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ACh

Biosynthesis

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by choline acetyltransferase (ChAT)

rate-limiting: Availability of choline and acetyl-CoA

--> used choline:

  • recycling of choline from metabolized ACh
  • breakdown of the phospholipid, phosphatidylcholine

--> to increase ACh: substitution of ACh with food/diet eg egg yolk, vegetabels (soy, beans), meat (liver)

Lösung ausblenden
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ACh

Degradation

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  • by acetylcholinesterase (AChE)
  • after a briefly (kurze) binding to the pre- and postsynaptic receptors
  • hydrolyzed into acetat and choline
    • choline is transported back into nerve terminals (Nervenendigung) to resynthesize ACh
  • AChE: synthesized in neuronal cell body and distributes throught the neuron by axoplasmic transport (between soma (Zellkörper) and nerve terminal)
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Autonomic nervous system (Vegetatives NS)

Sympathetic 

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  • postganglionic neurotransmitter: norepinephrin (/noradrenalin)
  • "fight-or-flight"


specific reactions:

  • positive chronotrop
  • dilation of bronchial tubes and pupils
  • contraction of muscles
  • Release of adrenaline from the adrenal gland
  • Conversion of glycogen to glucose to provide energy for the muscles
  • Shut down of processes not critical for survival.
Lösung ausblenden
TESTE DEIN WISSEN

Autonomic nervous system

Parasympathetic

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  • postganglionic neurotransmitter: acetylcholine
  • "rest-and-digest"


specific reactions:

  • negative chronotrop
  • constriction of bronchial tubes and pupils
  • relaxation of muscles
  • Saliva (Speichel) production: stomach movement and increased secretions for digestion
  • Increase in urinary output
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Nicotinic receptors

muscular nicotine receptor

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  • located in muscles
  • 2 α, β, δ, γ 


Attacking muscle relaxans:

  • Non-depolarizing: tubocurarine (antagonist)
  • Depolarizing: suxamethonium (agonist)
Lösung ausblenden
TESTE DEIN WISSEN

Nicotinic receptors

differ between neuronal and muscular

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addition of α-bungarotoxin

  • neuronal: reversible binding
  • muscular: irreverseble binding
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Muscarinic receptors

general

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  • synonym: m-cholinoreceptors
  • G-protein coupled receptors (GPCR)
  • also activated by muscarine (agonist)
  • blocked by atropine (antagonist)
  • 5 Subtypes (M1-M5)


Subtypes:

M1: neuronal structures (stratium, cortex, hippocampus)

M2: heart --> neg. chronotrop (Forebrain, thalamus, heart, pupils, spinal cord, exorine)

M3: smooth muscles --> contraction; endokrine glands --> secretion (Brain, hypothalamus, pupils, exocrine, peripheral arteries)

M4: stratium, cortex, hippocampus, spinal cord

M5: Dopaminergic neurons, basal ganglia, brain vasculature

Lösung ausblenden
TESTE DEIN WISSEN

Muscarinic receptors

mechanism

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--> G-protein coupled receptors (Gs ?)

  1. ACh binds to receptor => corformation change
  2. GDP is replaced by GTP => α-subunit activated
  3. α-subunit dissolves from other 2 subunits and attaches to adenylat cyclase (AC)
  4. AC converts ATP to cAMP (--> second messenger)
  5. Hydrolysis of GTP to GDP at α-subunit => inactivation of AC 
Lösung ausblenden
TESTE DEIN WISSEN

Muscle relaxants

general

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--> peripherally acting agents have no effect on CNS - patient is fully conscious

Structual precondition: 2 four-membered nitrogen groups (2 pos. charged nitrogen groups)

Application:

  • reduction of motor activity
  • Anesthesia
  • in case of poisoning, which leads to increased motor activity

Disadvantages:

respiratory muscles are not very sensitive to muscle relaxants

--> nevertheless it may cause respiratory paralysis during use with short-acting narcotic agents


Lösung ausblenden
TESTE DEIN WISSEN

Muscle relaxants

Non depolarizing agents bzw. stabilisierend

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= kompetitive ACh-Rezeptor-Antagonisten --> verhindert Depolarisation der Endplattenmembran u. somit Verhinderung der Muskelkontraktion

--> Curare-Typ: Tubo-curarin-Chlorid (starke UAWs durch Histamin-Ausschüttung, daher obsolet), Pan-curonium-bromid, Ve-curonium-bromid

Struktur: 2 pos. geladene N, die in Ringsystemen gebunden sind (quartäre Ammoniumverbindunen)

WW:

  • Wirkung wird aufgehoben durch Cholinesterase-Inhibitoren (zb Neostigmin) --> verdrängt durch steigende ACh-Level
  • verlängern anästhesierenden Effekt der Isoflurane
  • verlängern Wirkung der Tetracycline u. Aminoglykoside

UAW:

  • gesteigerte Histamin-Freisetzung
  • p.lytische Effekte (Mundtrockenheit, Tachykardie, Akkomodationsstörungen, RR-Anstieg)
Lösung ausblenden
TESTE DEIN WISSEN

Muscle relaxants

Depolarizing agents

Lösung anzeigen
TESTE DEIN WISSEN

= ACh-Rezeptor-Agonisten

--> Suxamethonium-Typ: Suxamethonium-chlorid (auch Succinylcholin)

mechanism:

  • they bind to ACh receptors and generate an action potential (AP)
  • acetylcholine esterase can not metabolize and degrade
  • depolarization of the motor endplate is extended
  • no new AP can be generated => no contraction

Structure: 2 pos. charged nitrogen groups in chain

WW: Cholinesterase-Inhibitoren verstärken Effekt

UAW: maligne hyperthermie (rapid increase in body temp with muscle contraction), parasympathomimetic symptoms (zb neg. chronorop, RR-Abfall, Bronchokonstriktion)

Lösung ausblenden
TESTE DEIN WISSEN

Muscle relaxants

BOTOX - general

Lösung anzeigen
TESTE DEIN WISSEN

Bolulinum toxin (BTX / BoNT) produced by Clostridium botulinum (gram-positive anaerobic bacteria)

  • inhibits release of ACh from presynaptic motor neurons
    • action in neuromuscular junction
    • => muscle paralysis
  • 7 toxin-types are existing
    • only A and B are used clinically
Lösung ausblenden
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Q:

ACh

Biosynthesis

A:

by choline acetyltransferase (ChAT)

rate-limiting: Availability of choline and acetyl-CoA

--> used choline:

  • recycling of choline from metabolized ACh
  • breakdown of the phospholipid, phosphatidylcholine

--> to increase ACh: substitution of ACh with food/diet eg egg yolk, vegetabels (soy, beans), meat (liver)

Q:

ACh

Degradation

A:
  • by acetylcholinesterase (AChE)
  • after a briefly (kurze) binding to the pre- and postsynaptic receptors
  • hydrolyzed into acetat and choline
    • choline is transported back into nerve terminals (Nervenendigung) to resynthesize ACh
  • AChE: synthesized in neuronal cell body and distributes throught the neuron by axoplasmic transport (between soma (Zellkörper) and nerve terminal)
Q:

Autonomic nervous system (Vegetatives NS)

Sympathetic 

A:
  • postganglionic neurotransmitter: norepinephrin (/noradrenalin)
  • "fight-or-flight"


specific reactions:

  • positive chronotrop
  • dilation of bronchial tubes and pupils
  • contraction of muscles
  • Release of adrenaline from the adrenal gland
  • Conversion of glycogen to glucose to provide energy for the muscles
  • Shut down of processes not critical for survival.
Q:

Autonomic nervous system

Parasympathetic

A:
  • postganglionic neurotransmitter: acetylcholine
  • "rest-and-digest"


specific reactions:

  • negative chronotrop
  • constriction of bronchial tubes and pupils
  • relaxation of muscles
  • Saliva (Speichel) production: stomach movement and increased secretions for digestion
  • Increase in urinary output
Q:

Nicotinic receptors

muscular nicotine receptor

A:
  • located in muscles
  • 2 α, β, δ, γ 


Attacking muscle relaxans:

  • Non-depolarizing: tubocurarine (antagonist)
  • Depolarizing: suxamethonium (agonist)
Mehr Karteikarten anzeigen
Q:

Nicotinic receptors

differ between neuronal and muscular

A:

addition of α-bungarotoxin

  • neuronal: reversible binding
  • muscular: irreverseble binding
Q:

Muscarinic receptors

general

A:
  • synonym: m-cholinoreceptors
  • G-protein coupled receptors (GPCR)
  • also activated by muscarine (agonist)
  • blocked by atropine (antagonist)
  • 5 Subtypes (M1-M5)


Subtypes:

M1: neuronal structures (stratium, cortex, hippocampus)

M2: heart --> neg. chronotrop (Forebrain, thalamus, heart, pupils, spinal cord, exorine)

M3: smooth muscles --> contraction; endokrine glands --> secretion (Brain, hypothalamus, pupils, exocrine, peripheral arteries)

M4: stratium, cortex, hippocampus, spinal cord

M5: Dopaminergic neurons, basal ganglia, brain vasculature

Q:

Muscarinic receptors

mechanism

A:

--> G-protein coupled receptors (Gs ?)

  1. ACh binds to receptor => corformation change
  2. GDP is replaced by GTP => α-subunit activated
  3. α-subunit dissolves from other 2 subunits and attaches to adenylat cyclase (AC)
  4. AC converts ATP to cAMP (--> second messenger)
  5. Hydrolysis of GTP to GDP at α-subunit => inactivation of AC 
Q:

Muscle relaxants

general

A:

--> peripherally acting agents have no effect on CNS - patient is fully conscious

Structual precondition: 2 four-membered nitrogen groups (2 pos. charged nitrogen groups)

Application:

  • reduction of motor activity
  • Anesthesia
  • in case of poisoning, which leads to increased motor activity

Disadvantages:

respiratory muscles are not very sensitive to muscle relaxants

--> nevertheless it may cause respiratory paralysis during use with short-acting narcotic agents


Q:

Muscle relaxants

Non depolarizing agents bzw. stabilisierend

A:

= kompetitive ACh-Rezeptor-Antagonisten --> verhindert Depolarisation der Endplattenmembran u. somit Verhinderung der Muskelkontraktion

--> Curare-Typ: Tubo-curarin-Chlorid (starke UAWs durch Histamin-Ausschüttung, daher obsolet), Pan-curonium-bromid, Ve-curonium-bromid

Struktur: 2 pos. geladene N, die in Ringsystemen gebunden sind (quartäre Ammoniumverbindunen)

WW:

  • Wirkung wird aufgehoben durch Cholinesterase-Inhibitoren (zb Neostigmin) --> verdrängt durch steigende ACh-Level
  • verlängern anästhesierenden Effekt der Isoflurane
  • verlängern Wirkung der Tetracycline u. Aminoglykoside

UAW:

  • gesteigerte Histamin-Freisetzung
  • p.lytische Effekte (Mundtrockenheit, Tachykardie, Akkomodationsstörungen, RR-Anstieg)
Q:

Muscle relaxants

Depolarizing agents

A:

= ACh-Rezeptor-Agonisten

--> Suxamethonium-Typ: Suxamethonium-chlorid (auch Succinylcholin)

mechanism:

  • they bind to ACh receptors and generate an action potential (AP)
  • acetylcholine esterase can not metabolize and degrade
  • depolarization of the motor endplate is extended
  • no new AP can be generated => no contraction

Structure: 2 pos. charged nitrogen groups in chain

WW: Cholinesterase-Inhibitoren verstärken Effekt

UAW: maligne hyperthermie (rapid increase in body temp with muscle contraction), parasympathomimetic symptoms (zb neg. chronorop, RR-Abfall, Bronchokonstriktion)

Q:

Muscle relaxants

BOTOX - general

A:

Bolulinum toxin (BTX / BoNT) produced by Clostridium botulinum (gram-positive anaerobic bacteria)

  • inhibits release of ACh from presynaptic motor neurons
    • action in neuromuscular junction
    • => muscle paralysis
  • 7 toxin-types are existing
    • only A and B are used clinically
Acetylcholin

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