Renal Path

Question 1

Failure of alpha intercalated cells to secrete acid can cause which type of RTA?

Answer 1

Type I

Question 2

Type II RTA is usually associated w/ what syndrome?

Answer 2

fanconi syndrome

Question 3

The main cause of Type II RTA is what?

Answer 3

impaired ability of PT to reabsorb bicarbonate

Question 4

All RTAs will cause normal anion gap metabolic acidosis. All RTAs will cause hypokalemia except for which one?

Answer 4

Type IV (causes hyperkalemia)

Question 5

What is the main cause of Type IV RTA?

Answer 5

hypoaldosteronism

Question 6

Dehydration (inadequate fluid intake) can cause which electrolyte disturbance?

Answer 6

hypernatremia

Question 7

What is the main cause of an increased anion gap metabolic acidosis?

Answer 7

ketoacidosis and ingestion of fixed acids (such as ethylene glycol, aspirin, & methanol)

Question 8

Decreased HCO3- reabsorption cause normal anion gap metabolic acidosis. Why?

Answer 8

The net loss of negative charge in the plasma will compensated by reabsorption of more Cl- (another measured anion)

Question 9

How does the body initially compensate for metabolic acidosis?

Answer 9

It will decreases pCO2 via expelling more CO2 through hyperventilation

Question 10

In cases of chronic metabolic acidosis, how will the body compensate?

Answer 10

Production of Ammonia causes proton trapping in tubular lumen of CD via exchanging protons instead of potassium to make ammonium (NH4+)

Question 11

How can chronic cases of metabolic alkalosis lead to hypokalemia?

Answer 11

intracellular inorganic phosphate will exchange extracellular protons for intracellular K+, thus trapping K+ in the tubular lumen and increase K+ secretion

Question 12

Hypoventilation can compensate for acute metabolic alkalosis. How does hypoventilation decrease plasma pH?

Answer 12

If respiration is decreased, more acidic CO2 will remain in the bloodstream thus decreasing plasma pH

Question 13

How can recurrent episodes of emesis lead to metabolic alkalosis?

Answer 13

Excessive loss of gastric protons decreases pancreatic secretion of bicarbonate

Question 14

How does aldosterone affect plasma pH?

Answer 14

Increases pH due b/c aldosterone promotes H+ excretion in CD

Question 15

How can diarrhea lead to metabolic acidosis?

Answer 15

diarrhea decreases bicarbonate reabsorption in the colon thus decreasing serum bicarbonate

Question 16

In the context of plasma volume, what is the physiological consequence of enhanced response to ADH and how can diuretics counteract it?

Answer 16

Blood becomes overdiluted leading to edema; when blood becomes overdiluted, BP will be dangerously elevated; diuretics can counteract this by driving more fluid into intravascular compartments to be excreted through the kidneys

Question 17

How does SIADH cause hyponatremia?

Answer 17

ADH’s overall effect is to increases plasma volume and elevate BP; it does this by increasing water reabsorption which decreases plasma osmolarity

Question 18

How can ACE inhibitors cause hyperkalemia?

Answer 18

inhibition of RAAS will decrease K+ secretion in DCT & CD

Question 19

What conditions can cause pseudohyperkalemia?

Answer 19

Tumor lysis syndrome & rhabdomyolysis

Question 20

What is the pathogenesis of Bartter Syndrome?

Answer 20

mutations of genes that codes for NKCC channels

Question 21

Based on your understanding of how ADH & aldosterone influence electrolyte balance through their actions on ROMK & NKCC channels, what can you predict will be the physiologic consequences of Bartter Syndrome?

Answer 21

ADH & aldosterone work together to elevate BP; if these hormones cannot act on receptors that drive this process, hypotension will result; impaired ability of ADH to act on NKCC channels will decrease Ca & Mg reabsorption leading to hypercalciuria, hypocalcemia, & hypomagnesemia; additionally, insensitivity to ADH will impair the body’s ability to retain water leading to polyuria & polydipsia

Question 22

What is the pathogenesis of Gitelman syndrome?

Answer 22

mutations of the gene that encodes for NCC channels

Question 23

What are the diagnostic hallmarks of Gitelman syndrome?

Answer 23

hypercalciuria, alkalosis, low serum Cl & Mg

Question 24

How does renal artery stenosis impair kidney function?

Answer 24

decreased RBF into the kidney thus decreasing GFR

Question 25

What are the main causes of Hydronephrosis?

Answer 25

outlet obstruction due to a kidney tumor, enlarged prostate, or kidney stones; posterior urethral valves

Question 26

How does hydronephrosis affect glomerular hydrostatic pressure?

Answer 26

it increases it

Question 27

How can CHF lead to acute kidney injury?

Answer 27

decreased blood flow activates baroreceptor complex in cardiac atria which stimulates ADH release in posterior pituitary; this can cause fluid volume overload in the kidneys

Question 28

How can acidemia cause hypercalcemia?

Answer 28

in an acidic pH environment, protons will outcompete Ca ions for binding to albumin leaving ionized Ca in the plasma

Question 29

How can hypercalcemia cause arrhythmias?

Answer 29

hypercalcemia decreases excitability via stabalizing the action potential gradient (making it more neutral); Intracellular Ca is higher relative to the extracellular concentration

Question 30

How can hypocalcemia increases risk of tetany & clonus?

Answer 30

it increase neuron excitability due to lowered threshold

Question 31

what conditions can lead to an increased BUN?

Answer 31

decreased GFR; high protein diet; CHF; hypovolemia

Question 32

How does Cushing’s syndrome affect kidney function?

Answer 32

cortisol increases expression of NHE; too much cortisol can cause to much reabsorption of bicarbonate

Question 33

what conditions can lead to a decrease in BUN?

Answer 33

liver failure/disease; SIADH

Question 34

What effect does increased intracranial pressure have on serum glucose levels?

Answer 34

it decreases serum glucose concentration

Question 35

What is the pathogenesis of Alport syndrome & what are common associated symptoms?

Answer 35

x-linked mutation of type IV collagen; associated with hearing & vision loss; renal disease; hematuria, proteinuria (nephritic syndrome); progresses to ESRD

Question 36

urothelium is what type of epithelium?

Answer 36

transitional epithelium

Question 37

What kind of metabolic disturbances can result in hypermagnesiumenima?

Answer 37

ESRD; inhibition of K+ & Ca2+ channels; hypoparathyroidism

Question 38

ANGII does what to the efferent arteriole to increase GFR?

Answer 38

vasoconstricts it

Question 39

Why would you want to decrease GFR in a pt. that has hypoalbuminemia?

Answer 39

If the pt. is losing albumin to urine, it would make sense decrease GFR, b/c this will cause more fluid to leave through the efferent arteriole and bypass the glomerulus

Question 40

What is a physiological consequence of prolonged use of loop diuretics?

Answer 40

Loop diuretics block transporting channels in the TAL which is the primary site for Magnesium reabsorption; so chronic use would lead to hypomagnesemia

Question 41

How would you expect chronic kidney disease to impact serum sodium levels?

Answer 41

Reduced kidney function will decrease sensitivity to ADH & aldosterone the two main hormones that regulate renal sodium reabsorption; this will decrease sodium reabsorption leading to hyponatremia

Question 42

How would you expect CKD to impact serum potassium levels?

Answer 42

reduced kidney function will decreases sensitivity to ADH & aldosterone, the two main regulators of potassium secretion leading to hyperkalemia

Question 43

How would you expect CKD to impact serum calcium & phosphate levels?

Answer 43

There are two main mechanisms that regulate renal calcium & phosphate reabsorption: PTH & Vit. D; when kidney function is reduced, it is not producing as much Vit. D. leading to hypocalcemia and is not as sensitive to PTH which will cause hyperphosphatemia

Question 44

how would you expect CKD to impact serum magnesium levels?

Answer 44

Mg2+ reabsorption is coupled to Ca2+ & K+ transportation in NKCC2 & ROMK channels in the TAL;