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MD2002 Arvin > Autonomic NS 3 > Flashcards

Autonomic NS 3 Flashcards

1
Q

Give examples of catecholamines.

A

Adrenaline, Dopamine, Noradrenaline

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2
Q

How may Tyrosine hydroxylase be inhibited ?

A

By catecholamines (hence negative feedback)

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3
Q

How may DOPA decarboxylase be targeted ?

A

Using Methyldopa

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4
Q

Where is Dopamine beta-hydroxylase enzyme located ?

A

Membrane bound

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5
Q

Where PMNT located ? How is its release induced ?

A

Mainly located in adrenal medulla

Induced by adrenal cortex hormone

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6
Q

Describe the process of Noradrenaline release.

A

Release facilitated by Ca2+ (hence ↓Ca2+ influx means ↓NA release)

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7
Q

Is there an equivalent of anticholinesterases for NA ?

A

No

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8
Q

What process occurs if excessive NA if release in the synapse ?

A

Binds to α2 adrenoreceptors on pre-synaptic terminal, which goes on to inhibit Calcium intake, thereby reducing NA release

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9
Q

What molecules, besides NA, do vesicles contain during NA release ?

A

ATP (has its own receptors on post-synaptic terminal)

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10
Q

How much of the NA is recaptured by neurons ?

A

75%

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11
Q

Which molecules are responsible for NA re-uptake and re-packaging ?

A
  • Norepinephrine transporter (NET)

- Vesicular monoamine transporter (VMAT) (re-packages it)

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12
Q

What are some drugs which can affect noradrenergic neurons ? Give examples for each.

A

DRUGS AFFECTING CATECHOLAMINE SYNTHESIS
– e.g. methyldopa

DRUGS AFFECTING CATECHOLAMINE RELEASE
– Indirectly acting sympathomimetics – e.g. amphetamines – By acting on α2 adrenoreceptors – e.g. clonidine

INHIBITORS OF CATECHOLAMINE UPTAKE
– NET inhibitors – e.g. cocaine, tricylic antidepressants

INHIBITORS OF CATECHOLAMINE METABOLIC DEGRADATION
– Monoamine oxidase inhibitors used in depression

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13
Q

Which kind of receptors are Adrenergic receptors ?

A

Metabotropic (G-protein coupled receptors)

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14
Q

What are the main groups of adrenoreceptors ?

A

α1, α2

β1, β2, β3

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15
Q

Are there exploitable differences in the selectivity of these receptors (α1, α2, β1, β2, β3) for catecholamines ? Which ones ?

A

Yes, differences in tissue distribution

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16
Q

Identify the main ANS locations of α1, α2, β1 and β2 adrenoreceptors.

A

α1
Cardiovascular
GI tract
Genitourinary

α2
Neuronal

β1
Heart
Kidneys

β2
Lungs
Smooth muscle
Skeletal muscle

17
Q

Identify the functional ANS response of α1, α2, β1 and β2 adrenoreceptors.

A

α1
Vasoconstriction
Smooth muscle contraction (GI sphincters and genitourinary)

α2
↓transmi tter release

β1
↑ cardiac rate
↑ cardiac force
Renin release

β2
Bronchodilation
Relaxation of visceral smooth muscle
Vasodilation (sk. muscle) Tremor

18
Q

Which kind of receptor should be targeted when treating nasal congestion ? Why ? Which drugs may used against Nasal Congestion ?

A

α1 because nasal congestion is mainly due to vasodilation in nasal mucosa and α1 stimulation can give rise to vasoconstriction

PHENYLEPHRINE (Constriction of airway blood vessels (α1))

19
Q

What are some symptoms of asthma ?

A

Coughing
Wheezing
Shortness of breath
Tightness in the chest

20
Q

Which kind of receptor should be targeted when treating asthma ? Why ? Which drugs may used against asthma ?

A

β2 because asthma involves brachoconstriction and β2 stimulation can give rise to brachodilation

SALBUTAMOL, SALMETEROL (all give cause brachodilation)

21
Q

What are some side effects of salbutamol and salmeterol ? Why ?

A

Muscle tremor and Cardiac arrhythmias
Because tremors are linked to β2 which is stimulated here, whilst arrhythmias are due to the fact that they have a little affinity for β1 leading to some β1 functional response (i.e. ↑ cardiac rate ↑ cardiac force)

22
Q

What is the main difference between Salbutamol and Salmeterol ?

A

Short-acting (Short Acting Beta2 Agonist = SABA) = salbutamol
Long-acting (Long Acting Beta2 Agonist = LABA) = salmeterol

23
Q

What is premature labour defined as ?

A

Occurring between 24 and 33 weeks of gestation

24
Q

Which kind of receptor should be targeted when delaying labour ? Why ? Which drugs may be used for this ?

A

β2 because it stimulates relaxation of visceral smooth muscle (including uterine muscle)

Salbutamol

25
Q

How does the sympathetic NS control BP ? Mention any important adrenoreceptors involved.

A
  1. INCREASES CARDIAC OUTPUT (HEART)
    - Increases heart rate
    - Increases volume pumped out at each stroke
    - β1 receptors mediates both ^
  2. INCREASES TOTAL PERIPHERAL RESISTANCE (ARTERIES)
    - Constricts blood vessels (mainly small arteries/arterioles)
    - α1 receptors mediates this
26
Q

Define Cardiogenic shock.

A

Damaged heart, unable to supply enough blood to the organs of the body

27
Q

Which kind of receptor should be targeted in cardiogenic shock ? Why ? Which drugs may be used for this ?

A

β1 because cardiogenic shock involves insufficient blood supply to the body, and the activation of β1 stimulates increased heart rate and increased force.

Dobutamine

28
Q

Which kind of receptor should be targeted in Hypertension ? Why ? Which drugs may be used for this ?

A

α1 (inhibiting it) because α1 causes vasoconstriction
β1 (inhibiting it) because β1 causes ↑ cardiac rate ↑ cardiac force and ↑ renin release by kidneys
α2 (stimulating it) because α2 causes ↓ NA release

PRAZOSIN (blocks α1 receptors)
Vasodilation

PROPRANOLOL (blocks β1 receptors)
↓ heart rate and force
↓ renin release by kidneys

ATENOLOL (blocks β1 receptors)
↓ heart rate and force
↓renin release by kidneys

CLONIDINE (stimulates pre-synaptic α2 receptors)
↓ NA release
Central effect

29
Q

What are cardiac dysrhthmias ?

A

Atrial fibrillations, with palpitations, rapid heart rate and inefficient cardiac output

30
Q

Which kind of receptor should be targeted in dysrhthmias ? Why ? Which drugs may be used for this ?

A

β1 (inhibiting it) because β1 causes ↑ cardiac rate ↑ cardiac force and ↑ renin release by kidneys

PROPRANOLOL (blocks β1 receptors)
↓ heart rate and force
↓ renin release by kidneys

ATENOLOL (blocks β1 receptors)
↓ heart rate and force
↓renin release by kidneys

31
Q

What is a cardiac arrest ?

A

Cessation of normal cardiac function

32
Q

Which kind of receptor should be targeted in cardiac arrests ? Why ? Which drugs may be used for this ?

A

α1 (stimulating it) because α1 causes vasoconstriction
β1 (stimulating it) because β1 causes ↑ cardiac rate ↑ cardiac force

ADRENALINE
Vasoconstriction
↑ cardiac rate ↑ cardiac force

33
Q

What are the symptoms of anaphylaxis ?

A
  • Narrowing of airways
  • Sudden drop in blood pressure
  • Red raised itchy skin rash
  • Swelling of eyes, lips, hands and feet
34
Q

Which kind of receptor should be targeted in anaphylaxis ? Why ? Which drugs may be used for this ?

A

α1 (stimulating it) because α1 causes vasoconstriction
β1 (stimulating it) because β1 causes ↑ cardiac rate ↑ cardiac force
β2 (stimulating it) because β2 causes bronchodilation and ↓ histamine release by mast cells

ADRENALINE
Vasoconstriction 
↑ heart rate and force  
Bronchodilation 
↓ histamine release by mast cells
35
Q

What is the main symptom of benign prostatic hyperplasia

A

Problems with passing urine due to swollen prostate

36
Q

Which kind of receptor should be targeted in benign prostatic hyperplasia ? Why ? Which drugs may be used for this ?

A

α1 (blocking it) in order to block smooth muscle contraction

PRAZOSIN
-Relax bladder neck and prostate capsule

TAMSULOSIN
-More prostate-specific

37
Q

Name all the main adrenoreceptor agonists.

A 
Adrenaline 
Clonidine
Dobutamine 
Noradrenaline
Phenylephrine
Salbutamol 
Salmeterol
38
Q

Name all the main adrenoreceptor antagonists.

A 
Atenolol 
Carvedilol
Phentolamine 
Prazosin 
Propranolol
39
Q

Describe the synthesis of these different catecholamines, naming the enzymes involved. Which is the RLS?

A

Tyrosine (enzyme: Tyrosine hydroxylase) –> DOPA (enzyme: DOPA decarboxylase) –> Dopamine (enzyme: Dopamine β-hydroxylase (DBH)) –> Noradrenaline (enzyme: PNMT) –> Adrenaline

The RLS is the initial state (conversion of Tyrosine into DOPA)

MD2002 Arvin (110 decks)

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