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Pharmacology > Pharm Quiz 3 > Flashcards

Pharm Quiz 3 Flashcards

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1
Q

Etomidate MOA

A

Potentiation of GABAa mediated Chloride shift

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2
Q

Etomidate- What is the limiting factor affecting use?

A

Transient depression of adrenocortical function

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3
Q

What would depression of the adrenocortical function do?

A

Adrenal glands on top of kidneys will release hormones in response to stress, so when you block or inhibit that, the body cannot respond to normal stressful situations.
Can have fatal complications from this because it suppresses the CV and Resp effects of the adrenal glands.
Pt in sepsis, this can be very dangerous because they need their adrenal glands to support them and create stress responses.

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4
Q

CNS effects of Etomidate

A

Decreased CBF.
Decreased CMRO2.
Decreased ICP, while maintaining CPP.
Decrease IOP.

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5
Q

CV effects of etomidate

A

Provides CV stability and is drug of choice for unstable cardiac system.
Minimal change in HR, BP, CVP.
Careful in pt with aortic or mitral valve disease.

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6
Q

Respiratory effects of Etomidate

A

Dose dependent decrease in MV,.
Compensatory increase in RR.
Decreased chemoreceptors.
May have brief period of apnea, followed by hyperventilation.

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7
Q

Does etomidate cause histamine release?

A

No histamine release. This is tied to the CV stability because histamine release would cause vasodilation/decrease in vascular tone.

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8
Q

Unique qualities of etomidate

A

Increase incidence of PONV.
No analgesic properties.
Low incidence of allergic reaction.
Involuntary myoclonic movement is common.

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9
Q

Chemical Structure of Etomidate

A

Has 5 sided Imadazole ring which is stable in big pH changes.
Only IV induction drug that is not a racemic mixture.
2 Isomers, but R isomer is hypnotic.

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10
Q

Pharmacokinetics of Etomidate

A

Rapid distribution half-life.
76% plasma protein binding.
Total body clearance is rapid.
Less accumulation compared to a lot of other induction drugs- useful for repeat doses and continuous infusions.

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11
Q

Etomidate onset/peal/duration

A

Rapid onset 30-sec.
Peak 1 min.
Duration 6-8min

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12
Q

Dexmedetomidine MOA

A

Highly selective Alpha2-Adrenergic Agonist.
Negative feedback loop.
Normally when Alpha 2 picks up Norepi, it sends a signal saying “we have enough epi/NE”, so secretion of these stops. Precedex acts as a false neurotransmitter and tricks the system into thinking it does not need any more secretion of NE/Epi.

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13
Q

What is the active component in dexmedetomidine?

A

D-Isomer of medetomidine.

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14
Q

How is dexmedetomidine metabolized?

A

By hepatic microsmal enzymes

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15
Q

How is dexmedetomidine more selective than clonidine?

A

1600:1 Alpha2:Alpha1.

Versus clonidine being 220:1

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16
Q

Dexmedetomidine has three sites of action. What are they?

A

Brain (locus ceruleus).
Spinal cord.
Autonomic Nerves.

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17
Q

CNS effects of dexmedetomidine

A

Decrease CBF.
No change in ICP or CMRO2.
Decrease MAC requirement for inhaled anesthetics.
Decrease plasma catecholamine concentration.

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18
Q

CV effects of Dexmedetomidine

A

Moderate decrease in HR.
Moderate decrease in SVR.
Bolus may cause more pronounced bradycardia (and rebound hypertension).

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19
Q

Respiratory effects of Dexmedetomidine

A

Small decrease in TV, but no significant change in respiratory rate.
Chemoreceptors remain intact.
Synergistic effects with other sedative/hypnotics.

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20
Q

JAMA Pediatrics Swedish Analysis

A

Single exposure to anesthetic drugs:
0.41% lower school grades.
0.97% lower IQ.
Summary: Children were NOT FOUND to be at increased risk of adverse child development outcomes compared with their biological sibling who did not have sugery/anesthetic.

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21
Q

MASK trial summary

A

Anesthesia exposure before age 3 was not associated with deficits in the primary outcome of general intelligence.
Multiple exposures may be linked to changed in behavioral and learning difficulties.

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22
Q

What does the FDA say about anesthetics?

A

Children <3yo and pregnant women in 3rd trimester= BLACK warning label; however, Am Coll of OB/GYN disagrees.

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23
Q

Describe the sleep associated with the administration of Precedex

A

Precedex is a more natural and restful sleep compared to other drugs because it puts the body into a more natural state of rest and digest.

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24
Q

What is Nociceptive pain

A

Pain you feel because something happens to your body structure. Usually referred to as sharp, stabbing.

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25
What is Neuropathic pain
Pain you feel, but nothing actually happen to your body. | Sometimes referred to as burning, or lightning bolt (shooting).
26
Four "Phases" of nociceptive pain.
1. Stimulation. 2. Transmission. 3. Perception. 4. Modulation
27
What happens during stimulation of nociceptors.
Noxious stimulus of nociceptors releases neural chemicals that also stimulate other nociceptors. (bradykinin, histamine, prostaglandins, leukotrienes, serotonin, substance P, Potassium.)
28
What happens during transmission of nociceptor's response?
Action potential moves from site of stimulus to the dorsal horn of the spinal cord, then to the CNS. From dorsal horn, neurotransmitters are released: Glutamate, Substance P, Calcitonin Related Peptide.
29
What helps us differentiate between types of pain?
Several pathways at the dorsal horn. | A delta and C.
30
A-Delta pathway detects what type of pain.
A-Delta is large diameter and sparsely myelinated: Sharp Localized pain.
31
C Pathway detects what type of pain?
Small diameter/unmyelinated: Dull, aching pain.
32
Which neurotransmitter has been targeted for migraine medications?
Calcitonin Related Peptide.
33
What happens during perception of nociceptive pain?
Conscious experience of pain. - Pain impulse relayed through thalamus. - Higher cortical structures transmit pain.
34
What happens during modulation of nociceptive pain?
Inhibition of impulses via the brain stem. | Releases endogenous opiods, serotonin, Norepinephrine, GABA.
35
Why do we not feel pain from a serious injury right away?
When we release Dopamine from painful stimuli, it briefly will stop you from truly feeling the pain. It naturally allows you some time to assess the situation and then react, before you actually feel the pain.
36
What are some causes of neuropathic pain?
Sustained by abnormal processing of sensory input; | Nerve damage, persistent stimulation, autonomic dysfunction.
37
What is allodynia?
Sensation of pain from a normally non-painful stimulus.
38
What is defined as chronic pain?
Chronic pain is >3 months or pain past the time of normal tissue healing.
39
Which age group has highest prevalence of opiate addition/overdose death?
Age 45-64yo.
40
Which group/groups are statistically less likely to be prescribed opiates?
``` Racial/ethnic minority. Women Elderly Persons with cognitive impairment. Cancer and at end of life. ```
41
What are optimal time lengths of opioid prescriptions?
4-9 days for general surgery procedures. 4-13 days for women's health procedures. 6-15 Days for musculoskeletal procedures.
42
Opioid Receptor Delta
Brain and peripheral nerves. | Analgesia/antidepressant/dependence.
43
Opioid Receptor Kappa
Brain, spinal cord, periphery. | Analgesia/sedation/miosis/dysphoria/ADH inhibition.
44
Opioid Receptor Mu
Brain, spinal cord, periphery, intestine. Mu1: Analgesia/dependence. Mu2: Resp depression/euphoria/reduced GI motility/dependence.
45
Which receptor is involved with most of the side effects of opioids?
Mu2
46
Morphine at the presynaptic fiber
When an opiate binds, it caused the G protein to have a confirmation shape change. That shape change sets off a cascade of events. Helps send the signal/ and helps amplify the signal. AC- takes ATP, and changes it to cAMP (cyclic AMP). When Morphine binds, it inhibits cAMP.
47
Morphine at the post-synaptic fiber
Morphine starts forcing K+ out The more K+ that comes it, the more hyperpolarized it becomes. Makes it more difficult for action potential to be carried through
48
Do Mu agonists work in an inhibitory or excitatory way?
Inhibitory.
49
What is an example of an agonist-antagonist?
Suboxone.
50
Which chemical structure do natural and semisynthetic opiates have in common?
Phenanthrene nucleus.
51
Which opiate isomer has agonist effects on pain receptors?
Levo-rotatory forms. These are the left sided isomers. Also called S-Antiomer.
52
Morphine is metabolized into 2 metabolites. What are they?
Morphine 3 Glucuonide and Morphine 6 glucuonide
53
Which morphine metabolite is active?
Morphine-6-glucuonide
54
Morphine-6-glucuonide causes what?
Analgesia. Depression of ventilation. M6G is 100x more potent than morphine.
55
What is biggest complication with Morphine-6-glucuonide?
Biggest issue is build up over time and respiratory failure (leading to death)
56
Morphine CV Effects
Bradycardia. Reduction in SNS response. Histamine release (itching, vasodilation
57
What happens to a patient in pain's BP after MSO4 given?
Patient is in pain, they are in a super stimulated state of SNS stimulation. SO when morphine is given, the reduction in SNS stimulation causes a greater swing than someone who is not in pain.
58
Morphine Respiratory side effects
Agonist effect at Mu2 Receptors causes depression of ventilation. Inhibition of chemoreceptors. CO2 Curve shift to right
59
What reflex to patients exhibit many times after Mu2 receptor agonism.?
You will see sometimes a patient will wipe their nose/face in a defense mechanism fashion to protect airway because of the respiratory depression. The body senses an issue and wants to react *cough supression*
60
Do men or women have higher prevalence of respiratory depression?
Women
61
Morphine CNS side effects
Caution with use in head injured patients. Increase ICP with decrease in spont resp. Pupil constriction
62
What do changes in BBB with head injury cause with opioid administration?
BBB integrity may be affected by head injury with resultant increased sensitivity to opioid.
63
Sedative effects of Morphine
Onset of sedation precedes onset of analgesia. Many yimes patient will feel sleepy prior to feeling good pain control. Sedation is not always equivalent to pain relief.
64
Morphine effects on biliary tract?
May cause spasm of biliary smooth muscle. | May increase intrabiliary pressures like colic and epigastric distress.
65
What medication can be given to treat spasm of biliary smooth muscle associated with morphine administration?
Glucagon 2mg IV. Increases cAMP.
66
Morphine side effects on GI tract
Constipation. Delayed gastric emptying. N/V from chemoreceptor trigger Zone Biliary colic.
67
Morphine side effects on Genitourinary
Urinary hesitance.
68
Morphine/dilaudid onset and peak
Onset 15-30mins. | Peak 30-90mins.
69
Why is morphine's onset slower than some drugs?
Poor lipid solubility. | High degree of ionization at physiologic pH
70
Why is hydromorphone a better choice for renal failure pt?
Lacks known active metabolites
71
Fentanyl MOA
Synthetic Mu2 agonist
72
Why does fentanyl have a more rapid onset and greater passage accross BBB than morphine?
Greater lipid solubility
73
How is fentanyl metabolized?
Via hepatic microsomal enzyme system. | 1st pass pulmonary reuptake.
74
Why does fentanyl have short duration of action?
Redistribution to inactive tissues: skeletal muscle, fat
75
What metabolite does fentanyl metabolism create?
Norfentanyl
76
Is the metabolite of fentanyl active or inactive?
Inactive. (technically limited pharmacological activity.
77
Fentanyl CNS side effects
6-9mmHg increase in ICP. | No seizure activity.
78
Fentanyl CV side effects
Bradycardia. Decreased BP and CO secondary to bradycardia. *No histamine release*
79
Fentanyl Respiratory side effects
Persistent depression of ventilation. | Can have recurrent depression with secondary peak in plasma concentration of drug.
80
What dosage changes must occur with fentanyl and CP bypass? and Why?
Increased dose may be required. | Drug adheres to the circuit of the CP bypass/pump
81
How much of the fentanyl dose is retained in a patch even after removal?
Approx 90%
82
What is the Peak plasma concenentration of transdermal fentanyl patch?
18hours
83
List these in order of potency: fentanyl, sufentanil, alfentanil
Sufentanil>fentanyl>alfentanil
84
What increases analgesic potency?
A greater affinity of the drug for opioid receptors.
85
List these in order of elimination half-life: alfentanil, fentanyl, sufentanil
Fentanyl>sufentanil>alfentanil.
86
Sufentanil CNS side effects
Decreased CMRO2 | Decreased CBF
87
Sufentanil CV side effects
Bradycardia | Decrease in CO secondary to bradycardia
88
Sufentanil Respiratory side effects
Dose dependent depression. | Chest wall rigidity risk
89
Sufentanil: Is Vd and elimination half time increased or decreased in obese patients and why?
Increased; high lipid solubility of sufentanil
90
Pros and cons of alfentanil
Pros: more rapid onset and short duration of effect. Cons: less potent
91
What is different about alfentanil?
Metabolized by two independent pathways. Less than half excreted unchanged in the urine. Highly dependent on live metabolism
92
Remifentanyl potency compared to fentanyl?
same or similar to fentanyl.
93
What makes remifentanyl structurally unique?
Its ester linkage.
94
How does remifentanyl's ester linkage effect it's use?
It is metabolized in the blood via esterases. | It is lipophilic, but does not accumulate in fat because of such a quick metabolism in the blood.
95
How do you dose remifentanyl differently between obese and lean individuals?
You don't. Similar profile between obese and lean d/t its extraordinarily quick metabolism/elimination.
96
Remifentanil side effects
Basically the same as fentanyl except more mild possibly d/t such quick metabolism.
97
Remifentanil post-operative pain management.
Patients who receive remifentanil appear to have high post-operative analgesic requirements.
98
Does an increased length of infusion cause accumulation of remifentanil?
No
99
What type of surgical procedures does remifentanil work well for an why?
Neuro procedures; so that you can assess their neuro status quickly by changing or stopping the infusion.

Pharmacology (9 decks)

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