Chapter 5: Renal and Acid-Base Physiology Flashcards
Total Body Water (TBW)
60% of body weight
High in newborns and adult males.
ICF
2/3 of TBW
Mg++ and K+ are major cations
Anions are Protein and Organic Phosphates
ECF
1/3 of TBW
Interstitial Fluid (3/4 of ECF) and PLasma (1/4 of ECF).. Ultrafiltrate of Plasma with little protein.
Cation: Na+
Anion: Cl- and HCO3-
TBW marker
H30, D2O and Atnipyrene
( distributes throughout body compartments)
ECF Marker
Mannitol, Inulin and Sulfate
goes into plasma and interstitial fluid
Plasma Marker
Evans blue, RISA
(binds albumin and cannot leave plasma fluid)
Equation for Volume
Volume = g/(g/ml) aka grams/Conentration
How can you calculate Interstitial Fluid ?
Interstitial = ECF (Mannitol, Innulin or sulphate) - Plasma (Evans Blue and Risa
How can you calculate Intracellular Fluid (ICF)
TBW (H30, D20) - ECF (Mannitol, Innulin)
What happens to ICF and ECF when you add an Isotonic fluid to a system ?
ECF will expand with no change in the osmolarity
ISOOSMOTIC VOLUME EXPANSION
Decreased hematocrit
What kind of fluid is lost in diarrhea ?
Isotonic Fluid
Leads to a decrease in the ECF only (Osmolarity is unchanged )
Increased Hematocrit
Hyperosmotic Fluid Expansion (Intake of excessive NaCL soulution)
Fluid will move from the ICF into the ECF expanding the ECF and decreasing the ICF
Hematocrit will decrease due to expanded ECF
Osmolarity of Both will be increased
Hyperosmotic Fluid Loss (sweating excessively)
ICF and ECF will become smaller (initially ECF then ICF )
Osmolarity of both will Increased.
Hematocrit does not increase despite ECF Fluid loss because fluid volume is lost from inside the RBC’s as well.
Hypoosmotic Fluid Expansion (SIADH)
Both the ECF and ICF will increase
Osmolarity Decreases
Hematocrit is unchanged since more water will go into the RBC’s expanding them.
Hypoosmotic Volume Contraction (Loss of NaCL. Adrenocortical insufficiency)
ECF osmolarity decreases leading to fluid shift into the ICF
ICF expands while ECF contracts
Osmolarity of Both Decreases
Hematocrit will increase due to loss of H20 from the ECF
Clearance
The amount of blood that can be cleared of solute per unit time ( mL/min)
C= UV/P
U= Urine Concentration (mg/mL) V= Urine Volume TIme (ml/min) P= Plasma Concentration (mg/mL)
Renal Blood Flow (25% of CO) Is directly proportional to …
The difference in pressure between Renal Artery and Renal Vein
Inversely proportional to Renal Resistance
What leads to Renal Arteriole vasoconstriction and decreased RBF ?
Sympathetic NS Angiotensin II (Dilates the EFFERENT arteriole leading to Increased GFR)
What leads to vasodilation of renal arterioles ?
Prostaglandins E2, I2 , Bradykinin, NO and DOPAMINE.
–> Increased Renal Blood Flow
What is the range of Renal blood pressures that renal blood flood is held constant due to Autoregulation ?
80-200 mmHg
Autoregulation: Myogenic Mechanism and Tubuloglomerular feedback
Tubuloglomerular feedback
Increased RBF leads to increased fluid being brought to the macula densa. Macula densa senses this and cause constriction of the AFFERENT arteriole to lower GFR and maintain proper blood flow.
Renal Plasma Flow
Amount of plasma that come through the kidney (measured by the clearance of PAH , a substance that is filtered and secreted only)
RPF = C(PAH) = UV/ P
U= Urine Concentration of PAH V= Urine Flow Rate P= Plasma Concentration of PAH
Renal Blood Flow
Amount of blood to come through the kidney over a set time
RBF = RPF/ (1-hematocrit)
1- hematocrit = Proportion of plasma in blood.
GFR
Calculated by clearance of INULIN ( Filtered not secreted or reabsorbed)
GFR = UV/P
U=Urine Concentration of Inulin
V= Urine flow Rate
P = plasma concentration of Inulin
What is the relationship between Decreasing GFR and BUN ?
BUN increases as GFR decreases
Pre-reanal azotemia
BUN:Creatinine of >20:1
Post renal : > 15
Primar Azotemia : <15
Filtration Fraction
Fraction of RPF that is filtered
FF = GFR/ RPF
Normally .2 !
Increased Filtration Fraction
Lead to increased [protein] of peritubular capillary blood –> Increased reabsorption in proximal tubule
Opposite is true of Decreased FF
Starling Forces For GFR
GFR = Kf ( Pc + Oi) - (Pi + Oc)
Glomerular Capilllary Hyrodstatic Pressure
Increased by dilation of Afferent or Constriction of Efferent .. Increasing this leads to increased GFR (all others held same)
Glomerular Capillary Oncotic Pressure
Increases along the capillary ( primary driving force is plasma proteins)
Increases in this decreases GFR and net filtration pressure
Bomans space Oncotic pressure
Essentially is zero
Bowmans Space Hydrostatic pressure
resists filtration, increases in this pressure leads to decreased GFR
Filtered Load
GFR x [Plasma] (g/min)
Excretion Rate
=Urine Flow (V) x [U]
Reabsorption Rate
FIltered Load - Excretion Rate
Less in blood than was filtered)
Secretion Rate
Excretion Rate - Filtered Load (More in urine than was filtered)
What is responsible for Glucose reabsorption in the proximal tubule
Na/Glucose co transport.
If plasma glucose is over 350 , you will see glucose in the blood (less than 250 all glucose is reabsorbed)
Splay is in between
Note: in the early proximal tubule, nearly all Glucose, HCO3 and Amino acids have been reabsorbed
What has higher clearance : A substance that is filtered and secreted or a Substance that is filtered ?
Filtered and secreted
In which conditions will The HA form of a weak acid be more prevalent than the A- form ?
At acidic pH
No reason to lose H+ to the solution
If it were basic solution, the A- would predominate since it would be easier to donate H+
In which conditions will The BH+ form of a weak base be more prevalent than the B form ?
In acidic environments. More readily accepts the B
Where is Reabsorption of Na+ the greatest along the nephron ?
Proximal Tubule
Reabsorbs 2/3’s of the filtered Na and H20
Done in Isoosmotic fashion so that reabsorption of Na is proportional to reabsorption of water.
What drives the Reabsorption of Na in the early prox tubule ?
Na/K+ pump on the basolateral side ** (sodium into the blood, K+ into the cell)
On the lumina side : Na/Glucose symport and Na+/H+ anti port
Note: Na/H+ antiport is due to activity of Carbonic ANhydrase. Carbonic Anhydrase inhibitors work as diuretics by blocking this (Acetozolamide, give this for Altitude sickness also to treat Respiratory Alkalosis)
How is Na+ reabsorbed in the Late Proximal Tubule ?
With Cl- ( Na/Cl- Symport)
How does ECF volume contraction affect tubular reabsorption ?
Increases it since ECF (Plasma and Interstitial fluid) decreases lead to increased plasma protein concentration and great Capillar oncotic pressures.
Opposite is true of ECF Expansion
How much of Na+ is reabsorbed in the Thick Ascending Loop of Henle ?
25% of filtered
NCCK Transporter
What diuretic class works on he NCCK transporter /
Loop Diuretics
What is different about the TALH and the Proximal tubule ?
Unlike in the Proximal Tubule, the TALH is impermeable to H20, so when The NCCK reabsorb ions, H20 cannot follow leading to a dilution of the Tubule osmolarity (
How much of Na+ is reabsorbed in the Distal Convoluted Tubule and Collecting duct ?
8%
Like in the Late Proximal Tubule, how is Na+ reabsorbed in the Early Distal Convoluted Tubule ?
with Cl- (Na/Cl- Symport
What diuretics work on the Na/Cl- Symport in the Early Distal Convoluted tubule ?
Thiazide Diuretics
Is the Early Distal Tubule permeable to H20 ?
NOPE (Just like the TALH)
What are the two types of cells important to ion regulation found in the Late Distal Convoluted Tubule/Collecting Ducts ?
Principal Cells
a-Interaclated cells
Pricinple Cells
Reabsorb Na+ and H20 , Secrete K+
Aldosterone mediates the function of Principle Cells !!!!! (Increases Na+ reabs and K+ secretion)… ENAC channels are placed on the lumenal side of Principal Cells and allow for the Movement of Na+ into the cell. Aldosterone also stimulates the activation of Na/K pump
Gradient is maintained by Basolateral Na/K+ Pump ( Na into blood, K+ into cell –> increased K+ which leave cell via lumenal K+ channel into urine)
Effect of Acidosis on K+ secretion
Acidosis leads to decreased K+ secretion
(H+ enters principal cell, this somehow causes K+ to leave the cell on basolateral side
H+/K+ anti-port ?