Basic - Renal, Urinary, Electrolytes Flashcards
How does chronic alcoholism cause hyponatremia?
impairs free water excretion -> dilutional hyponatremia
How does chronic alcoholism cause respiratory alkalosis?
- causes central and sympathetic nervous system activation –> increased respiratory drive
- ethanol metabolized to lactic acid -> metabolic acidosis -> compensatory respiratory alkalosis
How does chronic alcoholism cause hyperuricemia?
- Beer contains purines –> metabolized to uric acid
- Ethanol increases adenine degradation -> metabolized to uric acid
- Ethanol metabolism raises lactate levels -> inhibits renal excretion of uric acid
How does alcohol ingestion affect MAC of anesthetic agents?
Acute ingestion: decreases MAC
Chronic: increases MAC
Pts with denervation of muscle development have an (upregulation / downregulation) of the ACh receptor (AchR).
- What does this mean?
Upregulation
- upregulated receptors are immature and stay “open” longer than the mature receptors
- long activation times -> sig increase in potassium
Succinylcholine is metabolized by ____
plasma or butyrylcholinesterase
How do you test for the activity of butyrylcholinesterase (the thing that metabolizes succinylcholine)?
Dibucaine test
- 80 is normal
- 20 is abnormal (prolonged paralysis with single intubating dose of sux)
How much does serum potassium increase after succinylcholine admin in a healthy pt?
In a pt with ESRD?
- 5 mEq/L for both
* Chronic RF is NOT associated with upregulation of ACh receptors
After each a-subunit on the ACh receptor binds an ACh molecule, what happens?
opening of the ion channel
- INflux of Na, EFflux of K -> depolarization
How does an increase in the number of ACh receptors affect the administration of succinylcholine?
Exaggerated depolarization
-> exaggerated efflux of K+
Which NMB should be avoided in pts with renal disease?
Pancuronium
- 80% renally excreted
*Roc is 25% renally excreted
Neostigmine is eliminated by the kidney at __%
Edrophonium is eliminated by the kidney at ___%
50%
75%
*RF has significant effects on NMB AND reversal agents
Can sevoflurane cause kidney injury?
Controversial
- When exposed to CO2 absorbents, if low flow, sevo can be degraded into compound A in animals
Common causes of anion gap metabolic acidosis
MUDPILES Methanol Uremia DKA Paraldehyde Iron/INH Lactate Ethanol/Ethylene glycol Salicylates
Where is bicarbonate filtered?
in the renal glomerulus
- almost entirely reabsorbed
- 85% reabsorbed in prox tubule
- 10% in thick ascending LOH
Major independent preop risk factors for postop AKI in noncardiac sx? (6)
- Age > 59
- BMI > 32
- Chronic liver disease
- COPD requiring chronic bronchodilator use
- Peripheral vascular occlusive disease
- High risk/emergency sx
How is rocuronium cleared and excreted?
Cleared by hepatic uptake
- prolonged paralysis in pts with cirrhosis and liver failure
Excreted
- 75% hepatobiliary
- 25% renally
Which NMBs have minimal renal excretion and predictable durations of actions in pts with renal failure?
Succinylcholine
Cisatracurium
Why would a pt with ESRD who was last dialyzed 4 days ago have inadequate surgical hemostasis?
Uremia -> platelet dysfunction
- Impaired vWF formation and release
- Impaired GPIIb-IIIa (surface protein on platelets)
Reduced Antithrombin III –> (hypercoagulability/hypocoagulability). Why?
HYPERcoagulability
- ATIII is a protease that inactivates IIa (thrombin), VIIa, IXa, Xa, and XIa in the clotting cascade
Why is ketorolac nephrotoxic?
Vasoconstricts glomerular AFFerent arterioles
- especially in the setting of hypovolemia where RAAS is trying to dilate EFFerent arterioles
Prostaglandins dilate (afferent/efferent) arteriole
AFFerent (carries blood towards glomerulus)
- increase GFR
ACEi will antagonize production of ___, which will decrease cardiomyocyte remodeling of the heart induced by __.
Angiotensin II
AT1 receptor stimulation
Fenoldopam MOA
- selective D1 receptor agonist
- direct natriuresis and diuresis - Renal vasodilator
Nonanion gap acidoses are caused primarily by (3)
- Chloride containing acid administration (ie. NS, TPN)
- Increased HCO3- loss (GI or kidney)
- Decreased acid excretion (hypoaldosteronism or RTA1)
_____________
FUSEDCARS
- Fistula
- Ureteroenterostomy
- Saline
- Endocrine (hyperparathyroidism)
- Diarrhea
- Carbonic anhydrase inhibitor
- Ammonium chloride
- RTA
- Spironolactone
Substances commonly removed using dialysis
- Calcium
- Magnesium
- Phosphate
- Potassium
- Urea
- Creatinine
- Free water
*NOT sodium
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)
(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
(Hypernatremia/Hyponatremia) is associated with ESRD
Neither
During TURP procedures, how does glycine toxicity manifest?
Hyperammonemia
-> CNS symptoms and nausea and transient blindness
Calculate FENa
[(PCr x UNa) / (PNa x UCr)] x 100
*FENa < 1 = prerenal
> 2 = Intrinsic or Postrenal
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
Perioperatively, the most common cause of AKI is _____
ATN
- Death of renal tubular epithelial cells
- Ischemic vs toxic
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)
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
