tyrosine is converted to dopa via tyrosine hydroxylase

dopa is converted to dopamine via dopa decarboxylase

dopamine is converted to NE by dopamine B hydroxylase when it enters the vesicle

this docks wit the presynaptic cleft and releases NE

1. reuptake into the presynaptic cleft via reuptake pumps (reuptake 1)

2.broken down by COMT

3. taken up by alpha 2 on the presynaptic cleft which sends signals to stop the release of more NE

1. it is broken down in the mobile pool by MOA

or 

2. It is put back in to the vesicle to be released again in the future

1. inhibit MOA

2. displace stored NE from mobile pool

3.inhibit the re-uptake from the synaptic cleft

4.block pre junctional A2 receptors

5. stimulate the post synaptic receptors (only directly acting all the above are indirectly acting)

Tyramine

Amphetamine

Ephedrine

Metaraminol

(all above increase the release)

Cocaine (blocks reuptake)

dopamine (D> B1>>A)

norepi (A1=A2, B1>>B2)

epi (A=B)

ephidrine (A=B)

Phenylephrine

Mathoxamine

Metaraminol

Clonidine

Alpha methyl dopa

Terbutaline

Albuterol

Metaproterenol

Ritodrine

Salmeterol

What are the compensatory responses to 

1. Increase in arterial pressure

2. Decrease in arterial pressure

1. sensors in the aortic arch & carotid sinus send afferent impulses to the VMC which decrease sympathetic activity & increase parasympathetic activity (aka reflex bradycardia)

2. Sensors in the aortic arch & the carotid sinus send afferent impulses to increase sympathetic activity & decrease parasympathetic activity (aka reflex tachycardia)

A1 is on blood vessels and causes vasoconstriction on sympathetic activation causing a rise in BP (increase in CO =SV x HR)

B2 is present in skeletal muscle blood vessels and causes vasodilation during sympathetic activity leading to smooth muscle relaxation and decreased BP (decrease in CO= SV x HR)

pure B1 stimulation results in

what will a non selective B agonist do to BP?

Increase in BP (increase in CO = SV x HR)

Increases CO ( B1 activation), but will decrease TPR (B2 activation)

CNS stimulants

MOA

Name one and its ADR's

Amphetamine

Displaces stored catecholamines from mobile pool

ALL CNS stimulants have a high risk of causing convulsions 

Nasal congestion during cold/ allergie

1. what is given example of drug

2. ADR

1. A1 agonist to cause vasoconstriction reducing nasal congestion. - Phenylephrine, Ephedrine, Pseudoephedrine, Oxymetazoline & Xalometazoline

2. When an A1 agonist is overused - Rebound nasal congestion occurs.

1. A1a for the sphincter constriction

B2 for the bladder wall relaxation

**remember tap & pot**(A1a & B2)

Increase in insulin secretion

Decrease in insulin secretion

Increase in insulin secretion DECREASE oin blood sugar upon administration of B agonist

Decrease in insulin secretion INCREASE blood sugar upon administration of A2 agonist

A1=A2, B1 >>>>B2 (relativley little effect in B2)

thus increase in TPR - increased inotropic effects on the heart (increased contractility)

B non specific agonist

thus causes Increase in HR

Decrease in TPR due to B2 actions on skeletal muscle blood vessels

increases CO with a fall in diastolic and systolic pressure - positive chronotropic (increased pacemaker activity) and inotropic activity (increased in contractility)

1. low dose - D1 receptors  - increased renal, coronary & cerebral blood flow

2. Above 5mcg - D1 & B1 - Increase HR & Co

3. from 10-20mcg - D1, B1 & A - increase in HR & Vasoconstriction - Increase in TPR

Name the drugs used in nasal decongestion

what adrenergic receptor do they activate?

1. Phenylephrine

2. Ephedrine (displaces NE frommobile pool)

3.Pseudoephedrine

4. Xylometazoline

5. oxymetazoline

all are A1 agonists - vasoconstriction - except ephedrine

Clonidine

1.MOA

2.Use

3. ADR

1. A2 selective agonist - decreases release of NE via negative feed back (thus sympathetic antagonist, even though it is an A2 agonist))

2. HTN & DOC for most CNS withdrawal symptoms i.e alcohol withdrawal (as sympathetic nervous system is overactive during withdrawal)

3.postural hypotension, dry mouth, sedation & rebound htn

Cocaine

1. MOA

2. Use

1. Blocks the re-uptake of NE & DOPAMINE from the presynaptic cleft

2. it is a vasoconstrictor and an anaesthetic -Deviated Nasal Septum (NE) & it is addictive (dopamine)

Tyramine

1. MOA

2. Contraindicated?

1. Found naturally in cheese products, red whine & pickled fish products - Displaces stored NE from mobile pool

2. Do not take MOA inhibitors - pt suffering from depression takes MOA inhibitors, thus NE is not broken down - when cheese is taken along with this there is an increase in NE in the storage vesicle that is be displaced..

1. MOA inhibitors & Tyramine containing foods -

2.MOA is inhibited thus NE is not borken down and there is more ready for relase in the mobile pool

3. Tyramine displaces all the stored NE from the mobile pool leading to -  malignant HTN along with other symptoms

Modafinil

1.use

2. moa

1. narcolepsy

2. displaces stored NE from mobile pool

Name the irreversible non selective A blocker

all 'OCINS'

PrazOCIN

TamsulOCIN

Yohimbine

Mirtazepine

Pheochromocytoma

1. symptoms

2.what drug is used?

3. why?

1. VMA in uirne High BP space occupying in renal medulla

2. phenoxybenzamine & phentolamine

3. deceases BP before surgery

Tamsulosin

Doxazocin

(A1a blocker)

Vasodilation - Orthostatic / postural hypotension

Reflex tachycardia

nasal congestion

Decrease LDL & TG

Increase HDL

Cardio selective (blocks B1),

non selective B blockers (blocks B 1 & 2)

Mixed A & B blockers (B1, B2 & A1)

What is given for stage fright/anxiety?

what does it help?

B blockers

.tremmers, tachycardia etc

When are non selective B blockers contraindicated?

What other B blockers are also contraindicated?

Patient with COPD/ bronchial constriiction

as it will cause bronchoconstriction

Mixed A & B blockers

(starting with:)

A

B

E

A

M

(ending in olol)

Name the mixed A & B blockers

what do they block?

Carvidelol

Labetolol

block A1, B1 & B2

What drug is used for sexual dysfunction?

what class of drug is it?

What are its ADR?

1. Yohimbine

2. A2 blocker/ antagonist

2. impotence and orthostatic hypotension

1.What drug is used for depression

2.What class of drug is it?

1. Mirtazapine

2. A2 locker/antagonist

1. Bradycardia

2. Bronchoconstriction

3 Abnormal Lipid profile

What class of drugs Help the lipid profile?

What class of drugs are bad for te lipid profile

How?

A blockers/antagonists decrease LDL & TG, increase HDL, thus are good for the lipid profile

B blockers/ antagonists increase LDL & TG, Decreasing HDL thus are bad for the lipid profile

B blockers - beta receptors increase insulin, thus to block them would decrease it, this is not desired.

Pt will suffer from Hypoglycemia (B blockers will mask the symptoms i.e reduced sympathetic activity.. tremors tachycardia etc.)

Biphasic response - a rise in BP (B1 & A1 stimulation) followed by a decrease in BP (B2 stimulation)

TPR!!!!!!!!!!!!!

(B2 stimulation or A1 blockade)