Fluid And Electrolyte Balance Flashcards
The main objectives of fluid and electrolyte balance are to maintain internal
- Fluid volume
- overall osmolarity levels of specific ions and
- pH.
All of these have consequences on the function of different organs or organ systems
What percent of body weight is water and males and females and what percent is where inside the body
50%/30 L of body weight in females, 60%/42 L in males are made up of water. Most inside the cells 66%, 26% in interstitial fluids and 7% in plasma
Maintaining proper levels follows the rules of mass balance
Intake and output are balanced
We lose water through
Sensible/perceived and insensible/unperceived sweat, feces, lungs through exhalation, and a nearly obligatory amount of 1.5 L per day in urine production. Of these urine volume is the only thing that is able to be regulated
In order to maintain proper water levels
We need to eat/drink the equivalent of about 2 L per day some 0.3 L per day is made through metabolic reactions examples cellular reaction and dehydration synthesis
We will break this chapter into four parts
- Water balance,
- sodium potassium and ECF,
- behavioral mechanisms,
- acid base balance
Ground rules (5)
- Enough fluid/blood must maintain positive GFR at all times without over hydrating
- Kidneys can only conserve water not create it the only input is through ingestion
- Movement of water can only occur through osmosis not active transport pumps
* 4. Permeability of water changes between the descending/increasing Permeability and ascending/ decreasing Permeability limbs of the nephron loop. - Osmolarity steadily increases from the cortical regions of the kidneys about 300 mOsm to the medullary region about 1200 mOsm, establishing a Gradient of Increasing osmolarity
Water is conserved through reabsorption from
The nephrons since anything inside the tubule is technically considered outside the body if it’s not pulled back and you lose it for effort
Recall that GFR is always
Positive pushing Isosmotic ~300mOsm of fluid into the tubules 
To conserve water the
DCT and collecting duct together called the distal nephron alter their permeability to water and amount of sodium that is reabsorbed
Thick regions of the ascending limb and distal nephron
Are normally more or less impermeable to water unless aqua Porins are present. Pores on the apical surface that allow water to enter the cells
Thin regions of the descending Limb are comparatively
Permeable to water the increasing osmolarity of the kidney medulla creates the necessary gradient to allow water reabsorption but only when it’s allowed
When water intake increases
Nephrons produce dilute urine (as low as 50 mOsm; hypoosmotic to ECF) by maintaining normal basal rates of sodium reabsorption and not reabsorbing as much water, more water is excreted. Basically it traps water in the tubule and doesn’t let it diffuse back in!
When water intake decreases
Nephrons need to produce urine that is more concentrated (up to 1200 mOsm hyperosmotic) than the surrounding ECF which is a bit more complicated process. The distal nephron needs to re-absorb water without also reabsorbing more sodium than it needs to. Remember water can only move through osmotic gradients. 
Vasopressin a.k.a. antidiuretic hormone ADH/ no Pee
Is a small nine amino acid peptide hormone produced by the posterior pituitary gland that modulate permeability of the distal nephron to water by instructing cells to insert aqua Porins Increasing Permeability. It’s effects graded an increase in vasopressin causes an increase of water reabsorption back into the body 
Vasopressin initiates a
GPCR cAMP second messenger pathway that causes exocytosis of intracellular vesicular aquaporins (AQP2) into cells apical surface
Stimuli for vasopressin Secretion
- High plasma osmolarity greater than 280 mOsm: this is the most potent signal, osmo receptor neurons in the hypothalamus shrink in response to hyper osmolarity of ECF causing them to fire.
- Low blood volume and blood pressure: less potent signal, barrow receptors in carotid artery and aorta detect low BV and BP levels increasing vasopressin secretion
Sodium balance an ECF volume are intertwined. In the proximal tubule
 water freely follows sodium reabsorption. However water and sodium are independently regulated in the distal nephron when sodium is reabsorbed vasopressin must be present (aqua Porin ) for water to follow
The main stimulus for vasopressin (water conservation) Secretion
Is high osmolarity where is the main stimuli for sodium reabsorption are low blood volume and blood pressure
Aldosterone is a
- Steroid hormone produced by the adrenal cortex that regulates sodium reabsorption and secondly potassium Secretion.
- by Increasing activity of the sodium potassium pump‘s in the distal nephron
- the specific target are the principal P cells located there
Aldosterone mechanism of action (4)
- After secretion aldosterone diffuses from blood into P cells in distal nephron
- The receptor ligand interaction acts on the nucleus to increase DNA transcription and synthesis of new sodium, potassium channels and sodium potassium pump‘s and proteins that act on existing ones
- Sodium and potassium channels on the apical side are stimulated to stay open longer, new channels/pumps are inserted, more sodium is a reabsorbed and from filtrate and more potassium is secreted to filtrate
- Sodium is pumped out and potassium is pumped and by the sodium potassium pump on the basal lateral side into/from ECF which then diffuses into the blood
Stimulation for aldosterone Secretion falls into
Direct or indirect categories
Direct stimuli for aldosterone secretion
3
- Increase in potassium concentration in the extracellular fluid most common of these and an extreme cases namely dehydration
- Increase osmolarity
- Decrease sodium concentration
* when these stimuli are detected they act directly on adrenal cells which secrete aldosterone
The indirect stimulus for aldosterone Secretion is
A decrease in blood pressure which initiates the renin-angiotensin system (RAS) also known as the renin angiotensin aldosterone system (RAAS) and there are three ways that it can be initiated through detection of low BP.
What are the three ways that the RAAS pathway (indirect) can be initiated through a decrease in BP
- Directly by granular cells in JGA’s afferent arterioles
- Indirectly by CVCC increases SNS output to stimulate granular cells
- Indirectly by macula densa cells in JGA through decrease filtrate flow, sons paragon signals that stimulate granular cells. Conversely during increase filtrate flow macular densa cells will inhibit granular cells
* However it happens when stimulated granular Cells will secrete the enzyme renin and that’s begin the RAS cascade
The RAS cascade
Increase in renin > plasma angiotensin is converted to angiotensin I > converted to angiotensin 2 (by angiotensin converting enzyme ACE)
-ANG2 effects increasing BP (6)
Angiotensin two has the following affects which act to increase blood pressure via the RAS cascade (6)
- Increase secretion of aldosterone > increases osmolarity> increases thirst [&vasopressin secretion?] > increases extracellular fluid/blood volume
- Increase the secretion of vasopressin> increases water reabsorbed in DCT
- Increase sodium reabsorption in PCT through increase sodium hydrogen exchanger activity >increase osmolarity
- Increase vasoconstriction
- Increase SNS output on CVCC >increase cardiac output
- Increased thirst
While sodium and water reabsorption are handled by aldosterone and RAS the opposite sodium secretion and water loss are regulated by
Natriuretic hormones, Primarily atrial Natriuretic hormone ANP, but also brain natriuretic hormones BNP. Which are peptide hormones released by atrial and ventricular cells respectively. 
* BNP is used in hospital ER is to diagnose difficulty in breathing due to heart failure opposed to other causes and help indicate sudden death from cardiac arrhythmia
The main stimulus for ANP secretion is
The stretching of the atrial walls which indicates an increase in blood pressure. ANP then initiate a GPCR CGMP second messenger pathway in target cells.
ANP GPCR CGMP second messenger pathway in target cells causes (4)
- Decrease sodium reabsorption in collecting ducts (direct effect)
- Increase sodium excretion (indirect effect) by suppressing secretion of vasopressin, renin, and aldosterone
- Vasodilation of afferent arterial >increases GFR> increases water excretion and decreases plasma volume.
- Alter CVCC effects in medulla to decrease blood pressure
