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APEX > Unit 10 - Kidney part 2 > Flashcards

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

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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

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3
Q

how does ADH affect water and solutes

A

increases water reabsorption only (not solutes)

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4
Q

how does aldosterone affect water and solutes

A
  • increases Na+ and water reabsorption
  • increases K+ and H+ excretion
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5
Q

where in the nephron does PTH promote calcium reabsorption

A

distal tubules

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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)

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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

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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

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8
Q

2 effects of HCO3- loss to urine via carbonic anhydrase inhibitors

A
  1. akaline urine
  2. mild hyperchloremic metabolic acidosis
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9
Q

3 uses of acetazolamide

A
  1. open angle glaucoma
  2. high altitude sickness
  3. central sleep apnea
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10
Q

why can acetazolamide be used in high altitude sickness

A

mild metabolic acidosis ↑ resp drive

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11
Q

why is acetazolamide used in central sleep apnea

A

mild metabolic acidosis ↑ resp drive

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12
Q

why is acetazolamide used in open angle glaucoma

A

carbonic anhydrase inhibition ↓ aqueous humor production and ↓ IOP

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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)
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14
Q

function of carbonic anhydrase

A

facilitates production of H2CO3

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15
Q

location of osmotic diuretic action

A

inhibit water reabsorption in proximal tubule (primary site) & loop of Henle

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16
Q

dose of acetazolamide

A

200-500 mg

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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
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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)
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19
Q

complications of mannitol use

A
  • CHF
  • pulmonary edema
  • cerebral edema if blood-brain barrier is disrupted
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20
Q

adverse effect of osmotic diuretics in pts with CHF

A

transient increase in intravascular volume can cause pulmonary edema

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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
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22
Q

electrolytes lost to urine with loop diuretics

A
  • Na+
  • K+
  • Ca2+
  • Mg2+
  • Cl-
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23
Q

loop diuretic dosing

A
  • Furosemide: 20-200 mg
  • Bumetanide: 0.5-2 mg
  • Ethacrynic acid: 25-100 mg
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24
Q

clinical uses of loop diuretics

A
  • acute pulmonary edema
  • AKI
  • CHF
  • hypercalcemia
  • HTN
  • anion overdose
  • ↑ ICP
  • mobilization of edema fluid
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25
Q

complications assoc with loop diuretics

A
  • hypokalemic hyperchloremic metabolic alkalosis
  • hypocalcemia
  • hypomagnesemia
  • hypovolemia
  • ototoxicity
  • reduced lithium clearance

Ototoxicity ethacrynic acid > furosemide

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26
Q

MOA of thiazide diuretics

A

inhibit Na-Cl co-transporter in distal tubule

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27
Q

how do thiazide diuretics affect serum calcium

A

increase
* Inhibition in distal tubule activates Na-Ca antiporter
* ↑ Ca2+ reabsorption and ultimately increasing serum Ca2+

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28
Q

unique side effects of thiazide diuretics

A

hyperglycemia, hypercalcemia, hyperuricemia

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29
Q

clinical uses of thiazide diuretics

A
  • essential HTN
  • mobilize edema fluid
  • CHF
  • osteoporosis (↓ Ca2+ excretion)
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30
Q

MOA of Amiloride & triamterene

A

inhibit K+ secretion and Na+ reabsorption in collecting ducts

function is independent of aldosterone

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31
Q

MOA of spironalactone

A

aldosterone antagonist
by blocking aldosterone at mineralocorticoid receptors, it inhibits K+ excretion and Na+ reabsorption into collecting ducts

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32
Q

doses of K+ sparing diuretics

A
  • Spironolactone: 12.5-100 mg
  • Amiloride: 5-10 mg
  • Triamterene: 50-150 mg
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33
Q

uses of K+ sparing diuretics

A

to reduce K+ loss in a patient receiving a loop or thiazide diuretic, secondary hyperaldosteronism

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34
Q

adverse effects of K+ sparing diureics

A

hyperkalemia, metabolic acidosis, gynecomastia

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35
Q

increases risk of hyperkalemia with K+ sparing diuretics

A

concurrent NSAIDs, beta blockers, or ACE inhibitors

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36
Q

2 reasons amiloride is administered

A
  1. reduce K+ loss in pt on loop or thiazide diuretic
  2. secondary hyperaldosteronism
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37
Q

5 side effects of K+ sparing diuretics

A
  1. hyperkalemia
  2. metabolic acidosis
  3. gynecomastia
  4. libido changes
  5. nephrolithiasis
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38
Q

3 tests of glomerular function

A
  1. BUN
  2. Cr
  3. CrCl
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39
Q

normal BUN

A

10-20 mg/dL

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40
Q

normal serum Cr

A

0.7-1.5 mg/dL

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41
Q

normal CrCl

A

110-150 mL/min

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42
Q

tests of tubular function (concentrating ability)

A
  1. fractional excretion of Na+
  2. urine osmolality
  3. urine Na+
  4. urine specific gravity
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43
Q

normal fractional excretion of Na+

A

1-3%

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44
Q

normal urine osmolality

A

65-1400 mOsm/L

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45
Q

normal urine Na+ concentration

A

130-260 mEq/day

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46
Q

normal urine specific gravity

A

1.003-1.030

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47
Q

primary metabolite of protein metabolism in the liver

A

urea

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48
Q

etiologies of BUN < 8 mg/dL

A

Dehydration
Decreased urea production: Malnutrition, severe liver disease

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49
Q

etiologies of BUN 20-40

A
  • Dehydration
  • Increased protein input: High protein diet, GI bleed, Hematoma breakdown
  • Catabolism: trauma, sepsis
  • Decreased GFR
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50
Q

etiologies of BUN > 50

A

decreased GFR

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51
Q

metabolic byproduct of creatine breakdown

A

creatinine

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52
Q

production of creatinine is directly proportional to:

A

muscle mass (↓ in women and elderly)

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53
Q

lab test that is a useful indicator of GFR

A

Serum Creatinine

Undergoes renal filtration but not reabsorption

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54
Q

100% increase in serum Cr indicates:

A

50% reduction in GFR

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55
Q

why is BUN not a great indicator of GFR

A

Because urea undergoes filtration & reabsorption

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56
Q

how does BUN:Cr help evaluate hydration

A

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

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57
Q

normal BUN:Cr

A

20:1

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58
Q

BUN:Cr > 20 suggests:

A

prerenal azotemia

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59
Q

most useful indicator of GFR

A

CrCl

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60
Q

GFR calculation

A
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61
Q

calculating CrCl in women

A

Multiply value by 0.85 to account for smaller muscle mass

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62
Q

lab that relates sodium clearance to creatinine clearance

A

Fe(Na+)

Fractional Excretion of Sodium

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63
Q

what does Fe(Na+) < 1% suggest

A

prerenal azotemia
more sodium is conserved relative to the amount of creatinine cleared

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64
Q

what does Fe(Na+) > 3% suggest

A

impaired tubular function
more sodium is excreted relative to amount of creatinine cleared

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65
Q

what does urinary sodium level indicate

A

working kidneys can conserve sodium, failing kidneys waste sodium

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66
Q

UA result that indicates glomerular injury

A

Large amount of protein in urine (> 750 mg/day or +3 by UA)

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67
Q

what does urine specific gravity assess

A

weight of urine relative to sterile water

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68
Q

Measures kidney’s ability to concentrate or dilute urine

A

urine specific gravity

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69
Q

what does urine specific gravity indicate

A

Higher number = more concentrated urine (more solutes)
Lower number = less concentrated (less solutes)

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70
Q

Better test of tubular function than specific gravity

A

urine osmolarity

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71
Q

fractional excretion of Na+ in prerenal oliguria vs. acute tubular necrosis

A

oliguria: < 1
tubular necrosis: > 3

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72
Q

urinary Na+ in prerenal oliguria vs. acute tubular necrosis

A

oliguria: < 20
tubular necrosis: > 20

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73
Q

urine osmolality in prerenal oliguria vs. acute tubular necrosis

A

oliguria: > 500
tubular necrosis: < 400

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74
Q

BUN:Cr in prerenal oliguria vs. acute tubular necrosis

A

oliguria: > 20:1
tubular necrosis: 10-20:1

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75
Q

sediment prerenal oliguria vs. acute tubular necrosis

A

oliguria: normal, poss hyaline casts
tubular necrosis: tubular epithelial cells, granular casts

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76
Q

fundamental basis of AKI

A

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

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77
Q

The most common cause of perioperative kidney injury

A

ischemia-reperfusion injury

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78
Q

Patients at risk for AKI during perioperative period:

A
  • 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

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79
Q

problem with using UOP as surrogate of renal perfusion

A

oliguria is often result of physiologic response to perioperative stress (↑ ADH release during surgery)

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80
Q

RIFLE Criteria

A

Risk, Injury, Failure, Loss, End-stage kidney disease

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81
Q

Risk in RIFLE criteria

A

Cr > 1.5x baseline
UOP < 0.5 mL/kg/hr for > 6 hours

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82
Q

Injury in RIFLE Criteria

A

SCr 2x baseline
UOP < 0.5 mL/kg/hr for > 12 hrs

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83
Q

Failure in RIFLE criteria

A

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

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84
Q

Loss in RIFLE criteria

A

Need for renal replacement therapy > 4 weeks

85
Q

End-Stage in RIFLE criteria

A

Need for renal replacement therapy > 3 months

86
Q

End-Stage in RIFLE criteria

A

Need for renal replacement therapy > 3 months

87
Q

AKIN classification of kidney injury

A

Acute Kidney Injury Network

88
Q

Risk in AKIN classification of kidney injury

A

SCr increased > 1.5-2x baseline or > 0.3 mg/dL

UOP < 0.5 mL/kg/hr for > 6 hours

89
Q

injury in AKIN classification of kidney injury

A

SCr increased > 2-3x baseline

UOP < 0.5 mL/kg/hr for > 12 hrs

90
Q

failure in AKIN classification of kidney injury

A

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
Q

KDIGO classification of kidney injury

A

Kidney Disease Improving Global Outcomes

92
Q

risk in KDIGO

A

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
Q

failure in KDIGO criteria

A

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
Q

cause of prerenal injury

A

Hypoperfusion

Perfusion impaired as a result of hypovolemia, decreased CO, systemic vasodilation, renal vasoconstriction, or ↑ IAP

94
Q

treatment of prerenal injury

A

halt progression to ATN: restore RBF with IVF, HD support, PRBCs

95
Q

confirms diagnosis of prerenal azotemia

A

Improved UOP following IVF bolus

96
Q

why should NSAIDs be avoided in pts at risk of renal injury

A

decrease prostaglandin synthesis and cause constriction of renal vasculature

97
Q

cause of intrinsic renal injury

A

Parenchymal Dysfunction

98
Q

Intrinsic causes of acute tubular necrosis

A

ischemia & nephrotoxic drugs

99
Q

causes of intrinsic renal injury

A

Can be caused by injury of the tubules, glomerulus, or the interstitial space

100
Q

cause of postrenal kidney injury

A

obstruction

Source can arise anywhere between collecting system and urethra (Foley, ureteral stones, neurogenic bladder)

101
Q

cause of postrenal kidney injury

A

obstruction

Source can arise anywhere between collecting system and urethra (Foley, ureteral stones, neurogenic bladder)

102
Q

etiologies of prerenal injury related to depleted vascular volume

A
  • Hemorrhage
  • Dehydration
  • GI losses (V/D, NG tube)
  • Cirrhosis
  • Nephrotic syndrome
103
Q

etiologies of prerenal injury related to decreased CO

A
  • CHF
  • Sepsis
  • Cardiogenic shock
104
Q

etiologies of prerenal injury related to systemic vasodilation

A
  • Sepsis
  • Anaphylaxis
  • Cirrhosis
105
Q

etiologies of prerenal injury related to renal vasoconstriction

A
  • Early sepsis
  • Hepatorenal syndrome
  • Hypercalcemia
  • NSAIDs
  • Iodine-containing IV dye
106
Q

what kind of kidney injury does abdominal compartment syndrome cause

A

prerenal

107
Q

etiologies of intrinsic kidney injury that cause tubular injury

A
  • Ischemia – hypoperfusion
  • Myoglobin
  • Free hgb (transfusion rxn)
  • Antibiotics
  • Contrast agents
  • Chemotherapeutics
108
Q

etiologies of intrinsic kidney injury that cause Tubulointestinal Injury

A
  • Acute allergic interstitial nephritis
  • Infection
  • Infiltration
109
Q

etiologies of intrinsic kidney injury r/t glomerular injury

A
  • Inflammatory disease
  • Hemolytic uremic syndrome
  • Thrombotic thrombocytopenic purpura
110
Q

etiologies of intrinsic renal injury r/t renal vasculature

A
  • Toxemia of pregnancy
  • Hypercalcemia
  • Contrast agents
  • Malignant hypertension
  • Scleroderma
111
Q

etiologies of intrinsic renal injury r/t renal vasculature

A
  • Toxemia of pregnancy
  • Hypercalcemia
  • Contrast agents
  • Malignant hypertension
  • Scleroderma
112
Q

etiologies of postrenal injury

A
  • 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
Q

etiologies of postrenal injury

A
  • 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
Q

how is risk of prerenal azotemia decreased

A

by maintaining MAP > 65 and providing appropriate hydration

115
Q

fluids associated with an increased risk of renal morbidity

A

hydroxyethyl starches

116
Q

consequence of using diuretics to attempt to convert oliguric to nonoliguric AKI

A

increases risk of additional renal injury & mortality

117
Q

why does vasopressin maintain GFR and UOP better than NE or neo

A

preferentially constricts efferent arteriole

118
Q

antibiotics to avoid in pts at high risk for renal injury

A

aminoglycosides

119
Q

target serum glucose for preventing AKI in critically ill patients

A

110-149 mg/dL

120
Q

most common causes of CKD

A

1 - diabetes
2 - HTN

121
Q

stages of CKD

A
  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
Q

s/s uremic syndrome

A

anemia, fatigue, N/V, anorexia, coagulopathy

123
Q

most accurate predictor of bleeding risk in pt with uremic syndrome

A

bleeding time

124
Q

PT, PTT, and plt count in pts with uremic syndrome

A

normal

125
Q

1st line treatment of uremic bleeding

A

desmopressin (von Willebrand factor 8)

126
Q

when should dialysis be performed in uremic pt needing surgery

A

within 24 hours of surgery
improves bleeding time

127
Q

why are pts with CKD anemic

A
  • Decreased erythropoietin production leads to normochromic normocytic anemia
  • Excess PTH also contributes to anemia by replacing bone marrow with fibrotic tissue
128
Q

treatment of anemia in CKD

A

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
Q

side effect of exogenous EPO admin

A

HTN

130
Q

what causes HTN in CKD

A

result of RAAS activation leading to sodium retention and fluid overload

131
Q

most common cause of death in CKD

A

CAD
Assume all patients with CKD have CAD

132
Q

common CV complication with uremia

A

pericarditis

133
Q

acid-base balance in CKD

A
  • 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
Q

oxyhgb assoc curve in CKD

A

Acidosis shifts the oxyhgb dissociation curve to the right (partially compensates for anemia)

135
Q

serum K that necessitates dialysis

A

6

136
Q

treatments of hyperkalemia

A
  • 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
Q

why is CaCl given for hyperkalemia

A

does not alter serum potassium concentration but raises threshold potential in the myocardium and reduces the risk of lethal dysrhythmias

138
Q

2 causes of Renal osteodystrophy

A
  • Decreased vitamin D production
  • Secondary hyperparathyroidism
139
Q

why are pts with CKD at higher risk of bone fractures

A
  • 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
Q

phosphate level in CKD

A

increased

Phosphate clearance parallels GFR

141
Q

phosphate level in CKD

A

increased

Phosphate clearance parallels GFR

142
Q

respiratory effects of CKD

A
  • 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
Q

why do CKD patients have decreased baroreceptor response & delayed gastric emptying

A

ANS dysfunction

144
Q

when is PD favored over HD

A

in patients who can’t tolerate fluid shifts associated with HD (CHF or unstable angina)

145
Q

most common event during dialysis

A

hypotension

due to intravascular volume depletion and osmotic shifts

146
Q

most common event during dialysis

A

hypotension

due to intravascular volume depletion and osmotic shifts

147
Q

most common event during dialysis

A

hypotension

due to intravascular volume depletion and osmotic shifts

148
Q

leading cause of death in dialysis patients

A

infection

149
Q

5 indications for dialysis

A
  1. Volume overload
  2. Hyperkalemia
  3. Severe metabolic acidosis
  4. Symptomatic uremia
  5. Overdose with a drug that is cleared by dialysis
150
Q

what leads to gap metabolic acidosis in CKD patients

A

decreased excretion of non-volatile acids

151
Q

FDA recommended rate of sevo admin

A

1 L/min for no more than 2 MAC hours

After 2 MAC hours, FGF should increase to 2 L/min

152
Q

Factors assoc. with increased compound A production:

A
  • high concentrations over a long period of time
  • low FGF
  • high temp of CO2 absorbent
  • increased CO2 production
153
Q

is succs safe in renal failure?

A

Renal failure does not cause upregulation of extrajunctional receptors, so succinylcholine is safe in patients with renal failure and a normal potassium level

succs infusion shuold not be used - metabolite is renally excreted

154
Q

propofol dosing in CKD

A

may need an upward dose adjustment due to hyperdynamic circulation & disruption of BBB secondary to uremia

155
Q

is precedex safe to use in CKD

A

yes - biotransformed by liver
duration may be prolonged

156
Q

Primary function of the kidneys

A

eliminate toxins from the body

157
Q

what area of the kidneys is at particular risk from nephrotoxic agents

A

tubules

158
Q

what determines extent of nephrotoxic effects

A

Concentration of toxin & duration of exposure

159
Q

2 mechanisms by which radiographic contrast media causes nephrotoxicity:

A
  1. Ischemic injury due to vasoconstriction in renal medulla
  2. Direct cytotoxic effects
160
Q

when do s/s AKI begin after nephrotoxic agents are admin

A

Signs of AKI begin at 24-36 hours and peak between 3-5 days

161
Q

narcotics best for use in renal failure pts

A

fentanyl, sufentanil, remifentanil, alfentanil

162
Q

methods to prevent AKI from contrast dye

A
  • IV hydration with 0.9% NS before contrast
  • low or iso-osmolar contrast
  • bicarb
163
Q

sequelae of direct muscle trauma, muscle ischemia, or prolonged immobilization that damages kidneys

A

Rhabdomyolysis and myoglobinemia

164
Q

binds oxygen inside of the myocyte

A

myoglobin

165
Q

where is myoglobin filtered when released into circulation

A

at the glomerulus

166
Q

renal consequences of Rhabdomyolysis and myoglobinemia

A

tubular obstruction and acute tubular necrosis

167
Q

CK level assoc with increased risk of kidney injury

A

> 10,000 units/L

168
Q

prevention of AKI from myoglobin

A
  • 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
Q

side effects of tacrolimus

A

HTN, renal vasoconstriction

170
Q

neuraxial anesthesia level required for TURP

A

T10

171
Q

5 nephrotoxic antibiotics besides aminoglycosides

A
  1. ampho B
  2. vanc
  3. sulfonamide
  4. tetracyclines
  5. cephalosporins
172
Q

2 immunosuppressant agants that are nephrotoxic

A
  1. tacro
  2. cyclosporine
173
Q

5 conditions that cause rhabdomyolysis & myoglobinemia

A
  1. direct muscle trauma
  2. muscle ischemia
  3. immobilization
  4. MH
  5. succs in DMD
174
Q

absorbed irrigation volume in a TURP

A

estimated as 10 - 30 mL/min of resection time

175
Q

height of irrigation solution used in TURP

A

no more than 60 cm above OR table

176
Q

TURP time should be limited to:

A

1 hour

177
Q

TURP time should be limited to:

A

1 hour

178
Q

characteristics of ideal irrigation fluid used in TURP

A

provides good surgical visibility (should be clear), is isotonic, and nontoxic

179
Q

fluids that are contraindicated as irrigant solutions when monopolar electrocautery used in TURP

A

0.9% NaCl or LR

highly ionized - good conductors of electricity

180
Q

cons of using water in TURP

A

Increased risk TURP syndrome:

181
Q

classic triad in TURP syndrome

A
  • HTN with increased pulse pressure
  • reflex bradycardia
  • AMS
182
Q

cons of glycine use in TURP

A

Increased ammonia - dec LOC
Transient postop visual syndrome

183
Q

s/s transient postop visual syndrome with glycine in TURP

A
  • Blindness or blurry vision x 24-48 hours
  • Inhibitory neurotransmitter in the eye
184
Q

cons of 3.3% sorbital for TURP

A

Hyperglycemia
Osmotic diuresis
Lactic acidosis (w/ massive absorption)

185
Q

cons of 5% mannitol for TURP

A

Osmotic diuresis
Transient plasma expansion (risk LV failure)

186
Q

what causes TURP syndrome

A

absorption of a large volume of hypo-osmolar irrigation solution

187
Q

serum Na+ assoc with increased complications from TURP syndrome

A

< 120

188
Q

Serum Na+ level associated with seizure, coma, and lethal ventricular arrythmias

A

< 110 mEq/L

189
Q

hematologic effects of TURP syndrome

A

hemolysis

190
Q

treatment of TURP syndrome if Na+ > 120

A

restrict fluids and give lasix

191
Q

treatment of TURP syndrome if Na+ < 120

A

give 3% NaCl at < 100 mL/hr (d/c when Na+ > 120 mEq/L)

192
Q

complication of obturator n. stimulation in TURP

A

can cause lower extremity movement, which may cause the resectoscope to puncture the bladder wall

193
Q

presentation of bladder puncture in TURP

A
  • abdominal and shoulder pain
  • reduction of irrigation fluid return is an early sign of bladder rupture
194
Q

presentation of bladder puncture in TURP

A
  • abdominal and shoulder pain
  • reduction of irrigation fluid return is an early sign of bladder rupture
195
Q

management of pt with bladder perforation in TURP

A
  • HD support
  • serial assessment of H&H and transfusion as indicated
  • will require emergent suprapubic cystostomy or possibly exploratory laparotomy
196
Q

rough estimate of blood loss during TURP

A

2-5 mL blood per minute of resection time

197
Q

absolute contraindications to ESWL

A

pregnancy, bleeding disorder or anticoagulation (risk bleeding)

198
Q

relative contraindications to ESWL

A
  • 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
Q

Complications of ESWL

A
  • dysrhythmias
  • organ perforation
200
Q

common side effect after ESWL

A

hematuria

201
Q

common side effect after ESWL

A

hematuria

202
Q

Often used when ESWL has been ineffective

A

Percutaneous Nephrolithotripsy

203
Q

most common position for Percutaneous Nephrolithotripsy

A

prone

204
Q

complications of Percutaneous Nephrolithotripsy

A
  • TURP syndrome (large amount of irrigant used)
  • pneumothorax
205
Q

typical pt position for laser lithotripsy

A

lithotomy

206
Q

labs elevated in renal osteodystrophy

A

2 P’s
phosphate
parathyroid hormone

207
Q

most potent stimulators of ADH release

A

hypernatremia
hypovolemia

208
Q

why is vasopressin a good choice for a potent vasopressor when preserving renal function is particularly important

A

it constricts the efferent arteriole, increasing GFR

APEX (54 decks)

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