Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Pharm Quiz 2 > Flashcards

Pharm Quiz 2 Flashcards

1
Q

MOA of Barbiturates?

A

Barbiturates mostly enhance GABA mediated inhibitory neurotransmitters.

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

How does GABA react at GABAa receptor?

A

They increase the ion channel flow of chloride

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

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

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

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

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

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

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

Are IV Induction medications lipophillic or hydrophillic?

A

Lipophillic

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

Vessel Rich Group

A

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

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

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

Compartment 1

A

Blood vessels and blood volume

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

Compartment 2

A

All the highly perfused/highly vascular organs:

Brain, liver, kidneys, gut, etc.

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

Compartment 3

A

Fat and vessel-poor group

Same compartment, but different phases.

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

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

A

Barbiturates

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

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

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

CNS Effects of Barbiturates

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

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

A

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

22
Q

Metabolism of Barbiturates

A

Primarily by oxidation in liver
Produces inactive metabolites
Excreted in urine

23
Q

Absolute Contraindications to Barbiturate Use for induction

A

Allergy to barbiturates.

History of porphyria

24
Q

Imidazole Ring

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
Q

Midazolam MOA

A

Activation of GABAa receptors and enhancement of GABA mediated Chloride channels. Influx of Chloride makes neuron hyperpolarized and less excitable.

26
Q

CNS Effects of Midazolam

A

CMRO2 and CBF decrease
Little to no effect on ICP
Potent anti-convulsant, but can’t create isoelectric EEG
Paradoxical excitement occurs <1%

27
Q

CV Effects of Midazolam

A

Global CNS hyperpolarization causes a decrease sympathetic response.
Dose dependent decrease in SBP

28
Q

Resp Effects of Midazolam

A

Min dose dependent decrease in ventilation.
Transient apnea after fast IV administration (synergistic with opiods).
Swallowing reflex depression.

29
Q

Unique side effects of Midazolam

A

Amnesic effects- retrograde and anterograde.
Sleep is not restorative- do not hit REM cycle.
Phlebitis on administration d/t preservatives.

30
Q

Withdrawal Symptoms from Benzos and Barbs

A 
May last weeks to months 
 CNS: Anxiety, insomnia, seizures, coma, 
agitation, mania, psychosis, suicide 
 Cardio: Hypertension, tachycardia, 
postural hypotension
31
Q

Flumazenil

A 
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
Q

Remimazolam Metabolism

A

It does not rely on liver for metabolism.
Metabolized via esterases which are found in blood.
Allows for very, very fast metabolism.

33
Q

Chemical Structure of Propofol

A

Insoluble in dextrose or saline solutions.
Chemically distinct in that it needs a lipid vehicle.
Supports bacterial growth.

34
Q

Propofol MOA

A

Relatively selective modulator of GABAa receptors.

35
Q

Propofol Pharmacokinetics

A

Rapid onset of unconsciousness (30 sec).
CYP substrate and Inhibitor
Less hangover effect d/t rapid clearance from plasma through lungs, hepatic, etc.

36
Q

CNS effects of Propofol

A

Decrease CMRO2, CBF, ICP, IOP.
May see muscle twitching on induction.
Minimal reduction in seizure activity.

37
Q

CV effects of Propofol

A

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
Q

Respiratory effects of Propofol

A

Potent respiratory depressant.
Apnea after induction dose.
Less frequency of laryngo/bronchospasms.
Decrease ventilatory response to hypoxia/hypercarbia.

39
Q

Unique effects/properties of Propofol.

A

Anti-emetic
Does not potentiate muscle relaxants.
Significant reduction in upper airway reflexes.
Potential for pulm embolism d/t large fatty particles.

40
Q

Propofol Infusion Syndrome

A

Lactate Acidosis, unexpected tachycardia (first sign), kidney failure, rhabdomylysis, hypertriglyceridemia.
hyperkalemia in kids

41
Q

What is fospropofol?

A

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
Q

Ketamine MOA

A

Mixture of R and S enantiomers.

NMDA Receptor Antagonist which the end goal is to block flow of Calcium

43
Q

Pharmacokinetics of Ketamine

A

Not significantly bound to plasma protein.
Extremely lipid soluble.
Leaves blood rapidly and is distributed to the tissues.

44
Q

CNS Effects of Ketamine

A

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
Q

CV Effects of Ketamine

A

Associated with increase myocardial work.

Transient increase in BP, HR, CO.

46
Q

Respiratory Effects of Ketamine

A

No significant respiratory depression.
Preserved chemoreceptors.
Increased salivation.
Relaxes bronchial smooth muscle (good for asthmatic)

47
Q

Potential post-op problems of Ketamine

A

Prevalence of post-operative delirium.

Can be decreased with pre-operative administration of a benzo.

Pharmacology (9 decks)

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