Exam 1 Flashcards
Equation for renal plasma flow
UV/P—>
Excreted load/plasma concentration
How to prostaglandins affect afferent arterioles? NSAIDS
Dilation.
And NSAID oppose their effect—-> increase afferent resistance
name of the na/glucose transporters in pct?
SGLT1, secondary active transporter
transport max for SGLT1?
greater than 180 mg/DL
What are the channels in the principles cells
EnAC, K channel
What is RTA Type 1:
In Distal tubule —-> impaired
What are the ion channels located in the distal tubules and what do the absord/secrete?
late distal- ENaC and Potassium channel
Alpha intercalated cells
- –> h secretion
- –>K+ reabsorption
What are the ion channels located in the distal tubules and what do the absorb/secrete?
Late Distal-
- –> ENaC
- —>Potassium reabsorption channel
Alpha intercalated cells
- –> H secretion (H ATPase, H/K ATPase
- –> HCO3reabsorption
What is Type 4 RTA?
Hypoaldosteronism —> little production or resistance to aldosterone
-less NA absorbption, less K secretion
Why do low aldo levels leads to acidosis?
decreased reabsorption on sodium means increased retention of Hydrogen ions
What is RTA Type 1?
In Distal tubule —-> impaired
What are the ion channels located in the distal tubules and what do the absorb/secrete?
Late Distal Tubule (principal cells)
- –> ENaC
- —>Potassium reabsorption channel
Alpha intercalated cells
- –> H secretion (H ATPase, H/K ATPase
- –> HCO3reabsorption
What is RTAType 4 RTA?
Hypo aldosteronism —> little production or resistance to aldosterone
-less NA absorbption, less K secretion
Describe the pathogenesis of Syndrome of Apparent Mineralcortiocoid Excess?
a deficiency in an enzyme that converts cortisol to cortisone
—> results in .overstimulation of ENaC receptors
Leads to: -High blood pressure -Hypokalemia -Alkyosis Decreased Renin and Aldo
How does ADH act on princpal cells?
ADH inserts V2 receptors——> activates inserterion of Aquaporins 2 an 3
How does ADH act on prinicpal cells?
ADH inserts V2 receptors——> activates inserterion of Aquaporins 2 an 3
AND
Insertion of Urea channels, increasing medullary osmotic gradient
List the osmotic and non-osmotic stimuli for ADH release
1) osmotic = plasma osmolarity
2) non-osmotic=
- Extracellular fluid volume
- low blood pressure
- drugs, vomiting, SIADH
What aspect of urine will determine ADH levels?
Urine osmolality
–> with uOsm less than 100, urine is sufficiently dilute, no need for absorbption ————–»> no ADH
What is the mechanism of Atrial Natiuretic Peptide?
Counters effect of aldosterone—-> cause diuresiis
Released in response to ATRIAL VOLUME
Will ADH go up or down in Hypotonic Hyponatremia?
it will go up–even if there is low osmolality, it will try to preserve volume.
How do you calculate the ICF from the effective osmolality?
ICF= 1/effective osmolality
How do you estimate the ECF?
through physical examination!!!! High ECF: 1) EDEMA 2) lung crackles 3) venous congestion
Low ECF: low pulse, no edema
What is the pathology of SIADH?
Increased ECF but LOW BODY WATER
What are the 3 types of hypernatremia and what is their mechanism?
1) true volume depletion
- ——> causes increased RAAS (increased Na uptake)—> LOW SODIUM IN URINE
2) Hypervolemia– decreased EABV (HF, cirrhosis)
2) Euvolemic – extensive ADH, increased volume and sodium uptake ——> pressure naturesis causes water and high sodium to be released in urine
