Exam 1

Question 1

Equation for renal plasma flow

Answer 1

UV/P—>

Excreted load/plasma concentration

Question 2

How to prostaglandins affect afferent arterioles? NSAIDS

Answer 2

Dilation.

And NSAID oppose their effect—-> increase afferent resistance

Question 3

name of the na/glucose transporters in pct?

Answer 3

SGLT1, secondary active transporter

Question 4

transport max for SGLT1?

Answer 4

greater than 180 mg/DL

Question 5

What are the channels in the principles cells

Answer 5

EnAC, K channel

Question 6

What is RTA Type 1:

Answer 6

In Distal tubule —-> impaired

Question 7

What are the ion channels located in the distal tubules and what do the absord/secrete?

Answer 7

late distal- ENaC and Potassium channel

Alpha intercalated cells

• –> h secretion
• –>K+ reabsorption

Question 8

What are the ion channels located in the distal tubules and what do the absorb/secrete?

Answer 8

Late Distal-

• –> ENaC
• —>Potassium reabsorption channel

Alpha intercalated cells

• –> H secretion (H ATPase, H/K ATPase
• –> HCO3reabsorption

Question 9

What is Type 4 RTA?

Answer 9

Hypoaldosteronism —> little production or resistance to aldosterone

-less NA absorbption, less K secretion

Question 10

Why do low aldo levels leads to acidosis?

Answer 10

decreased reabsorption on sodium means increased retention of Hydrogen ions

Question 11

What is RTA Type 1?

Answer 11

In Distal tubule —-> impaired

Question 12

What are the ion channels located in the distal tubules and what do the absorb/secrete?

Answer 12

Late Distal Tubule (principal cells)

• –> ENaC
• —>Potassium reabsorption channel

Alpha intercalated cells

• –> H secretion (H ATPase, H/K ATPase
• –> HCO3reabsorption

Question 13

What is RTAType 4 RTA?

Answer 13

Hypo aldosteronism —> little production or resistance to aldosterone

-less NA absorbption, less K secretion

Question 14

Describe the pathogenesis of Syndrome of Apparent Mineralcortiocoid Excess?

Answer 14

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

Question 15

How does ADH act on princpal cells?

Answer 15

ADH inserts V2 receptors——> activates inserterion of Aquaporins 2 an 3

Question 16

How does ADH act on prinicpal cells?

Answer 16

ADH inserts V2 receptors——> activates inserterion of Aquaporins 2 an 3

AND

Insertion of Urea channels, increasing medullary osmotic gradient

Question 17

List the osmotic and non-osmotic stimuli for ADH release

Answer 17

1) osmotic = plasma osmolarity

2) non-osmotic=
- Extracellular fluid volume
- low blood pressure
- drugs, vomiting, SIADH

Question 18

What aspect of urine will determine ADH levels?

Answer 18

Urine osmolality

–> with uOsm less than 100, urine is sufficiently dilute, no need for absorbption ————–»> no ADH

Question 19

What is the mechanism of Atrial Natiuretic Peptide?

Answer 19

Counters effect of aldosterone—-> cause diuresiis

Released in response to ATRIAL VOLUME

Question 20

Will ADH go up or down in Hypotonic Hyponatremia?

Answer 20

it will go up–even if there is low osmolality, it will try to preserve volume.

Question 21

How do you calculate the ICF from the effective osmolality?

Answer 21

ICF= 1/effective osmolality

Question 22

How do you estimate the ECF?

Answer 22

through physical examination!!!!
High ECF: 
1) EDEMA 
2) lung crackles 
3) venous congestion 

Low ECF: low pulse, no edema

Question 23

What is the pathology of SIADH?

Answer 23

Increased ECF but LOW BODY WATER

Question 24

What are the 3 types of hypernatremia and what is their mechanism?

Answer 24

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