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169 Cards in this Set
- Front
- Back
what is considered the best measure of renal function
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GFR
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what is normal GFR
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~125 ml/min
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what is a potentially misleading test of renal function
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BUN
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serum creatnine is produced how
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at a relatively steady rate by hepatic conversion of skeletal muscle creatnine
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how is serum creatnine filtered
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freely at the glomerulus
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what is the normal value for serum creatnine for a female
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0.6-1.0 mg/dl
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what is the normal value for serum creatnine for a male
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0.8-1.3 mg/dl
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why is serum creatnine decreased in the elderly
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secondary to decreased muscle mass
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what lab test is slow to reflect acute changes in GFR
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serum creatnine
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what lab test is the most reliable measure of GFR
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creatnine clearance
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what is the normal value of creatnine clearance for a female
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85-125 ml/min
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what is the normal value of creatnine clearance for a male
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95-140 ml/min
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creatnine clearance decreases with what
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AGE
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urine specfic gravity is a assessment of what
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urine concentrating ability
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urine specific gravity of what implies adequate concentrating ability
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> 1.018
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what is normal protenuria
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</= 150 mg/day
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what are causes of proteinuria
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*glomerular damage
*failure of reabsorption *excessive plasma proteins *orthostatic proteinuria *microalbuminuria |
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with urinary sodium what value reflects decreased ability of the tubules to conserve sodium
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> 40 meq/l
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what is glycosuria
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tubules unable to reabsorb enough glucose to compensate for an increased load (typically r/t DM) and it is spilled into the urine
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with neurohormonal regulation the body protects against hypovolemia and hypotension through what mechanisms
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vasoconstriction and salt & water retention
(sympathoadrenal axis, renin-angiotension-aldosterone system, arginine vasopressin) |
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with neurohormonal regulation the body protects against hypervolemia and HTN through what mechanisms
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vasodilation and salt and water excretion
(prostaglandins, bradykinins, ANP) |
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sx and trauma may produce significant vasoconstriction and salt and water retention lasting for several days leading to what
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post-op oliguria and edema
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the kidneys lack which innervation PS or sympathetic
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PS
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the predominately a-adrenergic renal effects of sympathoadrenal stimulation result in what
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vasoconstriction from NE, epi, phenylephrine and high dose dopamine
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the predominately b-adrenergic renal effects of sympathoadrenal stimulation result in what
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*increase in renal blood flow secondary to increased CO
*unclear intrinsic renal effects from isoproteronol, dobutamine |
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renal effects of sympathoadrenal stimulation from dopaminergic agonists do what
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*selectively increase RBF
*may oppose a-adrenergic induced vasoconstriction |
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aldosterone is released from where
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adrenal cortex
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aldosterone is released in response to what
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*angiotension II
*hyponatremia *hyperkalemia |
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aldosterone does what to blood volume
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INCREASES it
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how does aldosterone affect blood volume
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*active sodium absorption
*passive H20 absorption |
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aldosterone acts via what
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mRNA transcription
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is the effect of aldosterone immediate or delayed
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DELAYED 1-2 hrs
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what is the function of arginine vasopressin
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regulates urine volume and osmolality
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where is arginine vasopressin synthesized
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in the hypothalamus
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where is arginine vasopressin stored
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in the pituatary
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arginine vasopressin is released in response to what
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*increasing plasma osmolality
*decreased intravascular volume *arterial hypotension |
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how does arginine vasopressin maintain adequate glomerular filtration
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*constriction of EFFERENT arterioles
*little to no effect on AFFERENT arterioles |
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what do prostaglandins do in regards to the kidneys
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*promote renal vasodilation
*maintain intrarenal hemodynamics *enhance Na & H2o excretion |
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what do kinins do
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*stimulate phospholipase a2
*act as vasodilators enhancing the action of prostaglandins |
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atrial natriuretic peptide is released when and why
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from atrial myocytes in response to increased atrial volume and subsequent wall stretch
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ANP does what to vascular smooth muscle
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dilates via formation of cGMP
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what does ANP do at phospholipase C receptor
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*competively blocks NE
*non-competively blocks angiotension II |
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what does ANP inhibit
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*renin secretion
*aldosterone secretion *AVP secretion |
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dopamine may produce benefit by
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*DA1 effects-increased RBF
*b-adrenergic effects-increased CO & renal perfusion |
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dopamines effectiveness is limited by what
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it mixed adrenergic effects
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dopamine is useful as an inotropic agent when
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oliguria persists despite adequate intravascular volume
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what is dopexamine
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synthetic analog of dopamine
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dopaxamine has found use in CHF producing what
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*afterload reduction
*increased RBF |
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what is fenoldopam
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selective DA1 receptor agonist
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what is fenoldopam approved for
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short term tx of severe HTN particulary renovascular
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prostaglandins do what to the effects of NE and angiotension II
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counteract the vascoconstrictive effects
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prostaglandins do what to the inner cortex
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maintain the perfusion
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Ca channel blockers do what in HTN pts
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increase RBF and GFR and induce natriuresis
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decreased renal reserve is a GFR of what
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60-75% of normal
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renal insufficiency is a GFR of what
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25-40% of normal
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what are the symptoms and abnormal labs with renal insufficiency
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*elevated creatnine and BUN
*nocturia may be the only symptom |
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what is the GFR with end stage renal dz
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<25% of normal
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what is the most severe form of chronic renal failure
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uremic syndrome
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what is the GRF with uremic syndrome
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<10% normal
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what are the s/s of uremic syndrome
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*anorexia
*nausea *vomiting *pruritis *anemia *fatigue *coagulopathy |
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what are the CV changes in chronic renal failure
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*systemic HTN
*uremic pericarditis |
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what are the pulmonary changes seen with chronic renal failure
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*low pressure pulm edema secondary to increased permeability of alveolar cap membranes
*peripheral vascular congestion appearing as a butterfly wing on CXR |
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what is the tx for chronic renal failure
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*aggresive management of HTN
*aggressive management of DM *dietary protein restriction <0.6g/kg/day *tx of anemia w/ erythropoietin *dialysis or transplant |
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what are the general goals with anesthetic drugs
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*maintain renal blood flow with adequate perfusion pressure
*suppress vasoconstricting salt retaining response to sx stimulation and pain *avoid or minimize nephrotoxic insults |
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sympathetic block of what areas effectively suppresses the sympathoadrenal stress response and release of catecholamines, renin and arginine vasopressin
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T4-T10
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with regional anesthesia renal blood flow and GFR remain adequate as long as what
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perfusion pressure is maintained
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with general anesthesia ALL anesthestic tech tend to reduce what
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GFR and urine output
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with general anesthesia what with the kidney is typically maintained
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renal autoregulation
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with volatile agents there is a mild to moderate reductions in what regarding the kidney that can be attenuated with fluid loading
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RBF and GFR
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what anesthetic tech has minimal effect on RBF and GFR
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high dose opioid tech
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what anesthetic tech is more effective than volatile in suppressing the vasoconstricting salt retaining effects of releasing catecholamines, angiotension, aldosterone and AVP
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high dose opiod
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IV induction agents with the exception of ketamine do what to RBF
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produce small decreases
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ketamine does what to RBF and urine output
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*increases RBF
*decreased UO |
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peak flouride levels of what rarely produce injury
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< 50
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peak flouride levels of what have a high incidence of injury
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>150
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methoxyflurane can produce what fluoride levels
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>100
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enflurane can produce what fluoride levels
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25
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isoflurane can produce what fluoride levels
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<4
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desflurane has what kind of fluroride levels
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MINIMAL
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positive pressure ventilation and PEEP may do what in regards to the renal system
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may decrease
*RBF *GFR *Na excretion *UO |
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the effect that positive pressure ventilation and PEEP has on RBF, GFR, Na excretion and UO can be attenuated how
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by adequate fluid load and maintenance of CO
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with deliberate hypotension what renal changes are commonly seen
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marked reduction in
*GFR *UO |
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nipride does what regarding the renal system
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*decreases renal vascular resistance but shunts blood away from the kidneys
*produces sig renin-angiotensin-aldosterone activation & catecholamine release |
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NTG does what regarding the renal system
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produces less reduction in RBF than nipride
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what kind of drug is fenoldopam
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selective DA1 receptor agonist
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what kind of effects does fenoldopam have regarding the renal system
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NO reduction in RBF
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what are the 2 major predictors of acute renal failure following aortic sx
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*pre-existing renal dysfunction
*peri-op hemodynamic instability |
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with suprarenal or infrarenal aortic crossclamp RBF is decreased to what of normal
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50%
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with suprarenal or infrarenal aortic crossclamp following release of cross clamp what occurs with RBF
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it increases to supranormal levels (reflex hyperemia)
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with suprarenal or infrarenal aortic crossclamp following release of cross clamp what is GFR at 2 hrs
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remains ~ 1/3 of control values
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with suprarenal or infrarenal aortic cross clamp following release of cross clamp what is GFR at 24 hrs
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still only ~ 2/3 of control values
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with suprarenal or infrarenal aortic cross clamp, clamp times longer than 50-60 min may do what
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produce prolonged decrease in GFR
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pts with hepatic failure and obstructive jaundice are particularly susceptible to what other system dysfunction
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RENAL
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what system dysfunction may occur in up to 2/3 of pts following liver transplant
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RENAL DYSFUNCTION
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has low dose dopamine shown advantage over pre-op hydration in preventing renal dysfunction in pts with obstructive jaundice
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NO
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nephrotoxic acute renal failure is usually oliguric or non-oliguric with what kind of concentrating ability
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*NON-OLIGURIC
*DECREASED concentrating ability |
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regarding nephrotoxic insults what drug class is directly related to high trough levels
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AMINOGLYCOSIDES
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with nephrotoxic insults and aminoglycosides toxicity may be reduced how
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by once daily dosing
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during stress what occurs with NSAIDs and the kidneys
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during stress impaired prostaglandin activity d/t NSAIDs results in failure of their protective activity w/ subsequent decrease in RBF & GFR
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what occurs with cyclosporin and a nephrotoxic insult
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induces sympathetic hyperreactivity, HTN & renal vasoconstriction
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with cyclosporin and nephrotoxicity what does concurrent use of Ca channel blockers do
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may allow dosage reduction & reduce incidence of ATN
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what is the mechanism of nephrotoxic insults with radiocontrast dyes
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*microvascular obstruction
*direct tubular toxicity |
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with radiocontrast dyes nephrotoxic insults are markedly increased when
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*in diabetic renal insufficiency
*hypovolemia *CHF *with a secondary insult (sx) in the 1st 3-5 days following contrast |
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what drugs may offer some protection when given prophylactically with radiocontrast dye
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*n-acetylcysteine
*fenoldopam |
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what are the symptoms of pigment nephropathy
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*rhabdomyalysis
*hemolysis *jaundice |
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what occurs with hemolysis in pigment nephropathy
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renal damage secondary to RBC stroma deposition
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with jaundice with pigment nephropathy at conjugated bilirubin > 8 mg/dl what occurs
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bile salt excretion ceases and portal septicemia occurs
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with jaundice with pigment nephropathy circulating endotoxins do what
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induce renal vasoconstriction
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what are the general goals of anesthetic drugs with renal disease
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*maintain renal blood flow w/ adequate perfusion pressure
*suppress vasoconstricting, salt retaining response to sx stimulation and pain *avoid or minimize nephrotoxic insults |
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with renal dz what would cause a pt to have attenuated sympathetic nervous system activity
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*anti-hypertensives
*uremia |
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with a renal pt with induction an exaggerated drop in BP may be seen secondary to what
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*positive pressure ventilation
*position changes *blood loss *drug-induced myocardial depression |
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what volatile anesthetic should be AVOIDED in the maintenance for a pt with renal dz
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SEVOFLURANE
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what are the ADVANTAGES of using volatiles for the maintenance of anesthetic for pts with renal dz
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*easily titratible
*allows reduction in dose of MR which might have prolonged duration |
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what are the DISADVANTAGES of using volatiles for the maintenance of anesthetic for pts with renal dz
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*high incidence of concurrent hepatic dz
*risk of depression of CO |
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what are the ADVANTAGES of using an opioid tech for the maintenance of anesthesia for a pt with renal dz
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*less myocardial depression
*avoid concerns over hepato- and nephrotoxicity |
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what are the DISADVANTAGES of using an opioid tech for the maintenance of anesthesia for a pt with renal dz
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*less able to control BP elevations
*not as titratable |
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what would be an example of a TIVA tech for a pt with renal dz
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propofol + remi + cisatracurium
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what muscle relaxants HAVE renal excretion
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*vecuronium
*rocuronium *pancuronium |
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what reversal agents HAVE renal excretion
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*neostigmine
*edrophonium *pyridostigmine |
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what muscle relaxants are INDEPENDENT of renal excretion
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*mivacurium
*atracurium *cisactacurium |
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succinylcholine is safe to use with renal dz with what exceptions
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*extensive neuropathy
*high or high-normal serum K+ |
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what anti-hypertensives are UNAFFECTED by impaired renal function
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*propranolol
*labetalol *esmolol *Ca channel blockers |
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what anti-hypertensives ARE affected by impaired renal function
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*furosemide
*thiazide duiretics *methyldopa *guanethidine |
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with deliberate hypotension how is trimethaphan affected
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UNCHANGED
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with deliberate hypotension how is NTG affected
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UNCHANGED
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with deliberate hypotension how is nipride affected
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potential for thiocyanate toxicity
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with deliberate hypotension how is hydralazine affected
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PROLONGED
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with deliberate hypotension how is esmolol affected
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UNCHANGED
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which vasopressor has the greatest negative impact on renal vasculature
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PHENYLEPHRINE
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which vasopressors are preferrable with renal dz but may increase myocardial irritability
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b-adrenergic agonists
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what type of fluid should be AVOIDED in fluid management of renal pts
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potassium containing fluids (LR)
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with renal dz pts the most likely etilogy of decreased UO is what
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inadequate circulating fluid volume
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is intra-op UO predictive of post-op renal function
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NO
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with IV access in a renal pt veins where need to be avoided
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veins in dominant arm
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what are the ADVANTAGES of a brachial plexus block for shunt placement
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*ideal sx conditions secondary to vasodilation
*good post-op analgesia *avoids many concerns with GETA |
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what are the DISADVANTAGES of a brachial plexus block for shunt placement
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*must assure adequate coagulation
*possible presence of diabetic or uremic neuropathies *metabolic acidosis lowers sz threshold following intravascular injection |
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for post-op management of pts with renal dz they will need smaller doses of narcotics particularly which ones
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*MS
*demerol |
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what are the most common causes of ESRD
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*DM (#1)
*glomerulonephritis *polycystic kidney dz *systemic HTN |
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a kidney can be preserved, cold and perfused for how long
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48 hrs
|
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a donor kidney is placed where in the body
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lower abd
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a donor kidney get blood supply how
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from iliac vessels
|
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what things are critical in the anesthesia of a renal transplant
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maintenance of euvolemia and adequate perfusion pressure
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with a renal transplant osmotic diuresis with mannitol does what
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facilitates urine formation by transplanted kidney without relying on renal tubular mech
|
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release of vascular clamps with a renal transplant does what
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*releases K+ and acid metabolites (vasodilating) into circulation
*addition of ~300 ml new capacity to intravascular space |
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hypotension after release of vascular clamps with a renal transplant usually responds to what
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fluid bolus
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acute renal failure is deterioration of renal function over hrs to days resulting in what
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*inability to maintain fluid & electrolyte homeostasis
*inability to excrete nitrogenous wastes |
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what are the common definitions of acute renal failure
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*increase in serum creatinine > 0.5 mg/dl
*50% decrease in creatnine clearance *decreased renal fxn resulting in need for dialysis |
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what is oliguric acute renal failure
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< 400 ml/day
|
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what is non-oliguric acute renal failure
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> 400 ml/day
|
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who is at the highest risk for acute renal failure
|
elderly pts with DM and baseline renal insufficiency
|
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what is PRERENAL acute renal failure
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acute circulatory problems which impair renal perfusion
|
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what is RENAL acute renal failure
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caused by primary or secondary renal dz, toxins or pigments
|
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what is POSTRENAL acute renal failure
|
caused by obstruction of the urinary tract
|
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what is the management for acute renal failure
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*supportive
*correct underlying causes *fluid resuscitation *vasopressors *diuretics *dialysis |
|
what is the supportive care for acute renal failure
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*limit further renal failure
*correct H2O, electrolyte & acid-base imbalances |
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what is the correction of underlying causes for acute renal failure
|
correct
*hypovolemia *hypotension *sepsis |
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what are vasopressors that can be used to tx acute renal failure
|
*norepi
*dopamine |
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in general attempts to convert oliguric to non-oliguric renal failure w/ diuretics are unsuccessful and potentially harmful w/ what EXCEPTIONS
|
*post transfusion ATN who receive mannitol w/ adequate hydration
*forced alkaline diuresis w/ mannitol useful in preventing ATN following renal crush injury |
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what may reduce ARF in high-risk pts who receive radiocontrast dye
|
N-acetylcysteine
|
|
what is the most common cause of new onset acute renal failure in the post-op period
|
SEPSIS
|
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what happens to renal autoregulation with sepsis
|
it is IMPAIRED
|
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what things may offer renal protection in sepsis
|
*anti-inflammatories
(U63557A, NSAIDs, high dose methylprednisolone) *supranormal O2 *low dose dopamine *norepi *arginine vasopressin |
|
how does U63557A offer renal protection in sepsis
|
protective effect against deterioration of creatinine clearance
|
|
how do NSAIDs offer renal protection in sepsis
|
decrease synthesis of renal vasodilating prostacyclin
|
|
what are the benefits of norepi in renal pts with sepsis
|
*increases stroke volume
*decreased HR *increased GFR |
|
norepi for renal protection in sepsis may be particularly advantageous in what pts
|
pts in whom high dose dopamine can be weaned by substitution with norepi
|
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norepi in renal pts with sepsis may require high doses d/t the refractoriness of peripheral vasculature secondary to what
|
*massive release of NO
*vasopressin deficiency |
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what type of pts have very low levels of arginine vasopressin
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*vasodilitory shock (hypotension, increased CI, decreased SVR)
|
|
arginine vasopressin deficiency is likely a result of what
|
excessive baroreceptor mediated release following sustained hypotension
|