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Diabetes > Polyuria/Polydipsia > Flashcards

Polyuria/Polydipsia Flashcards

1
Q

Major routes for water intake and loss (and regulatory mechanisms)

A

Intake: ~2400ml/day
2000ml/day from ingestion
400ml/day from metabolism

Kidney is the most important organ for water regulation (physiological)
Other (skin, intestine, lungs) become important in pathological circumstances

Regulated by:
1. Updake: mechanism of thirst
2. Elimination: reabsorption in the kidney
Without the kidneys, we’d balloon, have constant edema (accumulation of fluid in the body)

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2
Q

How does osmolarity influence fluid movement

A

Starling forces

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3
Q

How does osmolarity influence fluid movement

A

Starling: exchange of water depends on different forces

Arterial: BP 30mmHg arriving to capillaries (mean arterial pressure 100mmHg), 30 pushing out of capillaries

Oncotic pressure: Due to proteins present in body; brings water back in (about 20 mmHg) constant along vessel

Venous: BP drops to 10 mmHg

Difference of 20 mmHg between arterial and venous (equals oncotic pressure)

Creates a movement of fluid between vessel and interstitia

10mmHg is the difference favoring water efflux from vessel AND water entrance: it’s identical

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4
Q

Sensors and effector pathways involved in regulation of ECF volume

A
  1. Effective circulating volume is sensed
  2. Baroreceptors and volume receptor sensors
  3. Antidiuretic hormone (AVP), atrial natriueritc peptide (ANP), Renin-angiotensin-aldosterone, sympathetic nerve activity effector pathways
  4. Short term effects: heart, blood vessels; long term: kidney
  5. Short term regulation: blood pressure
    Long term regulation: Na+ excretion
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5
Q

Response of baroreceptors and volume receptors to changes in the effective volume and how these responses affect salt and water excretion by kidney

A

Maintaining ECF volume is 1 of 2 ways to regulate water balance

Total body Na+ is maintained through the diet
Leads to ECF volume
Baro/volume sensors located in veins, atrium, parts of vascular tissues signal effector pathways that signal Na+ excretion by the kidney (water will follow)

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6
Q

How do changes in osmolality caused by water and/or salt gain or loss alter the rate of urine production and the osmotic composition of urine

A

1 of 2 ways water balance is carried out: Maintaining osmolarity

Osmolarity is controlled by controlling the main electrolyte in our ECF (Na+)

Na+ regulated by adding or subtracting water

Water regulated by intake or excretion

Water follows solute

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7
Q

How does ADH change the ability of the kidney to produce diluted or concentrated urine

A

As pressure and volume go down, ADH goes up

Basal plasma osmolality: 285-290; beyond this, ADH increases

As ADH increases, urine flow rate will decrease. More water is being reabsorbed and less is being excreted

As ADH increases, osmolarity is increasing (urine becoming more concentrated, darker)

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8
Q

General functions of kidney (3)

A
  1. Homeostatic
    Regulation of ECF volume
    Regulation of electrolyte composition
    Regulation of ECF fluid acid-base balance (important for pH maintenance with specific electrolyte H+)
  2. Excretory
    Metabolic waste products
    Foreign substances and toxins
  3. Endocrine
    Regulation of blood pressure
    Erythropoiesis (production of RBCs when low O2 is detected by kidneys)
    Calcium metabolism
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9
Q

General functions of kidney (3)

A
  1. Homeostatic
    Regulation of ECF volume
    Regulation of electrolyte composition
    Regulation of ECF fluid acid-base balance (important for pH maintenance with specific electrolyte H+)
  2. Excretory
    Metabolic waste products
    Foreign substances and toxins
  3. Endocrine
    Regulation of blood pressure
    Erythropoiesis (production of RBCs when low O2 is detected by kidneys)
    Calcium metabolism

To filter everything from the blood except cells and proteins

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10
Q

Causes of Polyuria

A

Causes:

  1. Low solute reabsorption (if you aren’t absorbing the salt, water will not be reabsorbed- Solute diuresis)
  2. Abnormal ADH levels (water diuresis- if you don’t have ADH, you can’t reabsorb water)
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11
Q

Causes, diagnosis, and treatment of polydipsia

A

Excessive water ingested

Primary polydipsia is a form of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink. This includes psychogenic polydipsia (PPD), which is caused by psychiatric disorders, often schizophrenia, and often accompanied by the sensation of dry mouth.

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12
Q

How does the increase in glucose delivered to the kidney result in high urine output?

A

If glucose is not reabsorbed by the kidney, it appears in the urine, in a condition known as glucosuria.
This is associated with diabetes mellitus. Firstly, the glucose in the proximal tubule is co-transported with sodium ions into the proximal convoluted tubule walls via the SGLT2 cotransporter.

With regard to renal reabsorption of glucose, the kidneys normally retrieve as much glucose as possible, rendering the urine virtually glucose free. The glomeruli filter from plasma approximately 180 grams of D-glucose per day, all of which is reabsorbed through glucose transporter proteins that are present in cell membranes within the proximal tubules. If the capacity of these transporters is exceeded, glucose appears in the urine. The process of renal glucose reabsorption is mediated by active (sodium-coupled glucose cotransporters) and passive (glucose transporters) transporters

Hyperglycemia exceeds renal ability to resorb glucose

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13
Q

Solute diuresis (3 causes) - osmotic diuresis

A

Diuresis: production of urine by the kidney

When the production of urine depends on the solute
Causes:
1. Salt wasting
2. Diuretics (drug that make you pee more)
Treatment for hypertension, peeing makes you release water, lowering blood pressure; inhibits salt reabsorption, inhibiting water reabsorption
3. High glucose in renal tubule
High glucose in renal tubule, water follows glucose. why DM patient will have polyuria
4. Osmolytes in filtrate

Excess solutes in filtrate >
Decreased water reabsorption in proximal >
Partial, insufficient reabsorption compensation by distal >
Urine osmolarity isotonic or close to plasma >
Increased urine volume

Causes: 
Diabetes mellitus
Fanconi syndrome
Inhibition of salt reabsorption by drugs (diuretics)
Decreased aldosterone
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14
Q

Water diuresis

A

Excess water ingested (caused by polydipsia [psychogenic]- could be caused by polyuria or could cause) >
Decreased extracellular fluid osmolarity >
Decreased ADH secretion (also caused by diabetes insipidus) >
Decreased nephron permeability and water reabsorption >
Solute reabsorption continues >
Increased urine dilution

Causes:
Primary polydipsia - psychogenic
Diabetes insipidus (central or nephrogenic)

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15
Q

The countercurrent principle (loop of Henle)

A

In the loop of Henle: job is to create a very diluted fluid

Ascending loop
Has transporters that move Na+ out of the tubule and into the kidney (medulla gets saturated/salty with Na+). Some salt goes back into descending tubule (recycles around)

Descending loop:
Water follows the solute and goes into the intestitium

Ascending loop:
Water flows through but can’t move out into interstitium because ascending loop is completely impermeable to water

Fluid becomes more dilute because water is being retained but Na+ is lowing out

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16
Q

The countercurrent principle (loop of Henle)

A

In the loop of Henle: job is to create a very diluted fluid**

Ascending loop
Has transporters that move Na+ out of the tubule and into the kidney (medulla gets saturated/salty with Na+). Some salt goes back into descending tubule (recycles around)

Descending loop:
Water follows the solute and goes into the intestitium

Ascending loop:
Water flows through but can’t move out into interstitium because ascending loop is completely impermeable to water

Fluid becomes more dilute because water is being retained but Na+ is lowing out

17
Q

Countercurrent mechanism continued: What happens after the loop of Henle?

A

The very dilute fluid from the loop of henle now passes through a VERY salty medulla

Moving through distal and collecting tubules

Water wants to move out into the medulla to make it less salty, but can’t unless ADH is present to make tubule more permeable

ADH opens the gates, water follows gradient and is reabsorbed, less water comes out in the urine

18
Q

Diabetic nephropathy

A
  1. Thickening of membrane affects filtration mechanism
  2. Arteriolosclerosis increases pressure, thickened walls, decreased lumen, decreased blood flow,
  3. Messangial and glomerular expansion, creating protein deposits (Kimmestiel Wilson nodules)
  4. Disruption of podocytes (cells in Bowman’s capsule that wrap around capillaries of glomerulus, ruining glomerulus, leading to renal failure)
19
Q

Diabetic nephropathy

A
  1. Thickening of membrane affects filtration mechanism
  2. Arteriolosclerosis increases pressure, thickened walls, decreased lumen, decreased blood flow, more filtration
  3. Messangial and glomerular expansion, creating protein deposits (Kimmestiel Wilson nodules)
  4. Disruption of podocytes due to Hyaline deposits (cells in Bowman’s capsule that wrap around capillaries of glomerulus responsible for letting filtrate in)
    ruining glomerulus, leading to renal failure)
20
Q

Diabetic nephropathy (characteristics)

A
  1. Thickening of capillary and tubular basement membrane affects filtration mechanism
  2. Vascular changes: Atherosclerosis, Arteriolosclerosis increases pressure, thickened walls, decreased lumen, decreased blood flow, more filtration, more urine
  3. Messangial and glomerular expansion, creating protein deposits (Kimmestiel Wilson nodules)
  4. Disruption of podocytes due to Hyaline deposits ruins glomerulus (cells in Bowman’s capsule that wrap around capillaries of glomerulus responsible for letting filtrate in)
    Leads to hypofiltration, leading to renal failure)

Initially, this causes glomerular hyperfiltration (may be associated with transient increase in GFR),
but ultimately this leads to formation of nodular and hyaline deposits and glomerulosclerosis with the glomerular ischemia.
Eventually leading to tubular atrophy and interstitial fibrosis, with overall loss of cortical mass and decrease in renal size with scarring.

21
Q

Solute diuresis in DM

A

Glucose is reabsorbed in the tubules, but if the mechanisms that reabsorb it become saturated, glucose will appear in the urine

High plasma glucose >
Increased glucose filtration >
Glucose remains in tubule >
Increased diuresis

22
Q

Diabetes insipidus

A

Clinical features based on loss of free water

  1. Polyuria/polydipsia
  2. Hypernatremia or high serum osmolality
  3. Low urine osmolality or specific gravity

Water deprivation test fails to increase urine osmolality

Central: Lack of ADH
Due to hypothalamic or posterior pituitary pathology (tumor, trauma, infection, inflammation) genetic causes, hypoxic encephalopathy, or pituitary surgery
Treatment is desmopressin (ADH analog)

Nephrogenic: Receptors that respond to ADH are not working
Due to drugs (lithium) or reduced renal response from inherited mutations
No response to desmopressin

23
Q

Diagnosis of polyuria

A

Diagnosis: (tests)

  1. Water restriction (not drink water for a while), monitor urine osmolarity and volume, plasma and urine, plasma and urine levels
  2. Administer hypertonic saline (raise osmolarity and see how kidneys respond), measure plasma ADH levels, consider diabetes mellitus
24
Q

Graph for normal (plasma osmolarity and urine volume/osmolarity)

A

Plasma osmolarity increases, urine osmolarity increases
Plasma osmolarity increases, urine volume decreases

As plasma osmolarity increases, water is reabsorbed (ADH is released), urine comes at higher concentration

Injecting patients with vasopressin (ADH) won’t change anything because they have already absorbed water and ADH levels are maximal

25
Q

Graph for primary polydipsia (plasma osmolarity and urine volume/osmolarity)

A

Similar to normal, but urine will be a little less concentrated (lower osmolarity) and a little higher in volume
Because drinking so much water (lots of water going in, lots going out)

26
Q

Graph for diabetes insipidis (plasma osmolarity and urine volume/osmolarity)

A

Nephrogenic:
Kidneys do not respond to ADH or vasopressin

Increase in plasma osmolarity, very low increase in urine osmolarity, because water is not being reabsorbed.

Increase in plasma osmolarity, very low decrease in urine volume because water is not being reabsorbed.

Central:
Similar as nephrogenic, but when ADH is added, you’ll see some response (urine osmolarity inc, urine volume decrease)

Diabetes (4 decks)

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