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Pharmacology > Pharm Quiz 2 > Flashcards

Pharm Quiz 2 Flashcards

(47 cards)

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1
Q

MOA of Barbiturates?

A

Barbiturates mostly enhance GABA mediated inhibitory neurotransmitters.

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2
Q

How does GABA react at GABAa receptor?

A

They increase the ion channel flow of chloride

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3
Q

How does Chloride influx affect the neurotransmitter?

A

Chloride makes the cell more negative which increases the threshold that must be overcome in order for an action potential to occur/be transferred.

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4
Q

GABA Receptors

A

GABA binds to a GABAa receptor which causes an ion channel to open. Chloride rushes in and causes the cell to become more negative, therefore increasing the threshold that needs to be overcome for an action potential to occur.

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5
Q

Alpha 2 Receptors

A

Considered a negative feedback loop.

Alpha 2 receptors mostly in CNS, they recognize that there is enough norepi/epi so it stops more production of these two.

Precedex will bind to these alpha 2 receptors and ‘falsely’ make the CNS think that there is enough norepi/epi.

Precedex acts as a false norepi because the alpha 2 receptor believes it is norepi and the body stops sending norepi.

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6
Q

NMDA Receptors

A

Excitatory receptor.

Ion channel.
Glutamate binds in, opens ion channel, and POSITIVE ions (Ca++) are sent through. This is excitatory effect.
We will want to use antagonists to block this excitatory effect

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7
Q

Baroreceptors

A

Throughout the body that are small groupings of cells that sense pressure changes and this sends a message to release or stop releasing certain hormones.

Some medications will blunt these baroreceptors.

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8
Q

Chemoreceptors

A

Pick up O2 and CO2 changes in the body.
They can tell the CNS to “take a breath”.

Some medications will blunt these sensors so that the body will not respond normally to changes in O2 and CO2

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9
Q

Are IV Induction medications lipophillic or hydrophillic?

A

Lipophillic

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10
Q

Vessel Rich Group

A

Brain, heart, i.e. highly perfused/vascular organs.
Only 10% of body mass.
Receive 75% of cardiac output

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11
Q

Vessel Poor/Semi-poor Group

A 
Muscle/Fat semi poor group
Ligaments vessel poor.
Combined, they have..
90% of body mass, but
only 25% of Cardiac output
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12
Q

Why does a medication after one dose have to be re-dosed (or cont gtt started) before 9 minutes? Elimination, redistribution, or metabolism.

A

Redistribution

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13
Q

Compartment 1

A

Blood vessels and blood volume

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14
Q

Compartment 2

A

All the highly perfused/highly vascular organs:

Brain, liver, kidneys, gut, etc.

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15
Q

Compartment 3

A

Fat and vessel-poor group

Same compartment, but different phases.

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16
Q

What class of IV Induction drugs are some of the oldest drugs used?

A

Barbiturates

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17
Q

A drug that is protein binding. What happens if serum albumin level is low? High?

A

Low-
will be more “free” drug, so should require less drug
High/normal-
will be less “free” drug, so will require more/average drug

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18
Q

What are two factors that increase unbound fraction of barbiturates?

A
  1. Decreased plasma protein concentration.

2. Competition of other drugs for receptor sites (Aspirin, warfarin, naproxen.

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19
Q

CNS Effects of Barbiturates

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A

Prompt loss of consciousness 10-30 sec
No analgesic properties
Decrease CMRO2, CBF, ICP, IOP
Anti-convulsant properties

20
Q

CV Effects of Barbiturates

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A

Decrease Sympathetic outflow:

- Vasodilation--> Drop in Blood pressure
- compensatory increase in HR

Pronounced with large doses or quick administration

21
Q

Respiratory Effects of Barbiturates

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A

Cause transient apnea
Decrease in MV
Decrease in CO2 triggered response to breath
Can Cause laryngospasm/bronchospasm

22
Q

Metabolism of Barbiturates

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A

Primarily by oxidation in liver
Produces inactive metabolites
Excreted in urine

23
Q

Absolute Contraindications to Barbiturate Use for induction

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A

Allergy to barbiturates.

History of porphyria

24
Q

Imidazole Ring

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A

Chemical Structure of Midazolam. This ring stays closed and makes it more lipophillic
This makes versed versatile-it can withstand big changes in pH.

25
Midazolam MOA
Activation of GABAa receptors and enhancement of GABA mediated Chloride channels. Influx of Chloride makes neuron hyperpolarized and less excitable.
26
CNS Effects of Midazolam
CMRO2 and CBF decrease Little to no effect on ICP Potent anti-convulsant, but can't create isoelectric EEG Paradoxical excitement occurs <1%
27
CV Effects of Midazolam
Global CNS hyperpolarization causes a decrease sympathetic response. Dose dependent decrease in SBP
28
Resp Effects of Midazolam
Min dose dependent decrease in ventilation. Transient apnea after fast IV administration (synergistic with opiods). Swallowing reflex depression.
29
Unique side effects of Midazolam
Amnesic effects- retrograde and anterograde. Sleep is not restorative- do not hit REM cycle. Phlebitis on administration d/t preservatives.
30
Withdrawal Symptoms from Benzos and Barbs
``` May last weeks to months CNS: Anxiety, insomnia, seizures, coma, agitation, mania, psychosis, suicide Cardio: Hypertension, tachycardia, postural hypotension ```
31
Flumazenil
``` 200mcg q1-2mins until effect. Benzo competitive antagonist. Flumazenil can only last around 30 mins. Some benzos can linger in the body for 3-12hrs. Due to their lipophilia. So multiple doses are often needed ```
32
Remimazolam Metabolism
It does not rely on liver for metabolism. Metabolized via esterases which are found in blood. Allows for very, very fast metabolism.
33
Chemical Structure of Propofol
Insoluble in dextrose or saline solutions. Chemically distinct in that it needs a lipid vehicle. Supports bacterial growth.
34
Propofol MOA
Relatively selective modulator of GABAa receptors.
35
Propofol Pharmacokinetics
Rapid onset of unconsciousness (30 sec). CYP substrate and Inhibitor Less hangover effect d/t rapid clearance from plasma through lungs, hepatic, etc.
36
CNS effects of Propofol
Decrease CMRO2, CBF, ICP, IOP. May see muscle twitching on induction. Minimal reduction in seizure activity.
37
CV effects of Propofol
Significant decrease in Blood pressure by reduction in preload and afterload. Dramatic inhibition of baroreceptor reflexes- may not see compensatory increase HR with decrease in BP
38
Respiratory effects of Propofol
Potent respiratory depressant. Apnea after induction dose. *Less frequency of laryngo/bronchospasms.* Decrease ventilatory response to hypoxia/hypercarbia.
39
Unique effects/properties of Propofol.
Anti-emetic Does not potentiate muscle relaxants. Significant reduction in upper airway reflexes. Potential for pulm embolism d/t large fatty particles.
40
Propofol Infusion Syndrome
Lactate Acidosis, *unexpected tachycardia (first sign)*, kidney failure, rhabdomylysis, hypertriglyceridemia. *hyperkalemia in kids*
41
What is fospropofol?
Also called Lusedra. Same MOA as propofol, minus the lipid vehicle. When injected, the "fos" part is removed and the prodrug (propofol) works as propofol normally does.
42
Ketamine MOA
Mixture of R and S enantiomers. | NMDA Receptor Antagonist which the end goal is to block flow of Calcium
43
Pharmacokinetics of Ketamine
Not significantly bound to plasma protein. Extremely lipid soluble. Leaves blood rapidly and is distributed to the tissues.
44
CNS Effects of Ketamine
Dissociative Anesthesia- Dissociates the limbic system from the thalamocortical system. Cerebral Vasodilator= Increase CBF, CMRO2, and potentially Increase ICP. Anti-convulsant properties. May witness myoclonic movements with administration
45
CV Effects of Ketamine
Associated with increase myocardial work. | Transient increase in BP, HR, CO.
46
Respiratory Effects of Ketamine
No significant respiratory depression. Preserved chemoreceptors. Increased salivation. Relaxes bronchial smooth muscle (good for asthmatic)
47
Potential post-op problems of Ketamine
Prevalence of post-operative delirium. | Can be decreased with pre-operative administration of a benzo.

Pharmacology (9 decks)

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