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CVPR > Hypo/Hypernatremia (Brosnahan) > Flashcards

Hypo/Hypernatremia (Brosnahan) Flashcards

1
Q

What are all the names for Vasopressin?

A

Vasopressin, Arginine Vasopressin (AVP), and Anti-diuretic hormone (ADH).

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2
Q

What are the three determinants of the serum osmolarity?

A

Na (biggest)
BUN
Glucose

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3
Q

What are the two stimuli that trigger ADH release? Which is the more important? What is the consequence of this in extreme hypovolumetric situations?

A

Blood volume depletion and serum osmolality. Blood volume is the overriding (most important) factor. ADH increases exponentially to a decrease in blood volume of more than 6-8%, DESPITE a decrease in serum osmolality

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4
Q

What receptors in the kidney bind ADH? What is the signalling cascade/result? Where is all this happening?

A

The V2 receptors. Increase in cAMP (via Gs and Adenylate cyclase) increases PKA, which translocates water channels to the apical membrane (opposite the blood). This happens in the collecting ducts.

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5
Q

Causes of hypovolemic hyponatremia:

How would you treat?

A 
Hemorrhage
Plasma volume and EC fluid losses:
-GI losses
-Renal losses (excessive diuretic use, mineralocorticoid deficiency, osmotic diuresis)
-Excessive sweating
-Loss of sodium and Water

Treatment: normal saline (ADH will decrease)

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6
Q

Hypervolemic hyponatremia causes?

A

Either ADH mediated (CHF, liver cirrhosis)
HF–> CO is low, so the EABV is low. This leads to salt and H20 retention by the kidneys and ADH release.
Cirrhosis–> excessive vasodilation in splanchnic vasculature causes reduced EABV, stimulating ADH

OR

Independent from ADH (Severe renal failure)–> either the diluting mechanism in the distal tubules does not work or RBF and GFR are too low. Thiazide diuretics are a common cause because they impair dilution)

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7
Q

How do you treat hypervolemic hyponatremia.

A

DON’T give salt!

Treat the underlying disease. (Stop thiazide diuretics, treat CHF with inotropic drugs, etc.)

Can give loop diuretics.

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8
Q

Euvolemic hyponatremia causes

A

Generally, euvolemic hyponatremia is due to inappropriate ADH secretion. So:

Hypothyroidism
Adrenal insufficiency
Medications (SSIs, NSAIDs, antipsychotics, and more)
Nausea
Pain
Psychosis

SIADH is a diagnosis of exclusion (all above have been ruled out). Clinical defintion–> euvolemic hyponatremia and urine that is not maximally dilute. Can be caused by carcinomas (small cell lung cancer, classically), CNS disorders, pulmonary conditions.

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9
Q

Symptoms of hyponatremia:

A

Depends on the rapidity and severity

Anorexia, nausea, vomiting, weakness, lethargy, confusion, seizures, death.

Acute–> symptomatic with Na of 120 (25-48 hours) Symptoms generally due to cerebral edema. If seizures, give hypertonic saline.

Chronic–> can be as low as 95 without symptoms

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10
Q

What is the risk of correcting chronic hyponatremia too quickly?

A

Central Pontine Myelinolysis (osmotic demyelination syndrome). The brain adapts to chronic hyponatremia, so the brain sheds some electrolytes to become hypo-osmolar in an effort to avoid swelling. So if you give hypertonic saline, water rushes from the brain cells into the blood leading to brain shrinkage.

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11
Q

When will hypernatremia develop? (Only one condition)

A

When a patient is unable to drink. Increasing osmolality of the blood causes extreme thirst, so only patients who are intubated, unconsious, or some CNS defect suppressing the thirst reflex develop this condition.

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12
Q

Renal or extrarenal water losses that exceed sodium loss cause ____.

A

Hypovolemic hypernatremia

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13
Q

Addition of hypertonic fluids causes ______ .

A

Hypervolemic hypernatremia (generally iatrogenic, due to hypertonic saline, TPN, or bicarbonate administration)

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14
Q

Diabetes insipidus is associated with which -natremia?

A

Hypernatremia. Can be
Central –> ADH not secreted
Or
Nephrogenic–> ADH resistance (kidneys do not respond)

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15
Q

Diabetes patients with diabetes insipidus present with_____.

A

Polyuria.

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16
Q

What are causes of Central Diabetes Insipidus?

A

1) Due to diseases of the hypothalamus (head trauma, surgery, tumors, encephalitis)
2) 30-50% of cases are idiopathic (may be autoimmune)

***Kidneys still respond to exogenous ADH, so this can be used as a diagnostic test as well as therapy. Nasally administered DDAVP (form of vasopressin)

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17
Q

What are the causes of Nephrogenic Diabetes Insipidus?

A

1) Congenital: mutations in VP receptor, aquaporin water channels.
2) Acquired (more common): Medications, electrolyte disorders, chronic kidney disease.

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18
Q

Congenital Nephrogenic DI is due to which specific mutations?

A

90%: Mutation in AVP receptor (VR2 gene) –> X linked recessive

10%: Mutation in Aquaporin 2 gene –> autosomal recessive

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19
Q

What is gestational DI?

A

Happens in the last trimester. Placenta releases vasopressinase. Generally not treated, woman just drinks more water. DDAVP also works b/c is not degraded.

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20
Q

What is the treatment of hypernatremia?

A

Replace water defecit (D5 water in most cases). Slow correction of condition has been present for more than 48 hours.

21
Q

Do Hyper/Hyponatremia generally indicate severe or less severe illness?

A

Severe

22
Q

True/False: Hypo and hyper natremia can occur with increased or decreased total body sodium, and evaluation and treatment will depend on volume status?

A

True

23
Q

What is the proportional breakdown of the water (Intracellular/Extravascular(Interstisial)/Intravascular)

A

ICF: Intracellular ~28L (60%)
ECF: Intravascular ~3.5L (10%)
Extravascular ~10.5L (30%)

24
Q

What are the afferent sensors of the homeostatic Na/H20 system? What volume do these sense?

A 
Volume sensors. (4) Sense the EABV.
Low pressure baroreceptors
High pressure baroreceptors
Intrarenal sensors
Hepatic and CNS sensors (incompletely understood)
25
Q

Where are the Low-pressure baroreceptors located (there are 3)? What is their main purpose and how do they achieve it?

A

Located on the venous side of the circulation.

1) Cardiac atria
2) Left ventricle
3) Pulmonary vascular bed

Protect against ECF volume expansion by DECREASING RENAL SYMPATHETIC ACTIVITY. Net result is loss of sodium and water.

26
Q

Where are the high-pressure baroreceptors located (there are 2). What is their main purpose and how do they achieve it?

A

Located on the arterial side.

1) Carotid sinus body at the bifurcation of the carotid aa.
2) Aortic arch

Protect against volume depletion. In a state of low volume, these trigger INCREASED SYMPATHETIC RENAL ACTIVITY and are anti-natriuretic and anti-diuretic. In severe volume contraction, norepinephrine (noradrenaline) is also released. This catecholamine response raises blood pressure by increasing heart rate and vascular resistance.

27
Q

Where are the intrarenal sensors located? How do they work/what is their function?

A

Located at the junction of the efferent and afferent arterioles at the glomerulus. Hence, the juxtaglomerular cells (so named). They secrete renin.

Decrease in arterial pressure leads to an increase in renin secretion and an increase in sodium resorption.

28
Q

What are the main elements of the efferent limb of the homeostatic response?

A

The kidney is the major effector organ involved in fluid volume homeostasis. ECF volume is mainly regulated by changes in renal sodium excretion. Factors that influence the latter are:

1) GLOMERULAR FILTRATION is by far the most important
2) Physical factors at the level of the proximal tubule
3) Humoral effector mechanisms
4) Renal sympathetic nerves

29
Q

Describe renal autoregulation

A

Renal autoregulation is an ability of the kidney to keep RBF (renal blood flow) and GFR constant by the contraction of the vascular smooth muscle of the stretched afferent arteriole in response to a higher intravascular pressure or dilatation when perfusion pressure decreases.

30
Q

Describe Tuboglomerular feedback

A

TGF refers to a phenomenon whereby increased distal delivery of sodium chloride to the macula densa (part of the JGA) increases afferent arteriolar tone and returns the RBF and GFR towards normal values.

31
Q

Describe Glomero-tubular balance

A

Glomerulo-tubular balance is a fundamental property of the kidney whereby changes in GFR automatically induce a proportional change in the rate of proximal tubular sodium reabsorption. Thus, the fractional excretion of sodium is maintained constant in the setting of increases or decreases in GFR.

32
Q

What hormones increase sodium reabsorption? (anti-natriuresis)

A

ATII, Aldosterone, Catchecolamines, Vasopressin

33
Q

What hormones decrease sodium reabsorption? (natriuresis)

A

Natriuretic peptides, prostaglandins, bradykinins, dopamine.

34
Q

Talk about the proximal tubule. What are the transporters, what % of sodium is reabsorbed here, etc?

A

Most of the action happens here. 60-70% of glomerular filtrate is reabsorbed here. There are passive and active mechanisms. Gradient is obtained through the Na/K ATPase and active transport through the Na/H antiporter. Most sodium reabsorption is PASSIVE.

35
Q

Talk about the loop of Henle.

A

30% of filtered sodium is reabsorbed here. Impermeable to water, but impermeable to Na. Reabsorption by the Na/K/Cl/Cl is what loop diuretics (furosemide, etc) block. Cotransporter of all 4.

36
Q

Talk about the collecting duct.

A

Least reabsorption of sodium. ~10%. Happens through sodium channels. K sparing diuretics work here by blocking either sodium or aldosterone. Not as potent.

37
Q

2 mechanisms for renal losses of sodium and water

A 
Failure of effector mechanism:
Solute diuresis, glucosuria
Diuretic agents
Adrenal insufficiency
Selective aldosterone deficiency
Mutations in sodium transporters (Bartter’s &
Gitelman’s syndromes)

Intrinsic renal disease:
Non-oliguric acute renal failure Diuretic phase of acute renal failure
Post-obstructive diuresis “Salt-wasting” nephropathy
Medullary cystic disease Tubulo-interstitial disease

38
Q

_____ presents early in life, and is caused by a mutation in the Na/K/2Cl co-transporter in the TALH. This syndrome is characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, high plasma renin and aldosterone levels, increased calcium excretion, and normal blood pressure.

A

Bartter’s syndrome

39
Q

_______occurs usually in older individuals, and is caused by a mutation in NaCl co- transporter in the distal tubule. It is characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and reduced urinary excretion of calcium.

A

Gitelman’s syndrome

40
Q

ECF volume contraction extrarenal:

A

GI, dermal loss, 3rd space

41
Q

What changes will be seen in the serum during volume contraction?

A
  • ->Increased BUN: plasma creatinine ratio. A normal BUN: plasma creatinine ratio is 10-15:1. During volume contraction, the kidney avidly reabsorbs Na+ in the proximal tubule. Urea passively follows the Na+ causing the BUN: plasma creatinine ratio to rise to ≥ 20:1.
  • ->Metabolic alkalosis during upper GI loss of fluid.
  • ->Metabolic acidosis during lower GI loss of fluid.
  • ->Increased hematocrit and serum albumin because of hemoconcentration
42
Q

What changes will be seen in the urine during volume contraction?

A
  • ->UNa+ >20 for renal losses and FENa Specific gravity of urine will increase (>1.010)
  • -> Urine osmolality >300mOsm/kg
43
Q

What is the treatment for volume depletion?

A

Replacement of fluid. Rate/amount/route will depend on situation. Blood solutions are the best, but normal saline is the answer. (154mEq/L of NaCL; 0.9% NaCL)

44
Q

What are the main disease states leading to ECF volume expansion?

A

CHF, Nephrotic syndrome, Cirrhosis

45
Q

Diuretics acting at the proximal tubule:

A

Acetazolamide is a proximal tubular diuretic. It works by blocking carbonic anhydrase action and causes wastage of bicarbonate in the urine. Acetazolamide is unique as a diuretic in that it causes metabolic acidosis, and can actually be used to treat cases of metabolic alkalosis when isotonic saline can not be given because of ECF volume expansion

46
Q

Diuretics acting at the loop of Henle:

A

furosemide, bumetanide, and torsemide. These agents work by inhibiting the coupled entry of sodium, potassium, and chloride across the apical membrane in the thick ascending limb of the loop of Henle (at the Na/2Cl/K co-transporter). The side effects of loop diuretics are metabolic alkalosis, hypokalemia, hypocalcemia, and hypomagnesemia.

47
Q

Diuretics acting at the distal convoluted tubule:

A

Thiazides inhibit the sodium/chloride transporter and block sodium entry across the apical membrane into distal tubular cells. They have the same side effects as the loop diuretics, except that they increase calcium reabsorption and decrease urinary calcium excretion

48
Q

Diuretics acting at the collecting ducts:

A

Triamterene and amiloride are sodium channel blockers, and spironolactone is a competitive inhibitor of aldosterone. These diuretics cause mild natriuresis and potassium retention. These potassium-sparing diuretics can be used together with other classes of diuretics to prevent hypokalemia.

49
Q

What are the four causes of Euvolemic hyponatremia?

A
  • SIADH
  • 1° Polydipsia
  • Hypothyroidism
  • Adrenal Insufficiency

CVPR (18 decks)

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