Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
|
How BP is regulated in the ANS
|
regulated by arterial resistance and cardiac output
|
|
|
Baroreceptors
|
found in the carotid sinus and aortic arch, which is stimulated by stretch at high BP.
|
|
|
orthostatic reflex
|
low BP at baroreceptors -> activate sympathetic nervous systesm, results in HR and contractility increasing and vasoconstriction (skin). BP rises as a result
|
|
|
Give details of noradrenaline/adrenaline receptor and subunits
|
Adrenergic receptor (GPCR)
alpha 1 (smooth muscle around visceral blood vessels & papillary sphincters) and 2 beta 1 (heart), 2 (smooth muscles in the visceral organs) (3 adipose tissue, only) |
|
|
Adrenergic effects at alpha1, beta1 and 2 receptors and 2nd messengers
|
alpha1: Gq coupled, 2nd messenger - IP3/DAG, smooth muscle contraction
beta1: Gs coupled, 2nd messenger - cAMP, increases frequency, contractile force and conduction at AV node beta2: Gs coupled, 2nd messenger - cAMP, smooth muscle relaxation and decreased GI motility |
|
|
Effects of Adrenaline and Noradrenaline
|
Noradrenaline mainly acts on alpha receptors, while alpha 2 is a presynaptic receptor that inhibits noradrenaline release.
Adrenaline acts on all adrenoreceptors, and is one of the key factors that elevates blood pressure in the short term, which is useful for treating shock. |
|
|
Give details of ACh receptor
|
Nicotinic (cation channel)
Muscarinic (M1-M5 GPCR) |
|
|
What are the 3 drug classes and what actions they have on which receptors
|
Sympathomimetic drugs - agonist at a1, B1, B2
Sympatholytic drugs - antagonists at a1, B1, B2 (but agonist at a2) Indirect Sympathomimetic drugs - NA inhibitors, MAO inhibitors |
|
|
Why is adrenaline used as treatment for anaphylactic shock and what happens when it is injected i.m.
|
Causes a release of histamines that which causes system vasodilation: 1. drop in BP and 2. lung edema.
When injected i.m. it causes vasoconstriction and bronchodilation |
|
|
Why is adrenaline added to local anesthetics?
|
Limits the diffusion of the local anaesthetic by vasoconstriction
|
|
|
Name the agonist and antagonist of Alpha1 receptors and their effects and side effects
|
Agonist: Phenylephrine - nasal decongestant, side: hypertension
Antagonist: Prazosine - treatment for hypertension, side: postural hypotension |
|
|
What is Pseudoephedrine and what does it do?
|
An indirect sympathomimetic amine that is taken up into presynaptic terminals, displaces NA release and thus activation of adrenergic receptors.
|
|
|
B1 receptor agonist
|
Dobutamine: Increases cardiac contrictility, but causes dysarrhytmia
|
|
|
B2 receptor agonist
|
Salbutanol - used in asthma
|
|
|
Beta-blockers and functions
|
Often non selective B1/2 selective: propanolol
B1 blocker: Atenolol Treatment of hypertension, angina pectoris Side effects: bradycardia, few severe side effects B2-antagonists: (blank) in asthma patients |
|
|
What causes Feedback Inhibition and what is it's MOA?
|
a2 agonists - sympatholytic drugs
MOA: blocks NA release by reducing cAMP and inhibition of Ca channels. Used for hypertensive crisis |
|
|
NAT
|
Noradrenaline Transporter. Takes up noradrenaline on the presynaptic membrane into vesicles for degradation or storage
|
|
|
VMAT
|
Vesicular Monoamine Transporter is the actual vesicle which noradrenaline is stored and/or degraded
|
|
|
Reserpine
|
VMAT blocker, reduces levels of NA
|
|
|
Selegiline
|
MAO-imhibitor, increases NA levels
|
|
|
NAT inhibitors
|
Specific NA reuptake inhibitors, increased NA (and 5-HT)
levels in synaptic cleft due to uptake inhibition |
|
|
Indirect sympathomimetics
|
displace noradrenaline uptake into VMAT and NAT, causing a leaking of noradrenaline and other neurotransmitters like 5-HT and DA into the synaptic cleft
|
