Renal

Question 1

What proportion of sodium filtered by the glomerulus is typically excreted in the urine:

A. 95%
B. 75%
C. 50%
D. 25%
E. 5%

Answer 1

5%
The vast majority of sodium in the glomerular ultrafiltrate is reabsorbed in the nephron. Of the sodium that is reabsorbed, about 75% is absorbed in the proximal tubule, 15% in the ascending limb of henle, 5% in distal convoluted tubule, and 5% in the collecting tubule. Why is this important – it helps one understand and direct therapy when using diuretics.

Question 2

Is energy needed for absorption of solutes? What about how water is absorbed? How are solutes absorbed at proximal tubule?

Answer 2

Absorption of solutes in the kidney requires energy, either directly or indirectly; whereas water moves passively following concentration gradients. At the proximal tubule, water can move in direct proportion to solutes, so the ultrafiltrate is absorbed isotonically unlike the ascending loop of Henle which is impermeable to water.

Question 3

Which of the following areas of the nephron are most responsible for the concentrating urine:

A. Proximal tubule
B. Ascending loop of Henle
C. Distal convoluted tubule
D. Collecting duct

Answer 3

The correct answer is: D: Collecting duct

Whether you realize it or not, this is the hardest question to answer so far. To understand why D is correct you have to understand the entirety of renal physiology. Essentially, the ascending loop of Henle removes solute from the ultrafiltrate leaving a hypotonic filtrate in the tubules while the interstitium is hypertonic. Through the vasa recta, solutes are concentrated in the deeper medullary portions of the nephron and more superficial portions are diluted by water transfer from the descending limb of Henle. This creates a very hypertonic interstitium within the kidney medulla. The hypotonic ultrafiltrate moves out of the loop of Henle and into the distal convoluted tubule where minor modifications are made and then down to the collecting ducts. In the medullary portion of the collecting duct, the tubule is impermeable to water and the interstitium is very hypertonic. Anti-diuretic hormone (ADH) upregulates aquaporin-2 water channels, that when present, allow water to move towards the very hypertonic interstitium, therefore concentrating the urine.

Question 4

How does Furosemide work? In detail please-as far as the collecting ducts, etc.

Answer 4

Furosemide interrupts sodium absorption at the loop of Henle, therefore decreasing the tonicity of the medullary interstitium (and increasing the tonicity of the ultrafiltrate), and therefore decreasing the gradient between the filtrate and intersitium at the collecting duct….therefore decreasing water re-uptake in the kidney and diluting the urine. Slowly re-read this three or four times.

Question 5

How does aldosterone work? On which ducts? And what channels does it affect?

Answer 5

Aldosterone acts primarily on the cortical collecting duct by increasing the density of potassium channels and sodium potassium ATPase enzymes. By increasing Na/K ATPase activity the cortical collecting duct cells are constantly removing sodium out into the plasma creating a gradient for sodium uptake from the tubular ultrafiltrate. As sodium is taken up, potassium is moved out of the cells into the filtrate and excessive levels of aldosterone (such as seen in Conn’s syndrome) can lead to hypokalaemia. The renin-angiotension-aldosterone-system (RAAS) is partially responsible for increasing aldosterone production and release, in which angiotension II stimulates aldosterone release.

Question 6

What stimulates renin release? What does renin concert? What converts angiotensin 1 to angiotensin 2, and where? Angiotensin 2 causes mesangial cells in JGA to

Answer 6

Renin is released in response to B1 sympathetic stimulation and decreased afferent blood flow in the juxtaglomerular apparatus

In response to low afferent blood flow or sympathetic stimulation (indirectly), specialized cells in the juxtaglomerular apparatus release the enzyme renin which converts angiotensinogen to angiotension I. Angiotension I is converted into angiotension II by angiotension converting enzyme (ACE) in the lungs. Angiotension II causes mesangial cells in the juxtaglomerular apparatus to contract and decrease glomerular blood flow, thus further stimulating rennin release. Angiotension II also increases aldosterone release from the adrenal cortex. Angiotension II also has systemic effects on multiple organ systems which is complicated and only partially elucidated.

Question 7

What does dopamine due as far as renal arteries?

Answer 7

D1 receptors, responsive to low dose dopamine and fenoldapam, dilate both afferent and efferent arterioles and increase GFR.

Question 8

Which of the following are true regarding the regulation of renal blood flow (RBF) and glomerular filtration rate (GFR):

A. Creatinine clearance severely underestimates GFR
B. RBF is purely pressure dependent and is not autoregulated
C. Increased tubular flow rates increase RBF
D. Atrial natreutic peptide (ANP) decreases GFR
E. D1 dopamine receptors dilate glomerular arterioles

Explain why each one is right or wrong

Answer 8

E: D1 dopamine receptors dilate glomerular arterioles

This is an example of a question with an easy answer and difficult distracters, perhaps to the point where you will be tempted to second guess the correct answer. D1 receptors, responsive to low dose dopamine and fenoldapam, dilate both afferent and efferent arterioles and increase GFR. Creatinine clearance mildly overestimates GFR because creatinine is filtered and secreted. Like most organ systems, the kidney is autoregulated, often quoted to be MAP 80-180. Increased tubular flow rates (and therefore urine production) decreases RBF. ANP is released from atrial myocytes in response to distention (fluid overload) and dilate the afferent arteriole and constrict the efferent, causing increased glomerular pressures and hence increased GFR.

Question 9

A patient has a serum creatinine of 2.0 and a serum blood urea nitrogen (BUN) of 44; which of the following fractional excretion of sodium (FENA) ratios would be expected:

A. 0.5%
B. 1.5%
C. 2.5%
D. 25%
E. 105%

Explain this as it relates to FeNA, what BUN:act ratios mean

Answer 9

The FENA is a ratio that relates plasma and urine levels of sodium and creatinine, and employs the idea that a functioning kidney with low blood flow (pre-renal renal failure) will have increased creatinine and avidly reabsorb sodium (low urine sodium). A FENA less than 1% is typical of pre-renal etiologies for increased creatinine or low urine output. Furthermore, a ratio of BUN / Cr greater than 15-20 (depending on the source), as is the case in the stem, is also indicative of pre-renal eitiology. FENA can also be helpful when elevated above 2%, in this case it is indicative of a kidney that poorly concentrates urine due to renal (as opposed to pre- or post-renal) injury.

Question 10

A patient with an elevated baseline serum creatinine, diabetes, hypertension, and peripheral vascular disease (PVD) is to undergo fluoroscopy with contrast with possible iliac to popliteal bypass grafting. Which of the following strategies IS NOT helpful in preventing post operative renal failure:

A. > 1 liter of crystalloid administered prior to the procedure to produce > 150 cc of urine / hour
B. 600 mg of N-acetylcystine twice before and after contrast administration
C. 1 mg/ kg of lidocaine IV prior to contrast administration
D. Bicarbonate gtt before, during, and after procedure
E. Using low osmolality contrast

Answer 10

All of the above have theoretical utility in decreasing the rate of post-contrast renal failure except IV lidocaine. Volume administration probably has the best evidence. The evidence for isotonic bicarbonate and N-acetylcystine has been questioned, but likely results in no harm. The amount of data out there on this subject is enormous and there’s a lot of contradicting data, even regarding utilizing low osmolality contrast. Its worth adding that even statins have been thought to be protective of contrast induced nephropathy.

So what would a nephrologist say? Most likely they’ll tell you there’s no good evidence to give fluids, bicarb, and N-acetylcystine to prevent contrast induced nephropathy, but please go ahead and give fluids, bicarb, and N-acetylcystine.

Question 11

Treatment of AIN in a patient who was scheduled for a non-emergent case:

Answer 11

AIN is an inflammatory condition of the kidney, most commonly secondary to drugs, especially penicillin and some first generation cefalosporins like cefelexin. Treatment is supportive with steroids. You could treat patient with IV steroids and hospitalize

Question 12

What is the only proven therapy to improve the natural course of rhabdomyolyisis:

Answer 12

There are only two therapies proven to help: IV fluids and dialysis.

Question 13

Treatment for rhabdo:

Answer 13

Calcium, glucose, insulin, and bicarbonate

Question 14

Transfusion guidelines for patients with CKD? Anemia in CKD is secondary to what?

Answer 14

Current guidelines for transfusing patients with CKD are based on symptoms, not Hb level. Patients often tolerate Hb of 7 and even lower. Given the unlikely chance of blood loss and lack of fluid shift or surgical stress, a trigger finger release should not require stress test or blood transfusion in this setting. Anaemia in CKD is secondary to decreased erythropoietin production by the diseased kidneys.

Question 15

Why do people with CHF have increased renin levels and why are they given lisinopril?

Answer 15

Decreased GFR, as well as increased sympathetic discharge from low cardiac output causes increased renin secretion from the juxtaglomerular apparatus, which stimulates the RAAS finally resulting in aldosterone release and increased sodium retention. Afterload increases from angiotension II as well as fluid overload from sodium retention results in worsening cardiac function, decreasing cardiac output, and decreased GFR; which then further stimulates the RAAS. It is a pathological cycle that can be interrupted by ACE inhibitors or angiotensin II receptor blockers (ARBs).

Question 16

Acetazolamide works how? Why does this matter?

Answer 16

Acetazolamide is a carbonic anhydrase inhibitor, which works at multiple sites including the proximal tubule of the kidney. It indirectly inhibits the uptake of bicarbonate at the proximal tubule

Absorbed bicarbonate can accept a proton becoming carbonic acid which can either disassociate into CO2 and H2O or release the proton and become bicarbonate again. In the presence of carbonic anhydrase, the formation of CO2 and H20 is favored which forms a gradient for bicarbonate entry into the proximal tubule. When acetazolamide inhibits carbonic anhydrase, bicarbonate uptake is decreased as is H+ excretion, creating a non-gap acidosis.

Question 17

Now of thiazides:

Answer 17

It inhibits the Na-Cl transporter in the distal convoluted tubule

Question 18

Furosemide

Answer 18

It inhibits the Na-K-2Cl transporter in the thick ascending limb of the loop of Henle

Question 19

At what level of urine output would oliguria generally be defined:

Answer 19

A: < 0.5 cc/ kg/ hr

Question 20

What is the best treatment for acute tubular necrosis (ATN):

Answer 20

Re-establishment of renal blood flow (RBF)

Question 21

Oliguria in the OR:

Answer 21

The rules of oliguria are unpredictable and should not be taken dogmatically especially with laparoscopic surgery and trendelenburg position, both of which are associated with low urine outputs without sequelae.

Question 22

Normal Intraoperative fluids:

Answer 22

4 cc/ kg/ hr for surgical loss, 1:1 administration of 5% albumin for blood loss, and 1 L lactated ringer preop to cover NPO status.

Question 23

Which of the following would be expected with furosemide administration:

A. Hyperkalaemia
B. Hypercalcaemia
C. Metabolic alkalosis
D. Respiratory alkalosis
E. Hypermagnesaemia

Answer 23

The ABA has a love affair with metabolic acidoses and alkaloses in the setting of diuretics, so you may as well get your head around it. Loop and thiazide diuretics prevent sodium uptake at the ascending limb of Henle and distal convoluted tubule, respectively. The increased sodium load in the ultrafiltrate at the cortical collecting duct results in increased sodium uptake, which causes increased potassium uptake (by the principal cells to maintain electroneutrality) and leads to H+ secretion (into the ultrafiltrate which is now essentially urine) and a metabolic alkalosis. The metabolic alkalosis rarely results in a clinically significant alkalaemia. Furosemide also inhibits the uptake of potassium, calcium, and magnesium and leads to deficiencies of these electrolytes. An important distinction between loop and thiazide diuretics is that thiazide diuretics increase calcium reabsorption whereas loop diuretics lead to hypocalcaemia (not hypercalcaemia). Therefore one would utilize lasix and non-calcium containing crystalloid to treat hypercalcaemia.

Question 24

Why is digoxin and furosemide a bad idea?

Answer 24

Digoxin competes with potassium on the Na-K ATPase causing inhibition of this enzyme, increased intracellular sodium levels which are exchanged for calcium, therefore increasing intracellular calcium concentrations and contractility. In the setting of hypokalaemia, digoxin further out competes potassium for binding sites and leads to digoxin toxicity, which often manifests by arrhythmias

Question 25

Symptoms of uremia:

Answer 25

Digoxin competes with potassium on the Na-K ATPase causing inhibition of this enzyme, increased intracellular sodium levels which are exchanged for calcium, therefore increasing intracellular calcium concentrations and contractility. In the setting of hypokalaemia, digoxin further out competes potassium for binding sites and leads to digoxin toxicity, which often manifests by arrhythmias

Question 26

Why does HD lead to hypotension?

Answer 26

The reason that haemodialysis (HD) leads to hypotension is that it employs countercurrent exchange where large volumes of blood are rapidly driven through the dialysis circuit while dialysis fluid is driven at (at least) twice the rate in the opposite direction through a semi-permeable membrane. This process relies on rate and volume characteristic that leads to a relative hypovolaemia for the patient. Furthermore, fluid is removed from the patient but not returned, so this rapid process leaves a decreased intravascular volume.

Question 27

CRRT be HD:

Answer 27

CRRT has two major differences with HD. First it is pressure driven, not relying on high volumes and flows, so less blood is removed from the patient at any one time. Secondly, fluid removed from the patient can be given back within the circuit so the patient tolerates the procedure better. Although CRRT is less effective than HD, it is done continuously throughout the day, so that it essentially produces the same degree of filtration that would be expected from HD. Small runs of HD are not sufficient for effective dialysis and every-other day HD requires large volumes and rates

Question 28

What is normal plasma osmolality: and what is the formula? And when it’s higher than calculated what does that mean?

Answer 28

290. Plasma osmolality is (2X Na) + (Glu/18) + (BUN/2.8). When actual measured osmolality is higher than calculated, it is referred to as an osmolal gap, which, in general, is indicative of chronic more than acute renal failure.

Question 29

High glucose and sodium? Why? How to correct?

Answer 29

It is worth knowing that at a very high plasma glucose, the sodium is underestimated.
This is because the glucose is osmotically active and pulls in additional water into the plasma, essentially diluting the sodium. If the glucose were to be rapidly corrected, the plasma water would either be excreted from the body or move towards the next highest osmolality compartment (intracellular, interstitial, etc). The actual number for conversion is 1.6 (1.6 is the classic teaching, which is an oversimplification); in that for every increase of glucose of 100 mg/dl, the sodium will fall by 1.6 mEq/L. In this case, the glucose is about 1,000 points above normal so the sodium would be expected to rise by 16 points (140 +16 = 156), making the patients actual state hypernatraemic. Other common causes of hypernatraemia include diabetes insipidus and administration of hypertonic saline.

Question 30

Normal spot sodium urine:

Answer 30

Spot urine sodium should be under 20 mEq/L, especially in the setting of hypovolaemia (where the kidney should definitely be holding on to as much sodium as possible).

Question 31

In the setting of hyponatraemia and continuous salt wasting, intravascular volume should be replaced with:

Answer 31

In the setting of hyponatraemia and continuous salt wasting, intravascular volume should be replaced with isotonic fluids such as normal saline and supplemental salt administered. Hypertonic saline can be used instead of salt tabs

Question 32

D5W is iso, hypo, hyper?

Answer 32

Hypo

Question 33

Hypothermia does what to K+?

Answer 33

Decreases it

Insulin and B2 sympathetic stimulation increases Na-K ATPases’ activity, driving K intracellular.

Question 34

Which of the following is NOT an ECG finding consistent with hypokalaemia

A. U waves
B. Prolonged PR interval
C. T wave flattening
D. ST elevation
E. ST depression

Answer 34

Hypokalaemia leads to two cardiac manifestations: 1) increased myocyte automaticity (arrhythmia) and 2) delayed repolarization. All of the above are findings consistent with hypokalaemia except ST elevations. The most classic and notable of these is an increasingly prominent U wave

Question 35

When would you give fluids and diuretics? Hypercalcemia and going to the OR:

Answer 35

One of the few indications for fluid administration and diuretics together is hypercalcaemia. Hypercalacaemia can be life threatening and it is advised to treat the hypercalcaemia (with at least crystalloid) before heading to the OR.

Question 36

On the boards, hypophosphataemia is:

Answer 36

On the boards, hypophosphataemia is respiratory failure and/ or prolongation of muscle relaxants.

Question 37

A decrease in the strong ion gap (SIG) would be consistent with:

A. Metabolic Acidosis
B. Metabolic Alkalosis
C. Respiratory Acidosis
D. Respiratory Alkalosis

What is the SIG, what are examples of the answer above??

Answer 37

A: Metabolic Acidosis

The strong ion gap (SIG) is a measure of all of the cations (mostly Na+, but also K+, Ca2+, Mg 2+, etc) and the anions (mostly Cl-, but also lactate, HCO3-, and the conjugate bases (A-) of strong acids). The SIG is typically about 40 mEq/L, meaning that there are 40 mEq/L of unmeasured anions. When Cl- levels increase, the SIG decreases. With non-anion gap acidosis, increased Cl- leads to increased plasma H+ (as the sodium does not increase), leading to a metabolic acidosis. Because the Cl- increases, the anion gap (Na – (Cl- + bicarb)) will not be widened (nongap metabolic acidosis). Examples of this are renal tubular acidosis where (by definition) the Na+ excretion is greater than the Cl- excretion, leading to increased plasma Cl-. Another example is GI losses of fluid with low Cl- content (such as diarrhea), leading to sodium spilling in greater proportion to Cl-. Yet another example is large amounts of normal saline administration, where the Cl- load is high, leading to H+ being drawn out of the cells (acidosis). By thinking in terms of SIG, you come to realize that it is the handling of Na+ and Cl- that leads to acid-base disturbance, not H+ and bicarb.

Lets recap: A decreased SIG demonstrates a metabolic acidosis, an increased SIG demonstrates a metabolic alkalosis. An anion gap (AG) is different. A normal AG means that you are losing buffer and an increased AG means your’e retaining acid. Don’t let the terminology confuse you, you already learned all this in medical school and apply it daily in the OR.

Question 38

Acid base is really about which two ions? What does the kidney do when GO losses of chloride are high?

Answer 38

With the removal of HCl from the stomach, it is the Cl- loss, not the H+ loss leading to an alkalosis. With the loss of Cl-, the strong ion gap (all measured cations – all measured anions) increases (remember that the number of cations must equal anions in reality, this is what we can measure!). With the loss of Cl-, H+ must be moved out of the plasma, increasing the pH (alkalosis). By replacing the Cl- load, the alkalosis can be treated. Since normal saline has a higher Cl- load and, more importantly, an equal load of Cl- in proportion to Na+, it will be more effective in treating the alkalosis than lactated ringers (which has addition of lactate, allowing a lower Cl- load, which is good for treating the acidosis that appears with GI losses – making sense why surgeons use this??). By replacing the Cl-, the alkalosis will (partially) correct, making it Cl- responsive (answer A). This is a metabolic, not a respiratory process (answer B). With normal renal function, the kidneys will try to hang on to Cl- (as substantial losses are occurring in the GI tract), resulting in a low urine Cl- (< 10 mEq/L). Chloride-resistant metabolic alkalosis are related to excessive mineralocorticoids from a variety of reasons and will not be on your boards.

Question 39

A 55 year old man is to undergo cystoscopy, which of the following is the most likely nerve injury:

A. Ulnar neuropathy
B. Common peroneal neuropathy
C. Tibial neuropathy
D. Obturator neuropathy
E. Femoral neuropathy

How does that nerve injury happen? Who is at greatest risk for it? What are risk factors? What does the answer to the above proposed question present like?

Answer 39

Ulnar neuropathy

Common things being common, ulnar neuropathy is the most common position-related nerve injury. The reflex choice would be common peroneal (answer B), which is the most common lower extremity nerve injury.
This injury is more common when the lateral thigh (especially around the knee where the nerve is superficial) lies against a support and when the procedure lasts greater than 2 hours. Ulnar neuropathy is more common when the arm is pronated so that the cubital tunnel is being pressed against the arm board. Interestingly, even when perfect positioning is met, nerve injuries still occur, which argue for alternative causes. Risk factors for nerve injuries include hypotension, vascular disease, and diabetes. Fatter people are at increased risk of ulnar neuropathy and thinner people are at increased risk for common peroneal injury.

Common peroneal nerve injury presents with loss of dorsiflexion (foot drop). Lithotomy position can also lead to sciatic stretch injury, obturator injury (answer D), femoral nerve injury (answer E), and saphenous nerve injury. Tibial nerve injuries (answer C) are uncommon

Question 40

Explain the obturator reflex:
The urologist notes (i. e. complains like a child) that the patient’s thigh adducts whenever electrocautery is applied to the wall of the bladder under spinal anesthesia to the point it is interfering with the surgery. Which of the following is the most appropriate next step:

A. Place the patient in reverse trendelenberg to achieve a more complete saddle block
B. Place the patient in trendelenberg to achieve a higher spinal level
C. Placement of a “3 in 1” block
D. Induce general anesthesia

What can you do about it in the above situation? Obturator innervation comes from:
Are any regional techniques helpful?

Answer 40

obturator reflex” which occurs when electrocautery is applied to the (lateral) bladder wall and some of the current stimulates the obturator nerve. The only sure-proof way to treat this is general anesthesia with neuromuscular blockade. The obturator nerve is derived from L2-4, so a saddle block would not help (answer A). The bladder is innervated with general visceral afferent fibers that primarily derive from the hypogastric plexus (which itself receives innervation from as high as T10), so increasing the level of the block would not help as L2-4 are already presumably blocked (answer B). Multiple regional anesthesia techniques can address the obturator nerve (usually focusing on its sensory functions), with the easiest of these blocks to perform being the “3 in 1 block” (large volume of local anesthesia under the fascia illiaca). This block does not reliably block obturator sensory fibers much less motor function.

Question 41

What is TURP? What are side effects of the glycine solution?

Answer 41

TURP syndrome occurs when absorption of irrigating fluid enters the systemic circulation by way of compromised venous sinuses in the prostate. When a glycine solution is used, all the various manifestations of TURP syndrome are possible. First, large volumes of hypotonic nonelectrolyte containing fluids can decrease serum sodium, leading to hyponatraemia and seizures. This is more common with distilled water than glycine, sorbitol, and mannitol solutions. The length of the procedure as well as the bag height of the irrigation solution (increasing the back pressure) lead to a greater amount of fluid being taken up, which can also precipitate hypervolaemia and heart failure.

Glycine can be metabolized to ammonia (answer A) and both ammonia as well as glycine itself can be a CNS depressant. In fact, cases of transient blindness (answer D) are thought to be caused b the CNS depressing effects of glycine. Both glycine and sorbitol can lead to hyperglycaemia

Question 42

A patient is scheduled to have cystoscopy with stent placement under epidural anesthesia. At which level of loss of cold discrimination is minimally needed to cover surgical pain:

A. T6
B. T8
C. T10
D. T12
E. L2

Answer 42

The correct answer is: A: T6

Fibers as high as T8 need to be completely blocked to ensure loss of sensation of the bladder, ureters, and renal pelvis. Since loss of cold discrimination occurs approximately 2 dermatomes above the level of anesthesia, a T6 level would be appropriate. Below T8 not only surgical stimulation but potential complications such as bladder rupture can occur without specific signs (look for hypotension, confusion, referred pain instead).