Unit 10 - Kidney part 2 Flashcards
1
Q
objective of countercurrent system in descending loop of Henle
A
concentrate urine by transferring water from tubular fluid to peritubular interstitium & ultimately returning to blood
2
Q
why does UF become more dilute in the peritubular interstitium
A
water can’t follow Na+
fluid becomes more dilute, interstitium becomes more concentrated
3
Q
how does ADH affect water and solutes
A
increases water reabsorption only (not solutes)
4
Q
how does aldosterone affect water and solutes
A
- increases Na+ and water reabsorption
- increases K+ and H+ excretion
5
Q
where in the nephron does PTH promote calcium reabsorption
A
distal tubules
6
Q
where does the kidney expend most of its O2
A
Na/K-ATPase in basolateral membrane of tubular cells (the side that faces peritubular capillaries)
7
Q
MOA of carbonic anhydrase inhibitors
A
noncompetively inhibit carbonic anhydrase in cells that make up proximal tubule
reduces reabsorption of bicarb, Na+, and water
7
Q
MOA of carbonic anhydrase inhibitors
A
noncompetively inhibit carbonic anhydrase in cells that make up proximal tubule
reduces reabsorption of bicarb, Na+, and water
8
Q
2 effects of HCO3- loss to urine via carbonic anhydrase inhibitors
A
- akaline urine
- mild hyperchloremic metabolic acidosis
9
Q
3 uses of acetazolamide
A
- open angle glaucoma
- high altitude sickness
- central sleep apnea
10
Q
why can acetazolamide be used in high altitude sickness
A
mild metabolic acidosis ↑ resp drive
11
Q
why is acetazolamide used in central sleep apnea
A
mild metabolic acidosis ↑ resp drive
12
Q
why is acetazolamide used in open angle glaucoma
A
carbonic anhydrase inhibition ↓ aqueous humor production and ↓ IOP
13
Q
complicatinos of acetazolamide use
A
- metabolic acidosis
- hypokalemia
- may exacerbate CNS depression from severe hypercarbia in pts with COPD (loss of bicarb ions in urine = reduced buffer)
14
Q
function of carbonic anhydrase
A
facilitates production of H2CO3
15
Q
location of osmotic diuretic action
A
inhibit water reabsorption in proximal tubule (primary site) & loop of Henle
16
Q
dose of acetazolamide
A
200-500 mg
17
Q
MOA of osmotic diuretics
A
- They inhibit water reabsorption in proximal tubule (primary site) & loop of Henle
- Pull ECF volume into intravascular space - increases plasma osmolarity, which reduces brain water (↓ ICP) and augments RBF
18
Q
uses of mannitol
A
- preventing AKI (little evidence to support)
- ↑ ICP
- differential diagnosis of acute oliguria (mannitol ↑ UOP if prerenal, no effect with intrinsic injury)
19
Q
complications of mannitol use
A
- CHF
- pulmonary edema
- cerebral edema if blood-brain barrier is disrupted
20
Q
adverse effect of osmotic diuretics in pts with CHF
A
transient increase in intravascular volume can cause pulmonary edema
21
Q
MOA of loop diuretics
A
- disrupt Na-K-2Cl transporter in medullary region of thick portion of ascending loop of Henle (primary site)
- Amount of Na+ that remains overwhelms the distal tubule’s reabsorption capability - large amount of dilute urine excreted
22
Q
electrolytes lost to urine with loop diuretics
A
- Na+
- K+
- Ca2+
- Mg2+
- Cl-
23
Q
loop diuretic dosing
A
- Furosemide: 20-200 mg
- Bumetanide: 0.5-2 mg
- Ethacrynic acid: 25-100 mg
24
clinical uses of loop diuretics
* acute pulmonary edema
* AKI
* CHF
* hypercalcemia
* HTN
* anion overdose
* ↑ ICP
* mobilization of edema fluid
25
complications assoc with loop diuretics
* hypokalemic hyperchloremic metabolic alkalosis
* hypocalcemia
* hypomagnesemia
* hypovolemia
* ototoxicity
* reduced lithium clearance
## Footnote
Ototoxicity ethacrynic acid > furosemide
26
MOA of thiazide diuretics
inhibit Na-Cl co-transporter in distal tubule
27
how do thiazide diuretics affect serum calcium
increase
* Inhibition in distal tubule activates Na-Ca antiporter
* ↑ Ca2+ reabsorption and ultimately increasing serum Ca2+
28
unique side effects of thiazide diuretics
hyperglycemia, hypercalcemia, hyperuricemia
29
clinical uses of thiazide diuretics
* essential HTN
* mobilize edema fluid
* CHF
* osteoporosis (↓ Ca2+ excretion)
30
MOA of Amiloride & triamterene
inhibit K+ secretion and Na+ reabsorption in collecting ducts
| function is independent of aldosterone
31
MOA of spironalactone
aldosterone antagonist
by blocking aldosterone at mineralocorticoid receptors, it inhibits K+ excretion and Na+ reabsorption into collecting ducts
32
doses of K+ sparing diuretics
* Spironolactone: 12.5-100 mg
* Amiloride: 5-10 mg
* Triamterene: 50-150 mg
33
uses of K+ sparing diuretics
to reduce K+ loss in a patient receiving a loop or thiazide diuretic, secondary hyperaldosteronism
34
adverse effects of K+ sparing diureics
hyperkalemia, metabolic acidosis, gynecomastia
35
increases risk of hyperkalemia with K+ sparing diuretics
concurrent NSAIDs, beta blockers, or ACE inhibitors
36
2 reasons amiloride is administered
1. reduce K+ loss in pt on loop or thiazide diuretic
2. secondary hyperaldosteronism
37
5 side effects of K+ sparing diuretics
1. hyperkalemia
2. metabolic acidosis
3. gynecomastia
4. libido changes
5. nephrolithiasis
38
3 tests of glomerular function
1. BUN
2. Cr
3. CrCl
39
normal BUN
10-20 mg/dL
40
normal serum Cr
0.7-1.5 mg/dL
41
normal CrCl
110-150 mL/min
42
tests of tubular function (concentrating ability)
1. fractional excretion of Na+
2. urine osmolality
3. urine Na+
4. urine specific gravity
43
normal fractional excretion of Na+
1-3%
44
normal urine osmolality
65-1400 mOsm/L
45
normal urine Na+ concentration
130-260 mEq/day
46
normal urine specific gravity
1.003-1.030
47
primary metabolite of protein metabolism in the liver
urea
48
etiologies of BUN < 8 mg/dL
Dehydration
Decreased urea production: Malnutrition, severe liver disease
49
etiologies of BUN 20-40
* Dehydration
* Increased protein input: High protein diet, GI bleed, Hematoma breakdown
* Catabolism: trauma, sepsis
* Decreased GFR
50
etiologies of BUN > 50
decreased GFR
51
metabolic byproduct of creatine breakdown
creatinine
52
production of creatinine is directly proportional to:
muscle mass (↓ in women and elderly)
53
lab test that is a useful indicator of GFR
Serum Creatinine
| Undergoes renal filtration but not reabsorption
54
100% increase in serum Cr indicates:
50% reduction in GFR
55
why is BUN not a great indicator of GFR
Because urea undergoes filtration & reabsorption
56
how does BUN:Cr help evaluate hydration
Since BUN undergoes filtration AND reabsorption, but creatinine undergoes filtration but NOT reabsorption, the ratio of these substances in the blood can help evaluate state of hydration
57
normal BUN:Cr
20:1
58
BUN:Cr > 20 suggests:
prerenal azotemia
59
most useful indicator of GFR
CrCl
60
GFR calculation
61
calculating CrCl in women
Multiply value by 0.85 to account for smaller muscle mass
62
lab that relates sodium clearance to creatinine clearance
Fe(Na+)
| Fractional Excretion of Sodium
63
what does Fe(Na+) < 1% suggest
**prerenal azotemia**
more sodium is conserved relative to the amount of creatinine cleared
64
what does Fe(Na+) > 3% suggest
**impaired tubular function**
more sodium is excreted relative to amount of creatinine cleared
65
what does urinary sodium level indicate
working kidneys can conserve sodium, failing kidneys waste sodium
66
UA result that indicates glomerular injury
Large amount of protein in urine (> 750 mg/day or +3 by UA)
67
what does urine specific gravity assess
weight of urine relative to sterile water
68
Measures kidney’s ability to concentrate or dilute urine
urine specific gravity
69
what does urine specific gravity indicate
Higher number = more concentrated urine (more solutes)
Lower number = less concentrated (less solutes)
70
Better test of tubular function than specific gravity
urine osmolarity
71
fractional excretion of Na+ in prerenal oliguria vs. acute tubular necrosis
oliguria: < 1
tubular necrosis: > 3
72
urinary Na+ in prerenal oliguria vs. acute tubular necrosis
oliguria: < 20
tubular necrosis: > 20
73
urine osmolality in prerenal oliguria vs. acute tubular necrosis
oliguria: > 500
tubular necrosis: < 400
74
BUN:Cr in prerenal oliguria vs. acute tubular necrosis
oliguria: > 20:1
tubular necrosis: 10-20:1
75
sediment prerenal oliguria vs. acute tubular necrosis
oliguria: normal, poss hyaline casts
tubular necrosis: tubular epithelial cells, granular casts
76
fundamental basis of AKI
The nephron (particularly the proximal tubule and thick ascending limb of the loop of Henle) has a high ATP consumption, and research reveals that **impaired energetics** is the fundamental basis of AKI
77
The most common cause of perioperative kidney injury
ischemia-reperfusion injury
78
Patients at risk for AKI during perioperative period:
* Pre-existing kidney disease
* Prolonged renal hypoperfusion
* Congestive heart failure
* Advanced age
* Sepsis
* Jaundice
* High-risk surgery (Use of aortic cross-clamp and liver transplant)
| greatest risk: pre-existing kidney disease, CHF, advanced age, sepsis
79
problem with using UOP as surrogate of renal perfusion
oliguria is often result of physiologic response to perioperative stress (↑ ADH release during surgery)
80
RIFLE Criteria
Risk, Injury, Failure, Loss, End-stage kidney disease
81
Risk in RIFLE criteria
Cr > 1.5x baseline
UOP < 0.5 mL/kg/hr for > 6 hours
82
Injury in RIFLE Criteria
SCr 2x baseline
UOP < 0.5 mL/kg/hr for > 12 hrs
83
Failure in RIFLE criteria
SCr Increased to > 3x baseline **or** increase > 0.5 mg/dL to absolute value of > 4 mg/dL
UOP < 0.3 mL/kg/hr > 12 hrs **or** anuria for > 12 hrs
84
Loss in RIFLE criteria
Need for renal replacement therapy > 4 weeks
85
End-Stage in RIFLE criteria
Need for renal replacement therapy > 3 months
86
End-Stage in RIFLE criteria
Need for renal replacement therapy > 3 months
87
AKIN classification of kidney injury
Acute Kidney Injury Network
88
Risk in AKIN classification of kidney injury
SCr increased > 1.5-2x baseline or > 0.3 mg/dL
UOP < 0.5 mL/kg/hr for > 6 hours
89
injury in AKIN classification of kidney injury
SCr increased > 2-3x baseline
UOP < 0.5 mL/kg/hr for > 12 hrs
90
failure in AKIN classification of kidney injury
SCr increased > 3x baseline **or**
SCr increase > 0.5 mg/dL to absolute value > 4 mg/dL **or**
Need for renal replacement therapy
UOP < 0.3 mL/kg/hr > 12 hrs or
Anuria for > 12 hours
91
KDIGO classification of kidney injury
Kidney Disease Improving Global Outcomes
92
risk in KDIGO
Scr Increased > 1.5-2x baseline within past 7 days or increased > 0.3 mg/dL within 48 hours
UOP < 0.5 mL/kg/hr for > 6 hrs
93
failure in KDIGO criteria
SCr Increased > 3x baseline **or** increase to absolute value of > 4 mg/dL **or** need for renal replacement therapy
UOP < 0.3 mL/kg/hr > 12 hrs **or** anuria for > 12 hours
94
cause of prerenal injury
Hypoperfusion
## Footnote
Perfusion impaired as a result of hypovolemia, decreased CO, systemic vasodilation, renal vasoconstriction, or ↑ IAP
94
treatment of prerenal injury
halt progression to ATN: restore RBF with IVF, HD support, PRBCs
95
confirms diagnosis of prerenal azotemia
Improved UOP following IVF bolus
96
why should NSAIDs be avoided in pts at risk of renal injury
decrease prostaglandin synthesis and cause constriction of renal vasculature
97
cause of intrinsic renal injury
Parenchymal Dysfunction
98
Intrinsic causes of acute tubular necrosis
ischemia & nephrotoxic drugs
99
causes of intrinsic renal injury
Can be caused by injury of the tubules, glomerulus, or the interstitial space
100
cause of postrenal kidney injury
obstruction
## Footnote
Source can arise anywhere between collecting system and urethra (Foley, ureteral stones, neurogenic bladder)
101
cause of postrenal kidney injury
obstruction
## Footnote
Source can arise anywhere between collecting system and urethra (Foley, ureteral stones, neurogenic bladder)
102
etiologies of prerenal injury related to depleted vascular volume
* Hemorrhage
* Dehydration
* GI losses (V/D, NG tube)
* Cirrhosis
* Nephrotic syndrome
103
etiologies of prerenal injury related to decreased CO
* CHF
* Sepsis
* Cardiogenic shock
104
etiologies of prerenal injury related to systemic vasodilation
* Sepsis
* Anaphylaxis
* Cirrhosis
105
etiologies of prerenal injury related to renal vasoconstriction
* Early sepsis
* Hepatorenal syndrome
* Hypercalcemia
* NSAIDs
* Iodine-containing IV dye
106
what kind of kidney injury does abdominal compartment syndrome cause
prerenal
107
etiologies of intrinsic kidney injury that cause tubular injury
* Ischemia – hypoperfusion
* Myoglobin
* Free hgb (transfusion rxn)
* Antibiotics
* Contrast agents
* Chemotherapeutics
108
etiologies of intrinsic kidney injury that cause Tubulointestinal Injury
* Acute allergic interstitial nephritis
* Infection
* Infiltration
109
etiologies of intrinsic kidney injury r/t glomerular injury
* Inflammatory disease
* Hemolytic uremic syndrome
* Thrombotic thrombocytopenic purpura
110
etiologies of intrinsic renal injury r/t renal vasculature
* Toxemia of pregnancy
* Hypercalcemia
* Contrast agents
* Malignant hypertension
* Scleroderma
111
etiologies of intrinsic renal injury r/t renal vasculature
* Toxemia of pregnancy
* Hypercalcemia
* Contrast agents
* Malignant hypertension
* Scleroderma
112
etiologies of postrenal injury
* Retroperitoneal tumor
* Hematoma
* Fibrosis
* Surgical trama to ureter
* Hematoma
* Nephrolithiasis
* Blood clots/debris
* Tumor
* Stricture
* Infection
* Enlarged prostate
* Bladder obstruction
* Stones
* Neurogenic bladder
| urinary tract obstruction
113
etiologies of postrenal injury
* Retroperitoneal tumor
* Hematoma
* Fibrosis
* Surgical trama to ureter
* Hematoma
* Nephrolithiasis
* Blood clots/debris
* Tumor
* Stricture
* Infection
* Enlarged prostate
* Bladder obstruction
* Stones
* Neurogenic bladder
| urinary tract obstruction
114
how is risk of prerenal azotemia decreased
by maintaining MAP > 65 and providing appropriate hydration
115
fluids associated with an increased risk of renal morbidity
hydroxyethyl starches
116
consequence of using diuretics to attempt to convert oliguric to nonoliguric AKI
increases risk of additional renal injury & mortality
117
why does vasopressin maintain GFR and UOP better than NE or neo
preferentially constricts efferent arteriole
118
antibiotics to avoid in pts at high risk for renal injury
aminoglycosides
119
target serum glucose for preventing AKI in critically ill patients
110-149 mg/dL
120
most common causes of CKD
1 - diabetes
2 - HTN
121
stages of CKD
1. Normal = GFR > 90 mL/min
2. Mildly decreased = GFR 60-89
3. Moderately decreased = GFR 30-59
4. Severely decreased = GFR 15-29
5. Kidney failure (requires dialysis) = GFR < 15
122
s/s uremic syndrome
anemia, fatigue, N/V, anorexia, coagulopathy
123
most accurate predictor of bleeding risk in pt with uremic syndrome
bleeding time
124
PT, PTT, and plt count in pts with uremic syndrome
normal
125
1st line treatment of uremic bleeding
desmopressin (von Willebrand factor 8)
126
when should dialysis be performed in uremic pt needing surgery
within 24 hours of surgery
improves bleeding time
127
why are pts with CKD anemic
* **Decreased erythropoietin production** leads to normochromic normocytic anemia
* **Excess PTH** also contributes to anemia by replacing bone marrow with fibrotic tissue
128
treatment of anemia in CKD
exogenous EPO or darbepoetin + iron supplementation
Blood transfusion is **not** a first-line treatment because it increases the risk of HLA sensitization and future rejection of a transplanted kidney
129
side effect of exogenous EPO admin
HTN
130
what causes HTN in CKD
result of RAAS activation leading to sodium retention and fluid overload
131
most common cause of death in CKD
CAD
*Assume all patients with CKD have CAD*
132
common CV complication with uremia
pericarditis
133
acid-base balance in CKD
* Decreased excretion of non-volatile acid contributes to a gap metabolic acidosis
* Non-gap acidosis is the result of a loss of HCO3- ions
134
oxyhgb assoc curve in CKD
Acidosis shifts the oxyhgb dissociation curve to the right (partially compensates for anemia)
135
serum K that necessitates dialysis
6
136
treatments of hyperkalemia
* Glucose (25 - 50g) + insulin (10 - 20 units)
* Hyperventilation (for every 10 mHg ↓in PaCO2, the serum K+ level ↓ by 0.5 mEq/L).
* Sodium bicarbonate (50 - 100 mEq)
137
why is CaCl given for hyperkalemia
does not alter serum potassium concentration but raises threshold potential in the myocardium and reduces the risk of lethal dysrhythmias
138
2 causes of Renal osteodystrophy
* Decreased vitamin D production
* Secondary hyperparathyroidism
139
why are pts with CKD at higher risk of bone fractures
* Inadequate supply of vitamin D impairs calcium absorption in the Gl tract
* The body responds ↑ PTH, which demineralizes bone to restore serum calcium concentration
* decreased bone density = increased fractures
140
phosphate level in CKD
increased
| Phosphate clearance parallels GFR
141
phosphate level in CKD
increased
| Phosphate clearance parallels GFR
142
respiratory effects of CKD
* Increased intravascular volume and uremia create a restrictive ventilatory defect
* Volume overload may lead to pulmonary edema
* Metabolic acidosis is compensated by respiratory alkalosis (hyperventilation)
143
why do CKD patients have decreased baroreceptor response & delayed gastric emptying
ANS dysfunction
144
when is PD favored over HD
in patients who can’t tolerate fluid shifts associated with HD (CHF or unstable angina)
145
most common event during dialysis
hypotension
## Footnote
due to intravascular volume depletion and osmotic shifts
146
most common event during dialysis
hypotension
## Footnote
due to intravascular volume depletion and osmotic shifts
147
most common event during dialysis
hypotension
## Footnote
due to intravascular volume depletion and osmotic shifts
148
leading cause of death in dialysis patients
infection
149
5 indications for dialysis
1. Volume overload
2. Hyperkalemia
3. Severe metabolic acidosis
4. Symptomatic uremia
5. Overdose with a drug that is cleared by dialysis
150
what leads to gap metabolic acidosis in CKD patients
decreased excretion of non-volatile acids
151
FDA recommended rate of sevo admin
1 L/min for no more than 2 MAC hours
After 2 MAC hours, FGF should increase to 2 L/min
152
Factors assoc. with increased compound A production:
* high concentrations over a long period of time
* low FGF
* high temp of CO2 absorbent
* increased CO2 production
153
is succs safe in renal failure?
Renal failure does not cause upregulation of extrajunctional receptors, so succinylcholine is **safe** in patients with renal failure and a normal potassium level
## Footnote
succs infusion shuold not be used - metabolite is renally excreted
154
propofol dosing in CKD
may need an upward dose adjustment due to hyperdynamic circulation & disruption of BBB secondary to uremia
155
is precedex safe to use in CKD
yes - biotransformed by liver
duration may be prolonged
156
Primary function of the kidneys
eliminate toxins from the body
157
what area of the kidneys is at particular risk from nephrotoxic agents
tubules
158
what determines extent of nephrotoxic effects
Concentration of toxin & duration of exposure
159
2 mechanisms by which radiographic contrast media causes nephrotoxicity:
1. Ischemic injury due to vasoconstriction in renal medulla
2. Direct cytotoxic effects
160
when do s/s AKI begin after nephrotoxic agents are admin
Signs of AKI begin at 24-36 hours and peak between 3-5 days
161
narcotics best for use in renal failure pts
fentanyl, sufentanil, remifentanil, alfentanil
162
methods to prevent AKI from contrast dye
* IV hydration with 0.9% NS before contrast
* low or iso-osmolar contrast
* bicarb
163
sequelae of direct muscle trauma, muscle ischemia, or prolonged immobilization that damages kidneys
Rhabdomyolysis and myoglobinemia
164
binds oxygen inside of the myocyte
myoglobin
165
where is myoglobin filtered when released into circulation
at the glomerulus
166
renal consequences of Rhabdomyolysis and myoglobinemia
tubular obstruction and acute tubular necrosis
167
CK level assoc with increased risk of kidney injury
> 10,000 units/L
168
prevention of AKI from myoglobin
* Maintain RBF and tubular flow with IV hydration
* Osmotic diuresis with mannitol
* Keep UOP > 100-150 mL/hr
* Administer sodium bicarb and/or acetazolamide to alkalize urine
169
side effects of tacrolimus
HTN, renal vasoconstriction
170
neuraxial anesthesia level required for TURP
T10
171
5 nephrotoxic antibiotics besides aminoglycosides
1. ampho B
2. vanc
3. sulfonamide
4. tetracyclines
5. cephalosporins
172
2 immunosuppressant agants that are nephrotoxic
1. tacro
2. cyclosporine
173
5 conditions that cause rhabdomyolysis & myoglobinemia
1. direct muscle trauma
2. muscle ischemia
3. immobilization
4. MH
5. succs in DMD
174
absorbed irrigation volume in a TURP
estimated as 10 - 30 mL/min of resection time
175
height of irrigation solution used in TURP
no more than 60 cm above OR table
176
TURP time should be limited to:
1 hour
177
TURP time should be limited to:
1 hour
178
characteristics of ideal irrigation fluid used in TURP
provides good surgical visibility (should be clear), is isotonic, and nontoxic
179
fluids that are contraindicated as irrigant solutions when monopolar electrocautery used in TURP
0.9% NaCl or LR
highly ionized - good conductors of electricity
180
cons of using water in TURP
Increased risk TURP syndrome:
181
classic triad in TURP syndrome
* HTN with increased pulse pressure
* reflex bradycardia
* AMS
182
cons of glycine use in TURP
Increased ammonia - dec LOC
Transient postop visual syndrome
183
s/s transient postop visual syndrome with glycine in TURP
* Blindness or blurry vision x 24-48 hours
* Inhibitory neurotransmitter in the eye
184
cons of 3.3% sorbital for TURP
Hyperglycemia
Osmotic diuresis
Lactic acidosis (w/ massive absorption)
185
cons of 5% mannitol for TURP
Osmotic diuresis
Transient plasma expansion (risk LV failure)
186
what causes TURP syndrome
absorption of a large volume of hypo-osmolar irrigation solution
187
serum Na+ assoc with increased complications from TURP syndrome
< 120
188
Serum Na+ level associated with seizure, coma, and lethal ventricular arrythmias
< 110 mEq/L
189
hematologic effects of TURP syndrome
hemolysis
190
treatment of TURP syndrome if Na+ > 120
restrict fluids and give lasix
191
treatment of TURP syndrome if Na+ < 120
give 3% NaCl at < 100 mL/hr (d/c when Na+ > 120 mEq/L)
192
complication of obturator n. stimulation in TURP
can cause lower extremity movement, which may cause the resectoscope to puncture the bladder wall
193
presentation of bladder puncture in TURP
* abdominal and shoulder pain
* reduction of irrigation fluid return is an early sign of bladder rupture
194
presentation of bladder puncture in TURP
* abdominal and shoulder pain
* reduction of irrigation fluid return is an early sign of bladder rupture
195
management of pt with bladder perforation in TURP
* HD support
* serial assessment of H&H and transfusion as indicated
* will require emergent suprapubic cystostomy or possibly exploratory laparotomy
196
rough estimate of blood loss during TURP
2-5 mL blood per minute of resection time
197
absolute contraindications to ESWL
pregnancy, bleeding disorder or anticoagulation (risk bleeding)
198
relative contraindications to ESWL
* pacemaker/ICD
* calcified aneurysm of aorta or renal artery
* untreated UTI
* obstruction beyond renal stone
* morbid obesity (further distance from energy source to stone)
199
Complications of ESWL
* dysrhythmias
* organ perforation
200
common side effect after ESWL
hematuria
201
common side effect after ESWL
hematuria
202
Often used when ESWL has been ineffective
Percutaneous Nephrolithotripsy
203
most common position for Percutaneous Nephrolithotripsy
prone
204
complications of Percutaneous Nephrolithotripsy
* TURP syndrome (large amount of irrigant used)
* pneumothorax
205
typical pt position for laser lithotripsy
lithotomy
206
labs elevated in renal osteodystrophy
**2 P's**
phosphate
parathyroid hormone
207
most potent stimulators of ADH release
hypernatremia
hypovolemia
208
why is vasopressin a good choice for a potent vasopressor when preserving renal function is particularly important
it constricts the efferent arteriole, increasing GFR
