Basic - Renal, Urinary, Electrolytes Flashcards

1
Q

How does chronic alcoholism cause hyponatremia?

A

impairs free water excretion -> dilutional hyponatremia

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2
Q

How does chronic alcoholism cause respiratory alkalosis?

A
  1. causes central and sympathetic nervous system activation –> increased respiratory drive
  2. ethanol metabolized to lactic acid -> metabolic acidosis -> compensatory respiratory alkalosis
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3
Q

How does chronic alcoholism cause hyperuricemia?

A
  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
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4
Q

How does alcohol ingestion affect MAC of anesthetic agents?

A

Acute ingestion: decreases MAC

Chronic: increases MAC

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5
Q

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

A

Upregulation

  • upregulated receptors are immature and stay “open” longer than the mature receptors
  • long activation times -> sig increase in potassium
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6
Q

Succinylcholine is metabolized by ____

A

plasma or butyrylcholinesterase

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7
Q

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

A

Dibucaine test

  • 80 is normal
  • 20 is abnormal (prolonged paralysis with single intubating dose of sux)
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8
Q

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

A
  1. 5 mEq/L for both

* Chronic RF is NOT associated with upregulation of ACh receptors

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9
Q

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

A

opening of the ion channel

- INflux of Na, EFflux of K -> depolarization

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10
Q

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

A

Exaggerated depolarization

-> exaggerated efflux of K+

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11
Q

Which NMB should be avoided in pts with renal disease?

A

Pancuronium
- 80% renally excreted

*Roc is 25% renally excreted

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12
Q

Neostigmine is eliminated by the kidney at __%

Edrophonium is eliminated by the kidney at ___%

A

50%
75%

*RF has significant effects on NMB AND reversal agents

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13
Q

Can sevoflurane cause kidney injury?

A

Controversial

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

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14
Q

Common causes of anion gap metabolic acidosis

A
MUDPILES
Methanol
Uremia
DKA
Paraldehyde
Iron/INH
Lactate
Ethanol/Ethylene glycol
Salicylates
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15
Q

Where is bicarbonate filtered?

A

in the renal glomerulus

  • almost entirely reabsorbed
  • 85% reabsorbed in prox tubule
  • 10% in thick ascending LOH
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16
Q

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

A
  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
17
Q

How is rocuronium cleared and excreted?

A

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

Excreted

  • 75% hepatobiliary
  • 25% renally
18
Q

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

A

Succinylcholine

Cisatracurium

19
Q

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

A

Uremia -> platelet dysfunction

  • Impaired vWF formation and release
  • Impaired GPIIb-IIIa (surface protein on platelets)
20
Q

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

A

HYPERcoagulability

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

21
Q

Why is ketorolac nephrotoxic?

A

Vasoconstricts glomerular AFFerent arterioles

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

22
Q

Prostaglandins dilate (afferent/efferent) arteriole

A

AFFerent (carries blood towards glomerulus)

- increase GFR

23
Q

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

A

Angiotensin II

AT1 receptor stimulation

24
Q

Fenoldopam MOA

A
  1. selective D1 receptor agonist
    - direct natriuresis and diuresis
  2. Renal vasodilator
25
Nonanion gap acidoses are caused primarily by (3)
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
26
Substances commonly removed using dialysis
1. Calcium 2. Magnesium 3. Phosphate 4. Potassium 5. Urea 6. Creatinine 7. Free water *NOT sodium
27
What levels are usually increased after dialysis?
``` large molecules (ie. albumin) - transiently d/t concentrating effect from removal of free water (absolute amt is same) ```
28
(Hypercalcemia/Hypocalcemia) is associated with ESRD
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
29
(Hypernatremia/Hyponatremia) is associated with ESRD
Neither
30
During TURP procedures, how does glycine toxicity manifest?
Hyperammonemia | -> CNS symptoms and nausea and transient blindness
31
Calculate FENa
[(PCr x UNa) / (PNa x UCr)] x 100 *FENa < 1 = prerenal > 2 = Intrinsic or Postrenal
32
Why do pts taking ACE-i have trouble with hypotension intraop?
RAAS is chronically blocked by ACEi or ARbs Release of A2 by RAAS during episodes of acute hypotention is impaired - A2 mediates
33
Perioperatively, the most common cause of AKI is _____
ATN - Death of renal tubular epithelial cells - Ischemic vs toxic
34
How does hyperventilation result in hypocalcemia?
In response to respiratory alkalosis -> H+ bound to neg charged albumin is released -> Ca2+ then binds to albumin (decreases free/ionized calcium)
35
Vomiting vs Diarrhea | - what are their assoc metabolic disturbances?
Vomiting - metabolic alkalosis Diarrhea - metabolic acidosis *vomiting goes up, so does the pH diarrhea goes down, so does the pH