Water Balance Pt 3 | Physiology 2 Final

What are the two types of edema

• intracellular edema

• extracellular edema

What are the four common causes of intracellular edema

• hyponatremia (low Na levels in plasma; ECF)

• depression of metabolic systems of cells

• reduced nutrition of cells (ischemia)

• inflammation (inc membrane permeability)

What are the three common causes of extracellular edema

• abnormal leakage of fluid from plasma to interstitial spaces

• failure of lymphatic vessels to return fluid from tissues back into blood

What are the two action mechanisms of diurectics

1. inhibition of NaCl reabsorption

2. promoting water excretion

What is the function of carbonic anhydrase inhibitors as diuretics

carbonic anhydrase blocks Na/HCO3 reabsorption in PCT (lowering NaCl reabsorption → lowers H2O reabsorption → ECF volume)

What is the function of loop diuretics

loop diuretics block NKCC symport in TAL (lowering NaCl reabsorption → lowers H2O reabsorption → ECF volume)

What is the function of Thiazide diuretics

thiazide diuretics block Na/Cl symport in DCT (lowering NaCl reabsorption → lowers H2O reabsorption → ECF volume)

What is the function of aldoesterone antagonists

block aldoesterone which indirectly blocks Na channels to reabsorb in CD (lowering NaCl reabsorption → lowers H2O reabsorption → ECF volume)

What is the function of amiloride

block Na channels (ENaC) in CD (lowering NaCl reabsorption → lowers H2O reabsorption → ECF volume)

What is the function of aldosterone antagonists

block aldosterone receptor disabling ENaC at apical membrane of CD (lowering NaCl reabsorption → lowers H2O reabsorption → ECF volume)

What is the overall effect of diuretics in NaCl reabsorption and concentrations produced by the kidney

NaCl reabsorption dec (NaCl secretion) → H2O reabsorption dec (water secretion) → ECF volume dec → urine conc dec → dilution of tubular fluid

How does loop diuretics inhibit NKCC receptors in TAL

interfere w tubulo-glomerular feedback mechanism causing low Na reabsorption but high GFR favoring diuresis

What is diuresis

inc production of urine

What are the side effects of loop diuretics

• dec the lumen-positive transepithelial potential at TAL

  (→ negatively impacting interstitium reabsorption of Ca+ and Mg+)

• inc reabsorption of Na+ that arrives at CD at the expense of K+ secretion (hypokalemia)

What one of the side effects of loop diuretics is to decrease the lumen-positive transepithelial potential at TAL, what does this cause with other ions

Cl- is blocked by loop diuretics’ effect on NKCC channel preventing electron gradient → negatively impacting interstitium reabsorption of Ca+ and Mg+

What are the side effects of thiazide

inc reabsorption of Na+ that arrives at CD at the expense of K+ secretion (hypokalemia)

What are the side effects of thiazide and loop diurectics

inc reabsorption of Na+ that arrives at CD at the expense of K+ secretion (hypokalemia)

What drug would you use to counteract increased Na reabsorption preventing hypokalemia in CD from loop diuretics and thiazides

Potassium-sparing diuretics:

• amiloride

• aldosterone antagonists

What is the function of amiloride diuretics and aldosterone antagonists

blocks Na+ reabsorption in CD preventing hypokalemia (K+ excretion)

What diuretic prevents hypokalemia and what channel does it block

potassium-sparring diurectic that blocks ENaC (Na channels)

What is diabetes insipidus

large amount of dilute urine is excreted (low water reabsorption)

What are the two forms of diabetes insipidus

• diabetes insipidus centralis

• diabetes insipidus renalis

What are the three causes of diabetes insipidus centralis

• tumors

• hypothalamus/hypophysis damage

• genetic

What characterizes the cause of diabetes insipidus centralis

caused by lack of ADH synthesis in anterior hypothalamus and release from posterior pituitary gland

What characterizes the cause of diabetes insipidus renalis (nephrogenic)

ADH is produced but cannot act in the kidneys

What are the three causes of diabetes insipidus renalis (nephrogenic)

• kidney disease

• toxins

• genetic

What are the CS of diabetes insipidus

PU, PD, nocturia (waking up to urinate in the night)

What is an useful indicator of renal concentration ability

specific gravity of urine

In specific gravity of urine, what is the measurement of light refraction index

amount of refraction = amount of solutes in urine

What presence determines specific gravity of urine

type of solutes (i.e. glucose)

What presence determines osmolality of urine

osmolality depends on amount of active particles (regardless of size)

True or false: SG and osmolality correlate

true

True or false: SG and refraction of urine do not correlate

false; SG and refraction of urine correlate

How can you calculate osmolality of urine in dogs

using SG (multiplied by 36)

What is the purpose of water deprivation test

used to identify whether ADH is produced or not (centralis/renalis differentiation test)

What are three things you must perform before water deprivation test

1. patient should not be dehydrated and/or azotemic (excess nitrogenous product in plasma)

2. no UTI (as they are contradictory)

3. weigh animal

What is the protocol for water deprivation test

1. partial water restriction for 2-3 days prior to test

2. day 4 water deprivation then test begins

3. catheterization to collect urine for SG measurement

4. collect urine every 1-2 hours measuring SG

5. weigh animal before and after test

What results from water deprivation test indicate patient with concentration deficiency

SG of urine would be lower over time of water deprivation

What results from carter-robbins-test indicates patient with centralis

if SG increases after ADH administration (responding to ADH), patient has diabetes insipidus centralis

What results from carter-robbins-test indicates patient with renalis

if SG remains the same after ADH administration (not responding to ADH), patients has diabetes insipidus renalis

With osmoregulation, an increase in osmolality of ECF causes what

outflow of water from cell space to extracellular space → cell shrinkage

With osmoregulation, a decrease of osmolality of ECF (causing a higher solute concentration in cell) causes what

inflow of water to cell → cell swelling

In osmoregulation, when the ECF osmolality is low due to decreased solutes what occurs with water

water flows into the cell (concentration gradient) causing cell swelling

What are two types of water losses and their meaning

• insensible water loss - water loss that cannot be regulated

• sensible water loss - water volume that can be measured

What are types of insensible water losses

1. exhaled air (evaporation)

2. diffusion from skin (not sweating)

What are types of sensible water loss

1. urine

2. sweat

3. water loss with feces

What does cytolysis refer to

hypotonic solution that causes cell to swell to a point of rupture of plasma membrane

What does crenation/plasmolysis refer to

hypertonic solution causing a cell to shrink

What is the most common form of dehydration of the cell

hypertonic dehydration of the cell

What is hypertonic dehydration

water loss exceeds electrolyte loss leading to increased osmolality of ECF → water leaves the cell (cell shrinkage)

What is hypotonic dehydration

loss of electrolytes exceeds loss of water causing decreased osmolality of ECF

What is isotonic dehydration

water loss equals electrolyte loss → no change in ECF osmolality but hypovolemia

What is hypertonic overhydration

gain of electrolytes exceeds gain of water → increased osmolality of ECF

What is isotonic overhydration

gain of isotonic fluid → hypervolemia; osmolality unchanged

What is hypotonic overhydration

gain of water; electrolytes unchanged → decreased ECF osmolality

What is a common veterianian error from isotonic fluids (and what does it cause)

isotonic overhydration from fluid administration → elevated Na+ reabsorption in renal tubules

Where does fluid loss occur: ECF or ICF

ECF

Why does osmolality in ECF increase from hemorrhage or hyperventilation

fluids being lost causes ions to be more concentrated in ECF

Vomiting and diarrhea are examples of what type of dehydration or overhydration

isotonic/hypotonic dehydration (bec ions and fluid is being lost; ions more concentrated in ICF fluid shift causing dec conc in ECF)

hyperventilation and osmotic diurresis and diabetes insipidus are examples of what type of dehydration or overhydration

hypertonic dehydration = inc ECF

hemorrhage and burns are examples of what type of dehydration or overhydration

isotonic dehydration = hypovalemia

What are the three thirst stimuli that causes an increase in ADH

1. ECF volume decrease (from pathological cause of fluid loss i.e. vomiting, diarrhea)

2. increased osmolality of ECF (salt excess or water deficit - hypertonic)

3. hormones - angiotensin II

Where is the thirst center located

anterior hypothalamus

As the thirst stimulus is activated by decreased ECF volume from pathological fluid loss, what is the pathway of ADH release

1. ECF volume decreased by vomiting, diarrhea

2. stimulation of peripheral pressure and volume sensors

3. activation of Nucleus Tractus Solitarii

4. activation of central angiotensin II

5. (CA2) → stimulates subfomical organ (SFO) and organum vasculosum laminae terminalis (OVLT)

6. → stimulates nucleus paraventricund supraopticus

7. release of ADH

As the thirst stimulus is activated by increased osmolality of ECF from salt excess or water deficiency, what is the pathway of ADH release

1. increase osmolality of ECF

2. activation of centrale osmosensors

3. activation of central angiotensin II

4. (CA2) → stimulates subfomical organ (SFO) and organum vasculosum laminae terminalis (OVLT)

5. → stimulates nucleus paraventricund supraopticus

6. release of ADH

As the thirst stimulus is activated by hormones such as angiotensin II, what is the pathway of ADH release

1. hormones act as thirst stimuli

2. activates subfomical organ (SFO)

3. → stimulates nucleus paraventricund supraopticus

4. release of ADH