Flashcards in Proximal Tubular Dysfunctions and Disorders of Water Balance - Gosmanova Deck (32)
What structure does the proximal tubule have that facilitates increased absorption?
microvilli (brush border)
Functionally, the PT is divided into three parts. Explain
S1- initial short segment of PCT
S2 - remained PCT and cortical parse recta
S3 - medullary parse recta
What are the functions of the proximal tubule?
Reabsorption of filtered water, electrolytes and organic compounds
Secretion of organic compounds and drugs S2/3
Hormonal Function - final pathway in the synthesis active vitamin D
What percentage of glucose is reabsorbed in the pt?
What percentage of sodium is reabsorbed in pt?
What are the three types of transport ?
What drug targets Carbonic anhydrase
What is the function of carbonic anyhydrase
it mediates the conversion of h2c03 into h20 and c02, which can diffuse into the cell.
By inhibiting carbonic anyhydrase, you can cause mild diuresis
what transporters does angiotensin II work on?
it activates the H-Na transporter (bringing Na into the cell) and on the HCO3-Na co transporter, pumping both into the basolateral surface
Why is the PT highly susceptible to ischemia
it's depend on atp in the NKA PUMP
What are six potential defects in PT function?
defective solute influx
leakage back into the lumen
decreased solute flux into the blood
defective energy generation or transportation
increased backflux across tight junctions
defective transporter recycling
PT dysfunction can be due to what and what?
generalized: usually energy generation
genetic or acquired
What is hereditary renal glucosuria? and it's cause
Defect in glucose reabsorption.
Mutation in SGLT2 glucose transporter in PT that absorbs glucose.
What is the defect in amino acid reabsorption?and cause?
mutation of brush border transporter responsible for reabsorption of cystine, and ornithinem lysine and arginine
what is the common occurence in cystinuria?
what are the three common defects in phosphate reabsorption?
autosomal recessive hypophosphatemic rickets
oncogenic hypophosphatemic osteomalacia
What is the most common inherited phosphate wasting disorder? cause
increased levels of circulating factor FGF-23 that down-regulates activity of phosphate transporter rater than transport protein mutation itself.
What is commonly seen in children with x-linked hypophosphatemia?
adults have osteomalacia
t or f hartnup disease is a defect in neutral amino acid transporter in the pt
what is vitamine d-dependent rickets type 1?
causes by mutation of 1alpha-hydroxylase leading to hypophosphatemia and rickets
what are metabolic abnormalities associated with fanconis syndrome?
hyperchloremic metabolic acidsos
What are clinical manifestations of fanconis syndrome?
renal stones and nephrocalcinosis
extra renal organ involvement depending on underlying cause
What are inherited causes of fanconi syndrome
what are acquired causes of fanconi syndrome
multiple myeloma and tenofovir
an osmotic pressure above what will trigger thirst mechanisms?
What has a greater ability to stimulate adh secretion: change in Posm or decrease in blood volume?
Posm (change by 1%)
BV must decrease by 7% to stimulate ADH secretion
What is the mechanism of ADH action in the collecting duct?
AQP2 is the renal collecting duct water channel. It will cause a quick insertion of more aqp2 into the luminal surface. long term will increase the transcription of the aqp2 gene
What are two drugs that inh v2rc
conivaptan and tolvaptan
what is the cause of hyponatremia?
increased tbw. can have increased or decresaed Na levels as well. but water always predominates
what are specific causes of hyponatremia?
renal losses, gi losses, skin, all have volume depletion
normal volume status - SIADH, glucocorticoid deficiency hypothyroidism
volume overload - CHF, kidney failure, cirrhosis, nephrotic syndrome
what is central di
lack of adh