Renal - Conc/dilution

Front 1

Explain the osmotic control of ADH secretion in a state of increased plasma osmolality

Back 1

increased plasma osmolality
|
osmoreceptor (hypothalamus)
|
magnocellular neuron (supraoptic and paraventricular nuclei)
|
ADH secretion
|
water reabsorption by kidney
|
decreased plasma osmolality

Hint 1

pg 34

Front 2

Explain the volume and pressure control of ADH secretion.

-type and location of baroreceptors

Back 2

--some baroreceptors are located in low pressure areas (volume areas, cardiac atria and pulmonary vessels)
--some baroreceptors are located in high pressure areas (aortic arch and carotid sinus)

Hint 2

pg 35

Front 3

Explain the volume and pressure control of ADH secretion.

-signal and response

Back 3

Baroreceptor signal is relayed via CN IX and X to the medulla of the brain.

Baroreceptor responds to stretch by depolarizing (firing) --> inhibition of ADH secretion

A drop in filling pressure causes the nerves to stop firing --> ADH secretion is no longer tonically inhibited

Hint 3

pg 35

Front 4

Action of ADH on the kidney

-action, mechanism, consequence (2)

Back 4

1. Increase NaCl reabsorption by the thick ascending limb of Henle by stimulating the Na/K/2Cl transporter --> enhances the medullary interstitial osmotic gradient

2. Increases the permeability of the collecting duct to H2O and urea via synthesis of aquaporin 2 and insertion into the apical membrane --> increases the concentration of the urine as water flows from the lumen into the medulla down its gradient

Hint 4

pg 37

Front 5

Components of countercurrent multiplier

-anatomy and function (3)

Back 5

1. Descending loop of Henle -- high H2O permeability, low solute permeability

2. Thick ascending loop of henle -- water impermeable, actively resorbs solute

3. Medullary interstitium -- solute removed from TALH accumulates and raises interstitial osmolality

Hint 5

pg 38

Front 6

Urinary concentration/dilution

--requirements for excretion of hypo/hyperosmotic urine (3)

Back 6

1. Normal GFR and proximal tubule function

2. Functional thick ascending limb of henle

3. Absence/presence of ADH

Hint 6

pg 43/44

Front 7

Disorders of urinary concentration

--signs and symptoms (5)

Back 7

1. Polyuria
2. Polydypsia

--if H20 is unavailable and cant replace fluid loss from (1)
3. Confusion
4. Coma

If H20 loss is severe enough or accompanied by Na loss
5. Low BP, increase HR (signs of ECF volume depletion)

Hint 7

pg 49

Front 8

Disorders of urinary concentration

--causes (4)

Back 8

1. Decreased proximal tubular fluid reabsorption -- osmotic diuresis
2. Impaired TALH solute reabsorption -- inhibition of Na/K/2Cl symporter (diuretics); damage to TALH
3. Decreased medullary interstitial gradient
4. ADH derangments -- lack of ADH secretion, tubular unresponsiveness

Hint 8

pg 49

Front 9

Disorders of urinary concentration

--ADH derangements (2)

Back 9

1. Central diabetes insipidus -- lack of ADH secretion

2. Nephrogenic diabetes insipidus -- tubular unresponsiveness to ADH

-hereditary (abnormal structure of V2 receptor or aquaporin-2)
-acquired (high Ca, low K --> abnormal # of aquaporin-2)

Hint 9

pg 49

Front 10

Body fluid hyperosmolality

--causes (4)

Back 10

1. Thirst deficiency -- rare
2. Inability to obtain H2O -- most common
3. Intake of hypertonic salt without H2O
4. ADH derangements with inadequate H2O intake

Hint 10

pg 49

Front 11

Disorders of urinary dilution

--symptoms (4)

Back 11

Signs and symptoms of true hypoosmolality result from brain cell edema.

1. Headache, nausea, vomiting
2. Confusion, muscle cramps
3. Focal neurologic signs; seizures, coma
4. Death

Hint 11

pg 50

Front 12

Disorders of urinary dilution

--causes (4)

Back 12

1. Decreased GFR -- renal failure; low CO
2. Increased proximal tubular reabsorption -- profound heart fail; liver fail
3. Impaired TALH solute reabsorption -- inhibition of Na/K/2Cl symporter (loop diuretics); glucocorticoid or mineralcorticoid deficiencies; inhibition of NaCl transporter in cortex
4. Increased H2O permeability of collecting duct -- excess or inappropiate ADH levels

Hint 12

pg 50

Front 13

Body fluid hypoosmolality (hyponatremia)

--causes(7)

Back 13

1. H2O intake in excess of kidney's ability to excrete H2O
2. Pure H2O intake with salt and H2O losses
3. Abnormal osmoreceptor function
4. Stimulation of baroreceptors in induce ADH secretion despite hypoosmolality
5. Insensitivity of baroreceptors to volume/pressure stimuli
6. ADH secretion despite hypoosmolality -- hypoxia, hypercapnia, pain...
7. Enhanced ADH action on collecting duct -- drugs

Hint 13

pg 50

Front 14

Hyponatremia with decreased ECV

-causes (5)

Back 14

*relative excess TBW w/total body deficit of Na

1. hemorrhage
2. burns
3. GI loss
4. diuretics
5. adrenal insufficiency

Hint 14

pg 51

Front 15

Components of countercurrent multiplier

-anatomy and function (3)

Back 15

1. Descending loop of Henle -- high H2O permeability, low solute permeability

2. Thick ascending loop of henle -- water impermeable, actively resorbs solute

3. Medullary interstitium -- solute removed from TALH accumulates and raises interstitial osmolality

Hint 15

pg 38

Front 16

Urinary concentration/dilution

--requirements for excretion of hypo/hyperosmotic urine (3)

Back 16

1. Normal GFR and proximal tubule function

2. Functional thick ascending limb of henle

3. Absence/presence of ADH

Hint 16

pg 43/44

Front 17

Disorders of urinary concentration

--signs and symptoms (5)

Back 17

1. Polyuria
2. Polydypsia

--if H20 is unavailable and cant replace fluid loss from (1)
3. Confusion
4. Coma

If H20 loss is severe enough or accompanied by Na loss
5. Low BP, increase HR (signs of ECF volume depletion)

Hint 17

pg 49

Front 18

Disorders of urinary concentration

--causes (4)

Back 18

1. Decreased proximal tubular fluid reabsorption -- osmotic diuresis
2. Impaired TALH solute reabsorption -- inhibition of Na/K/2Cl symporter (diuretics); damage to TALH
3. Decreased medullary interstitial gradient
4. ADH derangments -- lack of ADH secretion, tubular unresponsiveness

Hint 18

pg 49

Front 19

Disorders of urinary concentration

--ADH derangements (2)

Back 19

1. Central diabetes insipidus -- lack of ADH secretion

2. Nephrogenic diabetes insipidus -- tubular unresponsiveness to ADH

-hereditary (abnormal structure of V2 receptor or aquaporin-2)
-acquired (high Ca, low K --> abnormal # of aquaporin-2)

Hint 19

pg 49

Front 20

Hyponatremia with normal ECV

-causes (3)

Back 20

*relative excess TBW w/normal total body Na content

1. Hypoxia
2. Hypercapnia
3. SIADH

Hint 20

pg 51

Front 21

Hyponatremia with high ECV

-causes (4)

Back 21

*relative excess TBW w/total body Na excess

1. Heart failure
2. Liver failure
3. Renal failure
4. Nephrotic syndrome

Hint 21

pg 51

Front 22

Hypernatremia with low ECV (most common presentation)

-causes (3)

Back 22

*relative deficit in TBW

1. GI losses
2. diabetic osmotic diuresis with coma
3. inability to gain access to H2O or food

Hint 22

pg 52

Front 23

Hypernatremia with high ECV

-causes (2)

Back 23

*relative deficit in TBW

1. Na-bicarb injection during CPR
2. hypertonic breast milk or formula

Hint 23

pg 52