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1.
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What are the functions of
the kidney?
·
excretion of
metabolic end products (urea)
·
control of
electrolyte and hydrogen ion concentrations
·
hormone
secretion (renin, erythropoietin)
·
hormone
metabolism (eg insulin)
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2.
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Describe renal blood flow
and its regulation
·
kidneys
receive 20% of CO (0.5% body weight)
·
autoregulation
(by modulating afferent arteriolar tone) between 60-150 mmHg
·
outside this
range, flow is pressure dependent
·
SNS (T4-L4)
stimulation à vasoconstriction
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3.
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Describe how the kidneys
filter blood
·
glomerulus
formed by invagination of a tuft of capillaries into Bowman’s capsule, the
dilated and blind end of the nephron
·
hydrostatic
pressure about 50mmHg forces water and low molecular weight substances (eg
electrolytes) through capillary walls
·
opposed by
oncopic pressure (25mmHg at afferent arteriole, up to 35 at efferent
arteriole due to concentration of proteins)
·
GFR about 125
ml/min
·
90% of
filtered fluid is reabsorbed in renal tubules
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4.
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Why might NSAIDs be
relatively contraindicated in the patient with renal disease?
Prostaglandins,
produced in renal medulla, are released in response to sympathetic
stimulation and increased levels of angiotensin II. They may modulate the
vasoconstrictive effects of catecholamines. NSAIDs may attenuate this
protection, allowing catecholamine-induced renal vasoconstriction. (This may
be clinically relevant only is settings of hypovolemia)
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5.
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Why is BUN not used as a
measure of GFR?
·
BUN does vary
with GFR, but also affected by many other factors
·
[BUN]
increased due to: high-protein diets, GI bleeding, increased catabolism (eg
during febrile illness), dehydration (à inc urea absorption due to slow movement
of fluid through renal tubules)
·
Nevertheless,
[BUN] > 50 mg/dl usually = decreased GFR
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6.
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How does Creatinine relate
to GFR?
·
a specific
indicator for GFR
·
changes in
[Cr] correlate with changes in GFR
·
Cr is a
product of skeletal muscle metabolism, therefore is related to skeletal
muscle mass
·
[Cr] does not
reflect GFR if decreased production of creatinine (e.g., decreased muscle
mass, GI excretion of Cr in patients with CRF)
·
at least 8
hours required for [Cr] to increase significantly from normal range in ARF
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7.
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What is normal protein
excretion?
·
< 150mg/d
·
increases
usually due to increased filtration of protein
·
may occur
intermittently in healthy people when standing
·
may be due
toxercise, fever, CHG
·
if
significant hypoalbuminemia results, can have decreased protein binding of
drugs and decreased plasma oncotic pressure
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8.
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What factors decrease urine
concentrating ability?
·
specific
gravity > 1.018 is OK (nl)
·
hypokalemia
·
hypercalcemia
·
increased fluoride
ion concentration
·
chronic
pyelonephritis
·
diuretics,
lithium
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9.
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How does surgery and anesthesia effect renal function?
·
decreases
from volatile anesthesia most likely related to decreases in blood pressure
(usually insignificant)
·
pain from
surgery can à ADH secretion (this effect is attenuated by prehydration)
·
Atrial
natriuretic factor (ANF) antagonizes release of ADH and renin à inc. UOP. PEEP inhibits ANF release
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10.
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Describe fluoride-induced nephrotoxicity
·
high-output
renal failure (dehydration, hypernatremia)
·
plasma
inorganic fluoride concentrations > 50mm/L (?lower level, if preexisting renal
disease)
·
*methoxyflurane*,
enflurane
·
?sevoflurane
·
depends on
duration of exposure and level of fluoride
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11.
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What changes are associated with chronic renal disease?
·
Anemia: Hgb
usu. 5-8 g/dl. Due to dec erythropoietin
·
Increased CO
·
Decreased
platelet adhesiveness à inc bleeding time. Normal PT, PTT, plt ct. Tx = desmopressin
or cryoprecipitate
·
Hyperkalemia
·
Unpredictable
intravascular fluid volume. Patients often respond to induction as if
hypovolemic
·
Metabolic
acidosis
·
Systemic
hypertension. Often due to fluid overload - Rx HD.
·
Pericardial
effusion
·
Decreased
sympathetic nervous system activity
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12.
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Describe induction and maintenance of general anesthesia
in the patient with CRI.
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Routine, with
some caveats
·
Cautious with
succinylcholine. Patients start with high K, and have high-normal increase in
serum K with sux (0.5-1 mEq/L)
·
May need
smaller dose induction agent; decreased protein binding à inc. free drug
·
May need less
volatile agent, because blood-brain barrier may not be intact (uremia)
·
Autonomic
nervous system dysfunction and impaired baroreceptor-mediated reflex
responses may contribute to exaggerated decrease in BP with induction
·
May avoid
halothane, because of high incidence of co-existing liver disease (viral
hepatitis)
·
Occasional
prolonged CNS and ventilatory depression from opioids, due to accumulation of
active metabolites when renal function is absent
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Ventilation:
normocapnia (resp alkalosis à left-shift of oxyhemoglobin dissociation
curve in face of anemia; acidosis à acute increase in [K]
·
IVF: avoid
K-containing solutions; may use CVP to guide volume replacement
·
NMB:
prolonged effect with pancuronium; vecuronium slightly prolonged; laudanosine
excretion delayed in renal failure; reversal like normal (excretion of NMB
AND reversal agent both delayed)
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13.
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Define oliguria. Compare diagnosis etiology and treatment
of prerenal causes vs. ATN.
Prerenal Oliguria ATN
Urine Na (mEq/L) <40 >40
Urine osm (mosm/L) >400 <400
Causes dec. RBF
(hypovolemia renal ischemia,
nephrotoxins, free hemoglobin
hypotension, decreased or myoglobin
cardiac output)
Treatment fluid
challenge, inotrope,
Lasix (0.1 mg/kg may re-
establish UOP if
oliguria due
to pain-induced release
of
ADH, but not if due to
decreased renal blood
flow)
Note: diuretics à impaired Na reabsorption for 6-12 hours,
making urine of prerenal oliguria indistinguishable from that of ATN
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14.
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What are the mechanisms of action of the various types of
diuretics?
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Thiazides:
inhibit Na and Cl reabsorption from tubules. Hypochloremic, hypokalemic
metabolic alkalosis with prolonged use.
·
Loop
Diuretics (e.g., ethacrynic acid, furosemide): inhibit Na and Cl
reabsorption, augment K secretion. 2-10 minute response time. Chronic use à hypochloremic, hypokalemic metabolic
alkalosis (rarely, deafness)
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Osmotic
Diuretics (e.g., mannitol): filtered by glomeruli, but not reabsorbed. Acute
increase in intravascular volume can cause pulm edema in patients with CHF
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Aldosterone
Antagonists (e.g., spironolactone): blocks renal tubular effects of
aldosterone, thus tending to offset loss of K associated with thiazides
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15.
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What are the complications of
transurethral surgery?
·
TURP
syndrome, from intravascular absorption of irrigating fluid (amount absorbed
depends on pressure of fluid, size and number of venous sinuses opened, and
duration of resection: increased risk with resection time > 1 hour, but
can happen much more quickly)
·
hemorrhage
·
perforation
of bladder or urethra
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16.
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What complications are associated with glycine? Cytal?
Glycine:
·
an amino acid
·
metabolites
include ammonia, but complications rare
·
prolonged CNS
depression may be related to ammonia toxicity
·
may act as an
inhibitory neurotransmitter in retina, causing transient blindness
Cytal:
·
mannitol +
sorbitol
·
good medium
for bacterial contamination
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17.
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What are the signs/symptoms of TURP syndrome?
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Hypervolemia
(HTN, bradycardia, increased CVP, pulmonary edema, CHF)
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Hyponatremia
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Hypoosmolarity
(cerebral edema, HA, restlessness, confusion, obtundation, seizures)
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18.
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What are the advantages of regional anesthesia (vs. GA)
for TURP?
·
can elicit
symptoms of bladder perforation (shoulder pain) or CNS changes in the awake
patient
·
good post-op
pain relief (SAB morphine)
·
NO proven
difference in morbidity/mortality
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