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Pharm > E3 > Flashcards

E3 Flashcards

1
Q

Boyles Law

A

Pressure and volume are inversely proportional

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2
Q

Ficks diffusion law

A 
Diffusion depends on:
Partial pressure gas gradient
Solubility of gas
Membrane thickness
Size of molecule
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3
Q

How does molecule size, membrane thickness, gas solubility, and pressure gradient affect gas effusion.

A

Molecule size
Big= slow
Small = fast

Solubility
High=
Low=

Pressure gradient
High=fast
Low=slow

Membrane thickness
Thick=Slow
Thin=Fast

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4
Q

What is a blood:gas partition coefficient?

What is it dependent on?

A

Equilibration ratio of pressure of volatile between gas in alveoli and blood

Dependent on:
CO
A-V pressure gradient

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5
Q

What is a blood:brain partition coefficent? What is it dependent on?

A

Equilibration ratio of pressure of gases between blood and brain.

Dependent on:
CBF
a-v pressure gradient

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6
Q

Influence of age on PK/metabolism of volatile.

A

<30 yo = INC met by 6% per decade

> 55 yo = DEC by 6% per decade

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7
Q

4 factors that alter volatile PK/metabolism

A

Age
DEC Lean body mass
INC fat
DEC hepatic fxn

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8
Q

What is the goal of volatile anesthetic

A

PA = Pa = PBr

End tidal PA = PBr

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9
Q

What does alveolar pressure indicate?

A

Depth of anesthesia
Recovery of anesthesia
Potency

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10
Q

What occurs to PA & PBr during anesthesia recovery

A

PA starts to INC

PBr DEC

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11
Q

What is concentration effect?

A
  • Impact of INSPIRED pressure (Pi) on rate of rise of PA

- Higher the Pi FASTER PA = Pi b/c HIGH delta-P

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12
Q

How does Pi r/t end tidal?

A

Picking up gas:
Pi > end tidal

Balance:
Pi = end tidal

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13
Q

How does Pi affect uptake & PA?

A

Low Pi = longer uptake and equilibration w/ PA

Higher Pi = more rapid uptake and equilibration w/ PA

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14
Q

8) What are some disadvantages of methoxyflurane

A

Disadvantage = dose related nephrotoxicity d/t fluroide

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15
Q

9) What are some advantages and disadvantages of enflurane?

A

Advantage= doesn’t sensitize myocardium to catechols
Not associated w/ hepatotoxicity
Disadvantage = Metabolism could lead to Sz in high concentration

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16
Q

10) What are some advantages and disadvantages of isoflurane?

A

Advantages= lack of cardiac dysrhythmias
lack of organ toxicity
rapid induction and emergence
Disadvantages = longer than sevo and des

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17
Q

11) What are some advantages and disadvantages of sevoflurane and desflurane?

A

Advantages = wholly fluorinated, low blood solubility

rapid induction

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18
Q

12) What characterizes the anesthetic state?

A

Characteristics of the anesthetic state include immobility, amnesia, analgesia and skeletal muscle relaxation

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19
Q

13) Which characteristics of the anesthetic state are achieved by the administration of inhaled volatile anesthetics?

A

Immobility
amnesia
skeletal muscle relaxation

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20
Q

14) Which characteristics of the anesthetic state are achieved by the administration of nitrous oxide?

A

Immobility, but not as sole anesthetic
Amnestic effects
No skeletal muscle relaxation

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21
Q

15) What is the mechanism of action of inhaled anesthetics in the central nervous system?

A

CNS depression by enhancing inhibitory ion channels and block excitatory ion channels
Affect release of NTs

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22
Q

16) Why are vaporizers required for the inhaled administration of volatile anesthetics?
How does this apply to N2O

A

Volatiles are liquid @ room temp and P_atm
They accurately deliver specified concentration of anesthetic
N2O is a gas at room temp so it doesn’t require vaporizer for delivery

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23
Q

4 purposes of anesthesia circuit

A

Deliver O2
Deliver inhaled drugs
Maintains temp and humidity
Removes CO2 and exhaled gases

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24
Q

3 Types of gas delivery systems

A

Rebreathing (Bain)
Non-rebreathing (self-inflating BVM)
Circle system

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25
Q

Set-up of Bain system, what it has and doesn’t have and its use?

A 
Set-up
Has APL valve, circuit tubing
No scavenger, CO2 absorver or HME
Use
Rebreathing circuit for transport
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26
Q

7 Component parts of circle system

A 
Fresh gas inlet
inspiratory and expiratory limbs
resevoir bag
CO2 absorbent
one-way valves (insp/exp)
Y piece
Scavenger system
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27
Q

Definition, advantages and disadvantages of high flow (HGF) anesthesia

A

Definition:
Gas flow exceeds Vm in L/min

Advantages:
Prevents rebreathing
Rapid change in anesthetic delivery, can INC anesthetic delivery

Disadvantages:
Wasteful (removes exhaled gas; no rebreathing)
Higher cost
Cools/Dries delivered volume (alters solubility and pressures)

28
Q

How does HGF affect solubility, pressure and rebreathing?

A

Flow is cooled and dried which alters solubility and pressure
INC flow removes exhaled gas leading to NO rebreathing

29
Q

Definition, advantages and disadvantages of low gas flow (LGF) anesthesia

A

Definition:
FGF < Vm

Advantages:
Allows for rebreathing
Low cost
Less cooling/drying

Disadvantages:
VERY slow anesthetic uptake

30
Q

Non-anesthetic effects of volatiles

A

Bronchodilation

Muscle relaxation

31
Q

How do anesthetics affect the airway? Descending order of most beneficial anesthetic?

A

Bronchodilation
Relax smooth muscle (that are already constricted)
Via VG Ca++ depletion in SR
DEC SM constractility

Sevo > Iso > Des

32
Q

Conditions for anesthetics to bronchodilate

A

Already constricted airway

Intact epithelium w/o inflammatory process

33
Q

Which anesthetic should be avoided in pts w/ asthma, COPD, and reactive airway and at what concentrations?

A

Desflurane

>2 MACs (according to Eger videos)

34
Q

Volatile gas effects on neuromuscular system? Relate to NMBD

A

Dose-dependent skeletal muscle relaxation
Potentiate depolarizing and ND-NMBDs
Enhances glycine at SC

35
Q

How do volatile gases mediate MR at the SC

A

Enhance glycine
Inhibit AMPA
Block glutamate release

36
Q

Anesthetic effects on CMRO2 and cerebral activity.
MAC burst suppression
MAC electrical silence

A

DEC in both
1.5 MAC = burst suppression
2 MAC = electrical silenc

37
Q

Which gas has no muscle relaxant properties and why?

A

N2O

B/c you can’t ever administer 1 MAC

38
Q

Anesthetic effects on sz

A

Anticonvulsant
At high concentration AND DEC CO2
LOWER CO2 in combination lowers Sz threshold

Proconvulsant
Enflurane not used in pts w/ h/o Sz
Esp >2MAC or PaCO2<30 mmHg

39
Q

Anesthetic effect on evoked potentials of SSEP and MEP.

A

Dose related @0.5-1.5 MAC
DEC amplitude
INC latency/freq

40
Q

What is SSEP and MEP and monitoring purposes

A

SSEP = somatosensory evoke potential
Monitors sensory/brain response

MEP = motor evoked potential
monitors motor response

41
Q

Anesthetic effects on CBF and ICP. Onset/dose of effects.

A

Dose dependent
INC CBF d/t DEC cerebral vascular resistance
May INC ICP
Onset >0.6 MAC w/in minutes

42
Q

Dose at which autoregulation ability is altered

A 
Halothane = lost @0.5 MAC
Sevo = lost>1 MAC
Iso/Des = lost @0.5-1.5
43
Q

How do anesthetics affect ICP and why? What pts are most at risk for INC and MAC onset

A

Parallel INC w/ CBF
b/c INC BF d/t vasodilation

At risk
pts w/ space occupying lesions or brain injury

Onset > 0.8 MAC

44
Q

Respiratory effects of anesthetics

A

Dose-Dependent INC rate and DEC Vt
Iso up to 1 MAC (celing)

Rate change is insufficient to maintain/counter DEC Vm or PaCO2 INC

Direct depression of medullary ventilatory centers

45
Q

MAC dose for apnea

A

1.5-2.0 MAC

except Iso

46
Q

Anesthesias effect on hypoxic response and at what dose

A

Blunts hypoxic response normally mediated by carotid bodies
T/F DEC drive to breathe

  1. 1 MAC = 50-70% depress initiated
  2. 1 MAC = 100% depression
47
Q

Anesthesia’s effect on hypercarbic response and at what doses

A

All anesthetics INC PaCO2 (according to Eger)
N2O doesn’t INC PaCO2
Substitution for part of MAC will provide less depression

48
Q

Anesthetic effect on HPV response. At what dose? Biggest concern?

A

Dose-dependent DEC in HPV response (no vasoconstriction to hypoventilated alveoli)

2 MAC = 50% depression

Most concerning = 1 lung ventilation and hypoxemia

49
Q

5 CV effects of anesthetics

A 
Direct myocardial depression
Peripheral autonomic ganglion blockade
Attenuation of carotid sinus reflexes
DEC formation of cAMP
DEC Ca++ influx
50
Q

Anesthetic effects on MAP and when is it worse?

A

MAP:
Direct myocardial depression alters CA++ into SR
DEC contractility, SV, CO
DEC MAP d/t DEC SVR

Worse:
w/ Iso
in diseased hearts

51
Q

Anesthetic effects on HR. Difference in anesthetics.

A

Dose dependent INC
To compensate for DEC SV/CO

Sevo only >1.5 MAC
Des VERY tachy w/ overpressurization

52
Q

Confounding variables to HR variability and anesthesia

A

INC:
Anxiety
Vagolytic admi

DEC:
Opioids
beta blockers

53
Q

Anesthetic effects on CO

A

DEC CO is offset by INC HR

N2O has mild sympathomimetic INC in CO

54
Q

Principle behind coronary steal and effects on heart

A

D/T coronary vasodilation
Coronary blood is rerouted from poorly perfused, sclerotic vessel collateral supply
Worsens injury to poorly perfused myocardium

55
Q
  1. Describe the physiologic effect of neuromuscular blocking drugs (NMBDs).
A

Interrupt the transmission of nerve impulses to the NMJ causing paralysis

56
Q

2.What are some clinical situations in which NMBDs are used to produce skeletal muscle relaxation?

A

ET intubation

Surgery

57
Q

What analgesic effects do NMBDs have

A

None

58
Q

4.How does the clinician evaluate the intensity of the neuromuscular blockade?

A

Monitoring twitch response from electrical stimulation of peripheral nerve from a nerve stimulator

59
Q

What are 5 characteristics of NMBDs that may influence the choice of which drug is administered to a given patient?

A

MOA, onset, duration, route of elimination and side effects

60
Q

7.Which NMBDs are the common offenders to triggering life-threatening anesthetic-related hypersensitivity reactions?

A

NMBDs Quaternary ammonium groups

Rocuronium and SCh are most common?

61
Q

8.What is component that is common to all NMBDs, resulting in possible allergic cross-reactivity of these drugs?

A

Quaternary ammonium group leads to possible allergic cross-sensitivity

62
Q

9.What is the most common side effects reaction to sugammadex?

A

N/V
Pruritis and urticaria
Anaphylaxis
Marked bradycardia

63
Q

Which NMBD class is associated w/ histamine release and which is not?

A

Benzylisoquinolinium = histamine release
Atracurium, mivacurium (Cisatracurium doesn’t in normal doses)

Aminosteroid = no histamine release
Pancuronium, Vecuronium, Rocuronium

64
Q

What is the neuromuscular junction (NMJ) and it’s components

A

Location where the transmission of neural impulses at motor nerve translate into skeletal muscle contraction

Consists of prejunctional MN ending, synaptic cleft and postjunctional membrane.

65
Q

11.What events lead to the release of neurotransmitter at the NMJ? What is the neurotransmitter that is released?

A

Events to release:
Impulse down MN fiber to axonal end of prejunctional nerve. Stimulation causes Ca++ influx into prejxn and stimulates the release of NT ACh into synaptic cleft.
NT
ACh is synthesized and stored in presynaptic terminal until released by CA++ influx

66
Q

12.What class of receptors is located at prejunctional and postjunctional sites?

A

nACh receptors are on both

67
Q

13.What clinical effect results from the stimulation of postjunctional receptors?

A

ACh binds to ligand-gated ion channels allowing influx of Na+ into postunctional membrane.
Results in potentiation of

Pharm (4 decks)

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