Basic - Renal, Urinary, Electrolytes

Question 1

How does chronic alcoholism cause hyponatremia?

Answer 1

impairs free water excretion -> dilutional hyponatremia

Question 2

How does chronic alcoholism cause respiratory alkalosis?

Answer 2

1. causes central and sympathetic nervous system activation –> increased respiratory drive
2. ethanol metabolized to lactic acid -> metabolic acidosis -> compensatory respiratory alkalosis

Question 3

How does chronic alcoholism cause hyperuricemia?

Answer 3

1. Beer contains purines –> metabolized to uric acid
2. Ethanol increases adenine degradation -> metabolized to uric acid
3. Ethanol metabolism raises lactate levels -> inhibits renal excretion of uric acid

Question 4

How does alcohol ingestion affect MAC of anesthetic agents?

Answer 4

Acute ingestion: decreases MAC

Chronic: increases MAC

Question 5

Pts with denervation of muscle development have an (upregulation / downregulation) of the ACh receptor (AchR).
- What does this mean?

Answer 5

Upregulation

• upregulated receptors are immature and stay “open” longer than the mature receptors
• long activation times -> sig increase in potassium

Question 6

Succinylcholine is metabolized by ____

Answer 6

plasma or butyrylcholinesterase

Question 7

How do you test for the activity of butyrylcholinesterase (the thing that metabolizes succinylcholine)?

Answer 7

Dibucaine test

• 80 is normal
• 20 is abnormal (prolonged paralysis with single intubating dose of sux)

Question 8

How much does serum potassium increase after succinylcholine admin in a healthy pt?
In a pt with ESRD?

Answer 8

0. 5 mEq/L for both

* Chronic RF is NOT associated with upregulation of ACh receptors

Question 9

After each a-subunit on the ACh receptor binds an ACh molecule, what happens?

Answer 9

opening of the ion channel

- INflux of Na, EFflux of K -> depolarization

Question 10

How does an increase in the number of ACh receptors affect the administration of succinylcholine?

Answer 10

Exaggerated depolarization

-> exaggerated efflux of K+

Question 11

Which NMB should be avoided in pts with renal disease?

Answer 11

Pancuronium
- 80% renally excreted

*Roc is 25% renally excreted

Question 12

Neostigmine is eliminated by the kidney at __%

Edrophonium is eliminated by the kidney at ___%

Answer 12

50%
75%

*RF has significant effects on NMB AND reversal agents

Question 13

Can sevoflurane cause kidney injury?

Answer 13

Controversial

- When exposed to CO2 absorbents, if low flow, sevo can be degraded into compound A in animals

Question 14

Common causes of anion gap metabolic acidosis

Answer 14

MUDPILES
Methanol
Uremia
DKA
Paraldehyde
Iron/INH
Lactate
Ethanol/Ethylene glycol
Salicylates

Question 15

Where is bicarbonate filtered?

Answer 15

in the renal glomerulus

• almost entirely reabsorbed
• 85% reabsorbed in prox tubule
• 10% in thick ascending LOH

Question 16

Major independent preop risk factors for postop AKI in noncardiac sx? (6)

Answer 16

1. Age > 59
2. BMI > 32
3. Chronic liver disease
4. COPD requiring chronic bronchodilator use
5. Peripheral vascular occlusive disease
6. High risk/emergency sx

Question 17

How is rocuronium cleared and excreted?

Answer 17

Cleared by hepatic uptake
- prolonged paralysis in pts with cirrhosis and liver failure

Excreted

• 75% hepatobiliary
• 25% renally

Question 18

Which NMBs have minimal renal excretion and predictable durations of actions in pts with renal failure?

Answer 18

Succinylcholine

Cisatracurium

Question 19

Why would a pt with ESRD who was last dialyzed 4 days ago have inadequate surgical hemostasis?

Answer 19

Uremia -> platelet dysfunction

• Impaired vWF formation and release
• Impaired GPIIb-IIIa (surface protein on platelets)

Question 20

Reduced Antithrombin III –> (hypercoagulability/hypocoagulability). Why?

Answer 20

HYPERcoagulability

- ATIII is a protease that inactivates IIa (thrombin), VIIa, IXa, Xa, and XIa in the clotting cascade

Question 21

Why is ketorolac nephrotoxic?

Answer 21

Vasoconstricts glomerular AFFerent arterioles

- especially in the setting of hypovolemia where RAAS is trying to dilate EFFerent arterioles

Question 22

Prostaglandins dilate (afferent/efferent) arteriole

Answer 22

AFFerent (carries blood towards glomerulus)

- increase GFR

Question 23

ACEi will antagonize production of ___, which will decrease cardiomyocyte remodeling of the heart induced by __.

Answer 23

Angiotensin II

AT1 receptor stimulation

Question 24

Fenoldopam MOA

Answer 24

1. selective D1 receptor agonist
   - direct natriuresis and diuresis
2. Renal vasodilator

Question 25

Nonanion gap acidoses are caused primarily by (3)

Answer 25

1. Chloride containing acid administration (ie. NS, TPN) 2. Increased HCO3- loss (GI or kidney) 3. Decreased acid excretion (hypoaldosteronism or RTA1) _____________ FUSEDCARS - Fistula - Ureteroenterostomy - Saline - Endocrine (hyperparathyroidism) - Diarrhea - Carbonic anhydrase inhibitor - Ammonium chloride - RTA - Spironolactone

Question 26

Substances commonly removed using dialysis

Answer 26

1. Calcium 2. Magnesium 3. Phosphate 4. Potassium 5. Urea 6. Creatinine 7. Free water *NOT sodium

Question 27

What levels are usually increased after dialysis?

Answer 27

``` large molecules (ie. albumin) - transiently d/t concentrating effect from removal of free water (absolute amt is same) ```

Question 28

(Hypercalcemia/Hypocalcemia) is associated with ESRD

Answer 28

HYPOcalcemia - kidney loses ability to reabsorb Ca - unable to convert 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is responsible for increasing Ca2+ absorption in GI tract

Question 29

(Hypernatremia/Hyponatremia) is associated with ESRD

Answer 29

Neither

Question 30

During TURP procedures, how does glycine toxicity manifest?

Answer 30

Hyperammonemia | -> CNS symptoms and nausea and transient blindness

Question 31

Calculate FENa

Answer 31

[(PCr x UNa) / (PNa x UCr)] x 100 *FENa < 1 = prerenal > 2 = Intrinsic or Postrenal

Question 32

Why do pts taking ACE-i have trouble with hypotension intraop?

Answer 32

RAAS is chronically blocked by ACEi or ARbs Release of A2 by RAAS during episodes of acute hypotention is impaired - A2 mediates

Question 33

Perioperatively, the most common cause of AKI is _____

Answer 33

ATN - Death of renal tubular epithelial cells - Ischemic vs toxic

Question 34

How does hyperventilation result in hypocalcemia?

Answer 34

In response to respiratory alkalosis -> H+ bound to neg charged albumin is released -> Ca2+ then binds to albumin (decreases free/ionized calcium)

Question 35

Vomiting vs Diarrhea | - what are their assoc metabolic disturbances?

Answer 35

Vomiting - metabolic alkalosis Diarrhea - metabolic acidosis *vomiting goes up, so does the pH diarrhea goes down, so does the pH