Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology - Urinary Tract > Disorders of Renal Concentration and Dilution > Flashcards

Disorders of Renal Concentration and Dilution Flashcards

1
Q

What do ECF volume expansion and depletion imply about Na levels?

A

ECF volume depletion -> total body Na deficit. Think about it like this -> if you have a normal amount of water in the body, but sodium is relatively depleted in the ECF compartment, the water will redistribute to the ICF

ECF volume expansion -> total body Na excess

However, this does not necessarily correlate with [Na+] in extracellular fluid, which may be high or low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is total body Na content estimated?

A

Based on clinical parameters on physical examination (not Na+ concentration)

Includes: skin turgor, mucous membrane moisture, edema / ascites, JVP, PCWP, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What parameter estimates the WATER CONTENT of extracellular and intracellular fluid compartments and how does it do this?

A

Plasma osmolality -> does this by assuming that except for some kidney tubules, osmolality will equilibrate across cell membranes in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is osmolality in units, and what would a low osmolality imply about total body Na content and water content?

A

It is moles solute / kg solvent (Water)

Low osmolality -> high relative water content (compared to solutes)

Low osmolality implies a high total body water content, but it implies nothing about the ECF volume (corresponds to total body Na content, since most Na exists in ECF and pulls water towards it).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does plasma osmolality relate to plasma Na concentration, conceptually?

A

Directly proportional. Thus, total body water content can be estimated by Na concentration, but ECF volume cannot be estimated by Na concentration (needs total body Na, a clinical assessment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the formula for calculating plasma osmolality? Give the normal value?

A

2*Na + (glucose / 18) + (BUN / 2.8)

Na in mmol/L - because each Na is accompanied by an anion

Glucose in mg/dL

BUN in mg/dL

Normal value is around 290 mOsm / kg water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the difference between water depletion and volume depletion? What is dehydration talking about?

A

Water depletion - depletion of total body water (increased Na concentration / osmolality) -> dehydration refers to this

Volume depletion - depletion of ECF volume - total body Na. Dehydration should not refer to this, but sometimes sloppily applied

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are sources of total body water gain?

A

Drinking fluids
IV fluids which are hypoosmotic to plasma
Bladder irrigation
Enemas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are sources of total body water loss?

A

Respiration, sweat (hypo-osmotic to plasma), GI tract (emesis, feces)

Renal - urine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two cases when plasma osmolality is NOT proportional to plasma [Na]?

A

Pseudohyponatremia:

  1. Artifactual hyponatremia
  2. Hyperosmolal hyponatremia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does artifactual hyponatremia occur and what are two disorders responsible for this?

A

Since Na only dissolves in the plasma water content, and not the 7% of undissolved solids, situations where there are elevated undissolved solids can make the measured Na+ be low relative to the whole volume of plasma pulled from the lab, while the Na+ / plasma WATER is relatively normal.

Examples:
Hyperlipidemia
Hypergammaglobulinemia (i.e. multiple myeloma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How would plasma osmolality be affected in artifactual hyponatremia?

A

Unaffected -> osmolality is a collagative property. Measured solutes dissolved per kg of WATER -> does not count the undissolved solids into the volume for the calculation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the concentration of injected normal saline and why?

A

154 mmol/L, since all the NaCl is dissolved in pure water.

154*0.93 = 140 mmol/L, the concentration we are used to, since 7% of plasma is normally undissolved solids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is hyperosmolal hyponatremia and when does it occur? How can this be corrected?

A

In hyperglycemia due to uncontrolled diabetes mellitus, plasma osmolality truly rises because insulin is not present to bring glucose into the cells. As water exits cells into the ECF, the ECF [Na] goes down, causing pseudohyponatremia. Na cannot simply move across the membrane.

When the hyperglycemia is corrected with insulin, the [Na] will renormalize.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

For a patient with a plasma glucose of 1,000 mg/dL, what is their true plasma [Na] after correction if their current [Na] is 120 mg/dL?

A

For every 100 mg/dL above 200 mg/dL, the plasma [Na] will go up 1.6 mM

(1,000-200)/100 = 8
8*1.6 = 12.8
12.8 + 120 = 132.8 mmol/L

Thus, this patient’s Na would still be low, and the patient would have excess TBW.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How will elevation of BUN in chronic renal failure affect plasma Na concentration?

A

No effect, since urea will increase plasma osmolality but not alter Na concentration because it doesn’t stay confined to one compartment (i.e. distributes equally to both compartments)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What three factors will stimulate thirst?

A
  1. Increase in plasma osmolality by 2-3%
  2. Decrease in blood volume
  3. Decreased blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What area of the brain regulates plasma osmolality? How do they relate to the BBB? how do they work? What are the osmoreceptors type?

A

Subfornical organ (beneath hippocampus) and organum vasculosum of lamina terminalis (OVLT)

Outside of BBB, have TRPV1 osmoreceptors and angiotensin II receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How will ADH release be affected by drinking?

A

Release will be decreased by the simple act of drinking (even before Posm decreases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does OVLT signal ADH secretion?

A

Signals thru the magnocellular neurons of the supraoptic and paraventricular nuclei of the hypothalamus. They transport ADH thru the pituitary stalk and release via neurophysin storage + release, increasing ADH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Other than angiotensin II, low BP, low blood volume, and high plasma osmolality, what other factors stimulate ADH release?

A

Other stress-related stimuli:

Nausea
Hypoxia
Hypercapnia
Pain (nociceptors)

-> keep these all in mind as causes of normal ECV hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where is blood pressure sensed and how does this relate to ADH secretion?

A

Low pressure baroreceptors - sense stretch in response to changes of filling volume. Located in cardiac atria and pulmonary vessels

High pressure baroreceptors - aortic arch and carotid sinus, in arterial areas, sense high pressure

They relay via the 9th and 10th cranial nerves, and when they fire they inhibit ADH secretion. When they stop firing they disinhibit ADH release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does the sensitivity and effect size of the baroreceptors relate vs osmoreceptor control of ADH? How do they interact?

A

Baroreceptors - lower sensitivity (need 10% drop in blood volume to stop firing and stimulate ADH release) but more steep effect

Osmoreceptors - higher sensitivity (1% change in osmolality) but lower slope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do the baroreceptors / osmoreceptors interact to control ADH?

A

The baroreceptors modify the rate of rise of ADH release based on blood volume. I.e. if blood volume is very high, a rise in plasma osmolality will not as greatly increase ADH levels

Likewise, if the blood volume is low enough, ADH secretion can be increased greatly even if plasma osmolality is low (baroreceptors have a greater effect despite lower sensitivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What effect does ADH have on the kidneys? What receptor does it bind?

A

Increases solute absorption via TALH (NKCC) and urea absorption by collecting duct to increase medullary osmotic gradient (greater concentrating power)

Binds V2 receptors. Increases Aquaporin 2 expression in collecting duct (cAMP mechanism). Aqp3 also has a minor effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the countercurrent “multiplier” and the size of the gradient?

A

Gradient of 200 mOsm between TALH and descending thin limb which is permeable to water but not solutes allows for multiplication of solute concentration between the two limbs and more concentration of the urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does the vasa recta relate to the loop of Henle?

A

Descending vasa recta are next to ascending limb, pick up solutes and lose water down the medulla

Ascending vasa recta are next to descending limb, gain water from the descending limb as osmolality falls, near the cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does tubular flow rate and blood flow rate through the vasa recta relate to the steepness of the osmotic gradient?

A

Tubular fluid flow rate - inversely related to gradient size (too fast = low gradient)

Vasa recta flow rate - inversely related to gradient size (more time to equilibrate is better), except when blood flow is super low and gradient cannot be maintained (too little nutrients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Where is urea synthesized, filtered, reabsorbed, and secreted?

A

Synthesized - liver
Filtered - glomerulus, freely
Reabsorbed - inner medullary collecting duct, taken up by ascending vasa recta
Secreted - proximal straight tubule - after acquisition from ascending vasa recta

Some urea from ascending vasa recta is also transferred to adjacent descending vasa recta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the mechanism of transport of urea in the kidney, and what is it under the control of?

A

Passive, facilitated diffusion through UT1 / UT2

Under the control of ADH (will put more transporters in membrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the requirements for excretion of optimal solute-free water and what is the lowest we can dilute our urine to?

A

Normal GFR and proximal tubule function

Functional TALH and distal convoluted tubule (NCC)

Absence of ADH (collecting duct impermeable to water)

50 mOsm / kg water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the definition of osmolal clearance and its corresponding formula?

A

Volume of plasma cleared of all solute per unit time

Clearance = Urine osmolality * urine flow rate / plasma osmolality

Cosm = (Uosm * V)/ Posm

33
Q

What is the definition of free water clearance? How do you calculate it?

A

Volume of urine per unit time that is solute free after removal of the volume of urine that is iso-osmotic plasma

Free water clearance = Urine flow rate - Osmolal clearance
Ch20 = V - Cosm

34
Q

What does it mean when free water clearance is positive, negative, or 0?

A

If Ch20 is 0 -> urine is iso-osmotic to plasma, meaning Uosm = Posm.

If Ch20 is positive -> substract a number which is less than V, Uosm/Posm <1, urine is hypoosmotic to plasma.

If Ch20 is negative -> Uosm/Posm >1 = urine is hyperosmotic to plasma (subtract a number that is greater than V)

35
Q

What is T(superscriptC)(subH20)? This relates to free water clearance.

A

Tubular water reabsorption

It is equal to the negative free water clearance (if free water clearance is -1.5L/min then water is being reabsorbed, and TcH20 = 1.5L/min)

36
Q

How much metabolic waste does the average person have person day?

A

About 600 mOsm, with catabolic patients having more, and small individuals / children having less

37
Q

Give TBW in terms of body weight, ECF / ICF in terms of TBW, and ISV and PV in terms of ECF.

ISV = interstitial volume
PV = plasma volume
A

TBW = 0.6 * wt in kg

ECF = 1/3 * TBW
ICF = 2/3 * TBW
ISV = 3/4 * ECF
PV = 1/4 * ECF
38
Q

How do you calculate the excess TBW for a patient who was ideally 70 kg before coming ill, and who now has a hypoosmotic plasma of 250 mOsm / kg water?

A

70 kg * 0.6 = 42 L = ideal TBW

M1V1 = M2V2

ideal Posm * ideal TBW = actual Posm * actual TBW

300 mOsm * 42 L = 250 mOsm * actual TBW

actual TBW = 50.4L

Actual TBW - Ideal TBW = Excess TBW

  1. 4L - 42 L = excess TBW = 8.4 L
  2. 4 L of solute free water needs to be excreted to correct the plasma osmolality
39
Q

What are the signs and symptoms of disorders of urinary concentration? What happens if it gets very advanced?

A

Polyuria, polydipsia, hypernatremia

More advanced: coma and confusion -> if individual cannot replace water loss

If water loss is also accompanied by Na loss (diarrhea / diuretics) -> signs of ECF volume depletion

40
Q

What are the signs of ECF volume depletion and what causes this?

A

Loss of Na from ECF (total body Na)

Signs include low blood pressure, increased heart rate, orthostatic vital changes, dry mucous membranes, poor skin turgor

41
Q

Why do diuretics (osmotic or loop) cause a urinary concentration defect?

A

Osmotic - decreased proximal tubule reabsorption, decreased interstitial gradient due to increased flow rate

Loop diuretics - impaired solute reabsorption which destroys gradient, loss of fluid reabsorption

42
Q

How do acute tubular necrosis and obstruction cause urinary concentration defect?

A

Damage thick ascending limb for reabsorption and maintaining gradient

43
Q

How does malnutrition cause urinary concentration defect?

A

Lack of sufficient urea

44
Q

How do sickle cell and analgesic nephropathy (i.e. NSAIDs) cause concentration defect?

A

Damage to vasa recta, destroys gradient

45
Q

What are the hereditary causes of ADH derangements?

A

Central diabetes insipidus (can also be acquired) - lack of ADH secretion

Nephrogenic diabetes insipidus - abnormal V2 receptor or AQP2 structure

46
Q

What are the acquired causes of nephrogenic diabetes insipidus?

A

Hypercalcemia, hypokalemia

-> impairs cAMP mechanisms, abnormal AQP2 number

Remember hypokalemia lecture mentioned impaired renal concentrating ability

Remember hypercalemic lecture (polyuria)

47
Q

What are the causes of inadequate water intake?

A
  1. Thirst deficiency - usually brain tumor in subfornical area
  2. Inability to obtain water (infants, unconscious, desert) - most common
  3. Intake of hypertonic salt without water
  4. ADH derangements with inadequate water intake
48
Q

Why do some babies not want to drink mama’s breast milk?

A

If it is too hypertonic, it is too salty and they need water and not da milk

49
Q

What is the diagnostic approach to hypernatremia?

A

First, determine clinically if the patient has low, normal, or increased ECF volume

Hypernatremia is usually associated with decreased ECF (lost total body Na content, but water relatively more than that), but can be with increased ECV (gained total body Na, not as much water was gained with it so Na concentration is high)

50
Q

If an individual has edema, pleural effusion, and ascites, what can we say about their total body water?

A

Absolutely nothing! We can say they have excess total body Na content though, because whatever total body water they have is being pulled into their extracellular fluid (out of cells) and leading to massive edema.

If plasma osmolality is low (low plasma Na concentration), then their total body water is high, and that water is exceeding their increased Na+ levels.

if plasma osmolality is high, then their total body water is low, and they have much more Na then they do water.

51
Q

What are the causes of hypernatremia with low ECV?

A

Loss of both Na and water, but water more than sodium (hence hypernatremia)

  1. GI losses - diarrhea or vomiting
  2. Inability to access food or water, with loss of water and salt in sweat
  3. Diabetic osmotic diuresis
  4. Drugs that impair water and salt reabsorption (diuretics)
52
Q

What is the only real cause of hypernatremia with (almost) normal ECV?

A

Diabetes insipidus - central or nephrogenic (sodium is absorbed fine, just can’t pull the water out of the urine at all)

Normal respiratory or dermal losses of water

-> lost water without loss of total body Na (by clinical assessment)

53
Q

What are the causes of hypernatremia with high ECV?

A

Situations where Na is gained in excess of water

  • > hypertonic breast milk / formula
  • > hypertonic dialysis
  • > primary hyperaldosteronism
  • > iatrogenic Na bicarbonate injections (hypertonic fluids)
54
Q

What is the treatment for all types of hypernatremia, and if you are low ECV vs normal or high ECV?

A

Treatment for all: permit acess to water, and give oral water if patient is awake / alert

Low ECV - BP is most important, give isotonic saline until BP improved, then switch to hypotonic to normalize hypernatremia

Normal / high ECV - Give D5W - basically giving pure water which is isotonic but does not raise sodium concentrations at all (ECV is already okay)

55
Q

What are the treatments for central and nephrogenic diabetes insipidus?

A

Central - ADH or desmopressin

Nephrogenic - hydrochlorothiazide - NCC channel in DCT is responsible for making iso-osmotic filtrate hypo-osmotic (down to 50mOsm / L). Knocking this out will make all the urine lost only iso-osmotic (300 mOsm/L) -> improves quality of life

56
Q

Why do disorders of urinary dilution cause their symptoms?

A

Plasma becomes hypoosmotic either due to decreased water loss (water retention) and a concomitant increase in solute loss (cannot reuptake solute)

Signs and symptoms are due to brain cell edema (water ends cells) -> skull has only 10% of space not occupied by brain tissue

57
Q

What will be the signs and symptoms of disorders of urinary dilution? What causes death?

A

Headache, nausea, vomiting, confusion, focal neurological signs, seizures

Death from brain herniation

58
Q

How can renal failure and heart failure contribute to impaired urinary dilution?

A

Renal failure - cannot make urine in order to lose water

Heart failure - decreased GFR so badly, causing increased proximal tubule reabsorption -> need to make enough urine that it actually reaches distal tubbule to lose water

59
Q

How could loop diuretics, thiazide diuretics, and glucocorticoid / adrenal insufficiency cause impaired urinary dilution?

A

Loop diuretics needed to dilute the urine (pull solutes out to lose water)

Thiazide diuretics - NCC needed to dilute urine

Glucocorticoid / adrenal / mineralocorticoid - Cortisol helps with aldosterone / solute reabsorption

60
Q

How can you think of the functional solute problem differences between problems of urinary concentration and urinary dilution? How can loop diuretics contribute to both?

A

Urinary concentration disorder - solutes are reabsorbed okay, just can’t seem to reuptake water. Loop diuretics can make this worse by not allowing formation of medullary gradient for water reuptake

Urinary dilution disorder - solutes are not reabsorbed well, water is not being lost adequately. Diuretics make this worse by not allowing reuptake of solute (makes blood hypoosmotic).

61
Q

How can ADH contribute to problems with urinary dilution? What things can cause this?

A

Inappropriate presence of ADH leads to hyperconcentration of urine -> too much water reuptake, retention of water

Things which cause increased ADH, especially heart failure (associated with hypoxia and hypercapnia, which increases ADH), certain drugs, and SIADH

62
Q

What is it called if you have hypo-osmolality / hyponatremia due to water intake in excess of kidney’s ability to excrete water?

A

Psychogenic polydipsia

63
Q

How can diarrhea cause hyponatremia?

A

If you have diarrhea, then drink water instead of chicken soup (not enough salt replacement)

64
Q

What drug is especially associated with hyponatremia?

A

Ecstasy - increases ADH levels + makes you ravenously thirsty

65
Q

How can osmoreceptors cause hyponatremia?

A

Some cancers reset the osmoreceptor threshold to a low value -> more ADH at a lower plasma osmolality

66
Q

What are some situations when ADH secretion may be physiologically stimulated despite hypo-osmolality?

A

Low blood volume - baroreceptors take priority over osmoreceptors in order to maintain blood pressure

i.e. hemorrhage, ECF depletion, hypotension

67
Q

Why does congestive heart failure cause hypo-osmolality?

A

Normal baroreceptors become insensitive overtime to the volume overload - they stop firing, ADH release is disinhibited, exacerbating heart failure

68
Q

What are some causes of low ECV hyponatremia?

A

Individuals lost more sodium than water, usually due to drinking water or hypotonic fluids after salt loss

GI losses
Burns: Loss of Na/water
Renal losses
Hemorrhage

69
Q

What are the renal loss causes of low ECV hyponatremia?

A
  1. Salt wasting nephritis
  2. Mineralocorticoid deficit (i.e. Addison’s disease)
  3. Osmotic diuresis
70
Q

What are the causes of high ECV hyponatremia? Why does each of them cause this?

A

They have high total sodium, but VERY high TBW

Big four:

  1. CHF - decreased baroreceptor responsiveness
  2. Cirrhosis - low BP due to profound splanchnic vasodilation to increase liver blood flow + fluid loss due to oncotic changes
  3. Renal failure - inability of kidney to excrete water in limited function
  4. Nephrotic syndrome - low intravascular volume due to oncotic changes
71
Q

How should you treat a patient with low ECV hyponatremia and why is this easier than high ECV hyponatremia?

A

low ECV hyponatremia - give isotonic saline. Na levels will normalize in body, and their baroreceptors work fine so they will lose the excess water through their kidneys

high ECV hyponatremia is bad because their baroreceptors are working badly, allowing too much ADH, or their kidneys aren’t working at all. -> kidneys will not allow them to lose water, and treating with isotonic saline would just exacerbate the problem.

72
Q

What does it mean if you have normal ECV hyponatremia?

A

Very difficult situation - total body Na is normal, but water is high. Usually due to too much ADH, but there are multitude causes and treatments (i.e. could be due to drinking too much water, like psychogenic polydypsia)

73
Q

Why does glucocorticoid deficiency cause normal ECV hyponatremia?

A

Cortisol-releasing hormone stimulates ADH release. If cortisol is not feeding back to inhibit ADH, it will build up.

If mineralocorticoids are normal, total body Na balance is normal in this situation

74
Q

What does hypothyroidism cause in hyponatremia?

A

Normal ECV hyponatremia -> in patients with myxedema

75
Q

What are the major causes of SIADH?

A

Ectopic ADH - malignancies, i.e. small cell lung cancer

Pulmonary disease - especially TB, but also asthma and other infections

CNS disorders / head trauma

Certain drugs

76
Q

What is the treatment for SIADH?

A

Water restriction
Normal saline -> especially if low ECV category
Hypertonic saline
Demeclocycline, lithium, and vaptans

77
Q

What are the vaptans? Two most important ones?

A

Aquaretics - block the resorption of water by antagonizing V2 receptor and thus actions of ADH

Tolvaptan and Conivaptan

Very dangerous because they can lead to true dehydration since they are so effective

78
Q

How do demeclocycline and lithium treat SIADH?

A

Demeclocycline - impairs AQP2 insertion into apical membrane

Lithium - prevents cAMP formation, so AQP2 can’t be moved to the membrane

79
Q

What is the risk of too rapidly correcting hyponatremia levels? What is most susceptible?

A

Osmotic demyelination syndrome

  • > rush of fluid out of myelin sheaths into extracellular space (there was lack of osmolytes in brain to prevent cerebral edema from all this water) causes damage
  • > need to give sodium back to ECF slowly to allow brain cells to generate osmolytes so fluid doesn’t leave the cells too rapidly

-> especially affects pons, can cause locked in syndrome

Pathophysiology - Urinary Tract (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions