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BIOM2402 > Module 2 part 2 > Flashcards

Module 2 part 2 Flashcards

1
Q

You are stimulating the sympathetic control center in a mouse.
What do you see?

A

Eye: Mydriasis
Lung: bronchodilation
GI-tract: Constipation
Heart: tachycardia
Blood vessels:
– Skin and viscera: vasoconstriction
– Skeletal muscle: vasodilation
– Adrenal gland: activation, NA and A release

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2
Q

Catecholamines:
Tyrosine-derived neurotransmitters

A

Tyrosine
DOPA
dopamine
Noradrenaline (Norepinephrine)
Adrenaline (Epinephrine)

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3
Q

Transmitters and Receptors in the
Sympathetic NS

A

Noradrenaline / Adrenaline
>
Adrenergic receptors GPCR
>
(α1, α2) (β1, β2)
*(β3 -adipose tissue, only)

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4
Q

α1

A

Gq
IP3/DAG ^

Smooth muscle contraction
Vasoconstriction in viscera,
M. dilator pupillae
GI sphincters

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5
Q

β1

A

Gs
cAMP
Heart:
Frequency, contractile force, conduction at A-V node

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6
Q

β2

A

Gs
cAMP
Smooth muscle relaxation:
Vasodilation in skeletal muscle GI motility
Bronchi: Dilation

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7
Q

andrenergic receptors

A

α1
Eyes: M. dil.pupillaecontraction (pupil dilation)
Arteries and veins: vasoconstriction in viscera and skin ; vasodilation in
skeletal muscle

β1
Heart: increased heart rate & force of beating (positive chronotropy and inotropy)
Arteries and veins: vasoconstriction in viscera and skin ; vasodilation in
skeletal muscle

β2
Lungs: relaxation of trachea & bronchi to facilitate respiration
Liver: increased glycogenolysis
Adrenals: NA and A release
Stomach & GI: decreased motility sphincter constriction

β3
Adipose tissue: increased lipolysis

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8
Q

Blood pressure

A

Blood pressure (BP) is regulated by the ANS through regulation of:
1) Resistance in arteries (vessel diameter)
+
2) Heart rate (cardiac output)

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9
Q

Baroreceptor reflex

A

mechanism that helps regulate blood pressure in the human body. It operates as a negative feedback system, meaning it works to maintain blood pressure within a relatively narrow range.

  • Stretch receptors -Baroreflex in carotid sinus
  • Stimulated by stretch or high BP
    –> activation of parasympathetic nervous system to lower BP.
  • When BP low at baroreceptors, such as after moving from a prone to standing position
    –> activation of sympathetic nervous system
    -> heart rate and contractility increase and vasoconstriction (skin)
    -> BP rises
    This is the orthostatic reflex.
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10
Q

Heart:

A

β1 - increased heart rate & force of beating (positive chronotropy and inotropy)

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11
Q

What happens to peripheral resistance and heart rate
when you give NA vs. Adrenaline ?

A

NA mainly acts on α receptors (no relaxation of smooth muscle)
A acts on all adrenergic receptors.

NA: (no vasodilation) -> peripheral resistance up, heart rate down (because baroreceptors sense increased BP leading to activation of vagus/ cranial nerve X)
NA: little effect on heart rate and lung.
Therefore NA is not used as a drug for shock

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12
Q

OVERVIEW OF DRUG CLASSES

A

Sympathomimetic drugs
Sympatholytic drugs
Indirect sympathomimetic drugs

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13
Q

Sympathomimetic drugs

A

Agonists at α1, β1, β2 adrenoceptors
Adrenaline and noradrenaline: little receptor selectivity

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14
Q

Sympatholytic drugs:

A
  • Antagonists at α1, β1, β2 adrenoceptors
  • α2 agonists
  • reserpine
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15
Q

Indirect sympathomimetic drugs:

A
  • NA uptake inhibitors
  • MAO-inhibitors
  • Amphetamine, ephedrine
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16
Q

Adrenaline as a drug (1)

A

Epipen or Anapen

Used for treatment of anaphylactic shock:
Release of histamines causes system
vasodilation -> 1) drop in BP and 2) lung edema (breathing problems)
Adrenalin injected i.m. will lead to
vasoconstriction in skin (alpha 1 rec), rise in BP and bronchodilatation

17
Q

Anaphylactic shock

A

treat with adrenaline

Alpha 1
+ vasoconstriction
+ blood pressure
- mucosal edema

beta 1
+ cardiac contraction force
+heart rate

beta 2
+bronchodilation
-mediator release

18
Q

Adrenaline as a drug (2)

A

Adrenaline is added to local anaesthetics (used s.c.), because it limits the diffusion of the local anaesthetic by vasoconstriction in the skin (alpha 1 rec).
Be careful with patients with uncontrolled hypertension.

19
Q

Alpha1-receptors:

A

Agonist:
e.g. Phenylephrine
- nasal decongestant
- Side effects: BP?
Hypertension

Antagonist:
- e.g. Prazosine
- treatment of hypertension
- Side effects ???
Postural hypotension

20
Q

Another decongestant:

A

Pseudoephedrine –
indirect sympathomimetic
amine (see ephedrine)

Both alpha (and beta) agonist properties, and acts as an
indirectly acting agonist (tyramine like effect).

21
Q

β1- adrenoceptors

A

Agonist:
Dobutamine
- increases cardiac contractility, thus used for (congestive) heart failure
- problem: dysarrhythmia (tachycardia)

22
Q

β2-agonists

A

Salbutamol
Terbutaline
Salmeterol
Formeterol

used for asthma

23
Q

β-blockers

A

Clinically very important!

Often non-β1/2 selective: propranolol
Or also β1-blocker: Atenolol

  • Treatment of hypertension, angina pectoris
  • Side effects:
    bradycardia, few severe side effects
    β2-antagonists: contraindicated in
    asthma patients.
24
Q

Feedback inhibition

A
  • α2 agonists -sympatholytic drugs:
    e.g. clonidine
  • MOA: blocks NA release by
    reducing cAMP and inhibition of
    Ca channels
  • Used for hypertensive crisis
     -Lowers arterial pressure by effect on heart and vasculature
 -Side effects: bradycardia, orthostatic hypotension, sedation, depression

Alpha2 antagonist:
Yohimbine – no clinical importance

25
Q

Other drugs affecting noradrenergic transmission

A

Monoamine
Oxidase

Noradrenaline
Transporter

Vesicular monoamine transporter

26
Q

Simplified actions of
neurotransmitters in the CNS

A

NA: alertness, anti-depressant
DA: pleasure, movement control
5-HT: feeling happy, relaxed, calm,
motivated, anti-depressant

27
Q

Block of vesicular monoamine
transporter

A

Reserpine

-> VMAT block
reduced amount of NA
in vesicles
 reduced NA release

(treatment of hypertension,
now obsolete; causes depression)

28
Q

Mono Amine Oxidase – inhibitors

A

Old antidepressants Selegiline (PD)

-> less NA degradation
-> increased NA levels
(problem: hypertension)

Note: dopamine is also degraded by MAO.

29
Q

NAT – inhibitors

A

Specific NA reuptake inhibitors
(SNRIs): e.g. reboxetine
anti-depressant, blocks anxiety,
stimulates CNS, motivation

Also:
Tricyclic anti-depressants:
(inhibit both NA and 5-HT uptake)
- imipramine, amytriptyline

MOA:
-> increased NA (and 5-HT)
levels in synaptic cleft due to
uptake inhibition

30
Q

Indirect sympathomimetics

A

Amphetamines, ephedrine
(NA displacers): uptake via NAT and VMAT
-> displacement of NA in vesicles
-> NA (DA, 5HT) leaks out
Central effects:
- CNS stimulation
- used for weight loss, narcolepsy,
ADHD (ritaline), decongestion

31
Q

Amphetamines

A

Drugs of abuse! “Crystal-Meth, Chalk, Ice, Glass, Crank, Speed.“

Short term: exhilaration, hyperactivity, loss of appetite, insomnia, increase in energy level and talkativeness

Long term: nervousness, irritability,
hallucinations, paranoia -> depression

Addicts (speed freaks ) do not eat, sleep, or care for themselves
 malnutrition, weight loss,
low resistance to disease, mental illness
-> eventually “Speed kills”

32
Q
A

BIOM2402 (9 decks)

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