Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology 1 > Induction Agents (2) > Flashcards

Induction Agents (2) Flashcards

1
Q

What neurotransmitters do most inhibitory neurons in the brain and spinal cord use?

A

GABA or glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What neurotransmitter do most excitatory neurons in the brain use?

A

Glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the purpose of an IV induction agent?

A

Move the patient from a state of consciousness to a state of unconsciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Moving from a state of consciousness to unconsciousness should happen how?

A

Rapidly, smoothly, without dysphoria, reversibly, reliably, and in an autonomically stable fashion (no current agent meets all these requirements)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What chart describes the stages of anesthesia and is used to assess the depth of general anesthesia?

A

The Guedel chart (created in 1937)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In general when GABA receptors are stimulated there is a ________ in neuronal activity

A

Decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What receptor is inotropic, and associated with binding sites for benzodiazepines, propofol, and barbiturates?

A

GABA-A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What type of channel are GABA-A channels

A

Ionotropic chloride channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of channels are GABA-B and what do they effect?

A

Metabotropic, when activated, GABA-B receptors cause potassium channels to open, allowing positively charged potassium ions to flow out of the neuron making it hyperpolarized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of channels are GABA-C channels and where are they located?

A

Ionotropic chloride channels, found primarily in the retina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

All anesthetics except ketamine and etomidate (barbiturates have little or no effect) stimulate what receptors

A

Glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

All anesthetics except ketamine stimulate what receptors?

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Most excitatory neurons in the brain use glutamate as their neurotransmitter. What channels does glutamate modulate?

A

Sodium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does NMDA stand for?

A

N-methyl-D-aspartate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What type of receptor is the NMDA receptor?

A

Excitatory glutamate receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Barbiturates work on what receptor and what subunit?

A

GABA-A (beta subunit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Barbiturates are metabolized by what?

A

CYP2C9 and 3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Barbiturate metabolites are:

A

Almost all inactive, water soluble, and excreted in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Barbiturates accelerate what related to blood?

A

Heme production; by stimulating D-aminolevulinic acid synthetase (acute porphyria risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If injected intra- arterially what risk do barbiturates have?

A

Venous thrombosis risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Patients treated with barbiturates for seizure disorders metabolized drugs ___ x faster than expected (especially muscle relaxants)

A

2 x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Barbiturates have what GI risk/side effect

A

PONV risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What drugs can cause exacerbations of Porphyria?

A

Barbiturates (in rare cases some antibiotics, birth control pills, ketamine, and etomidate)

24
Q

What is Porphyria?

A

rare group of disorders that affect the body’s ability to produce heme. These patients are deficient in enzymes within the heme biosynthetic pathway.

25
Q

What is the rate limiting enzyme in heme synthesis?

A

ALA (aminolevulinic acid)

26
Q

How do you pronounce Porphyria?

A

poor fear ya

27
Q

What genetic factors are involved with Porphyria?

A

Non sex linked autosomal dominant, variable expression (chromosome 11)
(Variable expression describes a range of symptoms that can occur in people with the same genetic condition)

28
Q

What are triggers of Porphyria?

A

Drugs are the most important trigger but other triggers can include infection, fasting, stress, menstruation and hormonal fluctuations

29
Q

Symptoms of Porphyria:

A

Symptoms usually occur as attacks that develop over several hours or days
~ Abd pain (severe) most common symptom
~ Cause, vomiting, constipation, pain in the back arms and legs, muscle weakness, urinary retention, palpitations, confusion, hallucinations, seizures

30
Q

Why can barbiturates cause a Porphyria attack?

A

barbiturates accelerate heme production, so it can accelerate the Porphyria process

31
Q

Methohexital onset:

A

15-30 seconds

32
Q

Methohexital Peak:

A

within 1 minute

33
Q

Methohexital E1/2T:

A

3-6 hr

34
Q

Methohexital VD:

A

2 L

35
Q

Methohexital Protein Binding:

A

75%

36
Q

Methohexital PKA:

A

Ph 10 - 11 of 1% solution

37
Q

Methohexital excretion:

A

Renal

38
Q

Methohexital metabolism

A

Hepatic oxidation via CYP2C9 and 3A4

39
Q

Methohexital DOA:

A

5-10 min

40
Q

Methohexital Class / structure:

A

~ Sedative/hypnotic/barbiturate
~ 6 carbon ring with O at C2 (oxybarbiturate) branched chain at C5 (hypnotic properties) and methyl group on N (decrease in seizure threshold)

41
Q

Methohexital MOA:

A

Acts on GABA-A (Beta subunit) increasing the duration of Cl- channels being open (hyper polarizes the neuron)

42
Q

Methohexital Dose:

A

Dose: Induction: 1 - 1.5 mg/kg IVP or 50-120mg (avg 70mg) at 10mg (1ml of 1% solution) over 5 seconds Maintenance: 20-40mg IVP q4-7min PRN; or 3ml/min (1gtt/sec); PEDS: induction dose- 6.6-10mg/kg IM once (5% conc); rectal 25mg/kg using 1% soln

43
Q

Methohexital SE:

A

SE: hypotension and tachycardia may occur post induction dose; histamine release, coughing, hiccoughing, movement, laryngospasm ↑PONV

44
Q

Methohexital Cautions:

A

~Long hangover/impaired judgment ~Decreases seizure threshold (ECT) ~Hyperalgesia with lower doses ~Can induce enzymes –> accellerate metabolism of other drugs ~CONTRAINDICATED in pts at risk for porphyria ~Intra-arterial injection- venous embolism

45
Q

Etomidate, Ketamein and Propofol onset time:

A

30-60 seconds

46
Q

Etomidate DOA:

A

3-5 min

47
Q

Etomidate Peak:

A

Within 1 min

48
Q

Etomidate E1/2T:

A

2-5 hours

49
Q

Etomidate VD:

A

Large 2.5 - 45. L/kg

50
Q

Etomidate Protein binding:

A

75%

51
Q

Etomidate PKA:

A

4.2 WB (99% non-ionized at physiologic pH)

52
Q

Etomidate excretion:

A

2% excreted unchanged, 85% renal, 13% in bile

53
Q

Etomidate class/structure:

A

Sedative/hypnotic, imidazole derivative (aromatic N ring) -predominately R (+) isomer for anesthetic effect (5x more potent than S(-) isomer)

54
Q

Etomidate MOA:

A

Binds to GABA-A (beta subunit) enhancing affinity for neurotransmitter GABA increasing its duration which increased dependent chloride channel opening thus hyperoplarizing the neuron.

55
Q

Etomidate SE:

A

SE: NO ANALGESIC EFFECT; can increase EEG activity (esp. in patients with seizure history) CV: MINIMAL CV effects, slight fall in PVR Resp: min depression of CO2 response GI HIGH INCIDENCE FOR PONV (30 - 40%) “vomidate”

56
Q

Etomidate Catuions:

A

Cautions: Pain on injection site d/t propylene glycol, **INHIBITS enzyme 11 beta hydroxylase (adrenocorticall suppression [lasting 4 - 8 hours]; acute porphyrias; Relatively hight margin of saftey (30-fold difference: effective dose vs. lethal dose)

57
Q

Etomidate metabolism:

A

hepatic ally by ester hydrolysis to ethyl alcohol

Pharmacology 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions