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Anesthesia based on Nebuchanedzzer II > Basic - Renal, Urinary, Electrolytes > Flashcards

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
Q

Nonanion gap acidoses are caused primarily by (3)

A
  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
Q

Substances commonly removed using dialysis

A
  1. Calcium
  2. Magnesium
  3. Phosphate
  4. Potassium
  5. Urea
  6. Creatinine
  7. Free water

*NOT sodium

27
Q

What levels are usually increased after dialysis?

A 
large molecules (ie. albumin)
- transiently d/t concentrating effect from removal of free water (absolute amt is same)
28
Q

(Hypercalcemia/Hypocalcemia) is associated with ESRD

A

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
Q

(Hypernatremia/Hyponatremia) is associated with ESRD

A

Neither

30
Q

During TURP procedures, how does glycine toxicity manifest?

A

Hyperammonemia

-> CNS symptoms and nausea and transient blindness

31
Q

Calculate FENa

A

[(PCr x UNa) / (PNa x UCr)] x 100

*FENa < 1 = prerenal
> 2 = Intrinsic or Postrenal

32
Q

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

A

RAAS is chronically blocked by ACEi or ARbs

Release of A2 by RAAS during episodes of acute hypotention is impaired
- A2 mediates

33
Q

Perioperatively, the most common cause of AKI is _____

A

ATN

  • Death of renal tubular epithelial cells
  • Ischemic vs toxic
34
Q

How does hyperventilation result in hypocalcemia?

A

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

35
Q

Vomiting vs Diarrhea

- what are their assoc metabolic disturbances?

A

Vomiting - metabolic alkalosis
Diarrhea - metabolic acidosis

*vomiting goes up, so does the pH
diarrhea goes down, so does the pH

Anesthesia based on Nebuchanedzzer II (38 decks)

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