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Patho > Exam 2 RA Cannabis Resp Psych > Flashcards

Exam 2 RA Cannabis Resp Psych Flashcards

1
Q

Length of time of tidal breathing to achieve an EtCO2 of 100%

A

4-5min

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2
Q

4 non-overlapping lung volumes:

A

1) inspiratory reserve volume (IRV)
2) tidal volume (Vt)
3) expiratory reserve volume (ERV)
4) residual volume (RV)

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3
Q

IRV=

A

inspiratory reserve volume = 3000mL

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4
Q

Vt=

A

tidal volume = 500mL
(dead space = about 150mL of that)

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5
Q

ERV=

A

expiratory reserve volume = 1100mL

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6
Q

RV=

A

residual volume = 1200mL

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7
Q

4 overlapping lung capacities:

A

1) inspiratory capacity (IC)
2) functional reserve capacity (FRC)
3) vital capacity (VC)
4) total lung capacity (TLC)

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8
Q

IC=

A

inspiratory capacity = IRV + Vt = 3500mL

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9
Q

FRC=

A

functional reserve capacity = ERV + RV = 1800mL

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10
Q

VC=

A

vital capacity = IRV + Vt + ERV = 4600mL

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11
Q

TLC=

A

total lung capacity = 5800mL

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12
Q

What two lung volumes can we actually quantify in real time?

A
  • Vt
  • dead space
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13
Q

How do you calculate dead space without drawing an ABG?

A
  • look at EtCO2
  • allow one full exhalation
  • look at EtCO2
  • calculate difference
  • the % difference in EtCO2 multiplied by Vt = dead space
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14
Q

What structures lie within the conducting zone?

A
  • trachea
  • bronchi
  • bronchioles
  • terminal bronchioles
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15
Q

What structures lie within the respiratory zone?

A
  • respiratory bronchioles
  • alveolar ducts
  • alveolar sacs
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16
Q

What occurs in the conducting zone?

A

movement of air

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17
Q

What occurs in the respiratory zone?

A

gas exchange

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18
Q

Describe the relationship between velocity of air movement and cross sectional area

A

inversely related

  • as CSA increases, the forward velocity of air decreases
  • decreased flow allows for diffusion of gas/deposition of pollutants
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19
Q

Air flow is turbulent in which airway structures?

A

upper airways:
- trachea
- lobar bronchi
- segmental bronchi

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20
Q

Air flow is laminar in which airway structures?

A

lower airways:
- conducting bronchioles
- terminal bronchioles

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21
Q

Ohms Law:

A

flow = change in pressure / resistance

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22
Q

Increasing Vt or RR has what effect on peak airway pressure?

A

increasing flow (Vt or RR) will increase the pressure gradient/peak airway pressure

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23
Q

Define peak airway pressure:

A

pressure in the airway with air flow = indicator of dynamic compliance of the lungs

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24
Q

Define plateau pressure:

A

pressure in the airway with no air flow = indicator of static compliance of the lungs

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25
Q

What effect does decreasing the tube radius have on resistance?

A

For laminar flow: magnified increase in resistance

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26
Q

Where is the highest resistance to flow in the respiratory system? Why?

A

trachea/bronchi:
- most turbulent (highest Re)
- lowest CSA
- transition from cartilage to smooth muscle

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27
Q

Plateau pressure correlates with which lung capacity?

A

FRC

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28
Q

Plateau pressure is associated with a (low/high) flow rate, (low/high) CSA, and (laminar/turbulent) flow

A
  • low flow rate
  • high CSA
  • laminar flow
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29
Q

Where is the lowest resistance to flow in the respiratory system? Why?

A

lower airways:
- laminar flow
- higher CSA
- smooth muscle to mucosae

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30
Q

You can control the radius of the upper airways by _____
You can control the radius of the lower airways by _____

A

upper: ETT size
lower: medications (Albuterol)

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31
Q

How do minute ventilation and alveolar ventilation differ?

A

MV = what you set on the ventilator = Vt x RR
VA = accounts for deadspace = (Vt-Vd) x RR

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32
Q

Normal amount of dead space:

A

2mL/kg or 150mL

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33
Q

Applying a mask to a patient (increases/decreases) dead space

A

increase (up to 300mL); “apparatus dead space”

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34
Q

Utilizing an ETT (increases/decreases) dead space

A

decreases (less anatomic dead space)

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35
Q

Insertion of a tracheostomy (increases/decreases) dead space

A

decreases (bypasses oral dead space)

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36
Q

Administration of glyco or atropine (increases/decreases) dead space

A

increases (more anatomic dead space d/t anticholinergic smooth muscle dilation in the conducting zone)

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37
Q

Dead space (increases/decreases) with age

A

increases

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38
Q

If a patient’s VCO2 increases, what must also increase proportionally?

A

alveolar ventilation

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39
Q

Phase I of a capnograph indicates

A

anatomic dead space

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40
Q

Phase 2 of a capnograph indicates

A

mixture of dead space and alveoli

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41
Q

Phase 3 of a capnograph indicates

A

gas exchange/effective alveolar ventilation

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42
Q

Phase 4 of a capnograph indicates

A

inspiration (drops off)

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43
Q

Which lung volume experiences the greatest change when a patient lays supine?

A

ERV decreases significantly –> decreases FRC

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44
Q

Apneic time for normal patient and for a supine/anesthetized/paralyzed patient

A

2 minutes for normal
3.5 minutes for supine/anesthetized/paralyzed

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45
Q

How does FRC change with induction?

A

-1L laying supine
-0.5L under anesthesia

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46
Q

Volume calculation for FRC

A

FRC = 34mL/kg

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47
Q

For a 40 y/o patient laying flat, how are FRC and CC related?

A

FRC=CC

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48
Q

Define closing capacity

A

the volume of gas within the lungs at the point at which airways closure begins; CV + RV

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49
Q

Equation/definition for compliance

A

compliance = volume / pressure
= the volume that can be achieved in the lungs per unit pressure change
(ability of the lungs to expand)

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50
Q

Equation/definition for elastance

A

elastance = pressure / volume
= the pressure change required to elicit a unit volume change
(measure of the resistance of lungs to expansion)

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51
Q

Describe the elastance and compliance of alveoli in geriatric/COPD patients

A
  • increased compliance
  • decreased elastance
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52
Q

Describe the elastance and compliance of the chest wall in geriatric/COPD patients

A
  • decreased compliance
  • increased elastance
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53
Q

Describe the elastance and compliance of alveoli in neonates/OB/pulmonary fibrosis patients

A
  • decreased compliance
  • increased elastance
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54
Q

Describe the elastance and compliance of the chest wall in neonates/OB/pulmonary fibrosis patients

A
  • increased compliance
  • decreased elastance
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55
Q

A pressure-volume loop is a graphical representation of what?

A

compliance versus elastance
- slope of the loop = static compliance / no air flow
- loop itself = dynamic compliance / inspiration & expiration

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56
Q

A pressure-volume loop that is laying down is indicative of what?

A

decrease in static compliance

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57
Q

A decrease in compliance is related to the (airway/alveoli)

A

alveoli

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58
Q

An increase in resistance is related to the (airway/alveoli)

A

airway

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59
Q

Definition of extrathoracic resistance

A

FEF is decreased
FIF is increased
FEF/FIF = 0.3

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60
Q

Definition of intrathoracic resistance

A

FEF is increased
FIF is decreased
FEF/FIF = 2.2

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61
Q

Source of extrathoracic resistance

A

pressures inside of trachea

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62
Q

Example of variable extrathoracic resistance

A

OSA
exhalation is OK, inhalation collapse of airway

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63
Q

Example of fixed extrathoracic resistance

A

epiglotitis

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64
Q

Source of intrathoracic resistance

A

pressures outside of trachea/bronchial tree

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65
Q

Example of variable intrathoracic resistance

A

tracheal malacia (usually is stented)
inhalation is OK; airway collapses on exhalation

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66
Q

Example of fixed intrathoracic resistance

A

tumor or mass or constriction (more dangerous)

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67
Q

Why are the volume-flow loops inverted on the ventilator

A

the vent measures inhalation as negative flow (out of the bag) away from the vent and exhalation as positive flow (fills the bag) back toward it

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68
Q

Gold standard for PFTs and assessing for disease

A

FEV1 = forced expiratory volume in 1 second

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69
Q

Define DLCO and when it is relevant

A

measurement of ability to transport CO2
- a decrease is reflective of emphysema
- 30% is when it is relevant

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70
Q

FEV1 is indicative of ____
DLCO is indicative of _____

A
  • FEV1 = bronchitis
  • DLCO = emphysema
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71
Q

PFT measurements indicative of obstructive lung disease

A
  • FVC increased
  • RV increased
  • FEF ratios decreased
  • FEV1/FVC <75%
  • DLCO 30% (emphysema)
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72
Q

PFT measurements indicative of restrictive lung disease

A
  • FVC decreased
  • RV decreased
  • FEV1/FVC >85%
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73
Q

What is the equation of motion of the respiratory system?

A

Paw = (volume x elastance) + (resistance x flow)

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74
Q

In VCV, what is set on the ventilator?

A
  • volume
  • flow
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75
Q

In VCV, what does Paw/Ppeak reflect?

A

the respiratory system

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76
Q

In VCV, a change in Paw/Ppeak indicates a change in _____

A

compliance and/or resistance

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77
Q

In PCV, what is set on the ventilator?

A

Paw/Ppeak

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78
Q

In PCV, what does Paw/Ppeak reflect?

A

settings on the ventilator

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79
Q

In PCV, changes in compliance and/or resistance will change _____

A

Vt and flow

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80
Q

What must you be conscious of when your ventilator is set to PCV?

A
  • Pmax is set to 40 and is “High Priority”, but you have set your Paw so you don’t really care
  • Vt and MV alarms are “Low Priority” and will not alert you to changes in the patient unless you are watching for them
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81
Q

PCV pressure waveform on the vent appears:

A

squared - it has a set pressure to achieve

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82
Q

VCV pressure waveform on the vent appears:

A

variable - the pressure reached with each breath changes but the delivered Vt is the same

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83
Q

PCV volume waveform on the vent appears:

A

triangular and variable - the volume achieved changes based on when Ppeak is met

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84
Q

VCV volume waveform on the vent appears:

A

triangular but consistent - the volume gradually increases but each delivered breath is the same

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85
Q

PCV flow waveform on the vent appears:

A

triangular and variable

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86
Q

VCV flow waveform on the vent appears:

A

squared - a set flow is delivered per breath and is not affected by effort, resistance, etc

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87
Q

In PCV-VG, what determines the Paw/Ppeak?

A
  • you set the volume
  • ventilator sets the Paw based on compliance
  • adjusts Pinsp based on compliance to achieve set volume
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88
Q

What parameters do you set in SIMV modes?

A
  • Vt
  • RR
  • PEEP
  • Pressure support
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89
Q

What parameters can be adjusted in “more settings” in SIMV?

A
  • flow trigger
  • Tinsp (I:E ratio)
  • Tpause
  • Trigger window %
  • End of breath % of peak flow
  • Rise rate
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90
Q

If you have a RR=10 and I:E of 1:2, what is your Tinsp and Texp?

A
  • Tinsp = 2 sec (20s / 10)
  • Texp = 4 sec (40s / 10)
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91
Q

What must you do to the Tinsp in synchronous modes if you increase your RR? Why?

A

adjust your Tinsp (under more settings) to achieve the I:E ratio you want - if you don’t, you risk breath-stacking the patient

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92
Q

In SIMV, what does a negative deflection in your pressure scalar indicate?

A

patient-initiated breath
(also should turn blue)

93
Q

What effect does increasing your trigger window % have?

A

increases the window in the expiratory phase so the vent is more likely to sense a patient-initiated breath and synchronize with both mandatory and initiated breaths

94
Q

What is the risk of adjusting the flow trigger?

A

it may falsely indicate that the patient is breathing enough and is ready for extubation

95
Q

Define End of Breath % of Peak Flow

A
  • stock setting = 30%
  • the lower you go, the longer the vent will support a patient-initiated breath
  • no real reason to change it
96
Q

Define Rise Rate

A
  • rate of breath delivery on a supported breath
  • range of 1-10
  • higher rise rate = faster breath delivery = sharper flow scalar
97
Q

To get a measurement for plateau pressure, what mode must you be in?

A

VCV

98
Q

How you find your plateau pressure in VCV?

A

reduce your RR and increase your Tpause (60%)

99
Q

In VCV, your Paw increases, but your Pplat stays the same. What does this mean?

A

increase in airway resistance with NO change in compliance

bronchospasm, mucous plug..

100
Q

In VCV, your Paw and Pplat both increase. What does this mean?

A

decrease in lung compliance

insufflation, Trendelenberg, high BMI, pneumothorax…

101
Q

The difference between PIP and Pplat indicates ____

A

resistance to flow

typically want it <10

102
Q

In PCV, what happens to the inspiratory limb of the flow curve when there is an increase in resistance?

A

taller and skinnier

103
Q

In PCV, what happens to the expiratory limb of the flow curve when there is an increase in resistance? Air trapping? Squiggly?

A
  • increased resistance = decreased flow
  • air trapping = doesn’t return to baseline
  • squiggly = obstruction/secretions
104
Q

On room air, what is the pressure of O2 in your lungs?

A

~100

105
Q

On 100% FiO2, what is the pressure of O2 in your lungs?

A

663

106
Q

What is the alveolar oxygen equation?

A

PAO2 = FiO2 (Pb-PH2O) - (PaCO2 / R)

107
Q

When calculating FRC you should use (IBW/TBW)

A

IBW

108
Q

When calculating total O2 needs, you should use (IBW/TBW)

A

TBW

109
Q

A PaO2 of 40 correlates with a SpO2 of ___

A

70

110
Q

A PaO2 of 50 correlates with a SpO2 of____

A

80

111
Q

A PaO2 of 60 correlates with a SpO2 of ___

A

90

112
Q

A PaO2 of 80 correlates with a SpO2 of ____

A

94

113
Q

SpO2 is calculated based on ____
SaO2 is calculated based on ____

A

SpO2 - light absorption
SaO2 - ABG analyzer, corrected for PaO2, temp, pH, HCO3-

114
Q

A leftward shift on the O2 dissociation curve indicates…

A

an increase in affinity of Hgb for O2

115
Q

A rightward shift on the O2 dissociation curve indicates…

A

a decrease in the affinity of Hgb for O2

116
Q

4 factors that cause a leftward shift in the O2 dissociation curve:

A

decreased
- temp
- CO2
- 2,3 DPG
- alkalosis
(fetal Hgb)

117
Q

4 factors that cause a rightward shift in the O2 dissociation curve:

A

increased
- temp
- CO2
- 2,3 DPG
- acidosis
(adult Hgb)

118
Q

Factors that can make your SpO2 inaccurate:

A
  • motion
  • low perfusion (systolic <80)
  • SpO2 < 70%
  • CO poisoning - falsely elevated
  • MetHgb - approaches 85% as it ^
  • NOT anemia unless significantly hypoxic
119
Q

Equation for O2 carrying capacity (CaO2)

A

CaO2 = (SaO2 x Hgb x 1.34) + (0.003 x PaO2)

120
Q

Define the P:F ratio

A

PaO2:FiO2 ratio
- Mild = 200-300
- Moderate = 100-200
- Severe < 100

121
Q

5 principle causes of hypoxia:

A

1) hypoxic mixture
2) hypoventilation
3) V/Q mismatch
4) shunt
5) diffusion impairment
the last 3 cause a A-a gradient

122
Q

Equation for delivered O2

A

DO2 = CO x CaO2

123
Q

Compare hypoxia to hypoxemia:

A
  • hypoxia means your SpO2 is low (but your CaO2 may be OK)
  • hypoxemia means your DO2 is low (d/t tissue deprivation, organ dysfxn)
124
Q

A shark fin appearance in the EtCO2 waveform indicates:

A

bronchoconstriction

125
Q

CO2 is transported in 3 main forms:

A

1) 7% dissolved in plasma
2) 23% carried by Hgb as carbaminohemoglobin
3) 70% as HCO3

126
Q

What equation describes dead space?

A

Enghoff’s equation

127
Q

Define shunt

A

perfusion of unventilated areas / gas exchange cannot occur

  • the part of the CO that returns to the L side of the heart without being ventilated

Va/Q = 0

128
Q

Define dead space

A

ventilation without perfusion

infinite Va/Q

129
Q

Vt should be based on (IBW/TBW)

A

IBW
(reduces lung injury)

130
Q

The majority of atelectasis occurs during which part of anesthesia?

A

within 5-10 minutes of induction

131
Q

What does the literature indicate is the most effective way to combat atelectasis?

A
  • FiO2 <0.6
  • VCM (+40cmH2O x 15sec)
  • PEEP (+10cmH2O)
132
Q

Define driving pressure

A
  • real time pressure the alveoli are experiencing
    = Pplat - PEEP
    ideally <15
133
Q

If you increase PEEP and perform VCM, and your driving pressure increases, what does this indicate?

A

lungs are overdistended

134
Q

If you increase PEEP and perform VCM, and your driving pressure decreases, what does this indicate?

A

lungs are recruitable

135
Q

If you increase PEEP and perform VCM, and your driving pressure is unchanged, what does this indicate?

A

you are in the linear portion of the compliance curve

136
Q

What was the tipping point for PEEP in the literature?

A

7

137
Q

2 most common causes of anesthesia related atelectasis

A

1) PEEP @ 5 (too low)
2) FiO2 >80% (too high)

138
Q

The source of rheumatoid arthritis is…

A

autoimmune

139
Q

Rheumatology accounts for what % of causes of disability in the US?

A

27% - making it #1

140
Q

3 potential causes of RA

A

1) genetics (50% risk)
2) hormonal influence
3) viral insult

141
Q

RA diagnosis typically occurs at what age?

A

40-50 years old
<40 3:1 female:male
>40 1:1 female:male

142
Q

Describe the pathogenesis of RA

A
  • injury to synovial endothelial cells (they are rich in Helper T cells that orchestrate cell mediated response)
  • cytokines released (tumor necrosis factor & interleukin-1)
  • necrosis of cartilage
  • joint narrowing
143
Q

4 stages of RA

A

1) synovitis
2) pannus (fibrous tissue)
3) fibrous ankylosis
4) bony ankylosis

144
Q

Effect of RA on mortality

A
  • 50% increased risk of premature death
  • 3-10 year reduction in lifespan
145
Q

RA joint symptoms

A
  • most commonly affects wrist/hand/knees/feet
  • morning stiffness
  • symmetrical swelling
  • possible C-spine involvement (esp. atlanto-axial subluxation)
146
Q

Body systems that RA can affect:

A
  • renal
  • hepatic
  • skin/eyes
  • lymphadenopathy
  • neuromuscular
  • hematological
147
Q

RA pulmonary effects

A
  • effusions
  • HTN
  • nodules
  • restrictive lung dz
  • resp myopathy
  • interstitial fibrosis
148
Q

RA cardiovascular effects

A
  • pericarditis
  • myocarditis
  • valvular dysfxn
  • vasculitis
  • conduction abnormalities
  • restrictive cardiomyopathy
  • accelerated coronary atherosclerosis
149
Q

Why are the CV risks associated with RA a significant contributor to mortality?

A
  • plaques more vulnerable to rupture
  • increased arterial stiffness
  • pro-thrombotic state
  • insulin resistance
150
Q

3 cardiac conditions that RA patients are at an increased risk for:

A
  • silent MI (6x)
  • sudden cardiac death (2x)
  • heart failure (2x)
    rheumatoid cachexia also increases CV mortality
151
Q

Define systemic lupus erythematosus

A

multi-system, chronic inflammatory disease characterized by antinuclear antibody production

152
Q

2 important groups that SLE affects most often:

A
  • young women (15-44)
  • women of color (2-3x)
153
Q

Proposed SLE theories:

A
  • genetics
  • drug-induced
  • viral (Epstein Barr)
  • hormones
154
Q

Which 2 associated conditions indicate a worse prognosis for patients with SLE?

A
  • nephritis
  • HTN
155
Q

SLE exacerbation during pregnancy has implications for…

A

poor fetal outcome

156
Q

Common factors associated with SLE:

A
  • presence of antinuclear antibodies
  • rash (butterfly)
  • photosensitivity
  • oral ulcers
  • arthritis
  • serositis
  • renal disorders
  • hematologic disorders
  • immunologic disorders
  • muscle aches
  • Raynaud’s
157
Q

SLE cardiac effects

A
  • pericarditis
  • myocarditis
  • CHF
  • MI
  • valve problems
  • conduction problems
158
Q

SLE pulmonary effects

A
  • lupus pneumonia
  • restrictive dz
  • alveolar hemorrhage
  • pulmonary HTN
159
Q

SLE musculoskeletal effects

A
  • non-erosive, symmetrical arthritis (90% of patients)
  • osteoporosis
  • atlanto-occipital subluxation
  • avascular necrosis (femoral)
  • tendonitis
160
Q

SLE GI effects

A
  • acute abd pain
  • oral ulcers
  • esophageal s/s
  • PUD (2* NSAIDS, steroid use)
161
Q

SLE hematologic effects

A
  • lymphoma
  • thromboembolism
  • increased r/f infection
  • thrombocytopenia
  • anemia
162
Q

SLE renal effects

A
  • glomerular nephritis with proteinuria
  • hematuria
  • reduced GFR
  • oliguric renal failure
163
Q

SLE laryngeal effects

A
  • mild inflammation
  • vocal cord paralysis
  • subglottic stenosis
  • laryngeal edema
  • complete obstruction
164
Q

SLE neurologic effects

A
  • cognitive dysfxn (30% of pts)
  • psychological changes (50% of pts)
  • HA
  • seizures (7-20% of pts)
165
Q

SLE skin effects

A
  • butterfly macular rash (50%, worse with sun)
  • discoid lesions (scalp, face, upper trunk)
  • alopecia
166
Q

What is the 2nd most common autoimmune rheumatic disease?

A

Sjogren’s syndrome

167
Q

Disease that Sjogren’s syndrome is commonly misdiagnosed:

A
  • fibromyalgia
  • MS
  • SLE
  • RA
168
Q

Sjogren’s syndrome more commonly affects (men/women)

A

women (9/10)

169
Q

How is Sjogren’s syndrome diagnosed?

A
  • labs (ANA, rheumatoid factor, SS-A and SS-B markers, erythrocyte sed rate, IGs)
  • ophthalmologic tests
  • dental tests (measure saliva fxn)
170
Q

SS signs/symptoms

A
  • DRYNESS (salivary, eye, lacrimal)
  • non-erosive arthritis
  • fever
  • fatigue
171
Q

SS other affected body systems

A
  • lymphadenopathy high r/f lymphoma
  • enlarged parotid glands d/t lack of drainage
  • peripheral neuropathy
  • lung involvement
172
Q

2 primary aims of rheumatologic management

A

1) symptom relief
2) reduction of immune response (prevent joint, organ, CV damage)

173
Q

Rheumatologic dz symptoms are commonly managed with what drug classes?

A
  • NSAIDs
  • COX-2 inhibitors
  • corticosteroids (flares)
  • opioids
174
Q

Drugs used to reduce immune response in rheumatologic dz:

A
  • Disease modifying anti-rheumatic drugs (DMARDs)
  • TNF inhibitors
  • human monoclonal antibody
  • Janus Kinase inhibitors
175
Q

MOA of DMARDs

A
  • reduce flare frequency
  • prevent erosions/long-term disability
176
Q

Examples of DMARDs

A
  • Methotrexate
  • Sulfasalazine
  • Lefunomide
  • Hydroxycholoroquine (Plaquenil)
177
Q

Methotrexate effects:

A
  • immunosuppression
  • interstitial lung dz/pulmonary tox
  • hepatotox
  • synergistic action with nitrous oxide?
178
Q

Drugs used for management of SLE:

A
  • Azathioprine (hepatotox)
  • Cyclophosphamide (cardiotox)
  • Mycophenolate
179
Q

Splenectomy may help manage which rheumatologic disease?

A

SLE (d/t source of the antiplatelet antibodies)

180
Q

Why are exogenous corticosteroids used in treatment of rheumatologic diseases?

A

stops the feedback loop with the HPA axis that results in the release of corticotropin releasing hormone

181
Q

Normal cortisol secretion in the absence of stress

A

10-20mg/day

182
Q

Cortisol secretion in the presence of stress:

A

150mg/day

183
Q

Cortisol regulates:

A
  • metabolism
  • CV fxn
  • growth
  • immunity
184
Q

Cortisone replacement for minor surgery

A
  • normal corticosteroid dose
  • 25mg hydrocortisone day of procedure
  • no taper
185
Q

Cortisone replacement for moderate surgery

A
  • normal corticosteroid dose
  • 50-75mg hydrocortisone day of procedure
  • taper over 1-2 days
186
Q

Cortisone replacement for major surgery

A
  • normal corticosteroid dose
  • 100-150mg hydrocortisone day of procedure
  • taper over 1-2 days
187
Q

What chronic steroid use patients do not need steroid supplementation?

A
  • daily prednisone 5mg or less
  • topical steroids only
188
Q

Dose equivalencies of Hydrocortisone - Dexamethasone - Methylprednisolone

A

Hydrocortisone 25mg
Dexamethasone 1mg
Methylprednisolone 5mg

189
Q

Important thing to remember for patients with SLE and regional anesthesia

A

may have clotting issues and struggle with resumption of anticoagulation

190
Q

Special anesthetic considerations for SS patients

A
  • no Scopolamine
  • lube eyes
  • monitor for QT prolongation
191
Q

THC acts on which receptors

A

CB1 and CB2 (partial agonist)

192
Q

CBD acts on which receptors

A

CB2 (allosteric modulator at CB2>CB1)

193
Q

CB1 receptors are located:

A

CNS and PNS
- nociception
- anxiolysis
- memory
- cognition
- emotion
- movement
- NO respiration

194
Q

CB2 receptors are located:

A
  • peripheral lymphoid and hematopoeietic cells
  • immunomodulatory function
195
Q

Rank the Delta strains of THC in order of strength

A

Delta 10 < Delta 8 < Delta 9

196
Q

Compare Delta 8 to Delta 9 side effects

A

Delta 9
- anxiety/tachycardia
- red eyes/dry mouth
- STM loss
- delayed rxn times
- coordination problems
- vomiting @ high doses

Delta 8
- pts with autoimmune disorders report redness/swelling of joints
- thermoregulation

197
Q

Delta 10 has a SE profile most similar to..

A

Delta 8

198
Q

List the Deltas and their receptors

A

Delta 9 - CB1
Delta 8 - CB1 and CB2
Delta 10 - CB1 and CB2

199
Q

CBD has effects on…

A
  • adenosine
  • serotonergic
  • glycine
  • nuclear PPARs
  • transient receptor potential channels
  • opioid
  • NDMA
  • GABA
200
Q

Cannabis is metabolized through which pathway?

A

CYP450 (2C9, 3A4, 2B6)

201
Q

Drug interactions with THC

A
  • increased effects of Clobazam, Warfarin, Hexobarbital
  • decreased effects of Theophylline
  • increased sedation with benzos, opioids, volatiles
202
Q

Effects of cannabis use on airway

A
  • hyperreactivity/bronchospasm
  • edema
  • obstruction
  • chronic cough
  • bronchitis
  • emphysema
    more irritating d/t burns at higher T
203
Q

THC effect on sympathetic/parasympathetic nervous systems

A
  • stimulates SNS
  • inhibits PNS
204
Q

Cannabis CV risks

A
  • endothelial dysfxn
  • platelet dysfxn
  • arrhythmias
205
Q

THC effects on CV

A
  • increased HR
  • increased myocardial O2 demand
  • increased BP
206
Q

CBD effects on CV

A
  • reduced HR
  • vasodilation
  • hypotension
207
Q

5 major anesthesia considerations for pts using THC/CBD

A
  • airway
  • CV/cerebrolvascular issues d/t endothelial/PLT dysfxn
  • delayed gastric emptying
  • drug interactions
  • increased analgesic/volatile requirements
208
Q

Some studies demonstrated an increased r/f ___ in cannabis users

A

MI
r/t PLT/endothelial dysfxn

209
Q

Acute s/s of cannabis intoxication

A
  • anxiety
  • paranoia
  • psychosis
210
Q

Cannabis CV risks

A
  • endothelial dysfxn
  • platelet dysfxn
  • arrhythmias
211
Q

3 classes of drugs used to treat depression:

A
  • TCAs
  • MAOIs
  • SSRIs
212
Q

MOA of TCAs

A
  • block reuptake of serotonin and NE
  • competitive antagonist at muscarinic ACh receptors
213
Q

SE of TCAs

A
  • anticholinergic (dry/red/blind/EPS)
  • antihistamine
  • conduction abnormalities (depresses cardiac impulses, prolonging intervals)
214
Q

TCA with most SE

A

Amitriptyline

215
Q

TCA OD looks like:

A
  • CNS depression
  • sz
  • hypoventilation
  • coma
  • anticholinergic s/s
216
Q

Treatment for TCA OD/anticholinergic toxicity

A

Physostigmine - reversible AChE inhibitor that crosses the BBB

217
Q

Patients on TCAs need (direct/indirect) acting agonists to treat low HR/BP

A

direct (Phenylephrine, then NE if that doesn’t work)

indirect can lead to HTN crisis

218
Q

Chronic administration of TCAs has what effect on the SNS?

A
  • downregulation of B-adrenergic receptors
  • decreased amount of NT
  • reduced sensitivity to that receptor
219
Q

MAO of SSRIs

A
  • increase serotonin by inhibiting reuptake
  • also inhibit reuptake of NE
220
Q

SE of SSRIs

A
  • insomnia
  • agitation
  • HA
  • sexual dysfxn
  • withdrawal symptoms if abruptly stopped
221
Q

Which SSRI is a CYP450 inhibitor?

A

Prozac (most potent inhibitor)

222
Q

Describe the effect of SSRIs on PLT activity

A
  • anti-PLT activity
  • block reuptake of serotonin in PLT
  • serotonin helps with aggregation
    relevant for pregnant women on SSRIs
223
Q

MOA of MAOIs

A
  • inhibit the enzyme monoamine oxidase to elevate serotonin, NE, and DA levels
224
Q

SE of MAOIs

A
  • orthostatic hypotension
  • sedation
  • blurred vision
  • peripheral neuropathy
  • agitation/tremor/sz
225
Q

Patients taking MAOIs should avoid what foods?

A
  • aged cheese
  • smoked fish
  • cured meats
  • some beers
    (tyramine)
226
Q

SE if a patient on MAOIs eats forbidden foods

A
  • HTN
  • hyperpyrexia
  • increased cerebrovascular resistance
227
Q

Drug to be avoided in pts taking MAOIs:

A

Demerol
- serotonin syndrome
- hyperthermia
- sz
- coma
- death

228
Q

Muscle relaxant to avoid with MAOIs

A

Pancuronium

229
Q

Risks associated with a spinal/epidural in pt on MAOI

A

hypotension

Patho (2 decks)

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