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assessment exam 3 > Renal Assessment > Flashcards

Renal Assessment Flashcards

1
Q

What is the role of antidiuretic hormone (ADH) in fluid and volume homeostasis?

A

ADH increases water and Na+ retention

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2
Q

What percentage of total body water (TBW) is water? What factors affect this composition?

A

~60%. TBW varies with age, gender and body fat % (higher muscle will lead to higher water)

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3
Q

Where is the fluid outside of cells located?

A

Extracellular fluid (ECF) (includes ISF and Plasma)

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4
Q

Which fluid compartement is more immediately altered by kidneys? ICF or ECF?

A

ECF

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5
Q

What regulates the majority of osmolar homeostasis? How is osmolar homeostasis maintained? (What does body do to improve fluid volume)

A

Osmlolar homeostasis mainly mediated by osmolality-sensors in anterior hypothalamus. These sensors stimulate thirst and cause pituitary release of ADH.
The cardiac atria release ANP which acts on kidneys to increase sodium and H20 excretion.

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6
Q

How is volume homeostasis regulated?

A

Volume homeostasis is maintained by juxtaglomerular apparatus.

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7
Q

What does a decrease in volume at the juxtaglomerular apparatus (JGA) trigger?

A

Renin-Angiotensinogen-Aldosterone system (RAAS) for Na+/H2O reabsorption

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8
Q

What is the normal range for sodium?

A

135-145mEq/L

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9
Q

What levels of sodium require correction prior to elective surgery?

A

sodium levels ≤125 or ≥155

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10
Q

What are the potential causes of hyponatremia in the Hypovolemic category?

A

From ppt notes section: Na+/H20 loss (diuretics, gi loss, burns, trauma)
Full list:
Renal losses: Mineralcorticoid deficiency, salt-losing nephritis, renal tubular acidosis, metabolic alkalosis, ketonuria, osmotic diuresis.
Extrarenal losses: vomiting, diarrhea, 3rd space lossed, burns, pancreatitis, muscle trauma

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11
Q

What are the potential causes of hyponatremia in the Euvolemic category?

A

Salt restriction, endocrine related -Hypothyroid, SIADH, gluccocorticoid deficiency, high sympathetic drive.

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12
Q

What are the potential causes of hyponatremia in the Hypervolemic category?

A

ARF/CKD, heart failure, nephrotic syndrome, cirrhosis

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13
Q

What percentage of hospitalized patients are hyponatremic?

A

15%

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14
Q

What is a contributing factor to hyponatremia in hospitalized patients?

A

Over fluid-resuscitation and increased endogenous vasopressin

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15
Q

Treatment of hyponatremia involves treating the underlying conditions. What are some common methods of correcting low sodium

A

electrolyte drinks, normal saline, diuretics (for dilutional hyponatremia). If ineffective hypertonic saline can be used.

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16
Q

What are the signs and symptoms of Na level 120-130 mEq/L

A
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17
Q

What are the signs and symptoms of Hyponatremia 130-135 mEq/L

A
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18
Q

What are the signs and symptoms of Na level <120 mEq/L

A
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19
Q

What are the two initial signs of hyponatremia

A

hyponatremia starts with headache and confusion

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20
Q

What is the dose for 3% NaCl?

A

80 mL/hr over 15 hours.

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21
Q

How often should Na+ level be checked while treating hyponatremia?

A

q 4 hr

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22
Q

What is the recommended rate for Na+ correction in hyponatremia?

A

Na+ should not exceed 1.5 mEq/L/hr

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23
Q

Why should Na+ correction be done slowly in hyponatremia treatment?

A

Rapid correction (>6 mEqL in 24 hr) can cause Osmotic Demyelination Syndrome (often leading to permanent neurological damage)

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24
Q

Hyponatremic seizures are a medical emergency that can lead to what?

A

neurological damage

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25
Q

What is the initial treatment for hyponatremic seizures?

A

3-5ml/kg of 3% over 20 min until seizures resolve.

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26
Q

What is DI often associated with?

A

Loss of dilute urine

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27
Q

What are common causes of hypernatremia?

A

Excessive evaporation, Poor oral intake, Overcorrection of hyponatremia, DI, GI losses, Excessive sodium bicarb (when treating acidosis)

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28
Q

What are the diagnostic algorithms for different types of electrolyte imbalances?

A

Hypo: Renal/GI loss
Euvo: DI/insensible loss (skin, respiratory)
Hyper: ↑Na+ intake (IV)/aldosteronism/Cushings

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29
Q

What are the causes of hypernatremia?

A

IV intake, hyperaldosteronism, Cushings

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30
Q

What are the symptoms of Hypernatremia?

A

Orthostasis, Restlessness, Lethargy, Tremor/Muscle twitching/spasticity, Seizures, Death

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31
Q

What is the initial step in treating Hypernatremia?

A

Identify root cause, Assess volume status (VS, UO, Turgor, CVP)

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32
Q

What treatment is recommended for Hypovolemic Hypernatremia?

A

Normal saline

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33
Q

What treatment is recommended for Euvolemic Hypernatremia?

A

Water replacement (PO or D5W)

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34
Q

What treatment is recommended for Hypervolemic Hypernatremia?

A

Diuretics

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35
Q

What is the target Na+ reduction rate to avoid cerebral edema, seizures, and neurologic damage in Hypernatremia?

A

≤0.5 mmol/L/hr, and ≤ 10 mmol/L per day

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36
Q

Normal Potassium Level?

A

3.5-5 mmol/L

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37
Q

Percentage of Potassium in ECF?

A

< 1.5%

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38
Q

What does Serum K+ level reflect?

A

Transmembrane K+ regulation

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39
Q

Effect of Aldosterone on K+?

A

Causes distal nephron to secrete K+ and reabsorb Na+

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40
Q

What happens to K+ excretion in renal failure?

A

Renal excretion of K+ declines and excretion of K+ shifts towards GI system.

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41
Q

What are the 3 major categories of causes for hypokalemia?

A

Renal loss, GI loss, Transcellular shift

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42
Q

What are common causes of hypokalemia related to renal loss?

A

Diuretics, Hyperaldosteronism

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43
Q

What are common causes of hypokalemia related to GI loss?

A

N/V/D, malabsorption

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44
Q

What are some common causes of hypokalemia related to intracellular shift?

A

Alkalosis, β-Ag’s, Insulin

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45
Q

What medical condition can lead to hypokalemia due to osmotic diuresis?

A

DKA

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46
Q

Which medication in blood pressure management can cause hypokalemia?

A

HCTZ

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47
Q

What dietary item in excess can lead to hypokalemia?

A

Excessive licorice

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48
Q

What are the symptoms of hypokalemia?

A

Generally cardiac (dysrhythmias, U wave) and neuromuscular (muscle weakness/cramps and ileus)

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49
Q

How can hypokalemia be treated?

A

Treatment of underlying cause.
Potassium PO > IV (CVC) may take days to correct.

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50
Q

What is the IV dose range for IV potassium? How much will IV potassium increase serum K+ levels?

A

Generally 10-20meq/L/hr IV.
EAch 10 mEq IV K+ will increase serum K+ by 0.1mmol/L

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51
Q

What should be avoided in the treatment of hypokalemia?

A

Avoic excessive insulin, β-agonists (decrease speed of Na+/K+ pump), bicarb, hyperventilation, diuretics

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52
Q

What are some symptoms of hyperkalemia?

A

Chronic may be minimally symptomatic (Malaise, GI upset)
Skeletal muscle paralysis, cardiac dysrhythmias, decrease fine motor function

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53
Q

What are some EKG changes associated with hyperkalemia?

A

Peaked T wave, P wave disappearance, prolonged QRS complex, sine waves, asystole

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54
Q

What can cause hyperkalemia?

A

Renal failure, hypoaldosteronism, drugs inhibiting RAAS/K+ excretion, Succinylcholine, Acidosis, cell death, massive blood transfusion.

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55
Q

How does succinylcholine affect serum K+ levels?

A

Increases by 0.5-1 mEq/L

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56
Q

What is the initial consequence of dialysis?

A

Hypovolemia

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57
Q

What is the initial treatment for hyperkalemia? Why is this the initial treatment?

A

Calcium administration. Calcium will stabilize cell membrane quickly.

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58
Q

How does hyperventilation affect potassium levels?

A

Hyperventilation will increase pH (more alkalotic). Increase of pH by 0.1 will decrease K+ by 0.4-1.5 mmol/L.

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59
Q

What is the dose of insulin and D50 in hyperkalemia treatment? How long will it take for insulin to work in hyperkalemia treatment?

A

10 units IV insulin: 25 g D50. Onset of 10-20 min

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60
Q

What should be avoided in hyperkalemia management?

A

Succs, hypoventilation, LR & K+ containing IV fluids

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61
Q

In addition to Calcium, hyperventilation and insulin what other drugs are utilized to decrease potassium?

A

Bicarb, loop diuretics, Kayexalate (hours to days)

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62
Q

How much of the body’s Calcium is in ECF? Where is the majority of Calcium stored? What percentage of plasma Ca++ is protein bound?

A

Only 1% of Calcium is in ECF; the other 99% is stored in bone.
Of the 1% of calcium in ECF 60% of it is bound to proteins (mainly Albumin)

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63
Q

How does pH affect the binding of Ca++ to albumin?

A

↑pH/Alkalosis→↑Ca++ binding

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64
Q

Which form of plasma Ca++ is physiologically active?

A

Ionized calcium is physologically active whereas protein bound calcium is not active.

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65
Q

What is the normal range for ionized Ca++?

A

1.2-1.38 mmol/L

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66
Q

Which hormones regulate Calcium

A

parathyroid, Vitamin D (calcitriol), Caclitonin.

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67
Q

What hormone stimulates the release of of Ca++ from the bones into plasma?

A

Parathyroid hormone

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68
Q

Which hormone augments intestinal Ca++ absorption?

A

Vitamin D

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69
Q

What hormone promotes calcium storage into the bone?

A

Calcitonin

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70
Q

What is required for PTH production?

A

Magnesium

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71
Q

How does pH influence the binding of Calcium to albumin?

A

increased pH/alkalosis leads to increase calcium binding to albumin (therefore decreasing ionized calcium levels)

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72
Q

When should iCa++ be checked in relation to PRBC transfusions?

A

After 4+ units

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73
Q

A major cause of Hypocalcemia is a decrease in what hormone?

A

PTH (Parathyroid hormone)

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74
Q

What role does Magnesium play in Hypocalcemia?

A

Deficiency can cause Hypocalcemia

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75
Q

How does Renal failure contribute to Hypocalcemia?

A

Kidneys not responding to PTH

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76
Q

What is a consequence of massive blood transfusion on calcium levels?

A

Citrate preservative binds Ca++, causing Hypocalcemia

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77
Q

Most common causes of hypercalcemia

A

Hyperparathyroidism or cancer

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78
Q

Hyperparathyroidism serum Calcium level range

A

<11

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79
Q

Cancer serum Calcium level range for those with hypercalcemia

A

> 13

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80
Q

Less common causes of hypercalcemia

A

Vit D intoxication, Milk-alkali syndrome (excess GI Calcium absorption), Granulomatous diseases (sarcoidosis)

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81
Q

What caution should be taken when extubating after parathyroidectomy?

A

Have laryngospasm plan

82
Q

What are signs and symptoms of hypercalcemia?

A

Confusion, lethargy, hypotonia/decreased deep tendon reflexes, abdominal pain, n/v, short QT interval.

83
Q

What are signs and symptoms of hypocalcemia?

A

Paresthesias, irritability, hypotension, seizures, myocardial depression, prolonged QT interval.

84
Q

What can chronic high calcium levels lead to?

A

Hypercalciuria & nephrolithiasis

85
Q

What is a life-threatening complication post-parathyroidectomy related to hypocalcemia?

A

Laryngospasm. Due to calcium absoprtion dependent on PTH.

86
Q

What are the causes of hypo-magnesium?

A

Low dietary intake or absorption, Renal wasting

87
Q

What are the symptoms of hypo-magnesium?

A

Muscle weakness or excitation, seizures, Ventricular dysrhythmia (polymorphic v Tach, Torsades)

88
Q

How is hypo-magnesium treated for torsades or seizures?

A

2g Mag Sulfate

89
Q

What are the symptoms of hypermagnesemia at 4-5 mEq/L?

A

Lethargy, N/V, Flushing

90
Q

What are the symptoms of hypermagnesemia at >6 mEq/L?

A

HoTN, ↓DTR

91
Q

What are the symptoms of hypermagnesemia at >10 mEq/L?

A

Paralysis, apnea, heart blocks, cardiac arrest

92
Q

How is hypermagnesemia treated?

A

Diuresis, IV Calcium (cell membrane stabilization), Dialysis

93
Q

Where are the kidneys located?

A

Retroperitoneal between T12-L4

94
Q

Which kidney is slightly caudal to accommodate the liver?

A

Right

95
Q

What is the primary structural and functional unit in the kidney? How many are present in each kidney?

A

Nephron. There are approximately ~1 million per kidney.

96
Q

What are the components of a nephron?

A

Glomerulus,
Tubular system: Bowman capsule, PCT, Loop of Henle, DCT, Collecting duct

97
Q

What percentage of cardiac output do the kidneys receive? What does this equate to in L/min

A

20% of CO, 1-1.25 L/min

98
Q

Which part of the kidney receives the majority of renal blood flow? What % of RBF does it receive?

A

Cortex receives majority of RBF (85-90%)

99
Q

Which part of the kidney is particularly vulnerable to necrosis in response to hypotension?

A

Loop of Henle

100
Q

What system is responsible for increasing Na+/H2O reabsorption?

A

RAAS (Renin Angiotensin Aldosterone system)

101
Q

What hormone, secreted from the cardiac atria, decreases Na+/H2O reabsorption?

A

Atrial Natriuretic Peptide (ANP)

102
Q

What is crucial for pH balance in the body?

A

Reabsorption & excretion of HCO3- & H+

103
Q

What role does EPO play regarding blood?

A

Involved in RBCs production. Renal patients often on EPO supplements.

104
Q

What maintains serum calcium levels?

A

Calcitriol

105
Q

What are prostaglandins’ roles in the kidneys?

A

Inflammatory modulators, vasodilatory effects, maintain renal blood flow

106
Q

What additional role do kidneys play in metabolism?

A

Gluconeogenesis and filtration & reabsorption of glucose

107
Q

How do kidneys help in regulating blood pressure?

A

RAAS, ANP

108
Q

Name a function of the kidneys related to excretion.

A

Excrete toxins/metabolites

109
Q

How do kidneys contribute to maintaining acid/base balance?

A

By managing the balance of HCO3- and H+

110
Q

Which hormones are produced by the kidneys?

A

Renin, Erythropoietin, Calcitriol, Prostaglandins

111
Q

What is the role of the kidneys in blood glucose homeostasis?

A

Gluconeogenesis, filtration & reabsorption of glucose

112
Q

What is the best measure of renal function over time? What is this lab heavily influenced by? How does aging affect this lab?

A

Glomerular filtration rate (125-140 mL/min) is best measure of renal function over time. GFR is heavily dependent on hydration status. GFR decreases by 10 mL/min per decade after 20’s.

113
Q

What does Creatinine Clearance measure? What is the normal range?

A

Most reliable measure of GFR. Conducted using 24 hour urine test. Normal level (110-140 mL/min)

114
Q

What is normal serum creatinine level? What is serum creatinine relationship to GFR?

A

Serum Creatinine (0.6-1.3 mg/dL).
It is inversely related to GFR.

115
Q

What can a double serum creatinine in an acute case indicate?

A

Drop in GFR by 50%

116
Q

What is the normal range for Blood Urea Nitrogen (BUN)?

A

10-20 mg/dL

117
Q

What could a low BUN level indicate?

A

Malnourished or volume diluted

118
Q

What could a high BUN level indicate?

A

High protein diet, dehydrated, GI bleed, trauma, muscle wasting

119
Q

What is the normal BUN:Creatinine ratio?

A

10:1

120
Q

Why is the BUN:Creatinine ratio a good measure of hydration status?

A

BUN reabsorbed, creatinine not reabsorbed

121
Q

Normal proteinuria level? What could proteinuria (>750 mg/day) suggest?

A

Normal level is (<150 mg/dL). >750 mg/day is indicative of Glomerular injury or UTI

122
Q

What is the normal range for specific gravity? What is it used to assess?

A

1.001-1.035. Measures nephron’s ability to concentrate urine.

123
Q

What should you consider when assessing volume status?

A

Hydration status, history, physical exam

124
Q

What is oliguria?

A

<500mL in 24h

125
Q

What is the normal range for urine output (UOP)?

A

0.5-1ml/kg/hr

126
Q

What does a compressed IVC indicate? How is this assessed?

A

compressed IVC is indicative of dehydration. It can be assessed via Ultrasound

127
Q

What does PCWP stand for and what does it stimulate?

A

Pulmonary Capillary Wedge Pressure; renal vasoconstriction

128
Q

What assumption is made when measuring stroke volume variation?

A

Patient is ventilated and in sinus rhythm

129
Q

What does >50% IVC collapse indicate?

A

Fluid deficit

130
Q

What can be considered to determine fluid responsiveness in addition to IVC collapsibility?

A

Passive leg raise

131
Q

What is a common hallmark of Acute Kidney Injury? Is Acute Kidney injury reversible?

A

Azotemia: buildup of urea and creatinine
Yes, it is Reversible with timely interventions

132
Q

AKI with Multiple System Organ Failure (MSOF) requiring dialysis results in a mortatility rate of?

A

> 50%

133
Q

What are some risk factors of AKI?

A

Primary risk: Pre-existing renal disease
Others: Advanced age (GFR decreases with age), CHF, PVD, Diabetes, Sepsis (via hypotension), Jaundice, Major operative procedures, IV Contrast

134
Q

What is the diagnostic criteria for AKI?

A

SCr increase by 0.3 mg/dL within 48h, SCr increase by 50% within 7 days, Creatinine clearance decrease by 50%, and abrupt oliguria (although not always seen in AKI)

135
Q

Physical symptoms of AKI

A

Can be asymptomatic, malaise, hypotension, hypo or hypervolemia

136
Q

What is the cause of pre-renal azotemia?

A

↓ renal perfusion

137
Q

What is the cause of renal azotemia?

A

nephron injury

138
Q

What is the cause of post renal azotemia?

A

outflow obstruction

139
Q

Which type of azotemia is the easiest to treat? Which is the most common form of AKI?

A

Postrenal Azotemia easiest to treat.
Pre-renal is the most common form of AKI.

140
Q

Name the causes of prerenal azotemia.

A
141
Q

Name the causes of renal azotemia.

A
142
Q

Name the causes of postrenal azotemia.

A
143
Q

What is the typical BUN:Cr ratio in Pre-Renal AKI?

A

> 20:1

144
Q

Is Pre-renal azotemia reversible? What can it lead to if it is not reversed in a timely manner?

A

Yes, pre-renal AKI is usually a volume issue.
If not reversed it can lead to Acute tubular necrosis (progressives from a pre-renal issue to a renal issue)

145
Q

What is the primary goal in treating Pre-renal azotemia? How is this achieved?

A

Restore RBF is primary goal and can be achieved via: fluids, mannitol, diuretics, maintain MAP, pressers.

146
Q

What is the typical BUN:Cr ratio in renal azotemia?

A

< 15:1

147
Q

In renal AKI, why does BUN:Cr decrease compared to pre-renal AKI?

A

Decreased urea reabsorption in proximal tubule

148
Q

What are the characteristics of renal azotemia?

A

Intrinsic renal disease, potentially reversible, decreased GFR (late sign), decreased urea reabsorption in proximal tubule (decreased BUN), decreased creatinine filtration (elevated blood creatinine)

149
Q

What is hydronephrosis?

A

Obstruction causing renal pelvis dilation

150
Q

What is post-renal azotemia?

A

Result of outflow obstruction

151
Q

How is reversibility related to the duration of obstruction in hydronephrosis?

A

Inversely related. (longer duration/less reversible) and vice versa

152
Q

What is the treatment for hydronephrosis?

A

Remove obstruction if possible

153
Q

What does persistent obstruction in hydronephrosis lead to?

A

Damage to tubular epithelium

154
Q

What are some neurological complications of AKI?

A

Uremic Encephalopathy (improved with HD), mobility disorders, neuropathies, myopathies, seizures, stroke

155
Q

What are the cardiovascular complications of AKI?

A

Hypertension (not excreting fluid), LVH, CHF, pulmonary edema, Uremic cardiomyopathy, Arrhythmias

156
Q

What is the order of cardiovascular complications in AKI?

A

HTN → LVH → CHF → ischemic heart disease →anemic heart failure →Arrhythmias → pericarditis (with or without effusion) →cardiac tamponade, Uremic cardiomyopathy

157
Q

What are some hematological complications of AKI?

A

Anemia (decreased EPO/RBC/RBC survival), Platelet dysfunction, vWF disruption (d/t uremia)

158
Q

What can be done prophylactically to address vWF disruption in AKI?

A

Prophylactic DDAVP (increased vWF/Factor VIII)

159
Q

What are some metabolic complications of AKI?

A

Hyperkalemia, Water/sodium imbalances, Hypoalbuminemia, Metabolic acidosis, malnutrition, hyperparathyroidism (parathyroid in overdrive to stimulate kidney reabsorption of Calcium)

160
Q

What is preferred pressor for maintaining renal blood flow in acute kidney injury?

A

Vasopressin

161
Q

What is the preferred fluid for renal issues? What is the preferred colloid?

A

NS preferred for renal (no K+)
Colloids: albumin is preferred over hetastarch

162
Q

How should mean arterial pressure be maintained in AKI anesthesia?

A

20% of baseline

163
Q

What role does sodium bicarb play in AKI prophylaxis?

A

decreases formation of free-radicals and prevents ATN from causing renal failure.

164
Q

Why may a patient with AKI need post-op dialysis?

A

Can’t clear drugs on their own

165
Q

What are some anesthesia implications for a patient needing dialysis?

A

Low threshold for invasive hemodynamic monitoring, prefer preoperative dialysis, recent labs especially K+, want POC equipment available, tailored drug dosing, avoid drugs with active metabolites, drugs that decrease RBF, and renal toxins.

166
Q

What are the leading causes of chronic kidney disease (CKD)?

A

Diabetes, Hypertension

167
Q

What are common presentations of chronic kidney disease (CKD) patients?

A

Surgery for dialysis access, Non-healing wounds, Diabetic toe/foot debridements/amputations, often frequent flyers

168
Q

What is the formula for estimating GFR?

A

GFR = 186 x (SCr)-1.154x (age)-0.203x (0.742 if female) x (1.210 if African American)

169
Q

What are the 5 stages of CKD based on GFR levels?

A
170
Q

How are CKD stages typically discovered?

A

Often found during routine testing (focus on trends)

171
Q

What are some cardiovascular effects of CKD?

A

Systemic hypertension

172
Q

How does CKD lead to retention of sodium and water?

A

Activation of renin-angiotensin-aldosterone system

173
Q

What is the 1st line treatment for CKD in terms of medications? What additional medications may be needed for CKD?

A

Thiazide Diuretics are 1st line.
Other meds: ACE-I/ARB

174
Q

Why ACE’s and ARB’s often used in CKD?

A

Reduces systemic BP and glomerular pressure
Reduces proteinuria by reducing glomerular hyperfiltration
Reduces glomerulosclerosis

175
Q

Why should ACE-I/ARBs be withheld on the day of surgery? If ACE-I/ARBs on board, what other medications may be required during surgery?

A

To reduce the risk of profound HoTN.
Vasopressin, NE, EPI may be needed if medication effects still present during surgery.

176
Q

Which populations are high risk for silent MI?

A

CKD, Women and Diabetics

177
Q

What are common lipid abnormalities in CKD patients?

A

Triglycerides often > 500, LDL often > 100

178
Q

What neuropathies may CKD patients experience?

A

Peripheral & autonomic neuropathy. Sensation may be blunted.

179
Q

What hematologic effects are associated with chronic kidney disease?

A

Anemia, Platelet dysfunction

180
Q

How is anemia in chronic kidney disease managed?

A

Exogenous erythropoietin with a target Hbg of 10

181
Q

What should be considered when transfusing blood in chronic kidney disease patients?

A

Risks vs benefits, Excess Hgb leads to sluggish circulation

182
Q

What are indications to consider dialysis?

A

Volume overload, Severe hyperkalemia, Metabolic acidosis, Symptomatic uremia, Failure to clear medications

183
Q

Why might peritoneal dialysis (PD) be more suitable for some patients?

A

Slower, less dramatic volume shifts, suitable for patients intolerant of fluid swings/volume shifts such as poor cardiac function

184
Q

What is the most common side effect of hemodialysis (HD)?

A

Hypotension

185
Q

What is the leading cause of death in dialysis patients?

A

Infection (due to impaired immune system/healing)

186
Q

What are some anesthesia concerns for patients with ESRD?

A

Stability of ESRD, glucose management, well controlled BP, body weight pre-post dialysis within 24 hrs post op, aspiration precautions, pressers, uremic bleeding.

187
Q

Why should body weight pre/post dialysis be assessed within 24 hours of surgery?

A

To monitor fluid shifts

188
Q

What is the onset time and duration of desmopressin? What is a limitation of desmopressin?

A

Peak 2-4h; lasts 6-8h
Can develop tachyphylaxis therefore should only be used when needed.

189
Q

What is important to consider about many anesthetic agents in patients with CKD?

A

Many anesthetic agents are lipid soluble, reabsorbed by renal tubular cells, lean towards agents not dependent on renal elimination, and avoid active metabolites (morphine and demerol)

190
Q

What are examples of lipid insoluble drugs? What is renal dosing usually based on?

A

Thiazide diuretics, Loop diuretics, Digoxin, Many antibiotics.
Renal dosing usually based on the GFR.

191
Q

What is important about lipid insoluble drug elimination? Especially with renal patients?

A

Lipid Insoluble meds are eliminated unchanged in urine. Longer duration of action in renal impaired patients.

192
Q

What is the class of the drug Edrophonium?

A

Cholinesterase inhibitors

193
Q

What percentage of Morphine is cleared through urine?

A

40%

194
Q

What is the inactive metabolite of Morphine? What is the active metabolite of Morphine?

A

Inactive: morphine-3 glucuronide
Active: morphine-6 glucuronide

195
Q

What is the main adverse effects of Demerol?

A

Neurotoxicity: nervousness, tremors, muscle twitches, seizures

196
Q

Why does multiple doses of meperidine result in the accumulation of normeperidine?

A

Long elimination half-life of normeperidine (15-30 h) compared to (2-4 hr) for meperidine.

197
Q

What level should potassium be under for elective surgery?

A

K+ < 5.5 mEq/L

198
Q

What is recommended for dialysis patients before elective surgery?

A

Dialyzed within 24 h before

199
Q

How do anesthesia and surgery affect renal blood flow (RBF) and glomerular filtration rate (GFR)?

A

Decrease RBF & GFR

200
Q

What effect does blood loss have on baroreceptors and sympathetic nervous system (SNS) outflow?

A

Activates SNS outflow

201
Q

How do catecholamines decrease renal blood flow (RBF)?

A

Catecholamines activate alpha 1 Receptors, this constricts afferent arterioles which decreases renal blood flow.

assessment exam 3 (4 decks)

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