Pathophysiology of Sodium Handling Flashcards
What is average daily sodium intake a day in the US? How about for a no added salt diet? Low salt diet?
3-7 g/day
4 g/day
2 g/day
How many grams is total body sodium?
50 g
How much sodium is filtered at the glomerulus per day?
600g/day
What is ICF and ECF sodium concentration in mEq/L?
ICF sodium concentration - 10 mEq/L
ECF sodium concentration - 140 mEq/L
True or False: Sodium is the major and most important determinant of ECF volume
True
Maintenance of ECF volume determines the _____ and _____ which are important for the existence of the organism
mean arterial pressure, left ventricular filling volume
What are the sensors that respond to changes in blood volume? (5)
- Low-pressure baroreceptors (located on venous side)
- High-pressure baroreceptors (located on arterial side)
- Intrarenal receptors (macula densa, juxtaglomerular cells)
- Hepatic receptors
- CNS receptors
What is tubulo-glomerular feedback and glumerulo-tubular balance?
Tubulo-glomerular feedback is when increased distal delivery of sodium chloride to the macula densa increases afferent arteriolar tone and returns RBF and GFR towards normal values.
Glomerulo-tubular balance is where changes in GFR automatically induces proportional change in the rate of proximal tubular sodium reabsorption.
True or False: There are physical forces, independent of GFR, that influence the renal reabsorption of sodium between the proximal tubule and the renal interstitium as well as the renal interstitium with the efferent arteriole.
True
What are 4 humoral effector factors (hormones) that increase sodium reabsorption? (Antinatriuresis)
- Angiotensin II
- Aldosterone
- Catecholamines
- Vasopressin
What are 4 humoral effector factors (hormones) that decrease sodium reabsorption (natriuresis)?
- Natriuretic peptides
- Prostaglandins
- Bradykinin
- Dopamine
True or False: Activation of renal sympathetic nerves have an anti-natriuretic effect.
True.
Nerve stimulation enhances the release of renin from the JGA.
At the proximal tubule, is movement of Na across the apical membrane passive or active? How about the basolateral membrane?
It is passive across the apical membrane and active (via Na/K-ATPase) across the basolateral membrane.
What channel does Amiloride block?
Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium reabsorption in the late distal convoluted tubules, connecting tubules, and collecting ducts in the kidneys. This promotes the loss of sodium and water from the body, but without depleting potassium.
Renal losses of sodium and water can happen due to failure of effector mechanisms or intrinsic renal diseases. Name 5 examples of each.
Failure of effectors
- 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
- Tubulo-interstitial disease
What are 3 examples of extra-renal sodium and water losses?
GI tract fluid losses (vomiting, diarrhea)
Dermal fluid losses
Fluid losses into the “third space”
Are extra-renal or intra-renal losses of sodium and water more common?
Extra-renal
What 6 things happen in the cardiovascular system and sympathetic nervous system when there is ECF volume contraction?
- Increased HR
- Increased cardiac inotropic function
- Systemic vascular resistance
- Increased angiotensin II
- Increased ADH (also called AVP apparently)
- Increased endothelin (peptides that are potent vasoconstrictors)
What 6 things happen in the kidneys when there is ECF volume contraction?
- decreased GFR resulting in a smaller filtered load of sodium
- activation of the renal sympathetic nerves
- decreased hydrostatic pressure and increased oncotic pressure in the peritubular capillaries
- stimulation of renin-angiotensin-aldosterone system
- increased secretion of ADH
- inhibited secretion of atrial natriuretic peptide (ANP) from the atrial myocytes
What are clinical manifestations of volume depletion? (12)
- Thirst
- Postural dizziness
- Weakness
- Heart palpitations (bc increased HR)
- Decreased urinary output
- Confusion
- Weight loss
- Orthostatic blood pressure
- Tachycardia
- Hypotension
- Decreased elasticity or turgor of skin
- Dry mucous membranes
Upper GI loss of fluid causes metabolic _____ and lower GI loss causes metabolic _____
Upper GI loss of fluid causes metabolic alkalosis
Lower GI loss of fluid causes metabolic acidosis
(just think that upper GI loss causes pH to go up and lower GI loss causes pH to go down)
True or False: Patients that are volume contracted get increased hematocrit and serum albumin
True. Because of hemoconcentration
True or False: volume contracted patients have a decreased BUN/plasma creatinine ratio
False. Their BUN/plasma creatinine ratio is increased.
What does urinary sodium tell you about a patient in a volume contracted state?
If the urinary sodium is greater than 20 mEq/L, the volume loss is renal.
If the urinary sodium is less than 20 mEq/L, the volume loss is extra-renal.
In patients with volume depletion, what SG and osmolality would you expect in urine?
Urine SG should be greater that 1.010 and the urine osmolality is greater than 300 mOsm/kg
What FENa value might you expect in a patient that is volume contracted?
FENa would be much less than 1%
A normal value for FENa is about 1%. In states of volume depletion, the body is trying to hold on to as much Na as it can so that it can hold on to water too. This causes the FENa (fractional excretion of Na) to fall much below the normal value.
If you give saline to correct for volume depletion, how much of the saline stays in the intravascular space?
About 25% of it.
The other 75% goes to the interstitial fluid.
Is D5W a good volume expander?
No. only about 9% of it will stay in the plasma/intravascular space.
Is plasma a good volume expander?
Yes, 100% of it stays in the intravascular space. However, it’s expensive.
ECF volume expansion can happen because of 3 general mechanisms. What are they?
- Disturbed starling forces
- Primary hormone excess
- Primary renal sodium retention
Give 3 examples of disturbed starling forces that can cause ECF volume expansion
- Congestive heart failure
- Nephrotic syndrome
- Liver cirrhosis
Give 3 examples of primary hormone excess that can cause ECF volume expansion
- Primary hyperaldosteronism
- Cushing’s syndrome (metabolic disorder caused by overproduction of corticosteroid hormones by the adrenal cortex and often involving obesity and high blood pressure)
- Syndrome of inappropriate secretion of anti-diuretic hormoe (SIADH)
What can cause primary renal sodium retention resulting in ECF volume expansion?
Acute glomerulonephritis
What are clinical manifestations of volume expansion? (10)
- Weakness
- Exercise intolerance
- Weight gain
- Difficulty breathing during exertion
- Orthopnea
- Swelling in extremities
- Increased urination at night
- Basilar pulmonary rales
- Distended neck veins
- CXR with fluid overload and cardiomegaly
How can liver cirrhosis cause sodium and water retention?
Cirrhosis causes severe vasodilation which causes activation of arterial baroreceptors. This causes activation of RAAS, SNS stimulation, and non-osmotic ADH stimulation resulting in water and sodium retention and increased peripheral arterial vascular and renal resistance.
