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Pharmacology > Lecture 12 (EXAM 3) > Flashcards

Lecture 12 (EXAM 3) Flashcards

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1
Q

The types of nicotinic antagonists

A

-Ganglionic blockers (in the autonomic ganglia)

-Neuromuscular blockers

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2
Q

Why do Ganglionic blockers have limited use?

A

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

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3
Q

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

A

Mecamylamine

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4
Q

Where are neuromuscular blockers used?

A

-Surgery for muscle paralysis

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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

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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

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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

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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

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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

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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)

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11
Q

Suffix for non-depolarizing steroidal neuromuscular blockers?

A

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

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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)

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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)

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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)

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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

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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??

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17
Q

Which type of drugs does Succinylcholine interact with?

A

-Aminoglycoside antibiotics

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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

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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)

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20
Q

What is a Catecholes?

A

Phenylring with 2 OH groups

Contained in Dopa, Dopamine, NE, Epinephrine

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21
Q

What determines which NT is formed from Tyrosine?

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A

The presence of the enzymes capable of building the specific NT

22
Q

What is the effect of Reserpine?

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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?

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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?

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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
What are the 3 ways a drug acts on a receptor?
-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
Similar structures of drugs to NT
-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
Major functions of receptors: α and Dopamine
α1: vasoconstriction increases BP α2 presynaptic (auto-receptor) and CNS: lowers BP Dopamine: Cardiac stimulation
28
How does α2 lower BP
By reuptake of NE into presynaptic neuron!
29
Major functions of receptors: ß
ß1: stimulates the heart ß2: bronchodilation
30
Location of ß receptors
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
Which NS is responsible for controlling the vascular smooth muscles?
Sympathetic NS vasoconstriction through α1receptors vasodilation through ß2 receptors
32
What is the α effect? What is the ß effect?
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
Why causes the decrease in HR in the α-effect?
Baroreceptors
34
Experiment to explain the decrease in HR in the α-effect Caused by the drug (Phenylephrine) or is it a reflex bradycardia?
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
Why is the change in HR bigger in the ß-effect than in the α-effect?
Because the heart has more ß-receptors than α-receptors -> ß-receptors are predominantly on the heart an kidneys to maintain bloodflow
36
What are the receptors causing vasoconstriction and vasodilation in the heart?
Vasoconstriction: α-1 Vasodilation: ß-2
37
What explains the initial vasodilation followed by vasoconstriction when Epinephrine is administered?
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
What is the effect of ß1-receptors?
increase in HR chronotrpic: faster ionotropic: harder dromotropic: conduction is quicker
39
What is the effect of NE as a drug?
-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
Effects of Epinephrine as a drug EMERGENCY signal
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
In what conditions is Epinephrine used?
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
Effects of Dopamine as a drug
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
Where is Dopamine used?
Heart failure the heart is not working hard enough to keep blood flow going
44
What is the ß agonist prototype
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
What is an example of a ß1 agonist
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
What are examples of ß2 agonists?
Short-acting: Albuterol, terbutaline Long-acting: salmeterol, formoterol Used for asthma and COPD, -> premature labor: Ritodrine is tocolytic
47
What are the adverse effects of ß2 agonists when they reach circulation?
(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
What are the compounds of ANORO ELLIPTA?
-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
What is BREO ELLIPTA?
- vilanterol: long-acting beta2-adrenergic agonist (LABA) Fluticasone: ICS (inhaled corticosteroid): reduction in the inflammatory process that leads to constriction of airways
50
Example of ß3-agonists
Mirabegron (Myrbetriq) -treats OAC (over-active bladder) -> men: BPH -Stimulates 3 receptors -> Relaxation of the detrusor mm (squeezes urine out of the bladder)
51
The function of ß3 receptors
-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)

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