ACE 8A Flashcards

1
Q

Regarding tocolytics: What class of drugs are contraindicated for additional tocolysis when magnesium sulfate is already being used?

A

Calcium channel blockers

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2
Q

Regarding tocolytics: What are the maternal side effects of calcium-channel blocking drugs?

A
  • Transient hypotension (with sequelae such as nausea, dizziness)
  • Flushing
  • HA
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3
Q

Regarding tocolytics: What class are NOT associated with fetal/neonatal side effects?

A

Calcium channel blocking drugs

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4
Q

Name four classes of tocolytics.

A
  • Calcium-channel blockers
  • Cyclooxygenase inhibitors (NSAIDs)
  • Beta-agonists
  • Magnesium
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5
Q

Regarding tocolytics: What conditions are contraindications for NSAID use as tocolytics?

A

A lot of common sense things here….

  • Significant renal/hepatic impairment
  • PUD
  • coag disorders/thrombocytopenia
  • NSAID-sensitive asthma
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6
Q

Regarding tocolytics: What are the fetal/neonatal side effects of NSAIDs?

A
  • PDA constriction
  • pulmonary HTN
  • reversible renal impairment
  • oligohydramnios (2/2 above renal impairment)
  • hyperbilirubinemia
  • +/- intraventricular hemorrhage (data is mixed)
  • +/-NEC (data is mixed)
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7
Q

Regarding tocolytics: What maternal conditions are contraindications to beta-agonist use?

A
  • Poorly controlled DM
  • Poorly controlled thyroid dz
  • cardiac dysrhythmias
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8
Q

Regarding tocolytics: What are the fetal side effects of maternal beta-agonist use?

A
  • tachycardia
  • hyperinsulinemia
  • hyperglycemia
  • myocardial and septal hypertrophy
  • myocardial ischemia
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9
Q

f c0-9p90-Regarding tocolytics: What are the neonatal side effects of maternal beta-agonist use?

A

This is actually different from the fetal side effects in many ways:

  • tachycardia (same as fetal)
  • hypoglycemia
  • hypocalcemia
  • hyperbilirubinemia
  • hypotension
  • intraventricular hemorrhage
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10
Q

Regarding tocolytics: What are the fetal/neonatal side effects of maternal magnesium sulfate use?

A
  • Lethargy
  • hypotonia
  • respiratory depression
  • demineralization (with prolonged use)
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11
Q

Regarding tocolytics: What maternal conditions are contraindications to magnesium sulfate use?

A
  • Myasthenia gravis
  • Myotonic dystrophy
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12
Q

Regarding tocolytics: What are the maternal side effects of magnesium sulfate?

A
  • Flushing
  • lethargy
  • HA
  • weakness
  • diploplia
  • dry mouth
  • pulmonary edema
  • cardiac arrest
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13
Q

What valvular anomaly is associated with constriction of the ductus arteriosus in a fetus?

A

Tricuspid regurgitation

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14
Q

What percentage of fetal cardiac output comes out of the right ventricle?

A

59%. (Thus 41% comes out of the left ventricle).

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15
Q

What percentage of combined ventricular output flows through the fetal pulmonary artery?

A

11%

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16
Q

What is it about congestive heart failure that causes increased production and release of brain-natriuretic peptide?

A

Stretch of atrial and ventricular cardiac myocytes

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17
Q

What is a normal value of BNP?

A

0 - 99

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18
Q

What value of BNP is consistent with heart failure?

A

Any value in excess of 100.

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19
Q

What is the gold standard for diagnosis of heart failure?

A

Echocardiography (…BNP values are generally used to follow the progression of CHF and the responsiveness of CHF to interventions)

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20
Q

Describe NYHA functional classification Class 1.

A

No symptoms and no limitation in ordinary physical activity.

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21
Q

Describe NYHA functional classification Class 2.

A

Mild symptoms and slight limitation during ordinary activity. COMFORTABLE AT REST.

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22
Q

Describe NYHA functional classification Class 3.

A

Marked limitation in activity due to symptoms, even during less-than-ordinary activity. Comfortable ONLY at rest

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23
Q

Describe NYHA functional classification Class 4.

A

Severe limitations. Experiences symptoms even while at rest.

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24
Q

What is the appropriate endotracheal tube position in a patient with bronchopleural fistula?

A

The tube should be placed in the mainstem of the unaffected side (regardless of whether single or double lumen is used) with position confirmed via FOB.

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25
Q

What is the recommended position of the patient with an infected bronchopleural fistula?

A

Head-up position with the side of the fistula in the dependent position will help minimize cross-contamination.

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26
Q

What nerve provides sensation to the plantar aspect of the foot?

A

posterior tibial nerve

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27
Q

What are the branches of the posterior tibial nerve and where does it divide?

A

The posterior tibial nerve divides as it passes through the flexor retinaculum.

It becomes the medial and lateral plantar nerves.

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28
Q

What is entrapment of the posterior tibial nerve called?

A

Tarsal tunnel syndrome (neuropathic pain in the feet analogous to carpal tunnel syndrome in the hands)

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29
Q

What nerve provides innervation to the web space between the 1st and 2nd toes?

A

Deep peroneal nerve

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30
Q

What innervates the dorsum of the foot?

A

The superficial peroneal nerve.

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31
Q

What nerve innervates the lateral foot?

A

The sural nerve.

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32
Q

List the Mapleson systems in greatest to least efficiency for prevention of rebreathing during spontaneous ventilation.

A

A > D = F > C > B

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33
Q

List the Mapleson systems in greatest to least efficiency for prevention of rebreathing during controlled ventilation.

A

D = F > B > C > A

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34
Q

Name this circuit.

A

Mapleson A

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35
Q

Name this circuit.

A

Mapleson C

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36
Q

Name this circuit.

A

Mapleson D

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37
Q

Name this circuit.

A

Mapleson F (Jackson Rees)

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38
Q

What is the minimum fasting period for breast milk? For formula?

A

Breast milk = 4 hours

Formula = 6 hours

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39
Q

During what perioperative period are adults and children most likely to aspirate?

A

Adults = emergence/extubation

Children = induction

Note: this is just a matter of likelihood, as anyone can aspirate anywhere, anytime. I aspirated a Chipotle burrito in California once. It was very tasty. My lungs said “gracias”.

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40
Q

Under what age are children at greater risk of aspiration?

A

Less than 3 years of age.

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41
Q

Is bradycardia or tachycardia a predictive indicator of a SEVERE allergic reaction?

A

Bradycardia

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42
Q

Why is immediate IV fluid adminstration vital for treatment of anaphylaxis?

A

Because increased vascular permeablity can lead to transfer of 50% (fifty!) of intravascular volume into the interstitium.

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43
Q

During anaphylaxis, what drug should be used in the event that epinephrine fails to achieve hemodynamic instability?

A

Vasopressin should be used in this condition which is called Anaphylactic Shock Refractory to Catecholamines.

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44
Q

A decelerating flow pattern is characteristic of what types of ventilation?

A

pressure support and pressure control

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45
Q

What type of ventilation is associated with these waveforms?

A

Assist control (volume targeted)

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46
Q

What type of ventilation is associated with these waveforms?

A

Controlled mandatory ventilation

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47
Q

What type of ventilation is associated with these waveforms?

A

Pressure controlled ventilation

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48
Q

What type of ventilation is associated with these waveforms?

A

Pressure support ventilation

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49
Q

What is the formula for left ventricular stroke work index?

A

LVSWI = (MAP – PAOP) x SVI x 0.0136 g • m • m–2

where

LVSWI = left ventricular stroke work index

SVI = stroke volume index

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50
Q

What is the formula for right ventricular stroke work index?

A

RVSWI = (MPAP – CVP) x SVI x 0.0136 g • m • m–2

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51
Q

Blockade of what nerve roots is required to prevent pain from traction on the uterosacral ligaments or bladder during c-section?

A

L5 - S4

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52
Q

What is the uppermost spinal level of entry of intraabdominal visceral pain afferents?

A

T2

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53
Q

Pain sensations from the pelvic organs enter the spinal cord at what levels?

A

T10 - L1 (although some pelvic nerves accompany sympathetic fibers to go as high as T4 – hence the higher level of neuraxial block needed for c-section)

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54
Q

What class(es) of neuromuscular blockers can cause histamine release?

A

Benzylisoquinoliniums, and succinylcholine.

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55
Q

What neuromuscular blockers block cardiac muscarinic receptors?

A

Pancuronium > Rocuronium. (Vecuronium does not)

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56
Q

What neuromuscular blocker blocks autonomic ganglia?

A

d-Tubocurarine

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57
Q

Name five physiologic effects of histamine.

A
  • Positive chronotropy (via H2 receptors)
  • positive or negative inotropy depending circumstances
  • coronary artery effects:
    • H1 = vasoconstriction
    • H2 = vasodilation
  • peripheral vasodilation
  • bronchospasm
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58
Q

What type of histamine receptor causes vasoconstriction of the coronary arteries?

A

H1

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59
Q

What type of histamine receptor causes vasodilation of the coronary arteries?

A

H2

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60
Q

What type of histamine receptor causes positive chronotropy?

A

H2

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61
Q

How does epidural analgesia affect maternal core temperature?

A

It increases it gradually over several hours! (typically less than 1°C total, but is also associated with a higher incidence of maternal fever during labor)

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62
Q

What is echothiophate?

A

It is an acetylcholinesterase inhibitor (organophosphate) that can be used as an eyedrop to lower IOP.

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63
Q

What is isoflurophate?

A

It is an acetylcholinesterase inhibitor (organophosphate) that can be used as an eyedrop to lower IOP.

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64
Q

What is xalatan?

A

It is a prostaglandin used as an eyedrop to lower IOP by increasing uveoscleral outflow of aqueous humor.

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65
Q

Patients receiving topical betablockers are at risk of developing what hemodynamic complication?

A

Exaggerated hypotension

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66
Q

What is the “mainstay” of hypercalcemia treatment?

A

Normal saline infusion.

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67
Q

Name the cardiovascular complications of lupus.

A

Pericarditis

Hypertension

CAD

Myocarditis

AS, MS, AR, MR

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68
Q

What are the pulmonary complications of lupus?

A

Pleural effusions

pHTN (2/2 recurrent pulmonary emboli)

Interstitial lung dz (rarely severe)

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69
Q

What are the renal complications of SLE?

A

Hematuria, proteinuria

nephrotic syndrome

rapidly progressive glomerulonephritis (rare)

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70
Q

What are the CNS consequences of SLE?

A

cerebral vasculitis

cognitive dysfxn

seizures

affective disorders

carotid artery dz

stroke

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71
Q

What are the hematologic consequences of SLE?

A

anemia

leukopenia

thrombocytopenia

antiphospholipid antibodies

recurrent pulmonary emboli

thromboses

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72
Q

Why might a pulse oximeter not work on a person with SLE?

A

Poor blood flow in the digits 2/2 vasospasm

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73
Q

What type of heat transfer is the most important cause of heat loss in the perioperative setting?

A

Radiation (which is why skin surface warming is the most effective way to decrease radiant heat loss)

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74
Q

A healthy subject has indwelling arterial catheters simultaneously transducing pressure from the brachial, radial, femoral, and dorsalis pedis arteries. Which catheter is likely to record the HIGHEST systolic pressure?

A

Dorsalis pedis

(because there are more branch points in the vasculature on the way there than at the other locations resulting in greater signal amplification)

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75
Q

What is another name for 15-methylprostaglandin F2alpha?

A

Hemabate

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76
Q

List the regional block locations according to their associated plasma local anesthetic concentrations from greatest concentration to least concentration.

A

Greatest concentration

Intercostal

Caudal

Lumbar epidural

Brachial plexus

Peripheral nerve

SubQ

Least Concentration

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77
Q

EMLA cream is a combination of what local anesthetics at what concentration?

A

Lidocaine and prilocaine, each at 2.5%

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78
Q

What does eutectic mean?

A

It refers to a mixture of substances whose melting point is lower than that of either of constituents alone. EMLA cream is an example of a eutectic mixture.

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79
Q

What is the metabolite of prilocaine responsible for methemoglobinemia?

A

O-toluidine

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80
Q

What age group is particularly susceptible to methemoglobinemia?

A

Infants < 3 -4 months of age

because their nicotinamide adenin dinucleotide methemoglobin reductase levels are only 50% of adult values at birth and do not reach adult levels until 3 - 4 months of age.

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81
Q

What type of receptors does dobutamine affect?

A

beta1 and, to a lesser extent, beta2 agonism

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82
Q

What effect does dobutamine have on afterload?

A

It reduces SVR thus decreases afterload.

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83
Q

Does dobutamine increase or decrease systemic blood pressure?

A

Unpredictable. Since dobutamine increases contractility and CO but also decreases SVR, it depends on how things play out between these two sides.

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84
Q

What receptors does norepinephrine affect?

A

alpha and beta1 (agonism)

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85
Q

What are the side effects of supraclavicular block?

A

Phrenic nerve block

Horner’s

pneumothorax (0.5% -5% with risk being experience-dependent)

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86
Q

What is the site of needle insertion for supraclavicular block without ultrasound guidance?

A

1cm superior to midpoint of clavicle which places it lateral to the clavicular head of the sternocleidomastoid.

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87
Q

What is normal P50 of oxygen-hemoglobin in adults?

A

26.7mmHg

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88
Q

Will hypothermia cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

left shift

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89
Q

Will alkalosis cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

left shift

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90
Q

Will decreased 2,3-DPG cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

left shift

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91
Q

Will fetal hemoglobin cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

left shift

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92
Q

Will carboxyhemoglobin cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

left shift

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93
Q

Will methemoglobin cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

left shift

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94
Q

Will hyperthermia cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

right shift

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95
Q

Will acidosis cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

right shift

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96
Q

Will increased 2,3-DPG cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

right shift

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97
Q

Will increased CO2 cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

right shift

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98
Q

Will pregnancy cause a left or right shift of the oxygen-hemoglobin dissociation curve?

A

right shift

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99
Q

What are some causes of hypovolemic hyponatremia?

A

Diarrhea

Diuretics

Cerebral salt wasting

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100
Q

What are some causes of normovolemic hyponatremia?

A

SIADH

Adrenal insufficiency

Hypothyroidism

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101
Q

What are some causes of hypervolemic hyponatremia?

A

cirrhosis

heart failure

nephrotic syndrome

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102
Q

If a patient is hyponatremic but has normal serum osmolality (280 - 300 mOsm), what is the differential?

A

Hyperlipidemia

Hyperproteniemia

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103
Q

If a patient is hyponatremic but has high serum osmolality (>300 mOsm), what is the differential?

A

Hyperglycemia

Hypertonic sodium-free solutions

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104
Q

If a patient is hyponatremic but has low serum osmolality (280 - 300 mOsm) and low urine sodium (<20mmol/L), what is the diagnosis?

A

water intoxication

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105
Q

If a patient is hyponatremic but has low serum osmolality (280 - 300 mOsm) and high urine sodium (>20 mmol/L), what is the differential?

A

If the patient is hypovolemic:

  • cerebral salt wasting
  • diarrhea
  • diuretics

If the patient is normovolemic:

  • SIADH
  • Adrenal insufficiency
  • Hypothyroidism

If the patient is hypervolemic:

  • cirrhosis
  • heart failure
  • nephrotic syndrome
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106
Q

Describe the effect of obstructive shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Obstructive shock

HR increased

MAP decreased

CVP increased

PAOP increased

SVR increased

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107
Q

Describe the effect of hypovolemic shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Hypovolemic shock

HR increased

MAP decreased

CVP decreased

PAOP decreased

SVR increased

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108
Q

Describe the effect of isolated RV failure cardiogenic shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Isolated RV failure cardiogenic shock

HR increased

MAP either increased or decreased

CVP increased

PAOP normal

SVR increased

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109
Q

Describe the effect of isolated LV failure cardiogenic shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Isolated LV failure cardiogenic shock

HR increased

MAP either increased or decreased

CVP normal

PAOP increased

SVR increased

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110
Q

Describe the effect of biventricular failure cardiogenic shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Biventricular failure cardiogenic shock

HR increased

MAP increased or decreased

CVP increased

PAOP increased

SVR increased

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111
Q

Describe the effect of early distributive shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Early distributive shock

HR increased

MAP decreased

CVP decreased or normal

PAOP decreased or normal

SVR decreased

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112
Q

Describe the effect of late distributive shock on HR, MAP, CVP, PAOP, and SVR (in terms of increase, decrease, or remains normal).

A

Late distributive shock

HR increased

MAP decreased

CVP increased or normal

PAOP increased or normal

SVR decreased

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113
Q

Describe how spinal shock may differ hemodynamically from all other forms of shock.

A

All forms of shock seem to be associated with tachycardia. In spinal shock, the HR could be decreased from normal.

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114
Q

Equalization of diastolic pressures and filling pressures is consistent with what pathological event?

A

Cardiac tamponade

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115
Q

In severe preeclampsia, what is the goal reduction of BP in terms of percentage?

A

No more than 15 - 20% reduction.

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116
Q

What is first line therapy for treatment of blood pressure in preeclampsia?

A

Labetalol and hydralazine

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117
Q

What nerve innervates the palmar aspect of the thumb?

A

Median nerve

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118
Q

What innervates the fifth digit and the intrinsic muscles of the hand?

A

ulnar nerve

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119
Q

Where is the ulnar nerve usually in relation to the axillary artery?

A

inferior (ulnar is under)

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120
Q

Where does the median nerve tend to lie in relation to the ulnar nerve in the axilla?

A

superior and superficial to the ulnar nerve

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121
Q

What nerve is subject to injury in a midhumeral fracture?

A

radial nerve

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122
Q

What innervates the dorsal webspace between the thumb and forefinger?

A

The radial nerve

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123
Q

The musculocutaneous nerve provides motor innervation to what muscles?

A

biceps brachii

coracobrachialis

brachialis

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124
Q

What nerve provides sensation to the lateral forearm?

A

musculocutaneous nerve

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125
Q

What provides sensory innervation to the medial hand and fifth digit?

A

ulnar nerve

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126
Q

What nerve provides sensory innervation to most of the palmar hand?

A

Median nerve (with the exception of the medial aspect of the hand which is provided by the ulnar nerve)

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127
Q

Which fingertips are innervated by the radial nerve?

A

None! The finger tips both dorsal and palmar are innervated by the median nerve (thumb - lateral half of ring finger) and the ulnar nerve (medial half of ring finger - pinky).

The radial nerve does innervate part of the dorsum of the proximal thumb and the dorsum proximal fingers.

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128
Q

What nerve provides somatic innervation to the perineum and pelvic floor?

A

pudendal nerve

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129
Q

What nerve innervates the distal two thirds of the vagina?

A

pudendal nerve

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130
Q

what nerve provides somatic innervation of the anus?

A

pudendal nerve

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131
Q

Neurolytic blockade of what nerve will affect control of urinary and anal sphincters?

A

pudendal nerve

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132
Q

What is the anatomical range of the visceral afferents contained by the celiac plexus?

A

From the distal esophagus to the splenic flexure of the colon. But NOT the body wall in the peritoneum.

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133
Q

What visceral afferents pass through the superior hypogastric plexus?

A

uterus, bladder, rectum (but NOT anal skin, perineum, or pelvic floor muscles–those go through the pudendal nerves).

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134
Q

What visceral afferents do the lumbar sympathetic ganglia contain?

A

They don’t. They contain efferent sympathetic fibers to the lower extremities.

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135
Q

What pressure in cm H20 is associated with compromised capillary blood flow in the tracheal mucosa?

A

> 30 cm H20

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136
Q

What is the single most important patient attribute affecting the risk of developing PDPH?

A

Patient age. Younger > older. Highest risk in late teens or early twenties.

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137
Q

Regarding risk of PDPH: is a higher or lower opening pressure at the time of dural puncture associated with PDPH?

A

A lower opening pressure is associated with a slight increase in risk for PDPH.

138
Q

Regarding risk of PDPH: Is a higher or lower BMI associated with an increased risk of PDPH?

A

lower BMI is associated with slight increase in risk

139
Q

What type of headache is associated with an increased risk of PDPH?

A

Chronic history of bilateral tension headaches. NOTE: there is NO association with a history of migraine headaches.

140
Q

Does a history of migraine headaches increase or decrease the risk of PDPH?

A

Neither. Migraine headaches have NO statistically significant association with PDPH.

141
Q

How does menstrual cycle affect the development of PDPH?

A

There is no association between menstrual cycle and PDPH.

142
Q

Does a history of PDPH have any bearing on risk of future PDPH?

A

Yes! Patients who have developed a prior PDPH are at a significantly increased risk of developing a PDPH.

143
Q

What are the two types of organic pain?

A

Neuropathic

Nociceptive

144
Q

What causes nociceptive pain?

A

Stimulation of nociceptors in visceral or somatic structures by things like pancreatitis, trauma, and cancer.

145
Q

What causes neuropathic pain?

A

Damage to or dysfunction of normal pain pathways involving afferent neural pathways. Diabetic peripheral neuropathy, MS, CNS injury, neuralgias, traumatic nerve injury, nerve entrapment are all causes of neuropathic pain.

146
Q

Why type of organic pain is involved in complex regional pain syndrome type II?

A

neuropathic pain

147
Q

What urine sodium level is consistent with the diagnosis of an intrarenal etiology for oliguria?

A

urine sodium > 40 mEq/L

148
Q

What urine specific gravity is consistent with the diagnosis of an intrarenal etiology for oliguria?

A

1.010-1.015

149
Q

What urine osmolality is consistent with the diagnosis of an intrarenal etiology for oliguria?

A

Urine osmolality < 350 mOsm/kg

150
Q

What FeNa is consistent with the diagnosis of an intrarenal etiology for oliguria?

A

FeNa > 2%

151
Q

What urinalysis finding is consistent with the diagnosis of an intrarenal etiology for oliguria?

A

casts on urinalysis (as well as gross proteinuria and gross hematuria)

152
Q

What urine specific gravity is consistent with a prerenal cause for oliguria?

A

> 1.020

153
Q

What urine osomolality is consistent with pre-renal oliguria?

A

> 500 mOsm

154
Q

What is formula for estimated weight by age?

A

Estimated weight in Kg = [ageyears x 2] + 10

155
Q

What is the sequence of treatment for a newborn whose heart rate is less than 60?

A

Chest compressions, consider intubation, monitor SpO2

If compressions fail to incr HR > 100, give epinephrine.

If HR < 60 despite resuscitation w/ lower FiO2, FiO2 should incr to 100% until HR returns to normal.

156
Q

How must a newborn present for a practitioner to provide only routine care immediately after birth?

A

Breathing, pink in color, HR > 100.

157
Q

If a newborn is breathing but cyanotic and has a HR > 100 what should the provider do?

A

Verify airway is clear

Measure SpO2 from a preductal location (right upper extremity)

consider CPAP

Titrate supplemental O2 to targeted preducal O2 sats

158
Q

When should vasopressin or atropine be used as part of the Neonatal resuscitation guidelines?

A

Neither drug is a part of the AHA Neonatal Resuscitation guidelines.

159
Q

Normal plasma cholinesterase is inhibited by dibucaine to what extent?

A

80% of normal plasma cholinesterase is inhibited by dibucaine. If the dibucaine number is 80, the patient is normal.

160
Q

What is the dibucaine number in a patient homozygous for atypical plasma cholinesterase.

A

Dibucaine 20

161
Q

Why does red blood cell transfusion in a premature neonate ultimately result in a lower Hgb concentration at the nadir of physiologic anemia?

A

The increased levels of Hgb A right-shift the O2-Hgb dissociation curve making more O2 available to the tissues resulting in decreased stimulus for erythropoeitin production.

162
Q

What is the average Hgb concentration in umbilical cord blood at birth in a healthy term neonate?

A

16.8 g/dL

163
Q

How does red blood cell survival compare between a neonate and an adult?

A

Neonates have shortened survival of 80 - 100 days vs an adult’s 120 days.

164
Q

At what age is the nadir in physiologic anemia of the neonate?

A

8 - 12 weeks

165
Q

What is the lowest normal value for the nadir of physiologic anemia in the neonate?

A

8 - 9 g/dL

166
Q

Why is the anemia of prematurity more profound than the physiologic anemia of the healthy, term neonate?

A

The red blood cell survival in the premature is 60 - 80 days which is even less than that of the term neonate (80 - 100). Additionally, premature infants tend to lose blood due to recurrent phlebotomy

167
Q

What effect does nitrous oxide have on CBF and ICP?

A

it markedly increases both

168
Q

What effect does xenon have on CBF and ICP?

A

It decreases CBF to gray matter, increases it to white matter, and either increases or leaves ICP unchanged.

169
Q

What effect do barbiturates have on CBF and ICP?

A

markedly decrease both

170
Q

What effect does etomidate have on CBF and ICP?

A

markedly decreases both

171
Q

What effect does propofol have on CBF and ICP?

A

markedly decreases both

172
Q

What effect does ketamine have on CBF and ICP?

A

markedly increases CBF, and increases ICP, sometimes markedly.

173
Q

What effect do benzodiazepines have on CBF and ICP?

A

decrease CBF

decrease or don’t affect ICP

174
Q

What effect do synthetic opioids have on CBF and ICP?

A

may cause slight decrease or increase in CBF

may cause slight increase ICP

but may leave both unchanged.

175
Q

What effect does dexmedetomidine have on CBF and ICP?

A

decreases CBF

leaves ICP unchanged

176
Q

What effect does isoflurane have on CBF and ICP?

A

increases or leaves CBF unchanged

may increase ICP

177
Q

What effect does sevoflurane have on CBF and ICP?

A

it may decrease, not affect, or slightly increase CBF and ICP

178
Q

What effect does desflurane have on CBF and ICP?

A

It will either increase or decrease CBF

it may increase ICP or leave it unchanged.

179
Q

What is the primary effect of mannitol on ICP and CPP?

A

decreases ICP

thereby increasing CPP

180
Q

What type of stabilization is recommended for direct laryngoscopy in a patient with possible cervical spine injury?

A

Manual in-line stabilization

181
Q

What effect do isoflurane, sevoflurane, desflurane and halothane have on hepatic blood flow?

A

Iso, Sevo, and Des maintain total hepatic and arterial blood flow while portal vein flow is increased.

Halothane decreases hepatic blood flow.

182
Q

What level of [HCO3] is consistent with metabolic acidosis?

A

< 20 mEq/L

183
Q

If you know the values of PaCO2 and pH, what equation can you use to calculate the bicarbonate concentration?

A

Henderson-Hasselbalch

184
Q

What mechanical event and phase of the cardiac cycle corresponds to a wave of the central venous waveform?

A

atrial contraction marking end diastole

185
Q

What mechanical event and phase of the cardiac cycle corresponds to c wave of the central venous waveform?

A

closure of TV, isovolumic ventricular contraction w/ motion of the tricuspid valve toward the RA

This markes early systole

186
Q

What mechanical event and phase of the cardiac cycle corresponds to v wave of the central venous waveform?

A

systolic filling of the atrium

corresponds with late systole

187
Q

What mechanical event and phase of the cardiac cycle corresponds to h wave of the central venous waveform?

A

diastolic plateau

marks mid to late diastole

188
Q

What mechanical event and phase of the cardiac cycle corresponds to the x descent of the central venous waveform?

A

atrial relaxation, descent of the base, systolic collapse

corresponds with mid systole

189
Q

What mechanical event and phase of the cardiac cycle corresponds to y descent of the central venous waveform?

A

early ventricular filling, diastolic collapse

corresponds with early diastole

190
Q

Draw a normal CVP tracing and label its components.

A

The central venous pressure (CVP) waveform consists of 3 positive components (a, c, and v) and 2 negative deflections (x and y).

  • a wave represents atrial contraction in systole
  • x descent reflects the fall in right atrial pressure following this event.
  • c wave reflects closure of the tricuspid valve with isovolumic ventricular contraction and motion of the tricuspid valve toward the right atrium.
  • v wave occurs during late systole and is generated by filling of the atrium.
  • y descent is caused by the fall in right atrial pressure after the tricuspid valve opens and the initiation of passive filling of the right ventricle.
  • At slow heart rates, an h wave, occurring between the y descent and the a wave, may be detectable; the h wave represents continued right atrial filling during diastole.

Correlation of the electrocardiographic (ECG) with the central venous pressure waveform is required to correctly identify these events.

191
Q

What rhythm creates this CVP tracing?

A

Atrial fibrillation.

Note the absence of the a wave, a prominent c wave, and a preserved v wave and y descent.

This arrhythmia also causes variation in the ECG R-R interval and left ventricular stroke volume, which can be seen in the ECG and arterial pressure (ART) traces.

192
Q

What rhythm creates this CVP tracing?

A

Isorhythmic atrioventricular dissociation.

In contrast to the normal end-diastolic a wave in the CVP trace (left panel), an early systolic cannon wave is inscribed (*, right panel). Reduced ventricular filling accompanying this arrhythmia causes decreased arterial blood pressure.

193
Q

What rhythm causes this CVP tracing?

A

Ventricular pacing.

Systolic cannon waves are evident in the CVP trace during ventricular pacing (left panel). Atrioventricular sequential pacing restores the normal venous waveform and increases arterial blood pressure (right panel). The ART scale is shown on the left; the CVP scale is on the right.

194
Q

What causes this CVP tracing?

A

Tricuspid regurgitation.

In TR, RA pressure increases and tall, prominent v waves occur in conjunction with loss of the x descent as blood is regurgitated into the right atrium during ventricular systole. The v wave is followed by a steep y descent, caused by the presence of an increased pressure gradient across the tricuspid valve, which allows rapid inflow into the right ventricle. The regurgitant wave of tricuspid regurgitation occurs concurrently with the carotid upstroke.

TR increases mean CVP, and the waveform displays a tall systolic c-v wave that obliterates the x descent.

(In this example the a wave is not seen because of atrial fibrillation.) Right ventricular end-diastolic pressure is estimated best at the time of the ECG R wave (arrows) and is lower than mean CVP.

195
Q

What causes this CVP tracing?

A

Tricuspid stenosis

TS increases mean CVP, the diastolic y descent is attenuated, and the end-diastolic a wave is prominent.

196
Q

What is Brown-Séquard syndrome?

A

Occurs with unilateral danage to the spinal cord. Ipsilateral weakness, loss of vibratory sensation, and proprioception with contralateral loss of pain and temperature sensation

197
Q

How does Guillain-Barre syndrome present?

A

Gradually progressive weakness typically over weeks usually accompanied by paresthesia and often back pain.

198
Q

Describe the mortality rate of a Stanford type A aortic dissection once symptoms begin if left untreated.

A

Left untreated, the mortality rate is 1 - 2% per hour after intial onset of symptoms for the first 48 hours.

199
Q

Describe the pathophysiology of amniotic fluid embolism.

A

Not a true embolic event, but rather caused by significant pulmonary artery vasospasm. Thought to be anaphylactoid in nature but not yet truly understood.

200
Q

What uterotonic drug is likely contraindicated in a patient with amniotic fluid embolism who also has uterine atony?

A

Hemabate (prostaglandin F2-alpha) because can produce pulmonary hypertension.

201
Q

What pH is associated with fetal acidemia?

A

pH < 7.2

202
Q

What is the difference between anterior and posterior ischemic optic neuropathy?

A

anterior refers to ischemia of the optic disc.

posterior refers to ischemia of the retrobulbar portion of the optic nerve

203
Q

What causes anterior ischemic optic neuropathy?

A

watershed infarct of the short posterior cilary arteries. It causes painless vision loss.

204
Q

Anterior ischemic optic neuropathy is associated with what type of surgery and when does it present?

A

AION is associated with cardiac surgery and presents 24 - 48 hours postoperatively.

205
Q

Posterior ischemic optic neuropathy is associated with what type of surgery and when does it normally present?

A

Associated with spine and neck surgeries and noted immediately upon awakening from anesthesia.

206
Q

How do the fundoscopic exams for AION and PION differ?

A

Anterior ischemic optic neuropathy demonstrates a pale edematous optic disc.

Posterior ION has a normal fundoscopic exam.

207
Q

What causes painful ischemic optic neuropathy?

A

An arteritic ION caused by temporal arteritis.

208
Q

How does cortical blindness differ from posterior ischemic optic neuropathy?

A

Both cortical blindness and PION have normal fundoscopic exams, but only PION has abnormal afferent papillary reflexes.

(AION also has abnormal afferent papillary reflexes, but the fundoscopic exam of AION is also abnormal and demonstrates a pale edematous optic disc).

209
Q

At what age does closing capacity equal FRC?

A

44 years in the supine position. 66 years in the upright position.

210
Q

What is Lambert-Eaton myasthenic syndrome (LEMS)?

A

LEMS is a presynaptic conidition caused by Ab to calcium channels of both motor and autonomic nerves.

It is most often associated with small-cell bronchogenic carcinoma as a paraneoplastic syndrome

211
Q

What pathology is Lambert-Eaton syndrome most often associated with?

A

Small-cell bronchogenic carcinoma

LEMS (Lambert-Eaton myasthenic syndrome) is most often a paraneoplastic syndrome.

212
Q

What is the pathophysiology of Lambert-Eaton syndrome?

A

A decreased release of Ach as a result of Ab to Ca+2 channels of both motor and autonomic nerves.

213
Q

What are salient features of LEMS (Lambert-Eaton myasthenic syndrome)?

A
  • proximal limb weakness (legs > arms)
  • increased strength with activity
  • muscle pain
  • decreased deep tendon reflexes
  • autonomic dysfunction
  • ptosis
  • increased sensitivity to both depolarizing and non-depolarizing muscle relaxants
  • resistance to anticholinesterases
214
Q

What muscles are most affected by Lambert-Eaton syndrome?

A

proximal muscles with legs more affected than arms

215
Q

What type of neuromuscular blocking drug is recommended for use with Lambert-Eaton syndrome?

A

No neuromuscular blocker is recommended (i.e.,the recommendation is “don’t use one”). If one is used, decreased doses are recommended.

216
Q

How does Lambert Eaton syndrome affect sensitivity to anticholinesterases?

A

Patients are resistant to anticholinesterases

217
Q

What is the first-line treatment for Lambert-Eaton syndrome?

A

Potassium channel blocker 3,4-diaminopyridine (3,4-DAP)

(it should be continued up to surgery and throughout the perioperative period).

218
Q

In a parturient with HOCM, is neuraxial anesthesia allowed or contraindicated?

A

Epidural anesthesia is generally safe provided that slow careful titration of the local anesthetic occurs.

Single-injection spinal is relatively contraindicated due to the rapid onset sympathectomy.

219
Q

What is the most common genetic cause of life-threatening obesity in children?

A

Prader-Willi syndrome

220
Q

What are the genetics and inheritance behind Prader-Willi syndrome?

A

abnormality in the 15th chromosome that produces an altered metabolism of fat and carbohydrates.

Thought to be autosomal recessive.

221
Q

What are the physical findings and signs of Prader-Willi syndrome?

A
  • Obesity
  • Short stature
  • low muscle tone (incl difficulty swallowing)
  • hypogonadism
  • endocrine abnormalities
  • developmental delays
  • Hyperphagia (love love love to eat, making them comply with NPO can be very difficult)
  • Behavior problems
222
Q

What are the airway concerns in Prader-Willi syndrome?

A

Difficult airway (OSA, micrognathia, viscous saliva, high-arched palate, poor dentition, small-for-age airway 2/2 growth hormone deficiency)

High aspiration risk due to weak muscles (weak ability to cough and swallow)

Chronic regurgitation of gastric contents (airway changes, poor dentition)

223
Q

What is Pickwickian syndrome?

A

Obesity hypoventilation syndrome:

  • Severe obesity
  • chronic hypoxemia
  • pHTN
  • right-sided heart strain
224
Q

What are the pain management concerns in Prader-Willi syndrome?

A

PWS patients show decreased response to painful stimuli (aka elevated pain threshold).

(Helpful in decreasing analgesic requirements but can also mask serious problems that in normals are heralded by pain).

225
Q

What endocrine abnormalities are associated with Prader-Willi syndrome?

A

Diabetes mellitus

hypogonadism

labile glucose levels

hypothyroidism

GH deficiency

226
Q

Should a patient with Prader-Willi get stress dose steroids?

A

No, they should not get stress dose steroids just because they’re Prader-Willi.

Because despite being hypothalamic, GH deficiency does not alter cortisol release in response to stress.

227
Q

Why type of glucose levels are expected perioperatively in Prader-Willi patients?

A

Labile levels with risk of hypoglycemia.

Because their metabolic disturbance results in a tendency to use circulating glucose to produce fat instead of applying it to basal metabolic needs.

228
Q

How does Prader-Willi affect thermoregulation?

A

Hyperthermic disturbances have been described.

229
Q

What are the recommendations for postoperative monitoring in pediatric patients with Prader-Willi syndrome?

A
  • recovery overnight in a monitored unit (either the pediatric recovery room or pediatric intensive care unit) for infants and children with PWS who undergo deep sedation or general anesthesia
  • continuous pulse oximetry monitoring for 24 hours after surgery
  • initial administration of reduced doses of opioids
  • a conservative start of oral intake 2/2 predisposition to postoperative ileus
  • direct supervision (1:1) to prevent postoperative foraging
  • monitoring for picking at wounds.
230
Q

What does the sciatic nerve branch to in the popliteal fossa?

A

Tibial and common peroneal nerves

231
Q

What does the tibial nerve branch in to?

A

medial and lateral plantar nerves

a branch to cutaneous sural nerves

muscular branches to the calf

articular branches to the ankle

232
Q

What structure does the common peroneal nerve follow?

A

It follows the fibula.

233
Q

What are the major and terminal branches of the common peroneal nerve?

A

terminal branches are superficial and deep peroneal nerves

also branches to the knee joint

cutaneous branches to the sural nerve

234
Q

A popliteal block is performed as the primary anesthetic for repair of an Achilles tendon rupture. During the surgery the patient begins to complain of pain along the medial aspect of his ankle. What nerve needs to be blocked and where should the injection occur?

A

the saphenous nerve

It may be blocked at the level of the tibial tuberosity a few centimeters below the patella with about 5–10 mL of local anesthetic injected subcutaneously in a ring starting at the medial surface of the tibial condyle and ending at the dorsomedial aspect of the upper calf.

235
Q

If the saphenous nerve needs to be blocked for anesthesia of the medial aspect of the foot alone, where should the injection occur?

A

Local anesthetic injected subcutaneously just above the level of the medial malleolus then posteriorly to the Achilles tendon and anteriorly to the tibial ridge should accomplish blockade of the saphenous nerve at this level.

236
Q

What provides sensation to the posterior lateral aspect of the foot and ankle?

A

The sural nerve

237
Q

What provides sensation to the dorsal aspect of the foot and lateral aspect of the ankle?

A

superficial peroneal nerve

238
Q

What nerve innervates the majority of the sole of the foot and what areas are the exceptions?

A

The posterior tibial nerve

Exceptions are the far lateral and heel area (sural)

and the far medial area (saphenous)

239
Q

Name the nerves that provide sensation to the different colored areas in this picture.

A
240
Q

What nerve provides sensation to the area indicated by the arrows?

A

Peroneal nerve (L4 - S2)

241
Q

What nerve provides sensation to the area indicated by the arrows?

A

Deep peroneal nerve

242
Q

What nerve provides sensation to the area indicated by the arrows?

A

Sural nerve (S1 - S2)

243
Q

What nerve provides sensation to the area indicated by the arrows?

A

Calcaneal nerve (S1 - S2 part of tibial nerve)

244
Q

What nerve provides sensation to the area indicated by the arrows?

A

Medial plantar nerve (L4 - L5)

245
Q

What nerve provides sensation to the area indicated by the arrows?

A

Superficial peroneal nerve (L5 - S1)

246
Q

What nerve provides sensation to the area indicated by the arrows?

A

Saphenous nerve (L3 - L4)

247
Q

What nerve provides sensation to the area indicated by the arrows?

A

Obturator nerve (L2 - L4, cutaneous branch)

248
Q

What nerve provides sensation to the area indicated by the arrows?

A

(anterior cutaneous) Femoral nerve (L2 - L3 contributions)

249
Q

What nerve provides sensation to the area indicated by the arrows?

A

Posterior femoral cutaneous nerve (S1 - S3)

250
Q

What nerve provides sensation to the area indicated by the arrows?

A

Lateral femoral cutaneous nerve (L2 - L3)

251
Q

What nerve provides sensation to the area indicated by the arrows?

A

Ilioinguinal nerve (L1)

The chart says genital branch of the genitofemoral nerve (L1 - L2) but this isn’t correct. The genital branch of the genitofemoral nerve provides skin sensation to the bottom of the scrotum and handles the cremaster reflex in men, and innervates the round ligament of the uterus labia majora sensation in women.

252
Q

What nerve provides sensation to the area indicated by the arrows?

A

Femoral branch of the genitofemoral nerve

(aka lumboinguinal branch of genitofemoral nerve, L1 - L2)

253
Q

What nerve provides sensation to the area indicated by the arrows?

A

Cluneal nerve

(posterior division of L1 - L3)

254
Q

What nerve provides sensation to the area indicated by the arrows?

A

Iliohypogastric nerve - lateral cutaneous branch (L1)

255
Q

What is R-time and what does it reflect?

A
  • R-time is the measure of the time from beginning of the test until beginning of clot formation
  • Reflects coagulation factor activity
256
Q

What is K-time and what does it reflect?

A
  • K-time measures the time from start of clot formation to the point at which the curve reaches a 20-mm amplitude
  • Reflects clot kinetics
257
Q

What is alpha-angle and what does it reflect?

A
  • Alpha-angle is the angle between the baseline and tangent to the TEG curve drawn through the point at which coagulation starts (R-time end point)
  • Reflects the acceleration and kinetics of fibrin formation as well as the process of fibrin cross-linking
258
Q

What is MA? What does it reflect? What particular factors does it depend on?

A
  • MA is a direct measure of the highest point on the TEG curve
  • Represents clot strength and is an indication of platelet function
  • Dependent on platelet concentration, function, and platelet-fibrin interaction
259
Q

What is LY30 and what does it reflect?

A
  • LY30 is the difference in amplitude between the MA and A30 (amplitude 30 minutes after MA)
  • Reflects fibrinolysis activity
260
Q

What is A30?

A

It is the amplitude 30 minutes after the occurence of the maximal amplitude.

261
Q

What local anesthetic is most likely to cause TNS after spinal?

A

lidocaine (It is NOT dose-dependent, NOR baricity dependent)

262
Q

What is the best treatment for TNS after spinal anesthesia?

A

NSAIDs are most effective

263
Q

What is the natural history of TNS after spinal anesthesia?

A

Self-limited. Symptoms begin 24 hours after uneventful spinal anesthesia and usually dissipate within 72 hours.

264
Q

Considering pKa alone, what is the relationship between a local anesthetic’s pKa and onset of action?

A

lower pKa = faster onset time

265
Q

What local anesthetic has the highest pKa of those used commonly?

A

2-chloroprocaine (pKa = 9.1)

The reason it has such a fast onset when we use it in OB is because we administer using both high concentration (3%) and high dose (which we get away with due to its low systemic toxicity).

266
Q

What is the primary determinant of a local anesthetic’s potency?

A

lipid solubility (the more lipid soluble, the more potent)

267
Q

What is the primary determinant of a local anesthetic’s duration of action?

A

protein binding

Local anesthetics work by binding to a protein receptor in the sodium channel of the nerve membrane. The greater the degree of protein binding of a local anesthetic, the longer it will bind to the channel and produce neural blockade.

268
Q

What is the goal plateau pressure when ventilating someone with ARDS?

A

< 30cm H20

because it reduces risk of VILI, reduces ICU mortality, reduces length of ventilation

269
Q

What is the goal tidal volume for ventilating someone with ARDS?

A

typically < 6 ml/kg based on predicted body weight

(with goal plateau pressure < 30 cm H20)

270
Q

What is the physiologic reasoning behind using low-tidal volume ventilation in a patient with ARDS?

A

attempts to minimize additional lung damage by preventing stretch injury to relatively healthy lung units (those units with compliance greater than the more diseased lung units).

271
Q

Where does baclofen act?

A

GABAB receptors pre- and post- synaptically

272
Q

Where do benzodiazepines act?

A

GABAA receptor (agonism)

273
Q

Define allodynia.

A

Pain due to a stimulus that does not normally provoke pain.

274
Q

What is reflex sympathetic dystrophy?

A

Complex regional pain syndrome type 1 (formerly reflex sympathetic dystrophy): A syndrome that usually develops after an initiating noxious event, is not limited to the distribution of a single peripheral nerve, and is apparently disproportionate to the inciting event.

275
Q

What physical exam findings is complex regional pain syndrome type 1 associated with?

A

It is associated at some point with evidence of edema, changes in skin blood flow, abnormal pseudomotor activity in the region of the pain, or allodynia or hyperalgesia.

276
Q

What is causalgia?

A

Complex regional pain syndrome type 2 (formerly causalgia): A syndrome of sustained burning pain, allodynia, and hyperpathia following a traumatic nerve lesion, often combined with vasomotor dysfunction and later trophic changes.

277
Q

Define hyperalgesia.

A

An increased response to a stimulus that is normally painful.

278
Q

Define neuralgia.

A

Pain in the distribution of a nerve or nerves generally in the absence of sensorimotor changes.

279
Q

What is the tell-tale difference between neurogenic claudication (pseudoclaudication) and vascular claudication?

A

Neurogenic (aka pseudo) claudication rapidly clears with rest, whereas vascular claudication often persists after stopping exercise.

Neurogenic claudication is caused by spinal stenosis.

280
Q

What happens to deep tendon reflexes in spinal stenosis?

A

They decrease.

281
Q

What positions attenuate the fatigue and pain of lumbar spinal stenosis?

A

any flexed position that opens the spinal canal (bike riding, bending forward, walking UPhill)

282
Q

What particular ambulatory activity worsens the pain and fatigue of lumbar spinal stenosis?

A

Walking DOWNhill

283
Q

What is a patient at risk for with a QRS duration > 160ms?

A

Ventricular dysrhythmias (risk > 50%)

284
Q

A patient is on amitriptyline and has a QRS > 100ms. What is the drug of choice to treat this?

A

Sodium bicarbonate

285
Q

How does sodium bicarbonate work as a therapy for TCA toxicity?

A

1) increase sodium gradient across neurons helping overcome blockade of sodium channels
2) elevates pH which keeps the TCA in neutral form (which can’t bind to cardiac sodium channels)

286
Q

Describe the drug-drug interaction between SSRIs and TCAs.

A

SSRIs (especially prozac) inhibit the metabolism of TCAs and can result in toxic TCA levels

Can also result in excessive central serotonin leading to serotonin syndrome.

287
Q

Aside from skin, where does angioedema primarily occur?

A

Mucous membranes primarily of the respiratory tract and bowel.

288
Q

What deficiency causes hereditary angioneurotic edema?

A

C1 esterase inhibitor deficiency (results in increased permeability with subsequent extravasation of plasma).

289
Q

What is the difference between Cinryze and Berinert P?

A

Both of these are concentrates of C1 esterase inhibitor. Berinert P is effective in the treatment of acute attacks in patients with hereditary angioneurotic edema. Cinryze is not.

290
Q

What is ecallantide?

A

An inhibitor of plasma kallikrein that results in symptomatic improvement in acute angioedema but is associated with anaphylaxis so needs to be administered by a physician in an setting that can deal with that potential complication.

291
Q

What is the approach to the airway in a patient with a history of hereditary angioneurotic edema presenting for a routine surgery?

A

Avoid airway manipulation entirely if feasible. Otherwise give:

  • Attenuated androgens (anabolic steroids) 2 days before surgery
  • C1 esterase inhibitors 24 hours before surgery
  • Fresh frozen plasma 6–12 hours before surgery
292
Q

What is Laplace’s law?

A

T = Pr/2h

Laplace’s law states that wall tension is proportional to pressure (P) and chamber radius (r) and inversely proportional to wall thickness (h)

293
Q

What is the effect of ventricular hypertrophy on ventricular wall tension?

A

It DECREASES it.

Laplace’s Law:

Tension = (Pressure x chamber radius) / (2 x wall thickness)

294
Q

What effect does epidural labor analgesia on uteroplacental blood flow?

A

Either no change or an increase.

295
Q

What is the justification for doing a caudal block over a dorsal nerve of penis block for elective circumcision?

A

There really isn’t any. DNBP showed no difference from caudal re: incidence of PONV nor the need for rescue medications for pain. The only difference found is greater risk of motor block/lower extremity weakness with caudal as compared with DNBP.

296
Q

By how much does caudal analgesia decrease the liklihood of PONV as compared to parenteral opioids for elective circumcision?

A

None. Caudal doesn’t have a lower incidence of PONV.

297
Q

How does SVR compare during pregnancy vs non-pregnancy?

A

SVR is decreased by 20% during pregnancy as compared to nonpregnant values.

298
Q

What physiologic factors cause the decrease in SVR seen during pregnancy?

A

1) development of a low-resistance placental vascular bed
2) vasodilatory effects of hormons like prostacyclin, estrogen, and progesteron

299
Q

How does intravascular fluid volume at term during pregnancy compare to non-pregnancy?

A

Intravascular fluid volume is increased by 35%.

300
Q

What causes the physiologic anemia of pregnancy?

A

The disproportionate increase in both plasma volume and red cell mass. Both increase, but plasma volume increases by 45% while red cell mass increases by 20%.

301
Q

How does CVP change during pregnancy?

A

It doesn’t. The increased venous capacitance during pregnancy offsets the increase in plasma volume.

HOWEVER femoral venous pressure typically increases by 15% during pregnancy – probably due to IVC compression by the gravid uterus

302
Q

To what extent does CO change during pregnancy broken down by the components of cardiac output?

A

CO increases throughout pregnancy to 40-50% above nonpregnany values at term.

SV increases by 30% (mostly in the 3rd trimester)

HR increases by 15 - 25% (beginning in early pregnancy)

303
Q

How does systemic blood pressure change during pregnancy?

A

Systemic (systolic, mean, and diastolic) blood pressure decreases during the first half of pregnancy, then returns toward baseline closer to term.

System blood pressure DOES NOT increase despite increases in CO and plasma volume because those changes are offset by the decrease in SVR.

304
Q

How does minute ventilation change during pregnancy?

A

By almost 50% during the 1st trimester continuing until delivery.

305
Q

How doe tidal volume and respiratory rate change during pregnancy?

A

TV increases by 40%

RR increases by 15%

306
Q

What factor has been shown to stimulate the respiratory drive and minute ventilation during pregnancy?

A

Elevated level of serum progesterone

307
Q

When do lung volumes begin to change during pregnancy?

A

3rd - 5th month

308
Q

How does FRC change during pregnancy?

A

It declines by 20 - 30% from prepregnancy values by term (this is in the upright position) due to the uterus pushing the diaphragm cephalad.

309
Q

How do total lung capacity and vital capacity change during pregnancy?

A

TLC stays the same (or only slightly decreases).

VC does not change.

310
Q

How does pregnancy affect closing capacity?

A

It doesn’t. Closing capacity remains relatively unchanged but due to the decrease in FRC, CC may exceed FRC during pregnancy.

311
Q

What pharmacologic agent is considered initial treatment for stable monomorphic VT according to ACLS recommendations?

A

Amiodarone IV

312
Q

If a patient is in stable monomorphic VT but no amiodarone is available, what are two acceptable pharmocologic alternatives according to ACLS?

A

Procainamide

Sotalol

(Although lidocaine has historically been the drug of choice for treatment of stable VT, current evidence suggests that other agents, including amiodarone, are more effective than lidocaine in this situation.)

313
Q

What medication is used for treatment of torsade de pointes?

A

IV magnesium

314
Q

What is the first intervention for witnessed ventricular fibrillation?

A

a single shock should be delivered with immediate resumption of cpr.

315
Q

When should vasopressors such as epinephrine or vasopressin be used during VF?

A

Indicated only after VF persists after failure of 1 or 2 episodes of defibrillation with ongoing chest compressions.

316
Q

Define odds ratio.

A

The odds ratio is the ratio of the odds of an outcome (e.g, pain) among the exposed group (e.g., those who had a paravertebral block) to the odds of the outcome (pain) among the unexposed group (those who did not have the block).

317
Q

What is a log-rank test?

A

The log-rank test is used in Kaplan-Meier analysis of time-to-end-point data to test for the statistical significance of changes in hazard rates. It is not useful in the analysis of categorical data.

318
Q

What are categorical data?

A

Categorical data are those that fall into distinct categories such as the presence of pain (yes/no). This is in contrast to continuous data, such as the severity of pain, that fall along a continuum (4.5 on a 0–10 scale).

319
Q

What are continuous data?

A

Continuous data, such as the severity of pain, fall along a continuum (4.5 on a 0–10 scale).

Categorical data are those that fall into distinct categories such as the presence of pain (yes/no).

320
Q

When is a chi-square test used?

A

The chi-square test statistic is used to compare the association of 2 categorical variables. A chi-square test will provide the probability that a large association arose by chance.

321
Q

In what patient population does neurogenic pulmonary edema occur and when does it occur?

A

Occurs in up to 20% of patient sith severe head injury commonly within the first hours of the injury.

322
Q

What physiologic factors contribute to the development of neurogenic pulmonary edema?

A
  • increased capillary permeability due to release of inflammatory mediators stimulated by disruption of the blood–brain barrier
  • increased transmural capillary pressures due to increased pulmonary artery pressures
  • impaired left ventricular function.
323
Q

What is the primary treatment of neurogenic pulmonary edema?

A

reduction of ICP

324
Q

What urine test can be used to help diagnose pheochromocytoma?

A

Metanephrine levels

325
Q

What urine test can be used to diagnose carcinoid syndrome?

A

Elevated levels of 5-hydroxyindoleacetic acid

326
Q

What are signs and symptoms of carcinoid syndrome?

A
  • cardiac lesions
  • intense flushing
  • diarrhea
  • wheezing
  • tachycardia
  • hyper or hypotension
  • abdominal pain
327
Q

What cardiac abnormalities occur in a patient with carcinoid syndrome?

A

More than half of patients have right-sided cardiac valve lesions including PS or TR 2/2 fibrosis of the endocardium.

328
Q

What humoral factor(s) is responsible for the diarrhea seen in carcinoid syndrome?

A

Serotonin

329
Q

What humoral factor(s) is responsible for the flushing and wheezing in carcinoid syndrome?

A

Release of many neurohumoral agents including histamine, substance P, vasoactive intestinal peptide, neurotensin, and somatostatin, is thought to be responsible for the flushing and wheezing.

330
Q

What drug should be given prior to surgery to a patient with carcinoid syndrome and for how long?

A

Octreotide (a somatostatin analogue) should be given for 24 - 48 hours before surgery and anesthesia and should be continued for the duration of the surgery.

331
Q

Describe emergence from anesthesia in a patient with carcinoid syndrome.

A

Patients with carcinoid syndrome might be slow to wake up after general anesthesia as increased serotonin levels have been associated with delayed awakening.

332
Q

What induction drug should be avoided in a patient with carcinoid syndrome?

A

Thiopental (… ketamine, too?)

333
Q

What neuromuscular blockers should be avoided in a patient with carcinoid syndrome?

A

Succinylcholine, atracurium, mivacurium

(Note: cisatracurium is considered safe)

334
Q

Which of desflurane, isoflurane, and sevoflurane should be avoided in a patient with carcinoid syndrome?

A

They are all considered safe.

335
Q

What is the first objective in assessment and treatment of a patient with delirium?

A

ensure that there are no significant physiologic derangements (eg, hypoxemia, hypoglycemia)

336
Q

What is the drug of choice to treat delirium?

A

Haloperidol (although there may be an emerging role for olanzapine, quetiapine, and risperidone)

337
Q

What is the only medication that is FDA approved for treatment of trigeminal neuralgia?

A

Carbamazepine, it is the gold standard for medical management.

338
Q

If medical management fails to treat trigeminal neuralgia, what is the next most appropriate therapy?

A

Local anesthetic blockade of the gasserian ganglion (aka trigeminal ganglion) (which could then be followed by glycerol ablative therapy if appropriate)

339
Q

What is a normal cardioplegia line pressure for retrograde cardioplegia?

A

10 - 40 mmHg

340
Q

Which has a higher risk of maternal mortality: Trial of Labor after C-section (TOLAC) or Elective Repeat Cesearean Delivery (ERCD)?

A

ERCD has a higher risk of maternal mortality

341
Q

Which has a higher risk of perinatal mortality: Trial of Labor after C-section (TOLAC) or Elective Repeat Cesearean Delivery (ERCD)?

A

TOLAC appears to have a higher risk of perinatal mortality.