Renal Physiology Part 1 Flashcards
Distribution of fluids within the body
- ICF: approximately 2/3 of total body water
- ECF: approximately 1/3 of total body water
- Interstitial fluid: approximately 3/4 of ECF
- Plasma Volume: approximately 1/4 of ECF
Extracellular Fluid
-plasma and interstitial fluid
Plasma broken down into
- venous compartment
- arterial compartment (effective circulating volume)
Vascular compartment
-contains blood volume which is plasma and cellular elements of blood, primarily RBCs
Effective circulating volume (ECV)
-the volume of arterial blood effectively perfusing thetissue
Transcellular fluid
- also included in ECF
- normally contains only a small amount of water such as epithelial secretions, synovial, CSF, etc
- said to occupy a “third space”
Components of ECF
-sodium, chloride, bicarbonate
Components of ICF
-potassium, magnesium, phosphate, and organic anions, proteins
Cell membrane between ECF and ICF is
- highly water-permeable
- not permeable to most electrolytes
- fluid distribution between 2 compartments is dependent on osmotic effects of Na
Capillary cell membrane
- between ECF compartments is highly permeable to small ions
- fluid distribution is due to balance between capillary hydrostatic pressure and colloid osmotic pressure
Maintenance of body fluid balance is regulated by 2 factors which over NaCl and water balance
-ECF volume and ECF osmolarity
Distribution of fluid between ECF and ICF compartments is determined primarily by:
- ion distribution (Na)
- ATPase activity
Distribution of ECF between plasma (vascular space) and interstitial (tissue) compartments is determined by
- balance of hydrostatic vs. oncotic pressures
- intravascular pressure in capillaries vs. plasma protein and solute concentration
Edema
- palpable swelling produced by expansion of interstitial fluid volume caused by:
- alteration in capillary hemodynamics (altered starling forces with increased net filtration pressure)–fluid moves from vascular space into interstitium due to decreased capillary oncotic pressure
- renal retention of dietary Na+ and water–expansion of ECF volume
Altered Starling foces role
- edema does not become apparent until interstitial volume is increased by 2.5-3L
- normal plasma volume is only 3L
- therefore, edema fluid is not derived from only plsma
- compensatory renal retention of Na+ and water to maintain plasma volume in response to underling of the vasculature must occur in this situation to cause edema
- this renal compensation is appropriate to restore tissue perfusion although it exacerbates edema (e.g. congestive heart failure)
Forces for filtration
-hydrostatic pressure and oncotic pressure
Hydrostatic pressure (blood pressure) in the capillary (Pc)
-directly related to blood flow; venous pressure; blood volume
Oncotic (osmotic) force in the interstitium
- determined by concentration of protein in the interstitial fluid
- normally the small amount of protein that leaks to the interstitium is minor and is removed by lymphatics
- thus, under most conditions this is not an important factor influencing the exchange of fluids
Forces for absorption
-oncotic pressure of plasma and hydrostatic pressure in interstitium
onctotic (osmotic) pressure of plasma
- the oncotic pressure of plasma solutes that cannot diffuse across the capillary membrane; i.e., the plasma proteins
- albumin is the most abundant plasma protein and biggest contributor to this force
Hydrostatic pressure in the interstitium
- in most cases close to zero and is not a signficant factor affecting filtration versus reabsorption
- can become significant if edema is present or it can affect glomerular filtration in the kidney (pressure in Bowman’s space is analogous to interstitial pressure)
Renal retention of Na+ and water
- results in overfilling of the vascular tree
- inappropriate renal fluid retention
- usually results in elevated blood pressure, expanded plsma and interstitial volumes
- E.g. primary renal disease (glomerulonephritis, nephrotic syndrome)
Non-pitting edema
-swollen cells due to increased ICF volume–does NOT respond to diuretics
Pitting edema
- increased interstitial fluid volume
- nephrotic syndrome, CHF, pregnancy, cirrhosis
- does respond to diuretics
Primary causes of peripheral edema
- increased capillary hydrostatic pressure
- increased interstitial oncotic pressure
- decreased vasscular oncotic pressure
- increased capillary permeability (k)
- lymphatic obstruction/removal (lymphedema)
Increased capillary hydrostatic pressure (Pc)
- marked increase in blood flow, e.g., vasodilation in a given vascular bed
- increased venous pressure, e.g., venous obstruction or heart failure
- elevated blood volume (typically the result of Na+ retention), e.g., heart failure
Increased interstitial oncotic pressure
primary cause is thyroid dysfunction (elevated mucopolysaccharides in interstitium)
- act as osmotic agents resulting in fluid accumulation and a non-pitting edema
- lymphedema can also increase this
Decreased vascular oncotic pressure
- liver failure
- nephrotic syndrome
Increased capillary permeability
-circulating agents, e.g., tumor necrosis factor alpha, bradykinin, histamine, cytokines related to burn trauma, etc., increase fluid filtration resulting in edema
Lymphatic obstruction/removal (lymphedema)
- filarial
- bacterial lymphangitis
- trauma
- surgery
- tumor
When there is a net gain of fluid by the body
- ECF volume always enlarges
- a net loss of body fluid decreases ECF volume
Intracellular volume is only altered if
extracellular osmolality changes
If ECF osmolality increases
cells lose water and shrink
If ECF osmolality decreases
cells gain water and swell
Renal microcirculation
- 2 sets of arterioles, 2 sets of capillaries in series
- first capillary network (glomerular capillaries)
- second capillary network (peritubular capillaries)
Glomerular capillaries
-high hydrostatic pressure; large fluid volume filtered into Bowman’s capsule
Peritubular capillaries
-low hydrostatic presuure; large amounts of water and solute are reabsorbed
Renal sympathetic innervation
-sympathetic neurons synapse on smooth muscle (causing arteriolar constriction) and granular cells (causing renin secretion) in afferent arterioles
Sensory fibers from bladder wall and posterior urethra are activated by
stretch
Parasympathetic fibers from sacral micturition center
- S2-S4 (pelvic nerve)
- stimulate detrusor muscle, inhibits contraction of internal urethral sphincter
Sympathetic fibers
- hypogastric nerve
- inhibits detrusor constriction; constricts INTERNAL urethral sphincter
Somatic motor neurons
- voluntary; pudendal nerve
- constrict external urethral sphincter
Glomerular membrane
- free passage of water, small solutes (glucose, amino acids, electrolytes): concentration are the same on both sides of membrane
- passage of large molecules (proteins) are formed elements is impeded
- normally, only very small amounts of protein are filtered into Bowman’s capsule
Structure of glomerular membrane
- 3 distinct layers
- fenestrated capillary endothelium: highly permeable to water, dissolved solutes
- glomerular basement membrane: collagen, proteoglycans contain anionic negative charges
- podocyte epithelium: slit pores between podocytes restrict large molecules
Physical forces affecting glomerular filtration
- GFR is remarkably high
- GFR is product of 3 physical factors
1. hydraulic conductivity (Lp) of glomerular membrane
2. surface area for filtration (product of 1 and 2 is ultrafiltration coefficient Kf)
3. capillary ultrafiltration pressure (Puf) - GFR=Kf x Puf
A primary glomerular disease may
-lower GFR by decreasing the surface area available for filtration due to damage to glomerular membrane
Ultrafiltration pressure (Puf)
- driving force for glomerular filtration
- determined by hydrostatic and colloid osmotic pressures in glomerular capillaries, Bowman’s capsule
- Puf=Pgc-(Pbc + oncotic pressure in glomerular capillaries)
- the difference of 3 pressures–>net filtration pressure
Net filtration pressure
glomerular hydrostatic pressure- (bowman’s capsule pressure- glomerular oncotic pressure)
Mechanisms for altering GFR
- altered Kf: mesangial cell contraction–shortens capillary loops, lowers Kf and thus lowers GFR
- altered Puf changes in Pgc
Pgc determined by 3 factors
renal arterial blood pressure
afferent arteriolar resistance
efferent arteriolar resistance
