deck_5112194 Flashcards
(41 cards)
How is the PT designed for large reabsorption?
The epithelial cells have microvilli (brush border) and basolateral surface is thrown into folds: both enhance surface area
T or F. Proximal tubular cells are reach in mitochondria which are needed to provide sufficient energy for the reabsorption
T. ISCHEMIA is bad here
What are the parts of the PT (structurally)?
First 2/3: proximal convoluted tubule (PCT)Remaining 1/3: proximal straight tubule (parse recta). In turn, parse recta has cortical and medullarly segments
What are the parts of the PT (functionally)?
Some differences in transporter proteins):- S1- initial short segment of PCT- S2- remaining PCT and cortical parse recta- S3- medullary parse recta
What are the main functions of the PT?
Reabsorption of filtered water, electrolytes, and organic compoundsSecretion of organic compounds including some drugs (S2, S3 segments)Hormonal function: final pathway in the synthesis of calcitriol
How much Na is reabsorbed in the PT?Water?K+?
55-65% (Na+ and water)K+- 65%
How much Pi is reabsorbed in the PT?Calcium?Glucose?Urea?
80-95%60%100%50%
What are some pathways of reabsorption in the PT?
1) transcellular (through the PT epithelium to the ISF)2) paracellular (through junctions to the ISF)
Passive diffusion typically requires what?
an electrochemical gradient of some kind
What is reabsorption in the tubular cells from the PT lumen driven by?
The electrochemical gradient created by the basolateral Na-K ATPase.
What does the basolateral Na-K ATPase do specifically?
transports 3Na+ to the ISF and 2K+ into the tubular cell
What things are typically coupled to Na+ as it is reabsorbed into the tubular cell via the electrochemical gradient formed by the basolateral Na-K ATPase?
sugars, AAs, phosphate, glucose in symport (or H+ into the tubular lumen in antiport)this is called 2ndary active transport
How is the K+ brought into the cell by the BL Na/K ATPase removed back to the ISF?
by passive transport couple to a negative ion (usually Cl-)
What is the basis of glomerulotubular balance?
The intrinsic ability of the tubules to increase their reabsorption rate in response to increased tubular load (increased tubular inflow). all segments have this capability
What things decrease the net reabsorption of sodium and water?
Arterial pressure (Pressure natriuresis): increase in peritubular capillary hydrostatic pressure reduces the net reabsorption of sodium and waterdiuretics, hypoaldosteronism
What hormones regulate PT reabsorption?
Angiotensin II: regulates NaCl and water re-absorption and H+ excretionParathyroid hormone and FGF23- regulate Pi excretion
Why is the PT highly susceptible to ischemia?
It has ATP dependence for the function of Na-K-ATPase, and Polarized (apical and basolateral) structure of PT cells is a dynamic and ATP dependent process relying on cytoskeleton. It involves the formation and maintenance of cell-cell and cell-substratum attachments and the targeted delivery of plasma membrane components to the appropriate domains.
What are some basic potential defects in PT function?
-defective solute influx-leakage back from lumen-increased back flux across tight junctions from ISF-defective energy-decreased solute flux into blood from ISF-defective transporter recycling
How is PT dysfunction classified?
A. Generalized: usually due to defect in energy generation, Na-K-ATPase activity, or dysfunction of cellular organelles affecting transport protein recycling B. Isolated solute transport disorders: typically due to defect in specific transport protein 2. Classification based on mode of inheritance: A. Genetic B. Acquired
What is Familial/Hereditary Renal Glucosuria (HRG)?
isolated PT dysfunction that causes defect in glucose reabsorption
What is the MOI for HRG?
AR (1:20000)
What causes HRG?
mutation of SGLT2 glucose transporter which transports Na and glucose from the tubular lumen to the epithelium (where GLUT1 and 2 then transfer it to blood)types:a- decreased thresholdb- transport max is lowered0- no functional SGLT2 at all
T or F. If glucose conc. exceeds the normal thresholds, patients with functional SGLT2 will also have glucosuria
T.
What is Cystinuria?
A type of amino acid uria caused by mutation of the brush border transporter responsible for reabsorption of cystine, and dibasic amino acids ornithine, lysine, and arginine cysteine is not water soluble so once its conc. in urine is above 250, it forms hexagonal stones under the microscope
