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Advanced Health Assessment TWU CRNA > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

At what spinal level would we find innervation to the kidneys and ureters?

A

T8-L2

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2
Q

At what spinal level would we find innervation to the pelvic organs?

A

Primarily lumbosacral with some lower thoracic input

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3
Q

At what spinal level would we find innervation to the bladder?

A

T11-L2 (Dome), S2-S4 (Neck)

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4
Q

At what spinal level would we find innervation to the prostate?

A

T11-L2 and S2-S4

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5
Q

How many thoracic nerves do we have?

A

12

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6
Q

How many lumbar nerves do we have?

A

5

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7
Q

What plexus does T11 and S2 come from?

A

Hypogastric

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8
Q

How much of the CO does the Kidneys receive?

A

25%

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9
Q

What makes the kidneys an endocrine organ?

A

Secretion of renin, erythropoietin and 1,25-dihydroxycholecalciferol

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10
Q

Where is the medulla of the kidneys located?

A

Central region, located under the kidney capsule

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11
Q

Where is the papilla of the kidney located?

A

Inner most tip of the inner medulla

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12
Q

What is the functional unit of the kidney?

A

Nephron

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13
Q

Describe the renal tubules

A

Lined with epithelial cells which serve the functions of reabsorption and secretion

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14
Q

What does a nephron consist of?

A

Glomerulus and a renal tubule

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15
Q

Describe superficial cortical nephrons

A

Glomeruli in the outer cortex, short loops of henle which descend only into the outer medulla

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16
Q

Describe juxtamedullary nephrons

A

Glomeruli near the corticomedullary border, larger nephrons with higher GFR, long loops of henle that descend deep into the inner medulla and papilla

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17
Q

Where does the glomerulus emerge from?

A

Afferent arterioles

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18
Q

What surrounds the glomerulus?

A

Bowman’s capsule

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19
Q

What is the goal in the OR in regards to BP and renal function?

A

Maintain a good BP because urine output is not a good indicator of renal fx

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20
Q

What consideration do we make with insufflation in regard to the kidneys?

A

Insufflation can compress blood flow to kidneys

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21
Q

3 Renal Vasoconstrictors

A
  1. Sympathetic nerves (catecholamines)
  2. Angiotensin 2
  3. Endothelin (21 amino acid peptide)
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22
Q

6 Renal Vasodilators

A
  1. PGE2
  2. PGI2
  3. Nitric Oxide
  4. Bradykinin
  5. Dopamine
  6. Atrial Natruiretic Peptide
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23
Q

What are the afferent and efferent arterioles innervated by?

A

SNS fibers that produce vasoconstriction by activating alpha 1 receptors

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24
Q

What does increased sympathetic nerve activity cause when acting on the afferent arteriole?

A

Decrease in RBF and GFR

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25
Q

What does the baroreceptor response in situations like blood loss cause?

A

Increased SNS activity and reduced GFR

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26
Q

Describe Angiotensin 2 in regards to the kidneys (2)

A
  1. A potent vasonstrictor of both afferent and efferent arterioles
  2. Constricts both arterioles, increases resistance, and decreases blood flow
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27
Q

Describe ANP in regard to the kidneys (2)

A
  1. Cause dilation of afferent arterioles and constriction of efferent arterioles
  2. Because dilatory effects on afferent is greater than constrictor effect on efferent arterioles, there is an overall decrease in renal vascular resistant and resulting increase in RBF
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28
Q

Describe Prostaglandins in regards to the kidneys (2)

A
  1. Several are produced locally in the kidneys (PGE2, PGI2)

2. Cause vasodilation of both afferent and efferent arterioles

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29
Q

Describe dopamine in regards to the kidneys (2)

A
  1. Dopamine, a precursor of norepinephrine, has selective actions on arterioles
  2. At low levels, dopamine dilates cerebral, cardiac, splanchic, and renal arterioles, and it constricts skeletal muscle and cutaneous arterioles
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30
Q

5 Things in the evaluation of renal function

A
  1. Hx and physical
  2. Estimates of disease duration
  3. Urinalysis
  4. Assessment of GFR
  5. Laboratory Tests
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31
Q

Describe GFR (2)

A
  1. GFR is the best measure of glomerular function

2. Normal GFR is 125 mL/min

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32
Q

Describe BUN (2)

A
  1. BUN is a less specific indicator of kidney function and is a reflection of ingested protein and muscle catabolism
  2. Elevated BUN can be precipitated by protein intake, TPN, steroids, fever, dehydration, and GI bleed
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33
Q

Describe creatinine and creatinine clearance (2)

A
  1. Creatinine is a product of muscle metabolism and the most specific indicator of renal function
  2. Normal values are 0.5 to 1.5 mg/100 mL
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34
Q

Describe Urine Specific Gravity (3)

A
  1. Measures the concentration of solutes in urine
  2. Provides information on the kidney’s ability to concentrate urine
  3. The reference range is 1.005-1.030
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35
Q

Describe protein excretion (3)

A
  1. Without renal disease may excrete 150mg/day
  2. Greater amounts of protein can be excreted after strenuous exercise
  3. Massive proteinuria (>750mg/day) is always abnormal and usually indicates severe glomerular damage
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36
Q

Describe glucose and the kidneys (2)

A
  1. Glucose is filtered at the glomerulus and is reabsorbed in the proximal tubule
  2. Glycosuria signifies that the ability of the renal tubules to reabsorb glucose has been exceeded by an abnormally heave glucose load and is usually indicative of DM
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37
Q

When do electrolyte tests become abnormal in regards to the kidneys?

A

When frank renal failure is present

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38
Q

When does hyperkalemia usually occur with patients and kidney disease?

A

Not usually until patients are uremic

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39
Q

What would a doubled creatinine level indicate?

A

50% reduction in renal function

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40
Q

What is indicative of oliguria?

A

400 cc/day urine output

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41
Q

Describe Prerenal acute kidney injury

A

Caused by reduction in effective circulating volume and renal perfusion or bilateral arterial occlusion (hypotension, decreased CO)

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42
Q

Describe Intrarenal acute kidney injury

A

Caused by glomerular or renal tubular injuries, or intrarenal vascular disruption

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43
Q

Describe Postrenal acute kidney injury

A

Caused by obstruction of the urinary tract or bilateral renal veins

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44
Q

What is pre renal acute kidney injury the direct result of?

A
  1. Hypoperfusion

2. Complete lack of blood flow to the kidneys for 30-60 minutes can result in irreversible cell damage

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45
Q

What does Acute Tubular Necrosis (ATN) involve?

A

Specific injury to the renal tubules and is most commonly the result of ischemia secondary to reduced RBF

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46
Q

5 Renal toxins

A
  1. Contrast dye
  2. NSAIDS
  3. Aminoglycoside ABX
  4. Cocaine
  5. Rhabdo pigment
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47
Q

What part of the EKG do we wait for before performing a lythotripsy?

A

R-wave

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48
Q

Examples of obstructions from the tubules to the urethra that can cause post renal kidney injury?

A
  1. Kidney stones
  2. Uric precipitate (gout)
  3. Kinking of urinary catheter
  4. Prostatic Hyperplasia
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49
Q

Anesthesia considerations in acute kidney injury (5)

A
  1. Anesthesia and surgery decrease RBF and GFR
  2. Catecholamines released during surgery cause reduction in RBF and GFR
  3. Long periods of hypotension decrease RBF
  4. Vasopressors reduce GFR
  5. Neuraxial blockade effects are variable depending on degree to which BP and CO drop
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50
Q

What is the best anesthetic approach for TURP/TURB?

A

Neuraxial anesthesia

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51
Q

At what spinal level are the cardio-accelerator nerves found?

A

T1-T4

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52
Q

Describe chronic renal failure (3)

A
  1. Progressive, irreversible deterioration of renal function
  2. DM is leading cause of ESRD followed by HTN in the US
  3. GFR to less than 25 mL/min eventually progressing to dialysis or transplantation
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53
Q

Clinical presentation of ESRD

A
  1. Anemia d/t decreased erythroproeiten
  2. Increased bleeding time d/t platelet dysfunction, but platelet count is not decreased
  3. Hyperkalemia and hypermagnesemia
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54
Q

Preop Anesthesia Considerations for pts with ESRD (9)

A
  1. Evaluate serum creatinine trend
  2. Compare body weight before and after dialysis, monitor vital signs (BP and HR)
  3. Glucose management
  4. BP well controlled before surgery
  5. ACE-i and ARBS d/c day of surgery to reduce risk of intraop hypotension
  6. K+ should not exceed 5.5 mEq/L day of sx
  7. Gastric aspiration prophylaxis
  8. H2 receptor blockers excreted renally so adjust dose
  9. Dialysis within 24 hours preceding elective sx
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55
Q

Induction considerations for patients with ESRD (4)

A
  1. Safe with most IV drugs, watch cardio effects of propofol
  2. Many ESRD respond to induction as if they were hypovolemic
  3. RSI with succinylcholine if K+ less than 5.5 mEq/L
  4. Short onset non-depolarizers such as roc at lower doses, nimbex is renal friendly
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56
Q

How much K+ does lactated ringers contain?

A

4 mEq/L

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57
Q

What is generally considered a urine output to maintain?

A

0.5mL/kg/hr

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58
Q

What consideration do we give intraop urine output in regards to post-op renal insufficiency?

A

Intraop-UO has not been shown to be predictive of post-op renal insufficiency

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59
Q

What is the most likely cause of oliguria and how do diuretics play into this setting?

A

Inadequate circulating fluid volume and admin of diuretics in this setting may further compromise renal function

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60
Q

Describe Fenoldopam

A

It is a dopamine-1 agonist, may provide renal protection in patients at high risk who are undergoing cardiac, vascular, or transplant surgery

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61
Q

When should we consider blood transfusion in ESRD patients?

A

If oxygen-carrying capacity must be increased or if blood loss is excessive

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62
Q

What is a useful tool to guide fluid replacement?

A

CVP

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63
Q

Regional anesthesia considerations for ESRD patients

A
  1. Neuraxial anesthesia can be considered
  2. Sympathetic blockade of T4-T10 by attenuating catecholamine-induced renal vasoconstriction and suppressing the surgical stress response
  3. Platelet dysfunction effects of residual heparin must be considered (aPTT and ACT)
  4. Adequate intravascular fluid volume must be maintained
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64
Q

Describe dermatome levels

A

Skin area innervated by a given spinal nerve

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65
Q

What dermatome landmark is used for S1?

A

Lateral aspect of foot

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66
Q

What dermatome landmark is used for L1?

A

Inguinal ligament area

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67
Q

What dermatome landmark is used for T10?

A

Umbilicus

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68
Q

What dermatome landmark is used for T6?

A

Xiphoid Process

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69
Q

What dermatome landmark is used for T4?

A

Nipple

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70
Q

What dermatome landmark is used for T1-T2?

A

Inner aspect of the arm and the forearm

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71
Q

What dermatome landmark is used for C8?

A

Fifth finger

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72
Q

Where is the phrenic nerve located?

A

C5

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73
Q

What do we know if a patient is feeling numbness of their thumb and how should we respond?

A

This corresponds to C6 and this will eventually move up to C5, we will raise the HOB and give O2

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74
Q

Dermatome level targeted for peri-anal surgery considered to be a “saddle block”?

A

S2-S5

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75
Q

Dermatome level targeted for foot and ankle surgery?

A

L2

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76
Q

Dermatome level targeted for Vaginal delivery and uterine procedure?

A

T10

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77
Q

Dermatome level targeted for lower abdominal procedures?

A

T6

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78
Q

Dermatome level targeted for for upper abdominal surgery such as a C-section?

A

T4

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79
Q

What is the problem with blocks placed at T4?

A

Problems with cardiac accelerator nerves, so have neo and ephedrine ready

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80
Q

Post-op management of ESRD patients?

A
  1. Caution with IV opioids due to hypoventilation even if small doses
  2. Admin naloxone may be necessary if depression of ventilation is severe
  3. EKG monitor for hyperkalemia
  4. O2 especially if anemia is present
  5. Check levels of electrolytes, BUN, Creatinine and Hct
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81
Q

What is the gold standard procedure for BPH?

A

TURP

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82
Q

What is the transurethral procedure for kidney stones?

A

Extracorporeal Shock Wave Lithotripsy

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83
Q

Which procedure do we do biopsy of the bladder?

A

TURBT

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84
Q

What is a serious intraoperative complication during a TURB?

A

Bladder perforation by the rigid cystoscope due to unexpected patient movement

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85
Q

Which nerve may be stimulated during a TURBT causing ipsilateral contraction of the thigh muscle?

A

Obturator nerve

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86
Q

What is the highest spinal level we use for regional anesthesia in TURBT which will prevent the obturator reflex?

A

T9

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87
Q

Describe post-op pain from TURBT

A

Postoperative pain is usually minimal and responds well to nonopiate and opiate medications

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88
Q

What position do we place patients in for TURBT procedures?

A

Lithotomy

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89
Q

What do we need to make sure to do when positioning patients for TURBT?

A

Adequate padding of pressure points and avoidance of common perineal nerve compression

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90
Q

What is the most common lower body nerve injury?

A

Common perineal nerve compression

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91
Q

What side of leg does the common perineal nerve lie?

A

Lateral (outside) side of the lower leg

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92
Q

What nerve damage is common in almost all surgical procedures?

A

Ulnar nerve damage

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93
Q

Describe TURP (4)

A
  1. Prostate removal of BPH
  2. Resectoscope is very rigid, inserted into the urethra
  3. SAB is preferred @ T10 for neuro assessments
  4. GETA is possible, but does not allow for neuro checks
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94
Q

Which patient populations are TURPs likely to be performed in?

A

Elderly and those with serious comorbidities such as DM, so we need to monitor CV and pulmonary status

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95
Q

What intraoperative changes are elderly and those with serious comorbidities respond to the most?

A

Intravascular volume change

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96
Q

Which patients undergoing TURP would we prefer GETA over spinal anesthesia?

A

Those on anticoagulant therapy

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97
Q

How long prior to regional procedures should we d/c ASA?

A

7 days

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98
Q

By what degree and time period does body temp decrease during surgery?

A

1 degree Celsius per hour

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99
Q

What percentage of patients who receive room-temperature irrigation fluids does shivering occur in?

A

16%

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100
Q

What percentage of patients undergoing TURP require transfusions?

A

2.5%

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101
Q

What is the average blood loss per minute during a TURP?

A

2 to 4 mL/min

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102
Q

What lab should we monitor with 4 to 6 hour surgeries?

A

Serial hemoglobin levels

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103
Q

What is the purpose of irrigation solutions in TURP?

A
  1. Continuous fluid to irrigate the bladder and the prostate

2. Improves visualization during surgery

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104
Q

Where is irrigation solution absorbed?

A

open venous sinuses of the prostate and a portion is absorbed in the systemic circulation

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105
Q

What are two possible side effects of irrigation solution being absorbed into systemic circulation?

A
  1. Circulatory overload

2. Toxicity for the solutes of the fluid

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106
Q

Whats the absorbed volume per time of irrigation solution?

A

10-30 mL/min

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107
Q

How does resection time of a TURP affect complication rate?

A

The longer the reception time the more complications

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108
Q

What must the resection time in a TURP be limited to?

A

1 hour

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109
Q

Describe the changes of height of the irrigation solution

A

Height of the irrigation solution must be 30 cm above the OR table at the beginning of the case then dropped to 15 cm at the end of the case

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110
Q

Relate the number of venous sinuses open to reabsorption rate

A

Too many open venous sinuses increases intravascular reabsorption

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111
Q

What is the ideal irrigation solution?

A

great visibility, clear, isotonic, free of toxicity, electrically inert and inexpensive (this does not exist)

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112
Q

What is the problem with 0.9% saline and LR for irrigation?

A

They are good choices but are very ionized and good conductors of electricity

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113
Q

What type of cautery is LR and 0.9% saline safe to use as irrigation?

A

Bipolar cautery

114
Q

What is the issue with using water as irrigation?

A

Clear but absent of electrolytes and free water absorption decreases serum osmolality, causes hyponatremia, hemolysis, electrolyte imbalance and hypervolemia

115
Q

Advantages/Disadvantages of distilled water solution as irrigation?

A

Advantages: improved visibility

Disadvantages: hemolysis, hemoglobinemia, hemoglobinuria, hyponatremia

116
Q

Advantages/Disadvantages of Glycine (1.5%) solution as irrigation?

A

Advantages: Less likelihood of TURP syndrome

Disadvantages: Transient postop visual syndrome (effects optic nerve), hyperammonemia, hyperoxaluria

117
Q

Advantages/Disadvantages of sorbitol (3.3%) solution as irrigation?

A

Advantages: Less likelihood of TURP syndrome

Disadvantages: hyperglycemia, possible lactic acidosis, osmotic diuresis

118
Q

Advantages/Disadvantages of Mannitol (5%) solution as irrigation?

A

Advantages: Isosmolar solution, not metabolized

Disadvantages: possibility of acute intravascular volume expansion

119
Q

Osmo of Distilled water?

120
Q

Osmo of Glycine?

121
Q

Osmo of Sorbitol?

122
Q

Osmo of Mannitol?

123
Q

What clinical symptom would we see with intraoperative volume overload?

124
Q

Describe TURP syndrome

A

Cluster of symptoms related to hypervolemic water intoxication

125
Q

What are the symptoms associated with TURP Syndrome?

A

Excessive volume expansion, respiratory distress, congestive heart failure, pulmonary edema, HTN (incr. PP), bradycardia, hypotension, hyponatremia

126
Q

What is the most serious complication of TURP syndrome?

A

Hyponatremia due to leading to mental confusion and nausea, this can only be assessed if spinal anesthesia was utilized

127
Q

Treatment for TURP syndrome? (6)

A
  1. Oxygenation and circulatory support
  2. Terminate procedure ASAP
  3. 12-lead EKG
  4. Labs for electrolytes, creatinine, glucose and ABG
  5. Mild symptoms symptoms with fluid restriction and loop diuretic
  6. D/c 3% sodium chloride when serum Na+ >120
128
Q

Site of nephrolithiasis?

129
Q

Site of ureterolithiasis?

130
Q

Site of Cystolithiasis?

131
Q

What is the lifetime prevalence of nephrolithiasis in men and women?

A

Men 10% and women 5%

132
Q

What is the reoccurrence rate of kidney stones?

A

50% in the first 5 years after the first

133
Q

Whats the most common type of stone that is radio-opaque?

A

Ureter stones

134
Q

How do patients with kidney stones typically present?

A

With intermittent or continuous moderate to severe colicky pain in the ipsilateral flank and upper abdomen, also have painless urinary infection or hematuria

135
Q

Treatment for Urolithiasis?

A
  1. Conservative nonsurgical therapy for smaller stones consists of NSAIDs and or opiates
  2. Aggressive fluid admin to promote urine flow and passage of the stone
  3. Medical Expulsive Therapy (MET) to promote ureter relaxation and spontaneous passage of small stones
136
Q

What meds are used in Medical Expulsive Therapy for stones?

A

Calcium channel blockers, alpha blockers and corticosteroids

137
Q

What does the likelihood of a stone passing without surgery relate to?

A

Size of the stone, its location and the presence or absence of urinary system anatomic abnormalities such as strictures

138
Q

3 surgical options for the removal of stones?

A
  1. Percutaenous nephrolithotomy
  2. Shock-wave lithotripsy (most common)
  3. Ureteroscopy
139
Q

What conditions should we assess patients with CKD for in the pre-op setting for Urolithiasis?

A

Platelet dysfunction, anemia, and electrolyte abnormalities

140
Q

What patients are bladder stones often diagnosed in?

A

Poor voiding capacity such as paraplegic patients

141
Q

Which paraplegic patients are at risk for autonomic hyperreflexia?

A

Those with sensory deficits below T6, they require anesthesia to block the afferent stimulation that can provoke this reaction (bladder distention)

142
Q

How would patients in the pre-op setting be treated for idiopathic hypercalciuria?

A

thiazide diuretics, which increase the reabsorption of calcium by the distal convoluted tubule

143
Q

Which patients should we suspect tolerance to intra and postoperative opioid therapy?

A

Those with recurrent nephrolithiasis and receiving chronic opioid therapy

144
Q

What is renal colic often associated with?

A

Nausea and vomiting and preoperative aspiration prophylaxis should be considered

145
Q

When would blood transfusion be needed for stone surgery?

A

Open surgery

146
Q

What is very important to start as prophylaxis to stone surgery?

A

Antibiotics especially with infected stones or pyelonephritis

147
Q

When should eye protection be used?

A

For the operative team and patient when lasers are being utilized

148
Q

3 Main overviews of the Endocrine System

A
  1. Secretes hormones such as peptide, steroids or amines
  2. Secretes hormones into the circulation to be delivered to target organs
  3. Once in target cells, they produce a physiologic response
149
Q

Describe the exocrine function of the pancreas (2)

A
  1. Hormones are secreted into the duodenum for digestion

2. Produced by the acini tissue

150
Q

Describe the endocrine function of the pancreas (2)

A
  1. Hormones are released into the circulation for metabolism

2. Produced in the islets of Langerhans

151
Q

What pancreatic cells secrete Glucagon?

A

Alpha cells

152
Q

What pancreatic cells secrete Insulin?

A

Beta cells

153
Q

What pancreatic cells secrete Somatostatin?

A

Delta cells

154
Q

What is the primary source of endogenous glucose production?

A

The liver through glycogenolysis and gluconeogenesis

155
Q

Briefly describe the body’s response after eating a meal

A

Following a meal, plasma glucose level increases, which stimulates an increase in plasma insulin secretion that promotes glucose utilization

156
Q

When does the body transition from exogenous glucose delivery to endogenous production to maintain normal plasma glucose levels?

A

Postprandial period (2-4 hours after eating)

157
Q

Where is approximately 70 to 80% of glucose released by the liver utilized?

A

Brain, GI tract, and RBC

158
Q

Factors that cause increased serum glucose (7)

A
  1. PNS stimulation after a meal
  2. SNS stimulation
  3. Glucagon release
  4. Catecholamine release
  5. Cortisol release
  6. Growth hormone release
  7. Beta-agonist use
159
Q

Factors that cause decreased serum glucose (4)

A
  1. Insulin release
  2. Somatostatin release
  3. Volatile Anesthetics
  4. Beta-antagonists
160
Q

Describe Glucagon (4)

A
  1. Catabolic hormone that promotes energy release from adipose tissue and the liver
  2. Secreted by the alpha cells
  3. Physiologic antagonist to insulin
  4. Increases myocardial contractility, HR and AV conduction
161
Q

How does glucagon cause myocardial changes?

A

Increasing intracellular cAMP

162
Q

What are the 4 things that Glucagon can be used for?

A
  1. Beta-blocker overdose
  2. CHF
  3. Low CO after bypass or MI
  4. Use to increase MAO during anaphylaxis
163
Q

Triangular shaped endocrine glands that sit on top of the kidney?

A

Adrenal Glands

164
Q

Two things the adrenal gland does?

A
  1. ) Synthesizes and stores essential hormones

2. ) Releases hormones in conjunction with stress

165
Q

The adrenal gland is divided into two parts:

A

cortex & medulla

166
Q

The adrenal cortex is inner or outer zone? Origin? 3

A

the outer zone of the gland, mesodermal origin

167
Q

What does the adrenal cortex secrete?

A

adrenocortical steroid hormones

168
Q

Adrenal cortex differentiates by what gestational week? What is it responsible for throughout intrauterine life? After birth does what?

A

differentiates by gestational week 8 and is responsible for the production of fetal adrenal steroids. Soon after birth the fetal cortex begins to involute and eventually disappears/replaced by 3 layered adult cortex

169
Q

What are the 3 distinct layers of the cortex and what do they secrete?

A

innermost zone of the cortex - zona reticularis glucocorticoids and adrenal androgens
middle (widest) zone - zona fasciculata - glucocorticoids and adrenal androgens
outermost zone - zona glomerulosa - secretes mineralcorticoids

170
Q

What are hormone in the adrenal cortex is synthesized and secreted by the zona glomerulosa, and what does it do?

A
  • Mineral corticoids (aldosterone) - responsible for regulation of extracellular volume via urinary sodium and potassium exchange in RAAS
  • Aldosterone - increases K+ secretion and excretion, increases Na+ reabsorption/retention
171
Q

3 organs involved in RAAS

A

Liver (angiotensin located), kidney (stimulus), lungs (ace)

*Pt’s on ACE-I tend to cough alot because ACE is in the lungs!

172
Q

Which is the more potent vasoconstrictor between ADH and Ang II?

173
Q

What 2 hormones are secreted and synthesized by the zonta reticularis and zona fasciculata of the adrenal cortex, and what do they do?

A
  1. ) Glucocorticoids (cortisol) - responsible for gluconeogensis, elevation of blood glucose, promotion of glycogen storge, protein, lipid and carbohydrate metabolism, anti-inflammatory actions, and BP maintenance
  2. ) Androgens (sex hormones)
174
Q

What two catecholamines does the adrenal medulla produce that function as hormones throughout the body?

A

Epinephrine and norepinephrine

175
Q

What kind of tumor is a pheochromocytoma? Where does it arise? What does it cause?

A
  • It is a tumor of neuroendocrine tissue
  • Arising in the adrenal medulla from chromaffin cells that synthesize catecholamines.
  • Neoplastic proliferation of these cells leads to a release of norepi/epi in varying amounts and can cause catechoalmine toxicity
176
Q

Most pheochromocytomas have what 3 characteristics? Mostly located in what region of the body?

A

solitary (85-90% occur in either right or left adrenal gland - usually RIGHT), benign, and sporadic! Mostly located in the abdomen.

(occasionally: multifocal, malignant, or part of a syndrome, ex. Multiple Endocrine Neoplasias aka MENS)

177
Q

What is the name for similar tumors that can arise in extraadrenal locations from paraganglial cells of the ANS and in the heart or pericardium?

A

Paragangliomas, less likely to be functional compared with adrenal tumors (extra adrenal sites)

178
Q

Incidence of pheochromocytoma in the US?

A

Approximately 1,000 cases per year

179
Q

What are the signs and symptoms of pheochromocytoma (6)?

A

The clinical presentation is variable:

  1. Hypertension(most frequent manifestation)
  2. Headache
  3. Sweating
  4. Pallor
  5. Palpitations
  6. Orthostatic hypotension d/t hypovolemia and impaired vasoconstrictor reflex response
180
Q

Hemodynamic signs are related to catecholamine excess and vary, depending on which one predominates. Which catecholamine is the most common and is usually sustained? What are the effects related to?

A

Norepinephrine - with effects related to alpha-adrenergic stimulation (systolic and diastolic HTN, reflex bradycardia)

(attacks range from infrequent to numerous a day, may last less than a minute or several hours, may be precipitated by physical injury/emotional stress/meds)

181
Q

Which catecholamine is less commonly released and therefore often paroxysmal? What are the effects related to?

A

Epinephrine - episodic effects related to beta-adrenoreceptor stimulation (systolic HTN, dyastolic hypotension, tachycardia)

182
Q

S/S of both Epi and Norepi (4)?

A
  1. Increased SVR
  2. Normal cardiac output
  3. Decreased plasma volume
  4. Hyperglycemia (secondary to stimulation of glycogenolysis - breakdown of glycogen to glucose, and inhibition of insulin release)
183
Q

Pheochromocytoma may first manifest during anesthesia and surgery for another unrelated condition? During pregnancy?

A
  • Thyrotoxicosis (thyroid storm), malignant hyperthermia

- Preeclampsia

184
Q

3 complications of pheochormocytoma?

A
  1. Cardiomyopathy (ECHO!!! Want to determine EF and look at LV function)
  2. Coronary vasoconstriction (catecholamine release)
  3. Reduces coronary blood flow and potentially creates ischemia
185
Q

What are the three diagnostic tests that can be used to determine if someone has pheochromocytoma? Which is the most sensitive? Which is safest/most specific/provocative?

A
  1. 24-hour urine metanephrines and catecholamines - screening test
  2. Plasma-free metanephrines MOST SENSITIVE TEST
  3. Glucagon stimulation test - safest/most specific/provocative
186
Q

What does plasma-free metanephrines test look at?

A

catecholamines are metabolized to free metanephrines within tumor cells and these metabolites are continuously released into circulation

187
Q

What does glucagon act on? What does a positive response for the glucagon stimulation test yield?

A
  • Glucagon acts directly on the tumor to induce release of catecholamines
  • A positive response yields a plasma catecholamine increase of at least 3X baseline values within 1-3 minutes of glucagon administration

(test should only be performed in pts with DBP < 100 mmHg)

188
Q

Clinical diagnosis via scans for pheochromocytoma (3)?

A
  1. CT
  2. MRI
    (for tumor localization and surgical planning)
  3. Echocardiography (to detect cardiomyopathy and monitor improvement after preop medical therapy)
189
Q

Preop management: what is the drug class DOC for pheo? 4 things this drug does?

A

Alpha-blockade (DOC-given 7-14 days prior to surgery)!!! - blocks the toxic effects of catecholamines and prevent and reverse end-organ damage.

  1. Lowers BP, increases intravascular volume
  2. Prevent paroxysmal hypertensive episodes
  3. Decrease myocardial dysfunction
  4. Protect myocardial performance and tissue oxygenation
190
Q

What specific drug is the traditional first-line agent for pheo?

A

PHENOXYBENZAMINE - noncompetitive, nonselective, alpha-adrenoreceptor antagonist.

(long acting drug, works for 24-48 hours)

191
Q

Goals of phenoxybenzamine (3)? What can overtreatment result in?

A
  1. Normotension
  2. Elimination of ST-segment and T-wave changes on the ECG
  3. Elimination of arrhythmias

-Overtreatment can result in severe orthostatic hypotension

192
Q

What is the definitive treatment for pheochromocytoma? What technique is used?

A

Surgical resection, open laparotomy technique or laparoscopic technique (with or without robotic assistance)

193
Q

Intraop period of pheo resection may be complicated by what?

A

Hemodynamic instability and blood loss (when resecting the tumor it will release norepi/epi and everything will be sympathetic; once tumor is removed - no production of epi/norepi so everything goes down)

194
Q

Should you d/c alpha blockade prior to surgery?

A

This is up for debate - because of the prolonged effect on alpha receptors it is recommended to d/c 24-48 hours before surgery to avoid vascular unresponsiveness immediately following removal (if you took the drug it will combine effects and everything will go down). Others say take 1/2 or 1/3 dose prior to surgery (don’t want HTN during manipulation of the tumor either); depends on the surgeon.

195
Q

Phenoxybenzamine is the DOC, but what other medications can you give for preop management? Two advantages it provides to avoid post op hypotension?

A
  • Selective, competitive alpha-1 adrenoreceptor antagonist - ex. prazosin, doxazosin, terazosin
  • less tachycardia (than phenoxybenzamine), shorter elimination timess
196
Q

Both classes of alpha blocking agents may cause what? What would alleviate it?

A

Postural hypotension, alleviated by fluid supplementation

197
Q

If tachycardia (HR>120) results after phenoxybenzamine, what is most frequently prescribed?

A

Beta-adrenergic blocker - ex. Propanolol which is a nonselective beta blocker with a half life longer than 4 hours

(atenolol, metoprolol, labetalol have also been used successfully)

198
Q

What drug would be administered for preop management of pheo in patients with predominately epinephrine secreting tumors and with CAD?

A

Beta-blocker - ex. Esmolol, beta-1-selective antagonist, has a fast onset and short elimination half life and can be administered IV immediately before surgery

199
Q

Can you give beta blockers before adequate alpha blockade is ensured?

A

No! A beta blocker should never be administered before alpha blockade because blockade of vasodilatory beta2-receptors results in unopposed alpha-agonism, leading to vasoconstriction and HTN crisis!

200
Q

When would Ca-channel blockers be used in pheo?

A

Used as a second agent in patients who have refractory HTN or in patients who have coronary vasospasm

(CCBs: diltiazem, nifedipine, nicardipine, verapamil)

201
Q

5 considerations for pheo patient preop?

A
  1. Large-bore PIV
  2. A-line
    (preop volume loading may be warranted)
  3. CVP (considered for vasoactive infusions/give volume)
  4. PA cath (exceptional cases of CV compromise)
  5. Thoracic epidural (postop pain mgmt)
202
Q

Triggers or stimuli implicated in provoking catecholamine surges (6)?

A
  1. Anesthesia induction
  2. Depolarizing NMB
  3. Tracheal intubation
  4. Patient positioning
  5. Skin incision
  6. Pneumoperitoneum
203
Q

Surgical manipulation and other events can trigger catecholamine release in pheo, resulting in what (2)? What drugs would you administer?

A
  • acute HTN and dysrhythmias
  • Short-acting agents may be perferable given the generally short-lived nature of the catecholamine surges
  • beta-blockers and lidocaine are effective for SVT and ventricular dysrhythmias
204
Q

What drugs are not desirable and should be avoided in regards to induction agents for pheo patients?

A
  • Succynlcholine-induced muscle fasciculations in the abdomen can cause tumor compression and catecholamine release
  • Meds associated with histamine release or undesirable autonomic effects should be avoided (ex. atracurium, pancuronium, morphine, meperidine, ephedrine, metoclopramide)
205
Q

Which preop meds can be used safely in pheo patients?

A

Induction agents, opioids, NMB, and inhaled anesthetics

206
Q

What are carcinoid tumors, where are they, and what do they secrete?

A
  • Carcinoid tumors are slow-growing neoplasms of neuroendocrine tissue.
  • Site: bronchus, jejunoileum, or colo-rectum (GI system)
  • Secrete an array of bioactive substances
207
Q

How are carcinoid tumors diagnosed?

A

Urine and plasma assays of serotonin and its metabolite 5-hydroxy-indole-acetic-acid (5-HIAA) - the main metabolite of serotonin

208
Q

4 scans that can be performed to diagnose carcinoid tumor and what are they useful for?

A

CT, MRI, abdominal ultrasound - help identify the primary tumor and if possible, any mets

Bronchoscopy - useful for locating tumor in bronchial tree

(Incidental diagnosis on chest or abdominal x-ray)

209
Q

Where are carcinoid tumors located (6)? Symptoms for each?

A
  1. *Small intestine - *abdominal pain (most common), intestinal obstruction, tumor, GI bleeding
  2. Rectum - bleeding, constipation, diarrhea
  3. Bronchus - asymptomatic
  4. Thymus - anterior mediastinal mass
  5. Ovary and testicle - mass discovered on physical exam or ultrasonography
  6. Metastases - in the liver, frequently presents as hepatomegaly
210
Q

Carcinoid syndrome is a result of what?

A

Occurs in approx 20% of patients with carcinoid tumors as a result of large amounts of serotonin and vasoactive substances reaching the systemic circulation

211
Q

Signs and symptoms of classic carcinoid syndrome (3)?

A

wheezing, diarrhea, and episodic cutaneous flushing of head/neck/trunk/upper extremities

212
Q

Medications for carcinoid syndrome depending on the symptom (3)?

A
  1. Diarrhea - serotonin overproduced; 5-HT3 antagonist
  2. Red, patchy, pruritic flush - histamine release; H1 and H2-receptor blockers
  3. Bronchoconstriction - histamine and serotonin; anticholinergic works, octreotide definitely works

(beta 2 agonist doesn’t work for bronchoconstriction!)

213
Q

Carcinoid syndrome releases bradykinin, what two things might bradykinin release cause?

A
  1. Profound vasomotor relaxation resulting in severe hypotension
  2. Bronchospasm particularly in asthmatics and in the presence of cardiac disease
214
Q

What is a potentially life-threatening complication of carcinoid syndrome? How does it manifest (6)? Treatment?

A 
Carcinoid crisis
1. flushing
2. diarrhea
3. abdominal pain
4. tachycardia
5. hypertension
6. hypotension
Octreotide - if not treated, can be fatal (also treat symptomatically)
215
Q

Pharmacologic agents associated with carcinoid crisis (promote release of bradykinin) that we should avoid (9)?

A
  1. Succs
  2. Mivacurium
  3. Atracurium
  4. D-tubocurarine
  5. Epinephrine
  6. Norepinephrine
  7. Dopamine
  8. Isoproterenol
  9. Thiopental
216
Q

If we are going to choose between 3 inhaled agents, what should we use for carcinoid crisis in patients that already have liver mets/liver damage?

A

Des is the best choice secondary to lower rate of metabolism

217
Q

What is the major preop goal to prevent precipitating carcinoid crisis?

A

prevent release of bioactive mediators - avoid triggering factors

218
Q

Physical exam preop for patient with carcinoid tumor is performed to determine what?

A

The presence and severity of s/sx of carcinoid syndrome (flushing, diarrhea, wheezing, heart murmur)

219
Q

What need to be done preop for patient with carrcinoid tumor (2)?

A
  1. Lab tests (blood count, chem and liver fn panels, blood glucose, ECG*)
  2. *Urinary 5-HIAA assay reviewed

(excess serotonin can cause hyperglycemia-monitor blood sugar in the OR)

220
Q

30-50% of patients with carcinoid tumors have carcinoid heart disease which usually manifests as what?

A

RIGHT SIDED <3 FAILURE! (even mild symptoms warrant cardiac workup; ECHO)

221
Q

What is the DOC for bronchospasm secondary to carcinoma tumor release fo bradykinsins in a carcinoid crisis that is NOT responsive to beta-2-adrenergic agonists, theophylline, or epinephrine? Adjuncts (3)?

A

DOC: OCTREOTIDE

Adjunct: corticosteroids, antihistamine, and anticholinergic (ipratropium bromide)

(Bradykinin can cause Bronchospasm)

222
Q

What is octreotide and what does it inhibit (4)? How and when should it be administered?

A
  • Somatostatin is a cyclic peptide that inhibits GI motility, gastric acid production, pancreatic enzyme secretion, and bile colonic fluid secretion
  • subQ, IV, or continuous IV infusions
  • administered 24-48 hours before surgery, then continued throughout the procedure
223
Q

Describe diabetes mellitus

A

DM is a metabolic disease arising from defects in insulin secretion (Type 1) or insulin resistance (Type 2)

224
Q

What is insulin responsible for?

A

Storing excess nutrients as glycogen in the liver, as fat in adipose tissue and as protein in muscle

225
Q

Diabetes cascade? (8)

A
  1. Hyperglycemia >180 mg/dL
  2. Glycosuria
  3. Osmotic diuresis
  4. Hypovolemia
  5. Classic symptom triad
  6. Polyuria
  7. Dehydration
  8. Polydipsia
226
Q

A1C levels for normal, pre-diabetes, and diabetes

A
  1. Normal: <5.7%
  2. Prediabetes: >= 5.7% to 6.5%
  3. Diabetes >= 6.5%
227
Q

Fasting plasma glucose levels for normal, pre diabetes, and diabetes

A
  1. Normal: <100 mg/dL
  2. Prediabetes: >=100 mg/dL to 126 mg/dL
  3. Diabetes: >= 126 mg/dL
228
Q

Oral glucose tolerance test for normal, pre-diabetes, and diabetes

A
  1. Normal: <140 mg/dL
  2. Prediabetes: 140 mg/dL to 200 mg/dL
  3. Diabetes: >= 200 mg/dL
229
Q

Describe the hemoglobin A1C test (3)

A
  1. Average blood glucose for 2-3 months
  2. Glucose enteres RBC and links up with Hgb
  3. The more glucose in blood, the more hemoglobin gets glycated
230
Q

Describe Fasting Plasma Glucose (FPG)

A

No caloric intake for greater than or equal to 8 hours

231
Q

Describe Oral Glucose Tolerance Test (OGTT) (2)

A
  1. Two hour plasma glucose greater than or equal to 200 mg/dL during oral glucose tolerance test
  2. Two-hour test that checks your blood glucose levels before and 2 hours after you drink a special sweet drink
232
Q

Describe random glucose test

A

Symptomatic hyperglycemia (polyuria, polydipsia, unexplained weight loss) and random plasma glucose greater than or equal to 200 mg/dL

233
Q

3 key points of diagnostic criteria for DM

A
  1. Any of the listed criteria can establish the dx, not all have to meet criteria (just one needs to meet it)
  2. In the absence of hyperglycemia symptoms the test is repeated before solidifying the dx
  3. In the acute setting, hyperglycemia symptoms include polyuria, polydipsia, weight loss and blurred vision
234
Q

Describe Gestational Diabetes (3)

A
  1. Glucose tolerance test with the onset first recognized during pregnancy
  2. Clinical recognition of gestational diabetes is important because therapy and antepartum fetal monitoring can reduce perinatal morbidity and mortality
  3. Maternal complications related to gestational diabetes include an increased rate of C-sections
235
Q

Describe DM Type 1 (5)

A
  1. Caused by absolute deficiency of insulin secretion
  2. Caused by autoimmune destruction of pancreatic Beta cells
  3. Commonly occurs in childhood and adolescence but can occur at any age
  4. Require exogenous insulin admin for survival
  5. Severe clinical presentation is DKA
236
Q

Describe DM Type 2 (2)

A
  1. Caused by relative beta cell insufficiency and insulin release (will still have some insulin secreted)
  2. As the disease progress and pancreatic cell function decreases, insulin levels are unable to compensate and hyperglycemia occurs
237
Q

What are the 3 defects associated with DM Type 2

A
  1. Increased rate of hepatic glucose release
  2. Impaired basal and stimulated insulin secretion
  3. Inefficient use of glucose by peripheral tissues (insulin resistance)
238
Q

What is the risk of developing Type 2 DM associated with?

A

Age, obesity and inactivity

239
Q

What does chronic complications does DM predispose us to?

A

More at risk for developing chronic microvascular and microvascular complications

240
Q

Describe metabolic syndrome

A

Also called insulin-resistance syndrome, is a constellation of clinical and biochemical characteristics frequently seen in patients who have or at risk of DM Type 2

241
Q

What are the criteria that must be met for a diagnosis of metabolic syndrome? (5)

A

The patient must have at least 3 of the following:

  1. fasting plasma glucose >= 110 mg/dL
  2. abdominal obesity (men >40 in. women > 35 in.)
  3. serum triglyceride level >= 150 mg/dL
  4. Serum HDL < 40 in men or < 50 in women
  5. BP >= 130/85
242
Q

What is metabolic syndrome associated with?

A

Premature atherosclerosis and subsequent cardiovascular disease

243
Q

What percentage of people in the United States are affected by Metabolic Syndrome?

244
Q

Which extreme complication do Type 2 Diabetics tend to lean towards?

A

Hyperglycemia Hyperosmolar Syndrome (HHS)

245
Q

3 treatment modalities for DM?

A
  1. Diet
  2. Exercise
  3. Drugs
246
Q

What are the Secretagogues and what do they do?

A

Sulfonylureas and meglitinides which increase insulin availability

247
Q

What are the Biguanides and what do they do?

A

Metformin which suppresses excessive hepatic glucose release

248
Q

What are the Thiazolidinediones and what do they do?

A

Rosiglitazone and pioglitazone which improve insulin sensitivity

249
Q

What are the alpha-glucosidasse inhibitors and what do they do?

A

Acarbose, miglitol which delay gastrointestinal glucose absorption

250
Q

Describe Metformin (3)

A
  1. An oral hypoglycemic agent that is typically the firstling treatment for newly dx Type 2 DM
  2. Potential life-threatening side effect of lactic acidosis is associated with this drug, although studies show variable results
  3. Should be held the morning of surgery and only resumed when renal function and circulatory status are stabilized postoperatively
251
Q

What causes DKA?

A

An absolute lack of insulin leads to diabetic metabolic decompensation with hyperglycemia and ketoacidosis

252
Q

What occurs during DKA to cause the formation of ketone bodies?

A

Reduction in glucose utilization and increases lipolysis leading to the formation of fatty acids that are oxidized in the liver to ketone bodies

253
Q

What occurs with fatty acids in DKA? (2)

A
  1. Increased mobilization of free fatty acids (FFA) from adipose tissue to the liver
  2. FFA mobilization is initiated by the effect of absolute insulin deficiency on fat cells
254
Q

What does the switch of hepatic lipid metabolism to ketogenesis occur due to in DKA?

A

Not only in response to insulin deficiency but additionally to the concomitant rise in levels of the stress hormones such as glucagon, corticosteroids, catecholamines, and growth hormones

255
Q

What are the hepatic effects in DKA? (3)

A
  1. Increased glycogenolysis
  2. Increased gluconeogenesis
  3. Increased ketogenesis
256
Q

What are the clinical manifestations of DKA primarily due to?

A

The result of abnormalities in carbohydrate and fat metabolism

257
Q

Clinical manifestations of DKA? (7)

A
  1. Serum glucose level >= 300
  2. Hypovolemic shock (avg deficit of 5L) from hyperglycemic osmotic diuresis
  3. Anion gap metabolic acidosis due to ketoacids
  4. Kussmaul respirations
  5. N/V
  6. Confusion and coma
  7. Fatigue, blurred vision, polydipsia, polyuria, weight loss
258
Q

3 Ketoacids

A
  1. Beta-hydroxybutyrate
  2. Acetoacetate
  3. Acetone
259
Q

What is acidosis that causes anion gap widening caused by?

A
  1. Lactate
  2. Ketones
  3. Increased organic acids
260
Q

How do you calculate anion gap?

A

(Na + K) - (Cl +HCO3)

261
Q

What reading of an anion gap is too high?

262
Q

Lab issues associated with DKA? (7)

A
  1. Hyponatremia
  2. Blood glucose >= 300 mg/dL
  3. Low bicarbonate <= 18 mEq/L
  4. Low pH <= 7.3
  5. Moderate to high ketones in blood and urine
  6. Elevated lactate levels
  7. Hyperosmolarity >300 mOsm/L
263
Q

3 Triggers of DKA?

A
  1. Infection
  2. Omission or inadequate use of insulin
  3. New-onest diabetes (esp. Type 1)
264
Q

3 Treatment modalities for DKA

A
  1. Hydration
  2. Insulin
  3. Electrolyte Replacement
265
Q

Describe Hyperosmolar Hyperglycemia Nonketotic Syndrome

A
  1. Usually Type 2 DM
  2. Hyperosmolar condition triggered by hyperglycemia
  3. Evovles over days to weeks with a persistent glycosuric diuresis
266
Q

What is the issue with insulin in Hyperosmolar Hyperglycemia Nonketotic Syndrome?

A

There is enough insulin, but the hyperglycemic episode overwhelms the pancreas and produces severe hyperglycemia and glycosuria

267
Q

What is the amount of Insulin sufficient for in Hyperosmolar Hyperglycemia Nonketotic Syndrome?

A

To prevent lipolysis and ketone production

268
Q

What occurs when the glucose load exceeds renal tubular maximum for glucose reabsorption?

A

A massive solute diuresis occurs with total body water depletion

269
Q

What does the patient experience with Hyperosmolar Hyperglycemia Nonketotic Syndrome?

A

Polyuria, polydipsia, hypovolemia, hypotension, tachycardia and organ hypo-perfusion

270
Q

Clinical manifestations of Hyperosmolar Hyperglycemia Nonketotic Syndrome? (2)

A
  1. CNS changes

2. Dehydration (average deficit of 9L)

271
Q

Labs associated with Hyperosmolar Hyperglycemia Nonketotic Syndrome?

A
  1. Blood glucose >= 600 mg/dL
  2. ph >= 7.3
  3. HCO3 >= 15
  4. Hyperosmolarity (>340 mOsm/L) is responsible for mental confusion, lethargy or coma
272
Q

Triggers for Hyperosmolar Hyperglycemia Nonketotic Syndrome? (5)

A
  1. Infection
  2. Sepsis
  3. Pneumonia
  4. Stroke
  5. MI
273
Q

3 treatment modalities associated for Hyperosmolar Hyperglycemia Nonketotic Syndrome?

A
  1. Fluid Resuscitation
  2. Insulin
  3. Correct electrolytes
274
Q

Describe Hypoglycemia (2)

A
  1. Blood glucose <50 mg/dL

2. Obscured by general anesthesia

275
Q

When does neurologic and EEG depression appear in non-diabetic patients and when does it occur in diabetic patients?

A
  1. Non-diabetic: 50-55 mg/dL

2. Diabetic: 70 to 85 mg/dL

276
Q

CNS signs of Hypoglycemia? (6)

A
  1. Sluggishness
  2. Headache
  3. Confusion
  4. Irritability
  5. Seizures
  6. Coma
277
Q

CV signs of Hypoglycemia? (5)

A
  1. Initial stimulation of the sympathetic system
  2. Tachycardia
  3. HTN
  4. Diaphoresis
  5. Lacrimation
278
Q

What do the signs of hypoglycemia mimic?

A

They are very similar to signs of inadequate depth of anesthesia (too light)

279
Q

What does intraoperative hypoglycemia manifest as?

A
  1. Bradycardia
  2. Hypotension
  3. Respiratory failure
280
Q

When are manifestations of intraoperative hypoglycemia suppressed?

A

With beta-blockers or high MAC (get a finger stick!)

281
Q

3 Objectives in the treatment for Hypoglycemia

A
  1. Goal is to achieve blood glucose level >100 mg/dL
  2. Hypoglycemia is more likely to occur in the diabetic surgical patient
  3. Initial dose is 0.5g/kg given as 50% dextrose in water (D50W)

Advanced Health Assessment TWU CRNA (4 decks)

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