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51 Cards in this Set

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Diuretics
Inc UOP by DEC NaCl reabsor (and water) at diff places in nephron
Each part of nephron has a unique sodium entry mechanism. Diuretics work by inhibiting these mechanisms
Diuretics: how do they work
Protein bound--how do they get into tubule then...
They are secreted by proximal tubule anion pump that allows proteins to pass

In patients with renal insuff, the tubules don't work properly and they develop diuretic resistance
Osmotic Diuretics--Mannitol
Most commonly used osmotic diuretic
Six carbon sugar
Fully filtered--filtered at glomerulus unlike the others that are protein bound
Only means of clearance is via renal tubules
Mannitol--how does it work
Increases osmolarity of renal tubules and plasma--has two effects:

1) decreases water reabs in renal tubules leading to relative water diuresis--losing mostly water, little bit of Na, Cl, HCO3

2) expands intravascular volume by drawing water from intracellular sites. Leads to inc RBF and decreased brain bulk
Mannitol--why do we use it
1) To reduce intracranial pressure

Cranial vault is a fixed structure. Inc in brain, blood, or CSF may be offset by a dec in antoher
Mannitol--When do we use it
To reduce ICP
0.25 - 1gm/kg (usually 0.5g/kg)
Draws water from tissues in brain
Dec CSF volume by dec fluid formation
effect within 10-15 min
Duration 2 hr
Infuse slowly bc in theory you could develop acute inc in ICP d/t rapid fluid shifts
Must have intact BBB b/c it could get trapped in brain and fluid couldn't get out ?
Other Uses of Mannitol
1) Reduce IOP
-glycerin typically used here
-can lead to INC in blood glucose as it's metabolized

2)Differential diagnosis of Acute Oliguria
-if cause is dec volume (pre-renal) then mannitol should work
-if damage is in glomerulus or tubes mannitol will not work

3) Convert oliguric to non-oliguric renal failure

4) Prophylaxis agst ARF in setting of CV surgery, aortic surgery, or trauma--giving mannitol before ischemic insults seems to dec damage
Mannitol--who should we worry about
Pts with heart failure--volume overload

Electrolyte changes following admin--hyponatremia, hypokalemia, and hypovolemia

Pts without an intact BBB
Loop Diuretics
Powerful diuretics that work on the L of H
Sulfonamide derivates WATCH WITH SULFA ALLERGY
Loop Diuretics--how does it work
1) Inhibit NaCl reabs via competition with Cl for its postioin on Na K 2Cl transporters
-located on teh thick ascending limb and early distal tubule
-effect in 2-10 min
-at max doses can cause excretion of 20% of flitered sodium load
-ultimate effect: hypotonic urine, losses of sodium, potassium, calcium
Loop Diuretics--when do we use them
1) Mobilize edema
-help reduce pulm and cardiac overload in pts with heart failure, cirrhosis, renal insuff, and nephrotic syndrome
-causes peripheral dilation even prior to diuresis activ which is great for pulm edema
-helps forward flow, breathe better even before they start diuresing

2)Dec cerebral edema
-Dec total fluid volume
-dec CSF prod
-Dec Na transport to glial tissue
-not as good as mannitol, best if used together
-doesn't matter if BBB intact--no change in CBF or osmolarity

3) Tx of HTN

4)Eval of acute oliguria
-will help if problem was redistribution of blood flow to medulla
-if prob was hypovolemia then you just made matters worse

5) Tx of hypercalcemia
-ca reabs in loop is passive and gradient is created by the NaCl transporter. So, calcium reabs is inhibited wtih Loop diuretics
Loop Diuretics--what do we worry about
1) Hypokalemia
2) hypercalcuria--can cause stones
3) Enhance non-depolarizer--may act on presyn nerve endings causing dec release of Ach
4) enhances renal conc of aminoglycosides and cephalosporins--enhancing toxicity risk
5) SULFA ALLERGY
6) INC risk of lithium and dig toxicity
7) Deafness
Thiazides
Lower potency diuretic that works on distal tubule
Thiazides--how does it work
Competes for Cl site on NaCl luminal carrier protein at distal tubule
-results in an inc excretion of Na, Cl, and HCO3 ions
-leads to an excretion of 3-5% of filtered sodium load
-augment calcium reabs in distal tubule
-usually ok to take DOS
Thiazides--when do we use it
1) Manage essential HTN
-initially dec ECF volume
-peripheral dilation 2 to diminished sympathetic nervous system--overall dec in total body Na (needed for APs) thought to reduce sympth activ

2) Edema
-only if state is 2 to sodium overload

3) Hypercaluria--to reduce stone formation

4) Tx Nephrogenic DI
-ability to impair diluting capacity of tubules
Thiazides--what should we worry about
1) Hypokalemia, hypochloremia, metabolic alkalosis
-cardiac dysrhythmias, skeletal muscle weakness, GI ileus, dig toxicity, potentiation of non-dep
2) Be wary of hypovolemia, orthostatic hypotension, and hemoconcentrated labs

3) hyperglycemia--inhibits insulin release from pancreas
Potassium sparing Diuretics
even more weak diuretics that spare potassium via effect on Na resabs in collecting tubules
Potassium sparing diuretics---how does it work
1) act on principal cells in cortical collecting tubule decreasing the # of open sodium channels--so Na leaves and K doesn't
-Amiloride and Triamterene--directly dec sodium channel activity
-Spironolactone and Eplerenone--inhibit mineralocorticoid receptors---where aldosterone works

Only about 1-2% of filtered Na load excreted
Potassium sparing diuretics--when do we use it---Triamterene and Amiloride
1) HTN--combined with thiazides to prevent hypokalemia

2) CHF--added to loop diuretics to preven hypokalemia
Potassium sparing diuretics---when do we use it--Spironolactone
1) Primary and secondary Hyperaldosteronism
- direct antagonist to aldosterone therefore effect tx for edema assoc with above states

2) Pts with secondary ascites (liver failure and heart failure)
Potassium sparing diuretics--what should we worry about
1) Hyperkalemia
2)Metabolic acidosis
3) diarrhea and n/v
4) gynecomastia and sexual dysfxn
Carbonic anhydrase inhibitors
Diamox (Acetazolamide)

Summary:
Work by impairing H secretion in proximal tubule and impair HCO3 reabsor.

Used to treat metabolic alkalosis and alkalinize the urine

Produce HYPERCHOLREMIC METABOLIC ACIDOSIS
Anesthesia and Surgery--Effect on the Kidneys
RBF, GFR, UOP, Na excretion all REVERSIBLY DECLINE under both general and regional anesthesia

MAINTENANCE OF NORMAL BP AND INTRAVASCULAR VOLUME IS KEY!!!
Cardiovascular influences
Inhaled agents--

DOSE DEPENDENT MYOCARDIAL DEPRESSION AND VASODILATION

regional anesthesia--

HYPOTENSION AND LOSS OF VENOUS CAPACITANCE

Kidneys autregulate at MAP 80-180
-decreased GFR, RBF, UOP, and Na excretion outside this range
-RBF ceases at 40-50 MAP
So what do we do to help...IVFs!
Nervous System influences
Pts are SYMPATHETICALLY ACTIVATED!
1) INC SVR
2) Activ of Renin-Angiotensin system
3) INC Na and water retention
4) Redistrib of blood flow from cortex to medulla
Endocrine influences
Stress response:

1) Increase in circ catecholamines--epi and norepi
2) Increases in renin-angio syst
3) Inc in ADH, Aldosterone, ACTH, and cortisol

TAKE HOME: Endocrine system intimately responsible for the renal changes seen under anesthesia
Flouride induced nephrotoxicity
A state of high output renal insufficiency charac by polyuria, dehydration, hypernatremia, hyperosmolality, and eleveated BUN and Crt.
Difficult to treat.

Causative agents:
1) Methoxyflurane--extensive metab in the kidney leads to high plasma level of flourine causing renal injury
2) Enflurane--less metab than methoxy but is assoc with transient inc in flouride
3) Sevoflurane--even less metab <5%, can cause small inc in plasma flouride
Flouride induced nephrotoxicity
Severity of injury is related to:
1) Peak plasma flouride concentrations--want less than 50 micromoles

2) Duration of elevated plasma conc
-Methoxy has longest duration of elevation

3) Specific location for metab of the agent
-Methoxy undergoes much metab in the kidney by specific renal related cytochrome p450 enzymes
Flouride induced nephrotoxicity
TAKE HOME MESSAGE:

Methoxyflurane and Enflurane are the only anesthetics that have been clinically assoc with flouride induced nephrotoxicity or high levels of plasma flouride concentrations
Sevoflurane and Compound A
-CO2 absorbants degrade Sevo into this compound
-production of Comp A is enhanced by LOW FLOWS & WARM/DRY CO2 ABSORBANT

-Barium Lime makes MORE than Soda Lime

-High Levels of Comp A in rats have been shown to cause nephrotoxicity by causing cell necrosis of tubules
More about Compound A
Use Sevo if you want.
Most data on animals.
Recent studies with humans found no indications of renal effects
Average conc of Comp A during low flow Sevo is 8-24 ppm/hr
IV agents and renal changes during surgery
OPIATES/BARBS--same effect as inhaled agents when compared with N2O

KETAMINE--can help preserve renal fxn in settings of trauma d/t sympathomimetic effect

PROPOFOL & ETOMIDATE--safe to use if BP stays within autoregulation

OTHERS:
-Ketorolac--inhibit prostaglandins which normally act on afferent arteriole to inc RBF

-ACE inhibitors--potentiate anesthetic effects on kidneys, block Ang 2 mediated kidney protection

ABX--pay attention to redosing guidelines
Certain surgeries affecting Renal Function
1) Laparascopic--pneumoperitoneum causes compartment syndrome state in abdomen and therefore produces oliguria

2) CPB

3) Cross clamping of aorta

4) Clamping in and around renal vessels

5) Neurosurgical procedures around the pituitary can also affect UOP (SIADH)
Summary: Anesthesia and Healthy Kidneys
1) Use any agent you like--Sevo 2L/min flows recc

2) Use any IV induction agent appropriate

3) Use whatever narcotic you like

4) Maintain MAP 80-180 to preserve GFR and Give IVFs to compensate for surgical and anesthetic renal effects
Anesthesia and Sick Kidneys---Induction agents

BARBITURATES
Metabolism in liver hepatocytes and to a small extent renal--metabolites are usually INACTIVE and water soluble

Decreased protein stores=increased free circ drug=exaggerated clinical effects

Chronic acidosis thought to facilitate fast brain uptake of non-ionized portions of drug
Thiopental
Most commonly used BARB

Highly lipid soluble

Most protein bound 72-86%

REDUCE DOSE--reduce to 75% of normal dose (ex. if normal dose is 100mg then give 75mg)
Sick kidneys and Induction Agents

KETAMINE
Metabolism--hepatic to Norketamine 1/3 potency, then hydroxylated to water soluble form for excretion

Prob not a good choice for HTn pts.

TAKE HOME: Renal dysfxn has no effect on drug
Sick Kidneys and Induction Agents

PROPOFOL
Metabolism--hepatic, rapid, and extensive--inactive metabolites

TAKE HOME: Renal dysfxn does not affect clearance of propofol
Sick Kidneys and Induction Agents

ETOMIDATE
Metabolism--lipid soluble with large volume of distribution

76% bound to albumin--pharmacology may be enhanced but not significantly

TAKE HOME: Safe to use in renal pts and a good choice when cardiac failure is present
Sick kidneys and benzos

MIDAZOLAM
Extensively protein bound--therefore inc free fraction in renal dx

exaggerated resp to benzos

MIDAZOLAM--
-highly lipid soluble, ext protein bound
-metab extensively by hydroxylation in liver to 1 & 4-hydroxymidazolam and ACTIVE METABOLITE

TAKE HOME: Pts will have exagg effects so DECREASE DOSE. Elimination and clearance not altered by renal failure. CAN USE IT BUT USE LESS
Sick kidneys and opiods

FENTANYL
Lipid soluble, extensively protein bound
Liver metab with no active metabolites

REDUCE DOSE. Good choice for ESRD.
Sick kidneys and opiods

SUFENTANIL
lipid soluble, even more protein bound
Liver metab--ACTIVE metabolite, desmethyl sufentanil 10% as potent
-Prolong depression of ventilation can be seen with renal failure
Sick kidneys and opiods

ALFENTANIL
Renal failure does not alter clearance or elimination
Sick kidneys and opiods

REMIFENTANIL
Ester hydrolysis to weakly potent compound, makes safe choice in renal failure
MORPHINE and renal failure
Hepatic metabolism to:
Morphine-3-glucoronide (85%) INACTIVE
Morpine-6-glucoronide (10%) ACTIVE

Morphine-6-Glucoronide: Potency and duration are GREATER than Morphine--elimination of this metabolite IMPAIRED in renal failure

TAKE HOME: Not a good choice. Use sparingly
MEPERIDINE and renal failure
Extensive hepatic demethylation to less potent but active normeperidine

Normeperedine has elimination half-time of 15 hrs in normal pt

Normeperidine aslo produces CNS stim and is assoc with seizures

TAKE HOME: Not a good choice. Do NOT use.
Sick kidneys and Muscle Relaxants
SUCCINYLCHOLINE: safe to use with K<5

CISATRACURIUM, ATRACURIUM, MIVACURIUM: Drug of choice in renal failure d/t non-organ dep metab--ester hydrolysis and Hoffman elimination

VECURONIUM & ROCURONIUM: Both undergo primarily hepatic metab, 20% eliminated in urine. Use smaller doses.

PANCURONIUM: renal dependent excretion--don't use if you have to use small doses.
Moderate Renal Failure
-Monitor blood loss closely, replete volume and maintain BP
-Avoid large amts of phenylephrine, use as temp measure to inc BP and maintain RBF
VOLUME OVERLOAD IS EASIER TO TREAT THAN ARF
Crt levels and renal impairment
MILD RENAL IMPAIRMENT:
CrCl= 40-60 mL/min

MODERATE RENAL IMPAIRMENT
CrCl = 25-40 mL/min

FOCUS IS ON PRESERVING WHATEVER RENAL FUNCTION IS LEFT
Moderate Renal Failure: Preoperative Preparation
consider generous hydration coupled with solute diuresis

consider diuretics like mannitol 0.5 g/kg--has renal presrevation properties d/t solute diuresis

Consider having Dopamine agonists available

Maintain adequate UOP--0.5 mL/kg/hr) prevent fluid overload
Induction
Most IV agents are acceptable. Adjust dose as needed

Make sure adequately hydrated before induction to avoid a sudden decrease in RBF and RPP

Remember the sympathetic innervation our pts exhibit pre-op is detrimental to healthy renal fxn and even worse if diminished fxn