Na / Water Balance Flashcards

1
Q

What percentage of water is intra / extracellular

Where is most of the Na?

A

2/3 water intracellular. 1/3 extracellular

Most Na is extracellular.

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2
Q

Osmolality equation

Normal range for osmolality

A

2xNa + glucose/18 + BUN/2.8

Normal range is 280-300

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3
Q

Where are osmol receptors?

A

Hypothalamus

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4
Q

Where are baroreceptors?

A

Carotid sinus and aortic arch

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5
Q

3 non-osmotic factors that can trigger ADH

A

Pain, nausea, meds

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6
Q

Causes of hypovolemic hypoosmolar states (5)

A
  • Renal losses (urine Na is inappropriately high [>20 mEq/L]) – kidney disease, diuretics, aldosterone deficiency
  • Non-renal losses (urine Na is appropriately low [less than 10 mEq/L]) – GI losses, skin / burns.
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7
Q

3 causes of hypervolemic hypo-osmolarity

A

CHF, cirrhosis, nephrotic syndrome

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8
Q

9 causes of SIADH

A

SIADH caused by excess pituitary secretion (tumor, infection trauma), ectopic ADH production (small cell lung cancer), drugs, pulmonary infection, COPD, nausea, or severe pain.

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9
Q

2 hormonal causes of euvolemic hypo-osmolarity that mimic SIADH

A
  • Hypothyroidism – decreased cardiac output → decreased intravascular volume → decreased GFR → increased proximal reabsorption of water / Na → less delivery to diluting segment of nephron. Stimulation of ADH via baroreceptors also occurs.
  • Cortisol deficiency – cortisol normally feeds back negatively on ADH production, so deficiency → more ADH than normal. May mimic SIADH.
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10
Q

Beer drinker’s potomania

A

Poor diet → low solute intake → low solute excretion → limits how much water can be excreted w/ maximally dilute urine

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11
Q

4 causes of hypernatremia

A

Osmotic diarrhea / diuresis, inadequate replacement of insensible water losses, diabetes insipidus

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12
Q

3 causes of central diabetes insipidus

A

Caused by CNS abnormalities (pituitary / sellar mass, head trauma, infiltrating disease of hypothalamus)

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13
Q

4 causes of nephrogenic diabetes insipidus

A

Caused by inherited / congenital receptor dysfunction, meds (lithium, demeclocycline), or hypercalcemia

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14
Q

5 effects of Ang II

A

Stimulates Epi / Norepi and promotes release of ADH. Constricts efferent arteriole to maintain GFR. Increases proximal tubular Na resorption via Na/H exchange. Triggers thirst

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15
Q

2 things that trigger aldosterone release

A

Ang II and hyperkalemia

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16
Q

Primary hyperaldosteronism
Presentation (3)
Diagnosis (2)
Treatment (3)

A
  • Presents w/ MILD volume expansion, HTN, and possibly hypokalemia
  • Confirmed by salt-loading or administration of normal saline.
  • Treat w/ surgery or drugs that block mineralocorticoid receptor: spironolactone, eplerenone
17
Q

Treating hypoaldosteronism

A

Fludrocortisone

18
Q

Syndrome of apparent mineralocorticoid excess
Presentation
Cause

A
  • Presents similarly to primary hyperaldosteronism but renin and aldosterone are both low.
  • Cortisol can activate mineralocorticoid receptor, but normally, 11b hydroxysteroid dehydrogenase type 2 in kidney metabolizes cortisol → cortisone to prevent this.
  • This enzyme may be inactivated by a mutation or by licorice (glycyrrhiazic acid).
  • This is why HTN is common in Cushing’s. Too much cortisol overwhelms 11b hydroxysteroid dehydrogenase
19
Q

Pheochromocytoma
Sxs (6)
Treatment (4)

A
  • Sxs – HTN (due to vasoconstriction) and paroxysmal headache / palpitations / sweating / pallor / tremor.
  • Treat w/ surgery, but BP must be controlled to avoid hypertensive crisis during surgery.
  • Alpha blockers are first line, which block α1 mediated vasoconstriction. Subsequent vasodilatation can lead to reflex tachycardia, so volume repletion + beta blockers can be used to control the HR.
  • If BB is given first, it will block β2 mediated vasodilatation → “unopposed α1” vasoconstriction → severe hypertension.
20
Q

What is considered polyuria

Diff Dx for polyuria (5)

A
  • Polyuria is defined as >3L / day

* Diff Dx of polyuria: psychogenic polydipsia, diabetes insipidus, DM, hyperglycemia / calcemia (osmotic diuresis)