Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Lecture 12 (EXAM 3) > Flashcards

Lecture 12 (EXAM 3) Flashcards

1
Q

The types of nicotinic antagonists

A

-Ganglionic blockers (in the autonomic ganglia)

-Neuromuscular blockers

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

Why do Ganglionic blockers have limited use?

A

Because of low specificity (neurons pass ganglia - so it will affect all autonomic nerves)

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

Which drug blocks nicotinic receptors of the autonomic (involuntary) NS?

A

Mecamylamine

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

Where are neuromuscular blockers used?

A

-Surgery for muscle paralysis

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

Two types of neuromuscular blockers?

A

Succinylcholine: Depolarizing muscle cells and keeping them depolarized -> limits the ability to contract

All others: Non-depolarizing (competitive antagonist on the receptors of the muscle cells) -> charged N+ (like Acetylcholine) and steroidal backbone

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

RECAP

A

Motorneuron on muscle:
AP comes down to the Axon -> Ca gets into the cell -> vesicle fuse with the presynaptic membrane -> ACh release -> ACh binds to ACh receptor (Na channel), which opens -> depolarizes of muscle membrane -> Ca level goes up -> Ca binds Troponin C -> movement of tropomyosin -> muscle contraction

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

Components of a nicotine ACh receptor in skeletal muscles and in the CNS?

A

-Skeletal muscles: 2 alpha, ß, gamma, and delta subunit -> has 2 binding sites for ACh at the alpha units - both have to be occupied to open the receptor (Na channel)

-CNS and ganglionic: different compositions of alpha and ß units

Blocking will result in PARALYSIS

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

Why does Succinylcholine have a depolarizing effect?

A

Because it is composed of two Acetylcholine, that binds on the two binding sites of the ACh receptors and keeps it open -> DEPOLARIZING

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

Why does Succinylcholine has a paralyzing effect?

A

The receptor opens, closes, and resets in order for muscle contraction to occur -> this cycle is disrupted with Succinylcholine

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

Properties of Non-steroidal neuromuscular blockers?

A

-suffix: curarine, curium
-non-steroidal
-non-depolarizing
-bulky
-charged N+ don’t cross BBB, work peripherally
(used for animal hunting as poison -> digestible bc the poison gets degraded in the stomach)

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

Suffix for non-depolarizing steroidal neuromuscular blockers?

A

-curonium
-don’t cross BBB
-non-depolarizing

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

Properties os Succinylacetlycholine

A

-short half-life -> giving through constant IV drops, the effect can be easily stopped by stopping the IV

-no detectable metabolites bc it is broken into ACh (ACh is abundant in the body, no evidence in murderer)

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

What would be an antidote for a competitive neuromuscular blocker? (NON-DEPOLARIZING) -> blocks the binding site -> Channel is closed

A

A drug that blocks the AChE -> so ACh will build up and outcompetes the competitor

f.e. in the Myasthenia Gravis test: Edrophonium (Tensilon)

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

RECAP Lecture 11
What are examples of AChE inhibitors?

A

doesnt cross the BBB
* Neostigmine (Prostigmin)
* Pyridostigmine (Mestinon or Regonol)
* Ambenonium (Mytelase)

Cross the BBB
* Physostigmine (Antilirium)
* Tacrine (Cognex)
* Donepezil (Aricept)
* Galantamine (Reminyl)

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

What are the effects of Succinylcholine on a patch clamp measure?

A

low dose: single depolarizations

high dose: Phase I: Flickering, Depolarization -> Phase II: loss of depolarization

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

What would be an antidote for Succinylcholine?
DEPOLARIZING -> blocks the binding site -> Channel is open

A

There is no antidote?
WHY? Wouldnt a non-depolarizing blocker at least stop the constant opening of the channel??

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

Which type of drugs does Succinylcholine interact with?

A

-Aminoglycoside antibiotics

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

What are the two types of sympathetic agents?

A
  • Sympathomimetics – mimic the effects of the sympathetic NS
    -> AGONISTS

-Sympatholytics – block the effects of the sympathetic NS
-> ANTAGONIST

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

Steps from Tyrosine to Epinephrine

A

Tyrosine -> Dopa (by Tyrosine hydroxylase: adds OH to Tyrosine)
Dopa -> Dopamine (by Dopa decarboxylase: removes the carboxylic group from C-chain)

Dopamine to NE (by Dopamine ß hydroxylase: adds OH to alpha carbon)
NE to Epinephrine by Phenylethanolamine-N-methyltransferase: adds CH3 to the amine)

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

What is a Catecholes?

A

Phenylring with 2 OH groups

Contained in Dopa, Dopamine, NE, Epinephrine

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

What determines which NT is formed from Tyrosine?

A

The presence of the enzymes capable of building the specific NT

22
Q

What is the effect of Reserpine?

A

It blocks the uptake of the present Catechol in the vesicles within the presynaptic neuron

23
Q

How is NE getting removed from the synaptic cleft?

A

-Reuptake by NET into the presynaptic neuron (blocked by Cocaine or antidepressants)
-Uptake by other cells and get metabolized by COMT and MOA
-Autoreceptor: negative feedback, decreases NE release

24
Q

Which enzymes metabolizes NE?

A

COMT: catechol-O-methyltransferase
-widely distributed: nervous tissue, liver, kidney, intestine
-> cant gives Epinephrine orally bc metabolized by COMT
-metabolizes catecholamines and drugs
-by transferring a methyl group

Monoamine oxidase: MAO
-metabolizes monoamines in NE, Epi, Dopamine, 5-HT (serotonin)

25
Q

What are the 3 ways a drug acts on a receptor?

A

-Direct acting
-Indirect acting: stimulates the release, affects reuptake, or prevention of breakdown by MAO(-), COMT(-)
-Mixed-acting: Mix of direct and indirect acting

26
Q

Similar structures of drugs to NT

A

-structures of the agonist drugs are often very similar to the NT.

-NT themselves are used for drugs; affinity for ß receptor increases with the increase of the molecule

27
Q

Major functions of receptors: α and Dopamine

A

α1: vasoconstriction increases BP
α2 presynaptic (auto-receptor) and CNS: lowers BP

Dopamine: Cardiac stimulation

28
Q

How does α2 lower BP

A

By reuptake of NE into presynaptic neuron!

29
Q

Major functions of receptors: ß

A

ß1: stimulates the heart
ß2: bronchodilation

30
Q

Location of ß receptors

A

ß1:
Heart stimulated (inotropic - the strength of contraction, chronotropic - faster heart rate, dromotropic - stimulates the rate of the signal goes to the heart)
Kidney Juxtaglomerular cells – renin release -> Angiotensin to Angiotensin I -> Angiotensin II -> increase BP

ß2:
Blood vessels (dilate – oppose α1)
 Bronchioles (dilate)
 Uterus (relax)
 Liver (glycogenolysis)
 Pancreas (mild insulin stimulation)
 Skeletal mm (increased contractility)
 Eye (relax ciliary mm for far vision)

31
Q

Which NS is responsible for controlling the vascular smooth muscles?

A

Sympathetic NS
vasoconstriction through α1receptors
vasodilation through ß2 receptors

32
Q

What is the α effect?

What is the ß effect?

A

opposite effect with similar drugs on the same organ due to different receptors

-α-effect: vasoconstriction -> increase in BP (systolic, diastolic) and decrease in HR
-ß-effect: vasodilation -> decrease in BP and increase in HR

(Epinephrine will cause an increase in systolic and a decrease in diastolic BP)

33
Q

Why causes the decrease in HR in the α-effect?

A

Baroreceptors

34
Q

Experiment to explain the decrease in HR in the α-effect
Caused by the drug (Phenylephrine) or is it a reflex bradycardia?

A

Pretreatment with mecamylamine (than Phenylephrine) -> a ganglionic nicotinic receptor blocker -> no transmission on the autonomic ganglia -> no effect on the HR

-> Baroreceptor-mediated reflex mechanism

35
Q

Why is the change in HR bigger in the ß-effect than in the α-effect?

A

Because the heart has more ß-receptors than α-receptors

-> ß-receptors are predominantly on the heart an kidneys to maintain bloodflow

36
Q

What are the receptors causing vasoconstriction and vasodilation in the heart?

A

Vasoconstriction: α-1

Vasodilation: ß-2

37
Q

What explains the initial vasodilation followed by vasoconstriction when Epinephrine is administered?

A

Hormetic effect !! -> different effects depending on the dose
at low doses epinephrine cause vasodilation (ß2) because there are more ß2 receptors than α1 receptors on the heart -> higher doses will cause vasoconstriction caused by the α1-receptors

38
Q

What is the effect of ß1-receptors?

A

increase in HR
chronotrpic: faster
ionotropic: harder
dromotropic: conduction is quicker

39
Q

What is the effect of NE as a drug?

A

-low dose/any dose: α-1 vasoconstriction (vasoconstriction persists at high dose)

-high dose: acts on ß1 receptors -> increase in HR (ionotropic, chronotropic, dromotropic)
-> Initially no effect on HR because of reflex bradycardia
-> Vasoconstriction and an increase in HR will stress the heart (DANGEROUS)

40
Q

Effects of Epinephrine as a drug

EMERGENCY signal

A

low dose: ß-effect
ß1: increase in HR (ionotropic, chronotropic, dromotropic)
ß2: bronchodilation, vasodilation

high dose: α-effect
α1: vasoconstriction

Hyperglycemia:
α2: blood glucose goes up bc insulin is inhibited
ß2: glucagon release -> glycogen breakdown to glucose; lipolysis, FFA release

41
Q

In what conditions is Epinephrine used?

A

Anaphylactic shock, cardiac emergencies, asthma emergencies

included in local anesthesia bc it is a vasoconstrictor and helps to keep the anesthetics longer in the area
-> high dose at a local spot -> restricts blood flow to keep locals local (also reduces bleeding)

42
Q

Effects of Dopamine as a drug

A

ß1: increase in NE release -> stimulates the heart
-> also improves renal blood flow (important in heart failure bc the kidney needs a lot of blood flow)

43
Q

Where is Dopamine used?

A

Heart failure
the heart is not working hard enough to keep blood flow going

44
Q

What is the ß agonist prototype

A

Isoproterenol

-demonstrated the ß-effect, stimulates ß1 and ß2!!

ß1: cardiac stimulant (ionotropic, chronotropic, dromotropic)
ß2: bronchodilation, vasodilation

-cardiac stimulation and bronchodilation and vasodilation is not needed at the same time

45
Q

What is an example of a ß1 agonist

A

Dobutamine (Dobutrex)
ß1: increase cardiac output -> This drug is predominantly ionotropic (stronger -> pumps more blood with each beat)

-> Stimulation of heart strength is bigger than stimulation of velocity of pumping -> bc it costs less oxygen when increasing SV (stroke volume) than making the heart to beat faster

46
Q

What are examples of ß2 agonists?

A

Short-acting: Albuterol, terbutaline
Long-acting: salmeterol, formoterol

Used for asthma and COPD,
-> premature labor: Ritodrine is tocolytic

47
Q

What are the adverse effects of ß2 agonists when they reach circulation?

A

(they usually don’t reach circulation when inhaled)

-Cardiac arrhythmia (bc they also stimulate ß1 to some extent)
-decrease in plasma K+
-blood glucose goes up

48
Q

What are the compounds of ANORO ELLIPTA?

A

-used for COPD - not asthma (increase mortality when used in asthma)

-umeclidinium: anticholinergic (blocks muscarinic receptor -> sympathetic effect -> Vasodilation?)

-vilanterol: long-acting beta2-adrenergic agonist (LABA)

49
Q

What is BREO ELLIPTA?

A

-

vilanterol: long-acting beta2-adrenergic agonist (LABA)
Fluticasone: ICS (inhaled corticosteroid): reduction in the inflammatory process that leads to constriction of airways

50
Q

Example of ß3-agonists

A

Mirabegron (Myrbetriq)

-treats OAC (over-active bladder) -> men: BPH
-Stimulates 3 receptors -> Relaxation of the detrusor mm (squeezes urine out of the bladder)

51
Q

The function of ß3 receptors

A

-Mediate lipolysis (breakdown of tri glycerols in fat cells)
-activate UCP (uncoupling proteins - breaks the link between electron transport and ATP synthesis in mitochondria) -> electron transport without producing ATP, but heat
-may cause relaxation of prostate smooth muscle

Pharmacology (14 decks)

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