Nephron

Question 1

Potter sequence

Answer 1

Causes: Olgihydramnios 2/2 to

1) Bilateral agenesis
2) Posterior urethral valves
3) ARPKD

Signs:

1) Flat face with low set ears
2) Retrognathia
3) Pulmonary hypoplasia
4) Skeletal defects like club foot and rocker bottom foot
5) Nodules of fetal epithelium on placenta

Question 2

Horseshoe kidney

Answer 2

Assc with Turner Syndrome (XO)

Fusion at inferior or superior poles causes kidney to get stuck at IMA and L3

Increased risk of:

1) Ureteropelvic junction obstruction
2) UTIs
3) Hydronephrosis
4) Renal calculi
5) Wilm’s tumor

Question 3

Multicystic dysplastic kidney

Answer 3

Improper interaction between uteric bud and metanephric mesencymal tissue

Kidney is cystic with increased CT

Usually asymptomatic as other kidney compensates

Question 4

Renal ectopia

Answer 4

Kidney where it shouldn’t be. Usually in pelvis.

Question 5

Ureteral abnormalities

Answer 5

Duplicated on one side

Question 6

Ureter course

Answer 6

Under the 1) vas deferens and 2) uterine artery.

Can be damaged in surgery.

Question 7

Fluid compartments

Answer 7

60% TBW is H20.
40% Intracellular
20% Extrcellular
15% of Extracellular is interstitial
5% of Extracellular is intrvascular

Question 8

Glomerular filtration barrier

Answer 8

Composed of:

1) Fenestrated capillaries
2) Podocytes
3) BM fused to heparan sulfate

Nephrotic syndrome disrupts the charge barrier to albumin in urine, hypoproteinemia, edeme, and hyperlipidemia

Question 9

Renal clearance

Answer 9

Clearance = volume of plasma completed cleared of a solute per unit time

Clearance = Urine concentration x Flow/ Plasma concentration

Question 10

GFR

Answer 10

GFR is measured with inulin, because it is filtered but no secreted or absorbed.

GFR = Urine concentration x Flow/ Plasma concentration

Creatinine is a estimate, but overestimates GFR because is is secreted as well.

Question 11

ERPF

Answer 11

Effective renal plasma flow is measured with PAH (para aminohippuric acid), because it filtered and secreted.

ERPF = Urine concentration x Flow/ Plasma concentration

RBF = RPF / (1 - Hct)

PAH underestimated by 10%.

Question 12

NSAID effect on kidney

Answer 12

NSAID block prostaglandins. Prostaglandins dilate afferent arteriole which increase GFR and RPF.

Question 13

ATII effect on kidney

Answer 13

ATII constricts EA. EA constriction increase GFR but dec RPF.

Question 14

What are the 5 ways to change the glomerular filtration dynamics?

Answer 14

Constrict AA
Constrict EA
Increase plasma protein
Decrease plasma protein
Block the ureter

Question 15

How do you calculate filtration load?

Answer 15

Filtration load = GFR x plasma concentration

Question 16

How do you calculate excretion rate?

Answer 16

Excretion rate = Volume of urine x urine concentration

Question 17

How do you calculate absorption?

Answer 17

Absorb = Filter - Excretion

Question 18

How do you calculate secretion?

Answer 18

Excretion - filter = Secrete

Question 19

What are the dynamics of glucose clearance?

Answer 19

Glucose is taken up entirely in proximal tubule with Na coporter.

If blood glucose is over 200mg/dL, then glucosuria found.

If blood glucose is over 375mg/dL, then all transporters are saturated.

Normal glucose and amino acids in pregnancy.

Question 20

What are the dynamics of amino acid clearance?

Answer 20

AAs are taken up completed in the proximal tubule.

In Hartnup disease (AR), there is a defect in AA uptake of tryptophan which causes pellagra (deficiency in niacin, or vitamin B3).

This causes:

1) Dermatitis
2) Diarrhea
3) Dementia

Other causes of pellagra:

1) Isoniazid bc depletes B6
2) Malignant carcinoid (uses too much tryptophan)

Question 21

What are the transporters in the PT?

Answer 21

PT goals are to:

1) Take up glucose and Na, using NA K basloaterally
2) Na/H anti porter using CA and bicarb transporter basolaterally
3) Take up amino acids, K, PO4, HCO3, CL -

Question 22

What molecules act at PT?

Answer 22

ATII increases N/H transporter, increasing H into the urine

CA inhibitors inhibit CA and inc HCO3 into the urine

PTH blocks PO4 reabsorption, dumping it into the urine

Question 23

What happens in thin descending limb?

Answer 23

H2o leaves the tubules and concentrates the filtrate

Question 24

What happens in the thick ascending limb?

Answer 24

1) NAK2CL send molecules into the medulla, using NAKATPase basolaterally
2) K+ back into lumen creates + charge, and Ca and Mg2+ are sent into medulla

Question 25

What molecules act at thick ascending limb??

Answer 25

Loop diuretics like furosemide blocks the NAK2CL transporter.

Question 26

What happens in the distal convoluted tubule?

Answer 26

1) NaCl is taken up from lumen using the NAKATPase basolaterally 2) Ca is taken up and exhanged with Na/Ca basolaterally

Question 27

What molecules act at distal convoluted tubule?

Answer 27

1) Thiazide diuretics block NaCl transporter. | 2) PTH increases Ca reabsorption

Question 28

What happens in the collecting duct?

Answer 28

In the proximal tubule cell: 1) Na is taken up and K+ is dumped using a NAKATPase basolaterally 2) H20 is reabsorbed when ADH acts at V2 receptor and increase aquaporins In the a intercalated cell: 1) H+ATPase dumps H+ using a HCO3/Cl transporter basolaterally 2) H+/K+ATPase dumps H+

Question 29

What molecules act at the collecting duct?

Answer 29

1) ADH -- H20 is reabsorbed when ADH acts at V2 receptor and increase aquaporins 2) Amiloride and trimaterene block Na+ reabsorption and act as K+ sparing diuretics 3) Aldosterone increases: 1) Enac at lumenal surface 2) NaKATPase are basolateral surface 3) K+ dumping in principal cell 4) K+/H+ exchange in intercalated cell

Question 30

What are the 4 common renal tubular defects?

Answer 30

The kidneys put out fabulous glittering liquid: 1) Fanconi 2) Bartter 3) Gitelman 4) Liddle