Renal and Acid-Base Physiology Flashcards
2/3 of TBW
intracellular fluid
K, Mg, protein and organic phosphates
1/3 of TBW
extracellular fluid
1/4 is plasma
3/4 is interstitial fluid
Marker for TBW
tritiated H2O, D2O
Marker for ECF
Sulfate, inulin, mannitol
Marker for Plasma
Radioiodinated serum albumin (RISA), Evans Blue
Interstitial Fluid marker
measured indirectly
ECF-plasma volume
Marker for ICF
measured indirectly
TBW-ECF
Infusion of isotonic NaCl - addition of isotonic fluid
isosmotic volume expansion
ECF volume increases but no change in osmolarity
Diarrhea - loss of isotonic fluid
isosmotic volume contraction
ECF volume decreases no change in osmolaritiy
Excessive NaCl intake - addition of NaCl
Hyperosmotic volume expansion
osmolarity of ECF increases and water shifts from ICF to ECF
ICF osmolarity increases until it equals that of ECF
sweating, fever, diabetes insipidus
hyperosmotic volume contraction
decrease in ECF, ICF volume and increase ECF osmolarity
SIADH
hyposmotic volume expansion
increase in ECF & ICF volume and decrease in ECF osmolarity
Adrenal Insufficiency
hyposomotic volume contraction
decrease in ECF volume, increase in ICF volume, ECF osmolarity is decreased
Clearance Equation
CL = (UV)/P
U is urine conc
V is urine vol/time
P is plasma conc
Vasoconstriction of renal arterioles on RBF
RBF will decrease
Low conc of Ang II
preferentially constricts efferent arterioles and increase GFR
ACE-inhibitors on GFR
dilate efferent arterioles thus decreasing GFR
Vasodilation of renal arterioles on RBF
increase in RBF, is produced by PGE2 and PGI2, bradykinin, NO and dopamine
Macula Densa
increases renal artery pressure leads to increased delivery of fluid to macula densa
increased load causes constriction of nearby afferent arteriole, increasing resistance to maintain constant blood flow
Measurement of renal plasma flow
clearance of PAH, it is filtered and secreted by renal tubules
RPF equation
Cpah = (Upah*V)/Ppah
Measurement of RBF
RBF = RPF/(1-Hb)
Measurement of GFR
clearance of inulin
Cin = (Uin*V)/Pin
BUN and serum [creatinine] increase
when GFR decreases
Filtration Fraction
FF = GFR/RPF
normal is ~0.20
increases in FF causes
increase in protein conc of peritubular capillary blood
increased reabsorption in proximal tubule
decreases in FF causes
decreases in protein conc of peritubular capillary blood
decreased reabsorption in proximal tubule
GFR Starling eqtn
GFR = Kf[(Pgc-Pbs)-(OSMgc-OSMbs)
Constriction of Afferent Arteriole (sympathetic)
decrease GFR, decrease RPF, no change in FF
Constriction of Efferent Arteriole (angII)
increase GFR, decrease RPF, increase FF
increased plasma [protein]
decrease GFR, no change in RPF, decrease FF
Kidney Stone
decrease GFR, no change in RPF, decrease FF
Filtered Load
GFR * [plasma]
Excretion rate
V * [urine]
Reabsorption rate
Filtered Load - Excretion Rate
Secretion Rate
Excretion Rate - Filtered Load
Splay (on Tm for glucose)
excretion of glucose before glucose is fully saturated
ususllay between 250 and 350
HA form predominates in which type of urine?
acidic urine
A- form predominates in which type of urine?
alkaline
How to excrete salicylate acid
increase excretion by alkalinizing the urine
compares the concentration of a substance in tubular fluid at any point along the nephron with the conc in plasma
Tubular Fluid/Plasma ratio
TF/P = 1
no reabsorption of substance or reabsorption of the substance is exactly proportional to the reabsorption of water
TF/P < 1
reabsorption of substance
TF/P > 1
secretion of substance
Reabsorbs 2/3 of 67% of filtered Na and H2O in nephron
Proximal Tubule
Isosmotic process in the renal tubules
in Proximal Tubules
Carbonic anhydrase inhibitor
diuretic that act in early PT by inhibiting the reabsorption of filtered HCO3-
Late Proximal tubules reabsorbs what
Sodium and Chloride
Reabsorbs 25% of filtered Na+
Thick Ascending Limb of Henle
inhibits Na-K-2Cl in TAL
loop diuretics like furosimide, ethacrynic acid and bumetanide
impermeable to water
Thick ascending limb of henle, early distal tubule
diluting segment
TAL, TF/P is <1
site of action of thiazide diuretics
Distal Convoluted tubules
Principal Cells
in late distal tubule and collecting duct
Aldosterone - reabsorb Na and H2O & secrete K
ADH - increases H2O permeability
K-sparing diuretics
spironolactone, triamterene, amiloride
alpha-intercalated cells
secrete H+ by H-ATPase, stimulated by aldosterone
reabsorbs potasium by H/K-ATPase
Causes of Hyperkalemia
insulin deficiency, acidosis
digitalis
exercise
cell lysis
Causes of Hypokalemia
insulin, beta-agonists, alkalosis, hypo-osmolarity
Hyperaldosteronism
increases K secretion and causes hypokalemia
Hypoaldosteronism
decreases K secretion and causes hyperkalemia
Increases the urea permeability of the inner medullary collecting ducts
ADH
Low urine flow rate
greater urea reabsorption
high urine flow rate
greater urea excretion
Phosphate reabsorbed in the PT
85% via Na-Phos Cotransport
PTH
inhibits phsophate reabsorption in PT by activating adenylate cyclase
increased Calcium reabsorption by activating AC in distal tubule
Treatment of idiopathic hypercalciuria
Thiazide diuretics
TAL competition
Mg and Ca compete for reabsorption, hypercalcemia causes an increase in Mg excretion
hypermagnesemia causes an increase in Ca excretion
hyperosmotic urine
when ADH levels are high, water deprivation, hemorrhage, SIADH
maintenance of the corticopapillary osmotic gradient
Countercurrent exchange in the vasa recta
countercurrent mulitplication in the loop of Henle
ADH has a big part in reabsorption of NaCl and Urea to make the gradient
Impermeable to water
TAL, therefore NaCl will be reabsorbed making the urine dilute therefore TF/P <1.0
Early distal convoluted tubule as well
Late Distal Tubules and high ADH
ADH increases the H2O permeability of principal cells
TF/P = 1.0
Collecting Ducts and high ADH
ADH increases the H2O permeability of principal cells
TF/P >1.0
Renal Tubules without ADH
PT: TF/P = 1.0 (isosmotic)
TAL, early DT, late DT, and CT: TF/P <1.0
Used to estimate the ability to concentrate or dilute urine
Free water Clearance
- no ADH: Ch2o is (+)
- yes ADH: Ch2o is (-)
Primary Polydipsia
decreased ADH, decreased serum Na, hyposmotic urine, High urine flow rate, positive free water clearance
Central Diabetes Insipidus
decreased ADH, increased serum Na, hyposmotic urine, High urine flow rate, positive free water clearance
Nephrogenic diabetes insipidus
increased ADH, increased serum Na, hypoosmotic urine, high urine flow rate, positive free water clearnace
Water Deprivation
increase ADH, high/normal serum Na, hyperosmotic urine, low uring flow, negative free water clearance
SIADH
really increased ADH, decreased Na because too much water reabsorption, hyperosmotic urine, low urine flow rate, negative free water clearance
Stimulates 1alpha-hydroxylase
PTH
secreted when hyperosmotic plasma and decreased blood volume
ADH
increases H2O permeability in LDT and CD principal cells
released when there is a decreased in blood volume and an icnrease in plasma [K]
Aldosterone
Actions of Aldosterone
increase sodium reabsorption in DT principal cells
increase K secretion in DT principal cells
increase H+ secretion in DT alpha-intercalated cells
what is release with an increase in atrial pressure and its MoA
ANP, cGMP
used to increase GFR, decrease Na reabsorption
MoA of AngII
increases Na/H-exchange and HCO3- reabsorption in proximal tubule
Volatile Acid
CO2
When are buffers most effective?
within 1pH unit of the pK of buffer
Most important extracellular buffer
HCO3-
Most important urinary buffer
Phosphate
Intracellular Buffers
Organic Phosphates & Proteins like Imidazole and alpha-amino groups and Hb
deoxyHb is better buffer than oxyHb
Henderson-Hasselbalch Eqtn
pH = pK + loh ([A-]/[HA])
Buffer is most effective in what part of a titration curve?
Linear portion
Primary reabsorption site for HCO3-
proximal tubule
pCO2 and HCO3-
increased pCO2 => increased rates of HCO3- reabsorption, basis for renal compensation for respiratory acidosis
decreased pCO2 => decreased rates of HCO3- reabsorption, renal compensation for respiratory alkalosis
ECF volume and HCO3-
ECF volume expansion results in decreased HCO3- reabsorption
ECF volume contraction results in increased HCO3 reabsorption
Diffusion Trapping
H+ is secreted into lumen via H-ATPase and combines with NH3 to form NH4
NH3 and acidosis
in acidosis, adaptive increase in NH3 synthesis occurs thus increasing gradient for NH3 diffusion
Inhibits NH3 synthesis
Hyperkalemia
Kussmaul Breathing
respiratory compensation for metabolic acidosis
Serum Anion Gap
For metabolic Acidosis
[Na]-([Cl]+[HCO3])
normal is 12mEq/L
Hypoventilation
respiratory compensation for metabolic alkalosis
Decerase in respiratory rate and retention of CO2
Respiratory Acidosis
increase in both H+ and HCO3-
Winter Formula
PCO2 = (1.5 x HCO3) + 8 ± 2
• If Measured < Expected = Respiratory Alkalosis
• If Measured > Expected = Respiratory Acidosis
Anion Gap with K+
= ([Na] + [K]) − ([Cl] + [HCO3])
Metabolic Acidosis increase anion gap
Increase Anion ( >12 ): MUDPILES Methanol Uremia Diabetic Ketoacidosis Paraldehyde Iron, Isoniazide Lactate Ethylene Glycol Salicylates, Starvation
Metabolic Acidosis non-gap
normal is between 5-12: Hypercholemic
GI Loss: diarhhea, Sx drain, Fistula, Cholestryamine
Renal Loss: Renal tubular acidosis
• Proximal RTA – Acetazolamide (Diuretic)
• Distal RTA – Inpaired H+ Secretion, Cannot Acidify Urine
Nasogastric suction
causes metabolic alkalosis
medical procedures that cayse metabolic alkalosis with chloride sensitivity
vomiting, NG suction, diuretics, LR, TPN, Blood
Metabolic Acidosis - pH, primary disturbance, compensatory response
decreased pH, decreased HCO3
compen - decrease pCO2
Metabolic Alkalosis - pH, primary disturbance, compensatory response
increased pH, increased HCO3
compen - increase pCO2
Respiratory Acidosis - pH, primary disturbance, compensatory response
decreased pH, increased pCO2
compen - increase HCO3
Respiratory Alkalosis - pH, primary disturbance, compensatory response
increased pH, decreased pCO2
Compen - decrease HCO3
Furosimide, ALbuterol, Na Polysterene Sulfonate
Cause Hypo-K
Spironolactone, ACEi, Ibuprofen
Cause Hyper-K
Grossest Food Ever?
Onions