Renal: Physiology 3

Front 1

Why is Na+ delivery to distal tuble more or less constant?

Back 1

- tubuloglomerular feedback mechanism: constriction of afferent arteriole in response to high tubular [Na+] sensed by macula densa.
- glomerulotubular balance: ability of proximal tubule to absorb more Na+ when GFR is increased

Front 2

What % of Na+ is excreted with max aldolsterone?

Back 2

0.1%

Front 3

What % of Na+ is excreted with no aldolsterone?

Back 3

5%

Front 4

Where is the receptor for aldolsterone located?

Back 4

on the nucleus of principal cells and type A intercalated cells

Front 5

Mechanism of aldolsterone.

Back 5

bind to receptors on nuclear membrane of principal cell and type A intercalated cells.
- stimulate Na+/K+ channels on principal cells
- stimulate H+/K+ channels on type A intercalated cells
- increase oxidative metabolism of taget cells

Front 6

What some stimulators of aldolsterone?

Back 6

- high plasma [K+]
- angiotensin II

Front 7

Where is aldolsterone produced?

Back 7

produced and released by zona glomerulosa cells of adrenal cortex.

Front 8

Size of ECF volume is determined by ___.

A. Na+
B. HCO3-
C. Glucose
D. K+

Back 8

A.

Front 9

Factors that regulate Na+ balance.

Back 9

1) renin-angiotensin-aldolsterone system:
- low ECF -> renin released from JG cells -> Ang converted to AngI -> AngI converted to AngII(vasoconstriction) by ACE in the lungs -> aldolsterone release -> increased Na+ reabsorption -> normal ECF restored
2) GFR regulation: high ECF -> increased GFR and decreased proximal fluid resorption
3) third factor
- increased venous filling pressure -> ANP release -> decreased sympathetic tone -> decrease Na+ reabsorption
- ourabain-like factor (hypothalamus/adrenal cortex) -> inhibit Na+/K+ pumps of collecting duct

Front 10

What happens when kidney is unable to maintain normal ECF as in severe blood loss and excessive sweating?

Back 10

>15% volume contraction -> creaving for Na+ -> ingestion of salt -> Na+ balance

Front 11

How does kidney react to volume depletion?

Back 11

volume depletion -> increase AngII and aldolsterone, release of NE -> increase in Na+ reabsorption -> increased osmolarity -> ADH release -> water reabsorption -> volume returns to normal

Front 12

What is the strongest stimulator of aldolsterone release?

Back 12

high [K+] > 5mM

Front 13

Mechanisms of aldolsterone causing K+ wasting (kaliuretic)

Back 13

- electrical coupling with Na+ influx
- insertion of additional Na+/K+ channels
- intracellular alkalosis

Front 14

Increase in UFR ___ (stimulates/inhibits) K+ secretion.

Back 14

stimulate
- increase flow rate -> decrease tubular [K+] -> favor secretion
- increase flow rate -> larger Na+ delivery to distal tubule -> increased Na+ absorption and K+ secretion by Na+/K+ transporters

Front 15

What type of cell is most active during K+ depletion?

Back 15

type A intercalated cell
- active uptake of K+ by H+/K+ pump

Front 16

What causes water diuresis?
What causes osmotic diuresis?

Back 16

- water diuresis: absence of ADH
- osmotic diuresis: increased excretion of a solute

Front 17

Drugs that cause natriuresis.

Back 17

- acetazolamide (weak): inhibition of carbonic anhydrase
- loop diuretics
- thiazide
- K+ sparing diuretics

Front 18

Why do loop diuretics cause stronger natriuresis than acetazolamide(carbonic anhydrase inhibitor)?

Back 18

- loop diuretics inhibit tubuloglomerular feedback
- loop diuretics disrupt the corticopapillary gradient

Front 19

How do loop diuretics, thiazide cause K+ wasting?

Back 19

natriuresis -> more Na+ delivered to distal tubule and collecting duct -> stimulation of Na+/K+ exchanger -> more K+ secreted -> hypokalemia

Front 20

What is a good drug of choice for treating life-threatening edema of the lung and brain?

Back 20

loop diuretics and thiazide
- high ceiling level

also good in treating congestive heart failure and hypertension

Front 21

What is the compatible blood pH range?

Back 21

7-7.8

Front 22

What is the most abundant acid in the body?

Back 22

CO2

Front 23

What are the sources of each of the following acid?

- phosphoric acid
- sulfuric acid
- uric acid
- carboxylic acid

Back 23

- phosphoric acid: lipid, nucleic acid
- sulfuric acid: AA. low pKa, minimal excretion
- uric acid: purines. low pKa, minimal excretion
- carboxylic acid:ketoacidosis, lactic acidosis

Front 24

On normal western diet, how much fixed acids are excreted by the kidney?

Back 24

50-70 mmol

Front 25

Where are HCO3- absorption in the nephron?

Back 25

- 90% in proximal tubule: Na+/H+ exchanger, brushborder carbonic anhydrase. Luminal pH = 6.7
- rest is absorned in distal tubule and collecting duct (intercalated cells: absorption in typeA, secretion in typeB cells). Final pH 4.5

Front 26

What is the max [HCO3-] before you see it in the urine?

Back 26

30mM

Front 27

What can cause a left shift of HCO3- curve?

Back 27

- alkalosis
- volume expansion

Front 28

What can cause a right shift of HCO3- curve?

Back 28

- acidosis
- volume depletion

Front 29

What can cause volume depletion alkalosis? Is it easy to correct?

Back 29

volume depletion alkalosis
- constant vomit: loss of acid and volume at the same time
- alkalosis hard to correct because volume depletion shifts HCO3- excetion to the right.

Front 30

Name the two mechanisms that fixed acids are excreted.

Back 30

- titratable acid: di-basic phosphate
- ammonium: glutamine -> NH3 -> NH4+ -> Na+/NH4+ exchanger

Front 31

pKa of phosphate and NH4+.

Back 31

- pKa (phosphate) = 6.8
- pKa (NH4+) = 9.3

Front 32

Where is ammonium reabsorbed?

Back 32

- thick ascending limb
- medullary collecting duct

Front 33

What happens to acid excretion during acidosis?

Back 33

- stimulate enzyme in deamination of glutamine
- increase amount of titratable acid

Front 34

What happens to acid excretion during diabetic ketoacidosis?

Back 34

- stimulate enzyme in deamination of glutamine
- increase amount of titratable acid
- additional proton acceptor in the urine (beta-hydroxybutyrate, acetoacetate)

Front 35

Henderson-Hasselbach equation for calculating pH in bicarbonate buffer system.

Back 35

pH = 6.1 + log ([HCO3]/(0.3xPCO2))

Front 36

Equation for anion gap calculation.

Back 36

anion gap = [Na+] - [Cl-] - [HCO3] = 12mM (8-16mM)

Front 37

What can cause this?

- increased anion gap

Back 37

diabetic acidosis
- anion gap = [Na+] - [Cl-] - [HCO3]

Front 38

What can cause this?

- normal anion gap

Back 38

HCL ingestion
- anion gap = [Na+] - [Cl-] - [HCO3]

Front 39

How does kidney compensate for respiratory acidosis?

Back 39

- increase in HCO3 absorption: type A intercalated cell
- increase in H+ excretion: titratable acid, ammonium

Front 40

How does kidney compensate for respiratory alkalosis?

Back 40

- spill over HCO3-: type B intercalated cell

Front 41

Name some etiology of metabolic acidosis.

Back 41

- diabetic ketoacidosis: increased production of acids
- aspirin overdose: ingestion of acids
- secretory diarrhea: loss of alkaline fluid
- renal failure: inability to excrete fixed acids

Front 42

Name some etiology of metabolic alkalosis.

Back 42

- lye poisoning: ingestion of alkali
- vomiting: loss of gastric juice
- volume depletion: retention of HCO3-.

Front 43

What can cause this?

- respiratory acidosis
- lactic acidosis

Back 43

severe asthma

- respiratory acidosis: insufficient expiration of CO2
- lactic acidosis: hypoxia

Front 44

What happens in acid/base balance when in altitude region?

Back 44

lack of O2 -> hyperventilate -> hypocapnea -> respiratory alkalosis -> decrease HCO3 absorption (kidney response) -> metabolic acidosis

Front 45

T/F: Metabolic acidosis may persist 1-2 days after descending from a high altitude region.

Back 45

T.