcemia

A

isotonic saline
then try saline diuresis
then furosemide

54
Q

What are the 2 causes of Hypocalcemia. What is the most common cause?

A
  1. low albumin

2. hypomagnesemia (most common) - also causes hypokalemia

55
Q

What are the symptoms of hypocalcemia

A

Acral parethesias, lethargy, ab pain/cramps, increased DTR, TETANY, prolong QT interval
Tetany = CHVOSTEK’S SIGN

56
Q

What are the causes of hyperphosphatemia

A

Vit D excess
Laxative abuse
Granulomatous disease (Sarcoidosis)
Most common causes: renal disease, endocrinopathies, sickle cell disease

57
Q

What are the signs/symptoms of Hyperphosphatemia

A

Tetany-cramps-hyperreflexia

58
Q

What are the causes of Hypophosphatemia

A

Vit D deficiency
ALCOHOL abuse
FGF23 producing tumor

59
Q

What is the treatment for SEVERE hyponatremia

A

3% saline (513meq NaCl/L)
infuse 1ml/kg/hr
STOP 3% once Na+ = 125meg/L

60
Q

What is the management for Hyperkalemia (Acute and Slow)

A

acute: calcium chloride IV push (protect heart)
bicarb
D5W
Beta agonists
Slow correction - loop diuretics, dialysis, enema

Nephrology (13 decks)

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