Renal and Formulas Flashcards
Clearance Formula
Cx = Ux * V/Px
Clearance = Urine Concentration x Flow rate/Plasma Concentration
Filtered Load Formula
Filtered load = GFR * Px
Glomerular Filtration Rate x Plasma concentration
Ohm’s Law
Q = DeltaP/R
Flow Rate = Pressure Change / Radius
Ultrafiltration Pressure Definition
Net Filtration Pressure of Glomerulus, caused by oncotic and hydrostatic pressure differences across the filtration membrane.
Ultrafiltration Pressure Formula
UP = (Pgc + πbs) - (Pas + πgc)
Filtration pressure is the difference between the sum of the glomerular capillaries’ hydrostatic pressure and the oncotic pressure of the filtrate (pressure pushing out of the capillaries and pulling into the capule) and the filtrate hydrostatic pressure (pushing back into the capillaries) and glomerular capillaries oncotic pressure (pulling back into the capillaries)
Compliance Equation
Compliance = ΔV / ΔP - Change in volume per change in pressure.
Dalton’s law of partial pressures
Px = Pb * F
Partial pressure of x in a mixed gas = the pressure of the gas * the fraction of the mixture that gas makes up.
Relationship between GFR and ultrafiltration pressure (UP)
GFR = UP * Kf (ultrafiltration coefficient)
Fractional excretion relationship
FE = (Ux * V) / (Px * GFR)
Fractional Excretion = (urinary concentration x urine flow rate) / (Plasma concentration * GFR)
Relationship between dead space, tidal volume, and alveolar ventilation
Va = (Vt - Vd) * RR
Alveolar ventilation = (Tidal Volume - Dead Space) * Respiratory Rate
Alveolar Gas equation - Arterial Oxygen pressure = ?
PAO2 = FIO2(PB-PH20) - PACO2
Pressure of Arterial O2 = Fraction of Inspired 02 * (Barometric Pressure - Partial Pressure of H20) - Pressure of Arterial CO2
Laplace’s Law
P = 2T/r
Collapsing pressure is inversely proportional to radius, meaning that small alveoli are harder to open than large ones.
Relationship between flow, pressure, and radius (Poiseuille’s Law)
Q = (Π* ΔP * r^4) / (8nL)
Big picture - as radius increases, flow increases by a factor of 4.
Fick’s Law of Diffusion
V = (AD (P1-P2)) / Δ x
Flow rate = area x diffusion coeffecient x pressure difference / thickness
High renin level effects on glomerulus
ATII constricts Afferent Arteriole, leading to decreased GFR
Low renin level effect on glomerulus
ATII dilates Afferent arteriole, leading to increased GFR
Chemical signals that dilate the afferent arteriole
low ATII, prostaglandins, ANP, NO - anything that lowers BP basically.
Chemical signals that constrict the afferent arteriole
High ATII, NE, ADH - anything that raises BP.
Effects of charge and size on glomerular filtration
The filtration membrane is negatively charged, and the slits are very small, so bigger and more negatively charged molecules don’t go through, while smaller and more positively charged molecules cross more easily.
Determinants of GFR
Permeability, surface area, pressure
Myogenic regulation of GFR in response to increased BP
As BP rises, the smooth muscle of the afferent arteriole “pushes back” by contracting, causing a decrease in GFR. This happens quickly.
Tuboglomerular regulation of GFR in response to increased BP
As BP rises, the macula densa senses increased NaCl, and releases ATP. This becomes adenosine, which acts as a paracrine signal, causing increased intracellular calcium release and constriction in the afferent arteriole, leading to decreased GFR.
Sympathetic stimulation effect on afferent arteriole
constriction
Natriuretic Peptides - Function?
Released in response to sudden increase in BP, cause Afferent arteriole to dilate, increasing GFR. They also cause increased blood flow to the vasa recta, decreasing the osmolarity of the medulla and leading to more dilute urine to decrease volume.
If more of a substance is filtered than excreted, what is happening to it in the glomerulus?
It is being reabsorbed, clearance < GFR
If more of a substance is excreted than filtered, what is happening to it in the glomerulus
It is being actively secreted, clearance > GFR
How can you accurately measure GFR?
Inulin Clearance
What do we actually use to measure GFR?
Creatinine Clearance
How much of filtered glucose and amino acids are absorbed in the PCT?
100% of both. They are brought in via secondary active transport using sodium cotransporters
What if the patient has glucosuria? What is happening to the glucose transporters?
They are saturated.
What role does the kidney play in regulating serum levels of glucose and amino acid.
None
How do peptides get out of the filtrate and back into the cells?
Via endocytosis - they are too big for transporters.
If the intraluminal pH drops, does this favor excretion or reabsorbtion of weak organic acids?
It favors reabsorbtion. The more free hydrogen ions there are in the lumen, the more acid will be in the protonated (netural) form, and be able to diffuse back into the cells.
Note - this is an oversimplification, but you get the idea,
If the intraluminal pH rises, does this favor excretion or reabsorption of weak organic acids?
They will be secreted, because they will be in their ionized form in the filtrate, so they won’t diffuse back out.
Urea Handling
50% is passively reabsorbed in the PCT. 50% is actively transported in the loop and collecting duct via UREA TRANSPORTERS.
Functions of urea
Excreted to rid the body of nitrogenous wastes, and transported into the medulla to help maintain a high osmotic gradient.
Sodium transport in the PCT
Cotransport with Glucose and AA’s, countertransport with H+ via Na/H antiporters
Sodium transport in thickascendinglimb,LoopofHenle
Cotransport with other electrolytes - Na+/K+/2Cl‐
Sodium transport in early DCT
Cotransport with Cl-
Sodium Transport in late DCT and collecting duct
Enac luminal sodium channels - these can be opened or closed to concentrate or dilute urine. They are sensitive to Aldosterone.
How do the luminal cells maintain a positive sodium gradient to keep importing sodium?
They use the sodium-potassium pump on the basal side to pump sodium out into the blood and keep the gradient going.
Reabsorbtion of HCO3- in PCT mechanism?
Ok, remember the Sodium - H+ antiporter? Those H+ ions are going to combine with HCO3- via carbonic anhydrase and make CO2 and H20, which can diffuse out of the filtrate. Then intracellular carbonic anyhdrase can reverse the process, re-using that H+ for the sodium antiporter and pumping the HCO3- into the blood.
Reabsorbtion of chloride in PCT?
Chloride follows sodium, mainly via the paracellular route (between the cells) - 60% is reabsorbed in PCT.
Reabsorbtion of chloride in loop?
Cotransport with other electrolytes - Na+/K+/2Cl‐
Reabsorbtion of chloride in DCT?
Cotransport with Na+
H2O reabsorbtion - basic mechanism
Always passive - Follows sodium.
ADH effects on the nephron
ADH (think Always Digging Holes) - causes increased H2O permeability, increasing water retention by increasing the number of aquaporins, and increasing urea reabsorbtion. It also decreases sweating, and causes vasoconstriction in smooth muscle.
Brain control of ADH release
osmoreceptors in the brain signal via the hypothalamus, and the pituitary releases ADH into the bloodstream.
Blood volume control of ADH release
Baroreceptors in the cardiopulmonary system sense large decreases in BP (5-10%) and cause a large release of ADH.
Blood pressure control of ADH release
Baroreceptors in the carotid sinuses and aortic arch sense large decreases in BP (10%, as in severe bleeding) and cause a large, emergency release of ADH.
Potassium reabsorbtion in PCT
67% reabsorbed via paracellular route
Potassium reabsorbtion in TALH
20% Cotransport with sodium and chloride Na+/K+/2Cl‐
What happens to potassium in the late DCT and Collecting Duct in a normal potassium diet.
It is secreted. This is driven by a positive gradient established by Na/K pumps pumping Na into the blood, which leads to high intracellular K, and diffusion into the filtrate.
Calcium Reabsorbtion in PCT
70% - Paracellular via solvent drag (comes along with water)
Calcium reabsorbtion in TALH
20% - paracellular due to lumen positivity
Calcium reabsorbtion in DCT
9% via calcium channels
Control of calcium reabsorbtion
Parathyroid hormone. When released, this activates calcium channels in the DCT. It also causes increased osteoclast activity in the bones, so both of those raise serum calcium.
Phosphate Reabsorbtion
80% - Mainly in PCT via Pi /2Na+ cotransporter (to balance out the charges. Additional cotransporters can be expressed in the PST and DCT if needed to absorb the rest.
Magnesium Reabsorbtion
95% reabsorbed - mostly in the TALH, unlike most solutes. Always goes paracellular.
Bicarbonate Reabsorbtion
100% reabsorbed. 80% PCT, 15% TALH, 5% CD. Combined with intraluminal H+ (remember the sodium/H+ antiporter?) via carbonic anhydrase to make CO2 and H20, which diffuse into the cells, then carbonic anyhdrase reverses the process, and pumps on the basal side export bicarbonate back into the blood. There are two pumps - Cl-/HCO3- exchanger, and Na+/HCO3- cotransporter.
Endocrine function of the kidney in erythropoeisis
When the kidney senses decreased O2 in the blood, it releases erythropoeitin, which targets the red marrow and increases RBC production. This is why chronic kidney disease can lead to anemia.
Role of kidney in vitamin D homeostasis
Converts precursor to the active form of vitamin D, which is needed to absorb calcium.
