AP 2 Test 3 Flashcards

1
Q

Glomerular filtration pressure is about __% of mean arterial pressure

A

60

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2
Q

What is the major function of the proximal tubule?

A

Sodium reabsorption

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3
Q

What part of the nephron is the site of aldosterone mediated Na+ reabsorption?

A

Distal tubule

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4
Q

How does aldosterone affect Na/K ATPase in the collecting duct?

A

It enhances the activity which increases the number of open K+ and Na+ channels to favor reabsorption into the plasma

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5
Q

What part of the nephron is the principle site of antidiuretic hormone?

A

Medullary portion of collecting tubule

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6
Q

What physiologic changes causes the kidneys to release renin?

A

1) Sympathetic stimulation
2) Hypotension
3) Decreased sodium delivery

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7
Q

Renal failure symptoms aren’t detected until less than __% of functioning nephrons remain

A

40

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8
Q

What is creatinine?

A

A byproduct of muscle metabolism that is fairly constant and a good indicator of renal health

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9
Q

What are normal creatinine levels in men?

A

0.8-1.3

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10
Q

What are normal creatinine levels in women?

A

0.6-1

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11
Q

How do you calculate creatinine clearance?

A

[(140-age) x lean body weight] / (72 x plasma creatinine)

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12
Q

What is normal creatinine clearance values?

A

100-200

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13
Q

Creatinine clearance below __ indicats renal failure

A

25

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14
Q

Creatinine clearance below __ indicates end stage renal failure

A

10

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15
Q

How are creatinine levels related to glomerular filtration rate?

A

Inversely proportional

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16
Q

What physiologic state can affect BUN levels?

A

Hypovolemia

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17
Q

What is the normal range for BUN?

A

10-20

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18
Q

BUN:Creatinine ratios greater than ____ are seen in volume depletion and edematous disorders

A

15:1

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19
Q

Urine pH above 7 in the presence of systemic acidosis indicates what?

A

Renal tubular acidosis

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20
Q

Protein excretion greater than ___ is significant when screening for proteinurea

A

150

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21
Q

What causes acute glomerular nephritis?

A

An antibody-antigen reaction

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22
Q

Acute glomerular nephritis usually occurs after infection from which bacteria?

A

Beta streptococci

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23
Q

What is Polycystic Kidney Disease?

A

An autosomal genetic disease that causes cysts on the kidneys

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24
Q

What conditions are associated with Polycystic Kidney Disease?

A

Aortic aneurysms, brain aneurysms, HTN, chronic renal disease

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25
Q

How does renal artery stenosis lead to hypertension?

A

The afferent arterioles read a decreased blood pressure due to the stenotic renal artery and release renin which increases BP

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26
Q

What causes diabetic renal neuropathy?

A

Glucose increases past the kidneys capacity to reabsorb. This causes more water to be excreted and the sodium in the urine becomes diluted which triggers macula densa cells to secrete renin and decrease blood flow to the kidney.

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27
Q

What is hepatorenal syndrome?

A

Rapid deterioration in renal function secondary to liver failure

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28
Q

Which surgeries have the highest incidence of patients with acute kidney injury?

A

Cardiac

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29
Q

What is azotemia?

A

The rapid deterioration in renal function that results in retention of nitrogenous waste products in the blood

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30
Q

What causes pre-renal azotemia?

A

Decrease in renal perfusion due to hypotension or hypovolemia

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31
Q

How can you treat pre and post renal failure to avoid renal azotemia?

A

Preoperative volume loading

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32
Q

How does most perioperative AKI occur?

A

Renal ischemia due to hypotension or hypovolemia

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33
Q

How does volume loading avoid AKI?

A

It suppresses renin and increases ANP release

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34
Q

Optimizing what 3 physiologic parameters reduces AKI and mortality by over 50%?

A

1) MAP
2) Preload
3) Cardiac output

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35
Q

MAP below __ mmHg is associated with AKI

A

60

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36
Q

There is a graded increase in AKI for pre-op Hbg less than __

A

12

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37
Q

Oliguria is defined as having a urine output less than ___ cc/day

A

400

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38
Q

What are the treatments available for improving renal perfusion?

A
  • Treat hypovolemia
  • Treat/raise MAP
  • Pressors
  • Dopaminergic dilators such as dopamine or fenoldapam
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39
Q

What fluid doubles the incidence of AKI when compared to LR?

A

Normal saline

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40
Q

How do most diuretics increase urinary output?

A

By decreasing reabsorption of Na/K and water

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41
Q

How do osmotic diuretics increase urine output?

A

Their presence in the proximal tubule limits passive water reabsorption

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42
Q

What is the dose for Mannitol (osmotic diuretic)?

A

0.25-1g/kg

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43
Q

How should you administer Mannitol? Why?

A

Give over 20 minutes b/c if its given too quickly it can increase blood osmolarity and draw fluid into the bloodstream, causing increase in intravascular volume and possibly initiating cardiac failure in susceptible patients

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44
Q

How do carbonic anhydrase inhibitors increase urine output?

A

They interfere with Na+ reabsorption and H+ secretion in the proximal tubules

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45
Q

What is the dose of Diamox (CA inhibitor) to increase urine output?

A

250-500mg

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46
Q

How do loop diuretics work to increase urine output?

A

Inhibit Na+ and K+ reabsorption in the thick ascending loop of henle

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47
Q

What is the dose of Lasix?

A

10-100mg

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48
Q

What is the dose of Bumetetanide/Bumex?

A

0.5-1mg

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49
Q

What can be caused by chronic usage of loop diuretics?

A

Hearing loss

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50
Q

How do diuretics work at the distal tubule?

A

Inhibit sodium reabsorption by competing for the Cl- site on the Na/Cl carrier protein

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51
Q

What is the dose of Diuril (distal tubule diuretic)?

A

500mg

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52
Q

How do aldosterone antagonists work?

A

Cause the excretion of Na+ and H2O follows, and keeps K+

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53
Q

What aldosterone antagonist is used to prevent oliguria?

A

Spironolactone

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54
Q

How do non-competitive K+ sparing diuretics work?

A

Inhibit Na+ reabsorption and K+ secretion by decreasing number of open Na+ channels

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55
Q

What is an example of a K+ sparing diuretic used to prevent oliguria?

A

Triamterene

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56
Q

What are the metabolic manifestations of renal failure?

A
  • High K+, Mg2+, uric acid

- Low phosphate, Ca2+, albumin

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57
Q

What are the hematological manifestations of renal failure?

A
  • Anemia

- Decrease white cell and platelet function

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58
Q

Why is there an increased cardiac output in chronic renal failure patients?

A

It increases to offset decrease in O2 carrying capacity and the increase in preload

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59
Q

What are the results of increased angiotensin levels in chronic renal failure patients?

A

Arterial hypertension –> increased SVR –> left ventricular hypertrophy –> congestive heart failure

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60
Q

What are the pulmonary manifestations of renal failure?

A
  • Increased minute ventilation due to metabolic acidosis

- Pulmonary edema

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61
Q

What are the endocrine manifestations of renal failure?

A

Abnormal glucose tolerance secondary to peripheral resistance to insulin

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62
Q

What are the GI manifestations of renal failure?

A
  • Anorexia
  • N/V
  • Delayed gastric emptying
  • Hepatitis
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63
Q

What is the mainstay of treatment for chronic renal failure?

A

Dialysis or transplant

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64
Q

What is dialysis?

A

The process of removing solute such as toxins, electrolytes, and water from the body

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65
Q

What drugs are considered nephrotoxins and should be avoided when renal function is compromised?

A
  • Antibiotics
  • Anesthetic agents (methoxyflurane and enflurane)
  • NSAIDs
  • Contrast media
  • Immunosuppressive agents
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66
Q

What is myoglobinuria?

A

Severe muscle breakdown that causes myoglobin to be filtered by the kidneys which clogs the system

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67
Q

What causes myoglobinuria?

A
  • Severe muscle wasting
  • Malignant hyperthermia
  • Transfusion rxn
  • Anaphylactic rxn
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68
Q

What treatments are available for myoglobinuria?

A
  • Keep urine flowing
  • Fluids
  • Diuretics (mannitol)
  • Alkanalize urine with sodium bicarb
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69
Q

What is the concern if renal patients were just dialyzed before surgery?

A

Anticoagulants might still be on board

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70
Q

What lab values should be assessed preoperatively for patients with compromised renal function?

A
  • Recent electrolytes especially K+
  • Recent CBC
  • Blood glucose level
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71
Q

We should not use succinylcholine in renal patients unless the pre-op K+ level is less than __

A

5.0

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72
Q

What are the EKG manifestations of hyperkalemia?

A
  • Peaked T waves
  • Very flat ST segment
  • Long QRS
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73
Q

What are the quick treatments for hyperkalemia?

A
  • Calcium chloride
  • Sodium bicarb
  • Glucose and insulin
  • Hyperventilation
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74
Q

When managing renal patients, we should exercise judicious use of what drug classes?

A
  • Narcotics
  • Benzos
  • Relaxants
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75
Q

How should fluids be managed for renal patients?

A
  • Very judicious use
  • Use phenylephrine for low BP instead of fluid loading
  • Fluids with no potassium such as normal saline
  • Glucose free fluids
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76
Q

Rapid respirations might not always mean pain in renal patients - what else could be causing it?

A

Metabolic acidosis compensation or pulmonary edema

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77
Q

What basic parameters should be assessed postoperatively in patients with renal failure?

A
  • Oxygen saturation
  • Electrolytes and hb/hct
  • Fluid balance
  • Blood sugar
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78
Q

On average, assume __ ml/min of irrigation fluid is absorbed during TURP and TURB procedures

A

20

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79
Q

What are the deleterious affects of dilution with irrigation during TURP/TURB procedures?

A

CV collapse, heart failure, hypotension, pulmonary edema, hyponatremia, cerebral edema, anemia, hyperglycemia, hyperammonemia

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80
Q

Clinical symptoms of deleterious effects of irrigant absorption from TURB/TURPs is classified as….

A

TURP syndrome

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81
Q

What are the early signs of TURP syndrome in awake patients?

A

Restlessness, headache, N/V, confusion/slurred speech, tachypnea

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82
Q

What are the later signs of TURP syndrome?

A

Seizure, tachycardia and HTN followed by bradycardia and hypotension followed by CV collapse

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83
Q

What lab value confirms TURP syndrome?

A

STAT serum Na+ less than 120

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84
Q

What are the treatments available for TURP syndrome?

A
  • Loop diuretics
  • Restrict fluids
  • Hypertonic saline for the low Na+
  • Benzos for seizures
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85
Q

What are other issues (aside from TURP syndrome) associated with TURP/TURB procedures?

A
  • Hypothermia
  • Bladder perforation
  • Coagulopathy
  • Septicemia
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86
Q

What is a good choice of anesthesia for TURP/TURB procedures?

A

Spinal/epidural for good pain relief and allows you to monitor mentation

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87
Q

What can ECG changes can be seen during lithotripsy procedures due to shock waves?

A

Dysrhythmias on R waves

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88
Q

What type of anesthesia is usually necessary for percutaneous nephrolithotomy tube placement?

A

General

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89
Q

What are the anesthetic considerations for prostatectomies and cystectomies?

A
  • Significant blood loss
  • A line
  • Good IV access
  • May need indigo carmen or methylene blue
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90
Q

What is the more popular anesthetic method for prostatectomies/cystectomies?

A

General anesthesia

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91
Q

What are anesthetic considerations for nephrectomies?

A
  • Potential for extensive blood loss

- Reflex renal vasoconstriction can occur at non-effected kidney and can cause post op renal failure, consider mannitol

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92
Q

What drugs should be considered prior to clamping the iliac vessels during renal transplants?

A
  • Heparin
  • Calcium channel blocker into graft to prevent reperfusion injury
  • Mannitol
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93
Q

How does the autonomic nervous system correct hypertensive states?

A
  • Decrease HR
  • Vasodilation
  • Increase vagal tone
  • Decrease sympathetic tone
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94
Q

How does the autonomic nervous system correct hypotensive states?

A
  • Increase HR
  • Vasoconstriction
  • Increase contractility
  • Decrease vagal tone
  • Increase sympathetic tone
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95
Q

What activates the RAA system?

A

Hypotension and decreased sympathetic tone

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96
Q

What is the ultimate result of RAA system activation?

A
  • Increased vasopressin levels

- Increased angiotensin II

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97
Q

What occurs during the initiation of the RAA system?

A

Macula densa cells sense low fluid or low sodium concentration and prompt the juxtaglomerular cells to secrete renin into the blood

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98
Q

What happens after renin from the kidney and angiotensinogen from the liver is released into the blood?

A

Renin converts angiotensinogen to angiotensin I

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99
Q

What happens once angiotensinogen is converted to angiotensin I?

A

ACE from the pulmonary blood converts angiotensin I to angiotensin II

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100
Q

What happens once angiotensin I is converted to angiotensin II?

A

Angiotensin II stimulates vasoconstriction and aldosterone secretion from the adrenal cortex

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101
Q

How does aldosterone affect blood volume?

A

Aldosterone stimulates Na+ uptake and water reabsorption, thus increasing blood volume and arterial blood pressure

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102
Q

What are common causes of secondary hypertension?

A
  • Renal disease
  • Endocrine disorders
  • Renal artery stenosis
  • Medications
  • Neurologic disorders
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103
Q

What is the neurologic manifestation of unmanaged hypertension?

A

Ischemic stroke

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104
Q

What are the cardiovascular manifestations of unmanaged hypertension?

A

Aneurysms, LVH, angina, heart failure, arrhythmias

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105
Q

What are the renal manifestations of unmanaged hypertension?

A
  • Sodium retention
  • Hyperuricemia
  • Diminished GFR
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106
Q

What is a hypertensive emergency?

A

Severe HTN with evidence of acute end organ damage i.e. stroke, encephalopathy, LV failure, MI, renal failure

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107
Q

What is hypertensive urgency?

A

High blood pressure without signs of acute end organ damage

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108
Q

What is the likely etiology of a hypertensive emergency?

A

A very acute increase in SVR leading to acute increase in BP

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109
Q

Blood pressure should be lowered by about __% in the first few hours following an acute hypertensive emergency

A

20

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110
Q

What factors do the JNC-8 guidelines for hypertension depend on?

A

The patient’s age and co-morbid conditions

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111
Q

Hypertensive patients with chronic kidney disease can be managed with what drug classes?

A
  • ACE inhibitors

- ARBs

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112
Q

African American hypertensive patients without chronic kidney disease can be treated with what drug classes?

A
  • Thiazide diuretics

- Calcium channel blockers

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113
Q

Non-african american hypertensive patients without chronic kidney disease can be treated with what drug classes?

A
  • Thiazide diuretics
  • Calcium channel blockers
  • Ace inhibitors
  • ARBs
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114
Q

What lifestyle modifications can be made to treat hypertension?

A
  • Weight loss
  • Reduce salt intake
  • Alcohol/tobacco cessation
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115
Q

How do thiazide diuretics (hydrochlorothiazide) work to treat HTN?

A

Reduces sodium reabsorption in DCT which causes water loss and decreased BP

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116
Q

How do loop diuretics such as Furosemide and Torsemide work to treat HTN?

A
  • Inhibits sodium and chloride reabsorption in loop of henle to cause water loss
  • Increase prostaglandin levels
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117
Q

How do ACE inhibitors such as Lisinopril work to treat HTN?

A

Blocks the conversion of angiotensin I to angiotensin II to cause vasodilation, smooth muscle relaxation, natriuresis, and decreased vasopressin release

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118
Q

How do angiotensin receptor blockers such as Losartan and Valsaratan work to treat HTN?

A

Blocks the activation of the angiotensin II receptor which causes vasodilation, smooth muscle relaxation, natriuresis, and decreased vasopressin release

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119
Q

How do calcium channel blockers such as Amlodipine and Nicardipine work to treat BP?

A

Block calcium channels thus decreasing Ca2+ levels and causing vasodilation, negative inotropy, negative chronotropy, and reduced aldosterone production

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120
Q

You should avoid using calcium channel blockers in patients with what co-morbid condition?

A

Heart failure

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121
Q

When are calcium channel blockers commonly used to treat HTN?

A

For otherwise fairly normal functioning patients who don’t respond to diuretics or ACE inhibitors

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122
Q

Where are B1 receptors primarily located?

A

Heart and kidneys

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123
Q

Where are B2 receptors primarily located?

A

Muscle

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124
Q

Where are B3 receptors primarily located?

A

Adipose tissues

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125
Q

How do beta blockers such as metoprolol and carvedilol work to treat HTN?

A

Negative chronotropy, negative inotropy, anti-arrhythmic effect, reduced aldosterone, smooth muscle relaxation

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126
Q

What is a true aneurysm?

A

Aneurysm encompassing all 3 layers of the aorta

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127
Q

What is a pseudo-aneurysm?

A

Aneurysm of just the bottom layer of the aorta

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128
Q

What are common etiologies of aortic aneurysms?

A

HTN, artherosclerosis, collagen vascular disease, bicuspid aortic valve, syphilis, hyperlipidemia, mycotic, inflammatory

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129
Q

What is an aortic dissection?

A

An intimal tear creating a false lumen for blood to enter

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130
Q

What is a Type A aortic dissection?

A

Dissection involving either the ascending aorta or both ascending and descending

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131
Q

What is a Type B aortic dissection?

A

Dissection involving just descending aorta

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132
Q

What are common etiologies of aortic dissections?

A

HTN, collagen vascular disease, biscuspid valve, inflammatory, trauma, heart surgery complication

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133
Q

What is carotid artery stenosis?

A

Narrowing of the carotid arteries primarily due to atherosclerotic disease

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134
Q

Which carotids are primarily affected by carotid artery stenosis?

A

Internals

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135
Q

Carotid artery stenosis greater than __% indicates intervention

A

70

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136
Q

What are common risk factors for carotid artery stenosis?

A

HTN, hyperlipidemia, DM, PAD, tobacco

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137
Q

What is Raynaud’s phenomenon? In what gender is it most common?

A

Vasoconstriction in extremities during periods of cold or stress. Most common in females.

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138
Q

What is a venous thromboembolism?

A

A deep vein thrombosis plus pulmonary embolism that primarily occurs in lower extremities

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139
Q

Total hepatic blood flow accounts for __% of cardiac output

A

25

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140
Q

Hepatic blood flow has ___ (high/low) flow, ____ (high/low) resistance

A

High flow, low resistance

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141
Q

Most patients with liver disease have ___ SVR (hi/lo), ____ cardiac output (hi/lo), and ___ arterial pressure (hi/lo).

A

low SVR, high cardiac output, low arterial pressure

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142
Q

Splanchnic volume has a major role in the body’s response to what perioperative condition?

A

Hypovolemia

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143
Q

What nerves have neural control of liver blood flow?

A

Vagus and splanchic

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144
Q

Sympathetic stimulation _______ (increase/decreases) blood flow

A

Decreases

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145
Q

How does epinephrine affect liver blood flow?

A

Initial vasoconstriction via alpha receptors, then dilation via beta receptors

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146
Q

How does glucagon affect liver blood flow?

A

Long lasting arterial vasodilation

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147
Q

How does angiotensin II affect liver blood flow?

A

Profound vasoconstriction

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148
Q

How does vasopressin affect liver blood flow?

A

Marked splanchnic vasoconstriction

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149
Q

What components of anesthesia will decrease total hepatic blood flow?

A
  • All anesthetics that decrease cardiac output
  • Controlled ventilation
  • Regional anesthesia
  • Controlled hypotension with sodium nitroprusside
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150
Q

What type of surgery decreases hepatic blood flow up to 60%?

A

Upper abdominal surgeries

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151
Q

What key protein that maintains intravascular oncotic pressure is produced by the liver?

A

Albumin

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152
Q

What is the normal range of albumin levels?

A

3.5-6

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153
Q

All coagulation factors except which 3 are produced by the liver?

A

3, 4, and 8

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154
Q

A deficiency in which coagulation factors is a good indication of hepatic dysfunction?

A

Vitamin K dependent factors

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155
Q

Which clotting test is a good indicator of acute hepatic dysfunction?

A

PT

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156
Q

Removal of what toxic metabolite is impaired in both acute and chronic liver disease?

A

Ammonia

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157
Q

How are glucose levels affect in patients with impaired liver function?

A

Blood glucose can rise several fold

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158
Q

The majority of cholesterol synthesized by the liver is converted to what?

A

Bile salts

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159
Q

What is jaundice?

A

The yellow-green tint of body tissue due to bilirubin accumulation in extracellular fluids

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160
Q

Skin discoloration is usually visible when plasma bilirubin reaches __ times normal values

A

3

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161
Q

Why does bilirubin accumulation occur

A
  • Increased breakdown of hemoglobin (indirect bilirubin)

- Obstruction of bile duct (direct bilirubin)

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162
Q

Which form of bilirubin (conjugated or unconjugated) travels to the liver bound to albumin?

A

Unconjugated

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163
Q

What is the normal daily production of bilirubin?

A

300mg

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164
Q

How do narcotics affect common bile duct pressure?

A

Increase common bile duct pressure

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165
Q

Which narcotic increases common bile duct pressure the most? The least?

A

Fentanyl - the most
Morphine - middle
Demerol - the least

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166
Q

What drugs can attenuate the increase in common bile duct pressure caused by narcotics?

A

NTG, naloxone, atropin, glucagon

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167
Q

What occurs during phase I of drug biotransformation in the liver?

A

Oxidation w/ cytochrome P-450

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168
Q

What occurs during phase II of drug biotransformation in the liver?

A

Conjugation to water soluble for excretion

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169
Q

What factors affect drug metabolism in the liver?

A
  • Blood flow, protein binding, intrinsic hepatic clearance
  • Enzyme inducing compounds
  • Self-induced drugs like ketamine and diazepam
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170
Q

What lab value is increased when bile ducts are blocked?

A

Alkaline phosphatase (ALP)

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171
Q

What lab test is the best for detecting hepatitis?

A

Alanine transaminase (ALT)

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172
Q

What lab test is a more sensitive marker for cholestatic damage?

A

Gamma-glutamyl transpeptidase (GGTP)

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173
Q

What enzyme level used to evaluate liver function is found in the liver, heart, and muscle?

A

Aspartate transaminase (AST)

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174
Q

What is the normal range for ALT levels?

A

5-40

175
Q

What is the normal range for ALP levels?

A

13-39

176
Q

What other tests are useful in assessing liver function?

A
  • PT
  • Total proteins
  • Albumin
  • Bilirubin
  • Platelets
  • Ammonia
177
Q

How are serum albumin levels changed in patients with chronic liver disease such as cirrhosis?

A

Decreased

178
Q

What is bilirubin?

A

The breakdown product of heme that is cleared from the blood by the liver

179
Q

If direct bilirubin levels are normal, what are the etiologies of impaired liver function?

A
  • Hemolysis
  • Hepatitis
  • Cirrhosis
180
Q

If direct bilirubin levels are elevated, what is the issue? What should be suspected?

A

The liver is unable to secrete the bilirubin.

  • Gallstones
  • Cancer
181
Q

What is the normal range for total bilirubin?

A

0.2-1.5

182
Q

What is the normal range for direct/conjugated bilirubin?

A

0-0.3

183
Q

What is the normal range for indirect/unconjugated bilirubin?

A

0.2-0.8

184
Q

How is Hep A transmitted?

A

Fecal/oral route. Contaminated shell fish common

185
Q

How does Hep A manifest?

A

Fever, jaundice, painfully enlarged liver

186
Q

How is Hep B transmitted?

A

Blood transfusion, needle stick, sexual contact, across the placenta

187
Q

How is Hep C transmitted?

A

Blood transfusion, needle stick, sexual contact, across the placenta

188
Q

What is Hep D?

A

A co-infection acquired with hep B

189
Q

How is Hep E transmitted?

A

Fecal/oral route due to contaminated water or poor hygiene

190
Q

What are the top causes of acute liver failure?

A
  • Viral hepatitis
  • Drugs (acetaminophen, amiodarone, volatile anesthetics)
  • Toxins
  • Vascular events (ischemia)
191
Q

Which hepatitis is an occupational risk for anesthesia care providers?

A

Hep B

192
Q

What should be assessed during preop of a patient with hepatitis?

A
  • Assess coagulation and treat with fresh frozen plasma if needed
  • Glucose levels
193
Q

What respiratory state should be avoided in patients with hepatitis?

A

Hypercarbia

194
Q

Which drug classes have a prolonged affect in patients with hepatic dysfunction?

A
  • Benzodiazepines
  • Opioids
  • Non-depolarizing muscle relaxants
195
Q

Which opioids have prolonged effects in patients with hepatic dysfunction?

A

Morphine and alfentanil

196
Q

Which muscle relaxants are a better choice for patients with hepatic dysfunction?

A

Cis and atracurium

197
Q

What is cirrhosis?

A

Chronic disease of the liver characterized by distortion of the normal hepatic structure or scaring caused by cellular destruction

198
Q

In what patients is cirrhosis most commonly seen?

A
  • Patients with chronic viral hepatitis

- Alcholics

199
Q

What is cholelithiasis?

A

Formation of stones in the gallbladder caused by cholesterol crystal precipitation

200
Q

What is cholecystitis?

A

Inflammation of the gallbladder caused by a gallstone in the cystic duct

201
Q

What may be considered for induction with patients presenting for cholecystectomy?

A

RSI b/c they may present with a recent history of N/V

202
Q

The use of which drug class may prevent flow of contrast dye during a cholangiogram?

A

Opioids

203
Q

An elevation in unconjugated bilirubin can lead to what condition?

A

Kernicterus, characterized by seizures and brain damage

204
Q

1 unit of PRBCs contains approximately how much bilirubin?

A

250mg

205
Q

What IV access/monitoring should be considered for a hepatic resection?

A
  • Large bore IV
  • A line
  • CVC
206
Q

How should post op pain be managed for a hepatic resection?

A

Epidural

207
Q

How should you manage the patients fluid status during the hepatic resection phase?

A

Keep them relatively hypovolemic to minimize EBL

208
Q

How many units of T&C blood should be available during a hepatic resection?

A

6

209
Q

What is the normal range for portal vein pressures?

A

6-12cmH2O

210
Q

What is portal hypertension?

A

Sustained elevation of portal vein pressure causing an increased resistance to blood flow in the liver

211
Q

What are collateral channels (varices)?

A

Channels caused by the overload of the portal circuit in an attempt to flow around the hepatic obstruction

212
Q

What causes prehepatic portal htn?

A

Thrombosis

213
Q

What causes intrahepatic portal htn?

A

Cirrhosis

214
Q

What causes posthepatic portal htn?

A

Budd-chiari syndrome, right heart failure, pericarditis

215
Q

What is the clinical manifestation of severe portal hypertension?

A

Bleeding of varicies, particularly from the esophagus

216
Q

What is ascites?

A

Accumulation of serous fluid in the peritoneal cavity

217
Q

Ascites can be a manifestation of what other conditions?

A
  • Cirrhosis
  • Portal htn
  • Increased lymph, Na+ retention
  • Impaired h2o excretion
  • Hypoalbuminemia
  • Decreased colloid osmotic pressure
218
Q

Patients with ascites often present with what condition?

A

Arterial hypoxemia

219
Q

What are the common PaO2 values in patients with ascites?

A

60-70mmHg

220
Q

What is the most likely cause of the arterial hypoxemia seen in patients with ascites?

A

Right to left intrapulmonary shunting as a result of pulmonary htn, cigarettes, or COPD

221
Q

What is the common medical management of ascites?

A

Aldosterone antagonists such as Spironolactone

222
Q

How should fluids be managed during ascites fluid removal?

A

Administer IV fluids, usually colloids, to prevent hypotension. No more than 1 L drained per day.

223
Q

What is the mainstay treatment of coagulopathy in patients with advanced hepatic failure?

A

FFP

224
Q

What is the greatest fear of massive blood loss in the coagulopathic liver patients?

A

Fibrinolysis

225
Q

How does hepatic encephalopathy (hepatic coma) manifest?

A
  1. Mental confusion
  2. Asterixis (flapping motion of hands)
  3. Fetor hepaticus (fruity breath)
226
Q

What are the anesthetic questions we should ask when presented with patients with advanced liver diseases?

A
1 - Stage of disease?
2 - Coagulopathy?
3 - Ascites?
4 - Renal compromise?
5 - Anesthetic drug issues with hepatic dysfunction?
6 - Anticipated blood loss?
227
Q

The posterior pituitary secretes

A. TSH
B. Prolactin
C. Vasopressin
D. Growth hormone

A

C. Vasopressin

228
Q

Which lobe of the pituitary gland produces hormones? Which hormones does it produce?

A

Anterior - ACTH, TSH, GH, FSH, LH

229
Q

Which hormones are secreted by the posterior pituitary?

A

ADH and oxytocin

230
Q

What are the principle hormones secreted by the thyroid?

A

Thyroxine (T4)

Triiodothyronine (T3)

231
Q

Which hormone secreted by the thyroid is more potent and less protein bound?

A

T3

232
Q

Graves Disease is an autoimmune disease causing

A) Hypothyroidism
B) Hyperthyroidism

A

B. Hyperthyroidism

233
Q

What is the pathophysiology of hyperthyroidism?

A

Hyperfunction of the thyroid gland with excessive secretion of T3 or T4

234
Q

What are common causes of hyperthyroidism?

A
  • Graves disease
  • TSH secreting tumors
  • Iatrogenic
  • Thyroiditis
235
Q

What are the symptoms of hyperthyroidism?

A
  • Weight loss
  • Fatigue
  • Arrhythmias (a fib, SVTs, widened pulse P)
  • Anxiety
  • Exopthalmos
236
Q

What are the common treatments for hyperthyroidism?

A
  • Antithyroids
  • Beta blockers
  • Thyroidecetomy
237
Q

What can be administered to patients with hyperthyroidism pre-op to decrease hormone release?

A

Steroids

238
Q

What beta blocker is good intra-op for patients with hyperthyroidism?

A

Esmolol

239
Q

What intra-op drugs should be avoided in patients with hyperthyroidism?

A

Drugs that cause SNS stimulation

  • Ketamine
  • Pancuronium
  • Meperidine
  • Atropine
240
Q

What exaggerated response can occur during induction of patients with hyperthyroidism?

A

Exaggerated hypotensive response

241
Q

What are the major post op concerns in patients with hyperthyroidism?

A
  • Unilateral RLN injury (manifests as hoarseness)
  • Bilateral RLN injury (stridor)
  • Hypocalcemia 1-3 days after surgery (parathyroid removal)
242
Q

How does hyperthyroidism change MAC requirements?

A

No change

243
Q

What is a thyrotoxic crisis (thyroid storm)?

A

A life threatening exacerbation of hyperthyroidism that can be caused by trauma, infection, surgery, or illness

244
Q

When do thyroid storms most often appear?

A

6-18 hours after operation

245
Q

What are the symptoms of thyroid storm?

A

Abrupt anxiety, fever, tachycardia, CV instability

246
Q

What is the treatment of a thyroid storm?

A
  • Cooled crystalloids
  • Esmolol infusion (50-300mcg/kg/min)
  • Dexamethasone (2mg every 6 hours)
  • Cortisol (100-200mg)
247
Q

What other condition does a thyroid storm mimic?

A

Malignant hyperthermia

248
Q

How can you decipher a thyroid storm from MH?

A

A thyroid storm doesn’t cause muscle rigidity, elevated creatinine kinase, or acidosis

249
Q

What drug can be given PO to inhibit conversion of T4 to T3 during a thyroid storm?

A

Propylthiouracil

250
Q

What is the pathophysiology of primary hypothyroidism?

A

Dysfunction or destruction of thyroid tissue

251
Q

What is the most common kind of hypothyroidism?

A

Hashimoto’s thyroiditis

252
Q

Patients with primary hypothyroidism have __ (hi/lo) TSH levels but ___ (hi/lo) T3 and T4 levels

A

High TSH, low T3/T4

253
Q

What causes secondary hypothyroidism?

A

HPA axis dysfunction iatrogenically (thyroidectomy, antithyroid meds, radioactive iodine) or due to myxedema coma

254
Q

What is myxedema coma? In which patients is it most common?

A

Loss of deep tendon reflexes with severe hypothermia, hypoventilation, hyponatremia, hypoxia, hypotension, delirium. Most common in elderly women with long history of hypothyroidism.

255
Q

What are the symptoms of hypothyroidism?

A
  • Lethargy
  • Weight gain
  • Cold intolerance
  • Hypoactive reflexes
256
Q

What is the treatment for hypothyroidism?

A

PO T4 (L-thyroxine aka Synthroid)

257
Q

What are intra-op considerations for patients with hypothyroidism?

A
  • Can have severe hypotension and increased sensitivity to agents
  • Diminished cardiac output
  • Blunted baroreceptor reflexes
  • Impaired pulmonary function
258
Q

What anesthetic approach is best in patients with hypothyroidism?

A

Regional

259
Q

If you must do a general anesthetic in patients with hypothyroidism, what induction med should be used?

A

Ketamine

260
Q

What are post-op concerns for patients with hypothyroidism?

A
  • Resedation
  • Hypothermia
  • Hypoventilation
261
Q

Parathyroid hormone increases the levels of serum:

A. albumin
B. calcium
C. potassum
D. sodium

A

B. calcium

262
Q

What serum electrolyte is decreased by parathyroid hormone?

A

Phosphate

263
Q

What percentage of calcium in the blood is protein bound?

A

40%

264
Q

How many parathyroid glands are there?

A

4

265
Q

What are the common causes of primary hyperparathyroidism?

A
  • Adenoma
  • Carcinoma
  • Hyperplasia
266
Q

What are the common causes of secondary hyperparathyroidism?

A

Compensatory increase in PTH secretion due to hypocalcemia caused by renal disease or GI malabsorption

267
Q

What are the symptoms of hyperparathyroidism?

A
  • Renal stones
  • HTN
  • Constipation
  • Fatigue
268
Q

What are the medical treatments for hyperparathyroidism?

A
  • Saline

- Loop diuretics

269
Q

What are the periop anesthetic considerations for patients with hyperparathyroidism?

A
  • Adequate hydration
  • Maintenance of urine output
  • Possible hypotension during induction
  • Altered response to muscle relaxants
270
Q

What are the EKG manifestations of hypercalcemia due to hyperparathyroidism?

A
  • Prolonged PR interval

- Short QT interval

271
Q

What is hypoparathyroidism?

A

Decreased PTH or resistance to PTH that causes decreased calcium - almost always iatrogenic

272
Q

What is pseudohypoparathyroidism?

A

A congenital condition where the patient has normal PTH but kidneys don’t response

273
Q

What are the symptoms of acute hypoparathyroidism after surgery?

A
  • Paresthesias
  • Neuromuscular irritability
  • Restlessness
274
Q

What are the symptoms of chronic hypoparathyroidism?

A

EKG changes, lethargy, cataracts

275
Q

What is a positive Chvostek sign when screening for hypoparathyroidism?

A

Facial muscle twitching with manual tapping at angle of mandible

276
Q

What is a positive Trousseau sign when screening for hypoparathyroidism?

A

Carpopedal spasm after 3 minutes of tourniquet ischemia

277
Q

What is the treatment for hypoparathyroidism?

A
  • Calcium infusion
  • PO calcium
  • Vitamin D
278
Q

How should respiration be managed perioperatively in patients with hypoparathyroidism?

A

Don’t hyperventilate so you can avoid alkalosis

279
Q

The Thymus is a specialized gland of the _________ system:

A) cardiovascular
B) Neurological
C) renal
D) Immune

A

D. immune

280
Q

What does the thymus do?

A

Differentiates developing lymphocytes into mature T cells of the adaptive immune system

281
Q

What is the pathophysiology of DiGeorge Syndrome (congenital thymic hypoplasia)?

A

Hypoplasia or aplasia of the parathyroid and thymus

282
Q

What are the symptoms caused by DiGeorge Syndrome?

A
  • Hypocalcemia
  • Increased infections
  • Congenital cardiac defects
283
Q

What symptom of DiGeorge Syndrome indicates a difficult DL?

A

Micrognathia

284
Q

What are periop considerations for patients with DiGeorge Syndrome?

A
  • Avoid hyperventilation bc it could exacerbate hypocalcemia

- Unpredictable NMB

285
Q

Cushing’s Disease is an excess of which hormone?

A) ACTH
B) Cortisol
C) Aldosterone
D) GH

A

B. Cortisol

286
Q

What is released from the adrenal cortex?

A
  • Glucocorticoids (cortisol)
  • Anti insulin
  • Minerocorticoids (aldosterone)
  • Androgens
287
Q

What is the net effect of aldosterone?

A

Increased extracellular fluid volume caused by fluid retention, decreased plasma potassium, metabolic alkalosis

288
Q

What imbalance can occur with high circulating levels of anti-insulin?

A

Hyperglycemia

289
Q

What endocrine disorder is assessed with the Chvostek and Trousseau tests?

A

Hypoparathyroidism

290
Q

What is the only important disease process associated with the adrenal medulla?

A

Pheochromocytoma

291
Q

What neurotransmitters are released from the adrenal medulla?

A

Catecholamines (NE, E, DA)

292
Q

What is Cushing’s Syndrome?

A

ACTH stimulates excessive cortisol secretions from the adrenal cortex

293
Q

What are the symptoms of Cushing’s syndrome?

A

Obesity, HTN, glucose intolerance, osteoporosis, muscle weakness

294
Q

What are the treatments for Cushing’s syndrome?

A
  • Radiotherapy

- Transsphenoidal resection if microadenoma is the cause

295
Q

What are the preop considerations of a patient with Cushing’s syndrome?

A
  • Consider BP
  • Check for electrolyte imbalances
  • Check blood sugar
  • May be hypervolemia
  • May be hypokalemic
  • Muscle weakness may indicate sensitivity to NMB
296
Q

What are the intraop considerations for a patient with Cushing’s syndrome?

A
  • Careful positioning due to osteoporosis

- Obesity

297
Q

What are the physiologic effects of excess cortisol that must be considered while managing a patient with Cushing’s syndrome?

A
  • Systemic HTN
  • Muscle weakness
  • Osteoporosis
  • Obesity
  • Poor wound healing
  • Susceptible to infections
298
Q

What post op considerations are important for a patient with Cushing’s syndrome?

A
  • Poor wound healing

- Infection prone

299
Q

If Conn Syndrome involves oversecretion of Aldosterone, you would expect a patient with it to have:

A) Hypokalemic Metabolic Acidosis
B) Hyperkalemic Metabolic Alkalosis
C) Hypokalemic Metabolic Alkalosis
D) Hyperkalemic Metabolic Acidosis

A

C) Hypokalemic Metabolic Alkalosis

300
Q

What is the cause of primary hyperaldosteronism (Conn syndrome)?

A

Excess secretion of aldosterone usually from a tumor, hyperplasia, or adrenal carcinoma

301
Q

What are the symptoms of Conn syndrome?

A

Often asymptomatic but may see

  • headache
  • muscle cramps
  • metabolic alkalosis
  • hypokalemia
302
Q

What are the treatments for Conn syndrome?

A
  • Supplemental potassium

- Competitive aldosterone antagonist (Spironolactone)

303
Q

What are periop considerations of a patient with Conn syndrome?

A
  • Correction of hypokalemia
  • Treatment of systemic HTN
  • Don’t hyperventilate
304
Q

What is the cause of primary adrenocorticoid deficiency (Addison’s disease)?

A

An autoimmune disease that causes

  • Decreased release of glucocorticoids and mineralocorticoids
  • Absence of cortisol and aldosterone
305
Q

What causes secondary adrenocorticoid deficiency?

A

Can be caused from iatrogenic use of synthetic steriods. Causes…

  • decreased ACTH from pituitary
  • No cortisol
  • Normal aldosterone
306
Q

What symptoms of adrenocorticoid deficiency are caused by the absence of cortisol?

A
  • Weakness
  • Fatigue
  • Hypoglycemia
  • Hypotension
  • Weight loss
307
Q

What symptoms of adrenocorticoid deficiency are caused by the absence of aldosterone?

A
  • Hyponatremia
  • Hypovolemia
  • Hyperkalemia
  • Metabolic acidosis
  • Hyperpigmentation of skin
308
Q

What is Addisonian crisis? How is it triggered

A

Severe hypotension leading to a coma that can be triggered in steroid-dependent patients who do not receive increased doses during periods of stress

309
Q

What are the treatments for adrenocorticoid defiency?

A

Replace steroids with hydrocortisone

310
Q

What are the periop considerations for patients with adrenocorticoid deficiency?

A
  • Be aware of addisonian crisis
  • Beware of steroid withdrawal and redose steriods
  • Infection prone
  • Assess if pressors and fluids are working to treat hypotension
311
Q

What induction drug should be avoided in patients with adrenocorticoid deficiency?

A

Etomidate

312
Q

What are the causes of hypoaldosteronism?

A
  • Congenital deficiency of aldosterone synthase
  • Hyporeninemia
  • unilateral adrenalectomy
313
Q

When is hypoaldosteronism suspected?

A

-When the patient has hyperkalemia but no renal insufficiency

314
Q

What metabolic condition could be due to hypoaldosteronism?

A

Hyperchloremic metabolic acidosis

315
Q

What is the treatment for hypoaldosteronism?

A

Fludrocortisone

316
Q

What are the periop considerations for patients with hypoaldosteronism?

A
  • Patients may have heart block due to hyperkalemia and orthostatic hypotension
  • Consider volume status
317
Q

What is the pathophysiology of pheochromocytoma?

A

Tumor of the adrenal medulla causes an oversecretion of epi, norepi, and dopamine

318
Q

What are the symptoms of pheochromocytoma?

A

Sudden onset of malignant hypertension, tachycardia, arrhythmias, headache, perspiration

319
Q
Acromegaly is associated with an oversecretion of which hormone?
A) ACTH
B) TSH
C) GH
D) ADH
A

C) Growth Hormone

320
Q

What is the most common cause of acromegaly?

A

Adenoma in the pituitary gland

321
Q

What symptoms of acromegaly can make airway management difficult?

A
  • Enlarged tongue and epiglottis
  • Elongated mandible
  • Narrowed glottic opening
322
Q

What sized OETT may be best for an acromegalic patient?

A

A smaller OETT because of the increased incidence of subglottic stenosis

323
Q

What test should be performed before placing an a-line on an acromegalic patient?

A

Allen’s test

324
Q

What is the pathophysiology of diabetes insipidus?

A

Deficiency or resistance to vasopressin causing poor reabsorption of water by the kidneys

325
Q

What are the symptoms of diabetes insipidus?

A
  • Extreme thirst (polydypsia)

- Dilute urine

326
Q

What are the periop considerations for patients with diabetes insipidus?

A

Watch for electrolyte imbalances like high Na+ and low K+/Mg2+

327
Q

What is diabetes mellitus?

A

Chronic disease caused by abnormal glucose metabolism that results in long-term morbidity

328
Q

What organ is the primary source of endogenous glucose?

A

Liver

329
Q

What is a normal Hemoglobin A1C?

A) Less than 6%
B) Less than 8 %
C) Less than 10%
D) Less than 15%

A

A. Less than 6%

330
Q

What is the function of beta cells in the pancreas?

A

Secrete insulin when blood glucose levels are high

331
Q

What is the function of alpha cells in the pancreas?

A

Secrete glucagon when blood glucose levels are low

332
Q

What is the function of delta cells in the pancreas?

A

Secrete somatostatin upon food ingestion and inhibits insulin, glucagon, growth hormone, etc to extend the time over which food nutrients are put into the blood

333
Q

What is the sympathetic innervation supplying the pancreas?

A

T5-T10, causes insulin inhibition and glucagon stimulation

334
Q

What is the parasympathetic innervation supplying the pancreas?

A

Innervation via the vagus to cause insulin release

335
Q

What is the function of insulin?

A
  • Triggers glucose transport into the cells for usage by the cells
  • Stimulates protein and lipid synthesis
336
Q

Is insulin required for brain utilization of glucose?

A

No

337
Q

What is the function of glucagon?

A
  • Increases glucose output from the liver
  • Stimulates glycogenolysis
  • Stimulates gluconeogenesis
  • Inhibits glycolysis
338
Q

What causes diabetes mellitus?

A

Decreased secretion of insulin from beta cells or increased resistance of receptors to insulin caused by either heredity or obesity

339
Q

What is Type I DM?

A
  • Immune related destruction of beta cells

- Insulin dependent

340
Q

What is Type II DM?

A

Insulin resistance, have normal to high plasma insulin levels but inappropriate for level of glucose

341
Q

What is gestational diabetes?

A

Glucose intolerance that first develops during pregnancy

342
Q

What is the classic triad of symptoms of diabetes melitus?

A

1) Polyurea
2) Polydypsia
3) Polyphagia (constant appetite)

343
Q

What are the acute complications associated with diabetes mellitus?

A
  • Diabetic ketoacidosis
  • Hyperosmolar coma
  • Hypoglycemia
344
Q

What are the long term complications associated with diabetes mellitus?

A
  • HTN
  • CAD
  • MI
  • CHF
  • Vascular disease
  • Neuropathy
345
Q

Patients with DM have a __ times greater risk of an MI perioperatively

A

20

346
Q

What preop testing should be done to avoid a periop MI in patients with DM?

A

EKG

347
Q

What symptoms of DM could indicate a difficult DL?

A

Stiff joint syndrome causes atlanto-occipital joint stiffness and possible TMJ stiffness

348
Q

Diabetic Ketoacidosis (DKA) is more common in patients with Type 2 Diabetes.

A) True
B) False

A

B) False

349
Q

What is the cause of diabetic ketoacidosis?

A

Decreased insulin activity causes the metabolism of free fatty acids and the accumulation of organic acid by products

350
Q

What is often the first manifestation of type I DM in adolescents?

A

Infection

351
Q

What are the clinical signs of diabetic ketoacidosis?

A
  • Kussmal breathing
  • Dehydration
  • N/V
  • BS 320-330
  • Polyuria
  • Ketones in urine
  • Fatigue
  • Altered mental status
352
Q

What is the treatment of diabetic ketoacidosis?

A
  • Correct hypovolemia with normal saline
  • Correct hyperglycemia with insulin
  • Correct electrolyte deficiencies
353
Q

What is a hyperosmolar nonketotic coma?

A

When hyperglycemia diuresis results in dehydrations and hyperosmolality

354
Q

What are the symptoms of hyperosmolar nonketotic coma?

A
  • Glucose over 600
  • No acidosis or ketones
  • Thirst
  • Confusion
355
Q

What is the treatment for hyperosmolar nonketotic coma?

A
  • Hypotonic saline

- Low dose insulin

356
Q

What causes hypoglycemia?

A

Excessive insulin relative to carbohydrate intake

357
Q

Which type of diabetes does hypoglycemia most often occur?

A

Type I

358
Q

Hypoglycemia is defined as a blood glucose less than __ mg/dL

A

50

359
Q

What are the symptoms of hypoglycemia?

A
  • Catecholamine discharge causing agitation, diaphoresis, tachycardia
  • Mental status changes
360
Q

Which type of diabetes is managed with regular insulin therapy?

A

Type I

361
Q

What is the only insulin that can be given IV?

A

Regular insulin

362
Q

How soon before surgery should metformin be discontinued?

A

24 hours

363
Q

Which insulin drug has a rapid onset?

A

Novalin

364
Q

Which insulin drug is intermediate?

A

Humalin

365
Q

Which drugs given to diabetics stimulates insulin secretion?

A

Sulfonylureas like tolazamide and tolbutamide

366
Q

Which drugs given to diabetics inhibit gluconeogenesis?

A

Biguanidines

367
Q

What biguanide is considered first line therapy in obese type II patients who dont respond to diet and exercise?

A

Metformin (glucophage)

368
Q

What are the four major classes of oral hypoglycemic agents? What are their MOAs?

A

1) Secretagogues (sulfonylureas) - increase insulin availability
2) Biguanides (Metformin) - suppress glucose release
3) Glitazones - improve insulin sensitivity
4) Alpha glucosidase inhibitors (Acarbose) - delay GI glucose absorption

369
Q

Hemoglobin 1Ac levels greater than __% indicate poor glycemic control

A

10

370
Q

Patients with hypoglycemia may have drug interactions with which classes?

A
  • Steroids
  • Catecholamines
  • Beta blockers
371
Q

What are the risks during induction of hypoglycemic patients?

A
  • Dramatic drop in BP

- Gastric aspiration risk

372
Q

How can you assess for autonomic neuropathy of the parasympathetic nervous system in hypoglycemic patients?

A

Valsalva maneuver or watch for sinus arrhythmia

373
Q

What is normal heart rate variability during voluntary deep breathing?

A

Greater than 10 beats per minute

374
Q

When should you treat high glucose levels intraoperatively?

A

Greater than 150

375
Q

How do you calculate the number of insulin units to give patients with high glucose intraop?

A

(Blood sugar-100)/40

376
Q

Insulin administration will decrease what serum electrolyte?

A

K+

377
Q

How often should you check blood glucose when administering insulin intraop?

A

Every hour

378
Q

What is the starting infusion rate for insulin?

A

0.1 units/kg/hour

379
Q

How much does 1 unit of insulin lower blood sugar?

A

25-30 mg/dL

380
Q

Carcinoid syndrome is caused by tumors in the GI tract that release massive amounts of what substances?

A
  • Serotonin

- Histamine

381
Q

What are the symptoms of carcinoid syndrome?

A
  • Flushing
  • Diarrhea
  • Hypotension
382
Q

What are the anesthetic considerations for patients with carcinoid syndrome?

A
  • A line
  • Zofran
  • Octreotide
383
Q

What drugs commonly given by anesthetists can cause a carcinoid crisis?

A
  • Succinylcholine
  • Atracurium
  • Epi
  • Norepi
384
Q

What are the 6 significant risk factors for a postoperative cardiac event?

A

1) High risk surgery
2) Ischemic heart disease
3) Creatinine over 2.0
4) History of TIA or CVA
5) Type I Diabetes
6) History of CHF

385
Q

Patients having __ or more risk factors are considered at an elevated risk for a postop cardiac event

A

2

386
Q

What are the indications for a pre-op 12 lead ECG?

A
  • CAD
  • PAD
  • Arrhythmias
  • Cerebrovascular disease
387
Q

What pre-op test gives us a good assessment of left ventricular function?

A

Echo

388
Q

A pre-op echo is reasonable for patients with what symptoms and medical histories?

A
  • Dyspnea of unknown origin
  • CHF with worsening dyspnea
  • Previous LV dysfunction
389
Q

ECG exercise testing requires the ability to exercise enough to get the heart rate up to __% of age predicted maximum

A

75%

390
Q

What is the dipyridamole-thallium stress test?

A

Assess for at risk areas by redistributing myocardial perfusion

391
Q

What is the range of positive predictive values for ischemic events with the dipyridamole-thallium stress test?

A

4-20%

392
Q

What is the dobutamine stress echo?

A

Assess for new regional wall motion abnormalities with increased heart rate

393
Q

What 3 components make up the preoperative cardiac assessment according to ACC/AHA guidelines?

A

1) Clinical predictors
2) Functional capacity
3) Surgical risk

394
Q

What are considered “active cardiac conditions” according to ACC/AHA guidelines?

A

1) Recent MI
2) Decompensated heart failure
3) Significant arrhythmias
4) Severe valvular disease

395
Q

What are considered high risk surgeries according to ACC/AHA guidelines?

A

1) Emergencies
2) Aortic and major vascular surgeries
3) Prolonged surgeries with large fluid shifts/loss

396
Q

What are considered intermediate risk surgeries according to ACC/AHA guidelines?

A

1) Carotid endarterectomy
2) Head/neck surgeries
3) Intraperitoneal/intrathoracic
4) Orthopedic
5) Prostate

397
Q

What are considered low risk surgeries according to ACC/AHA guidelines?

A

1) Endoscopic procedures
2) Superficial procedures
3) Cataracts
4) Breast
5) Ambulatory

398
Q

What activities are considered 1 MET?

A
  • Eat, dress, walk around house

- Walk 1 or 2 blocks on ground level

399
Q

What activities are considered 4 MET?

A
  • Climb 1 flight of stairs
  • Walk on level ground at 4mph
  • Heavy house work
  • Golf
  • Dance
400
Q

What activities are considered 10 MET?

A
  • Swim
  • Run
  • Aerobic exercise
401
Q

When is CABG indicated according to ACC/AHA guidelines?

A
  • Stable angina and L main stenosis
  • Stable angina and 3-vessel CAD
  • Stable angina and 2-vessel CAD with LAD stenosis and EF less than 50%
402
Q

Use of beta blockers in patients with CAD has shown an increased risk of what periop events?

A

Bradycardia and stroke

403
Q

Which beta blocker has been associated with an increased risk of stroke?

A

Metoprolol

404
Q

Patients with __ or more RCRI risk factors may need to begin beta blockers before surgery

A

3

405
Q

Why are ACE inhibitors usually held on the morning of surgery?

A

To prevent intraop hypotension

406
Q

What AAR monitoring is necessary for all aortic cases?

A
  • ASA standard monitoring
  • Large IV access
  • A line
407
Q

What AAR monitoring is necessary for patients with good LV function?

A

Central venous line

408
Q

What AAR monitoring is necessary for patients with poor LV function?

A
  • PA catheter

- TEE

409
Q

What are the renal affects caused by infrarenal aortic cross clamping?

A
  • Reduction in renal blood flow

- Reduced GFR

410
Q

What should be monitored during and after clamping of infrarenal aorta to assess renal function?

A

Urine output

411
Q

What diuretics should be considered during an infrarenal aortic cross-clamping?

A

Mannitol and furosemide

412
Q

What are the hemodynamic changes during clamping of the aorta?

A

Increase in catecholamines leading to venoconstriction which causes increased preload, afterload, and contractility

413
Q

What are the hemodynamic changes after the unclamping of the aorta?

A
  • Decrease myocardial contractility
  • Central hypovolemia
  • Decrease venous return
  • Decrease cardiac output
  • Hypotension
414
Q

Neuraxial anesthesia with abdominal aortic surgeries for post op pain relief has been found to decrease what postop incidence?

A

MI

415
Q

What IV access should be obtained for an infrarenal aortic endostent graft surgery?

A
  • Large IV access

- A-line

416
Q

What anesthetic techniques can be used for an infrarenal aortic endostent graft surgery?

A
  • Local
  • Regional
  • General
417
Q

What are the symptoms of anterior cord ischemia?

A

Loss of motor function, pain, and temperature sensation

418
Q

What are the symptoms of posterior cord ischemia?

A

Loss of proprioception and fine touch

419
Q

What are the hemodynamic changes associated with clamping of the thoracic aorta?

A
  • Shift of blood volume to the brain
  • Increased ICP
  • Decrease spinal cord perfusion
420
Q

What airway device should be used for an open thoracic aneurysm repair?

A

Double lumen ETT

421
Q

A spinal drain is used during an open thoracic aneurysm repair to keep CSF pressure less than __ mmHg

A

10

422
Q

What drugs should be administered during an open thoracic aneurysm repair for spinal cord protection?

A

Steroids

423
Q

Carotid endarterectomies are more prevalent for patients with which risk factors?

A
  • Angina
  • HTN 180/110
  • CHF
  • A fib
  • Over 75 y/o
  • Diabetes
  • Renal insufficiency
424
Q

What are the standard monitoring used in carotid endarterectomies?

A
  • Standard ASA
  • 5 lead ECG
  • A line
425
Q

Patients that had an rSO2 decrease by more than __% presented with neurological symptoms

A

30

426
Q

What are the advantages of regional anesthesia for a carotid endarterectomy?

A
  • Can keep patient awake to monitor cerebral function
  • Less hemodynamic variation
  • No postop sedation to confuse evaluation
427
Q

What are the advantages of general anesthesia for a carotid endarterectomy?

A
  • No patient movement
  • Control of airway
  • Can control CO2
  • Can provide HTN during clamping
428
Q

What physiologic states can increase cerebral protection during carotid endarterectomies?

A

1) HTN
2) Hemodilution
3) Hypothermia
4) Normoglycemia
5) Normocarbia

429
Q

What anesthetic drugs can increase cerebral protection during carotid endarterectomies?

A

1) Barbituates
2) Volatile agents
3) Propofol

430
Q

What are the symptoms of hyperperfusion syndrome?

A
  • Ipsilateral headache
  • Seizures
  • Focal neurologic signs
431
Q

What factors increase the risk of hyperperfusion syndrome?

A
  • Severe ICA stenosis
  • HTN
  • Contralateral ICA stenosis
432
Q

How should perfusion pressure be maintained before and during aortic crossclamping?

A

Maintain high pressures

433
Q

After aortic surgeries there should be close monitoring post-op for what issues?

A

1) Hypotension
2) Neck hematoma
3) Hyperperfusion syndrome