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Pain Control > Vasoconstriction > Flashcards

Vasoconstriction Flashcards

1
Q

amides in general characteristic

A

vasodilation except cocaine - so they would have a short duration if no addition of vasoconstriction

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2
Q

big difference between LA drug and other drugs

A

LA - has to stay in area - other drugs go to different target areas

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3
Q

vasoconstrictor - general and what are its advantages

A

*agent that causes narrowing of the blood vessels
advantages:
1. decrease blood flow to the site of injection
2. prolong and increase the depth of anesthesia
3. reduce the toxic effect of the drug
4. render the area of injection with less bleeding

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4
Q

reduce the toxic effect of the drug?

A

a vasoconstrictor has this characteristic

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5
Q

same anesthetic max dosage with and without vasoconstriction

A

less toxic with vasoconstrictor

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6
Q

chemical structure of vasoconstrictor

A

chemically identical / quite similar to the sympathetic nervous system mediators epinephrine and norepinephrine

*resemble the response of adrenergic nerves to stimulation and are classified as sypathomimetic nerves or adrenergic

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7
Q

catecholamines

A 
ones that we mainly use - 
epinephrine 
norepinephrine 
levonoproterenol 
isoproternol
dopamine
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8
Q

noncatecholamines

A 
still vasoconstrictors but not ones we clinically usually use 
amphetamine
methamphetamine
ephedrine
phenylephrine
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9
Q

direct acting drugs

A

exert their action directly on adrenergic receptors IN THE POST SYNAPTIC

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10
Q

Indirect Acting drugs

A

drug enhances release of catecholamine norepinephrine from adrenergic nerve terminals

neurotransmitter release from the vesicles at the pre-synaptic area

*Tachyphylaxis could occur? or associated with this method of action

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11
Q

mixed acting drugs

A

act on the pre-synaptic area and enhance release from vesicle - from the adrenergic nerve terminals and also work directly on the post synaptic receptors

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12
Q

vasoconstrictors we use - epi and norepi function in what type of method/action

A

Direct acting – stimulate the receptors at the post synaptic area

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13
Q

Two types of adrenergic receptors

A

Alpha –> vasoconstrict

Beta –> vasodilate

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14
Q

activation of alpha receptor by sympathomimetic drug

+ alpha 1 vs alpha 2

A

stimulates contraction of smooth muscle in vessels = vasoconstrict
alpha 1 = EXCITATORY post-synaptic
alpha 2 = INHIBITORY
- so NE release and Ach release would decrease in release

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15
Q

Beta 1 activation causes

A

Vasodilate and bronchodilatation and cardiac stimulation

increase in contractility of the heart and lipolysis by small intestine

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16
Q

Beta 2 activation causes

A

Vascular beds - VESSELS - produces vasodilation

Bronchi - bronchiodilatation * = relaxation

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17
Q

potential contraindication of patient taking non-selective beta blockers and using vasoconstrictors?

A

*stimulation of B receptors is BLOCKED - so vasodilation or bronchodilatation does NOT occur

this will block the activation of dilation in the VESSELS of the smooth muscle/heart so could increase HR too much in these patients
- giving a vasoconstrictor and wont have the effect of dilation produced normally by the activation of these receptors

18
Q

overview of administration of epinephrine

A

Stimulate alpha receptors and beta receptors

alpha – increase in contractility, gluconeogensis in liver and salviary gland secretion

beta - vasodilation of smooth muscle and bronchiodilation

19
Q

epinephrine works mostly on?

A

alpha and beta receptors

20
Q

norepinephrine works mostly on what receptors?

A

mainly alpha

21
Q

levonordefrin works on what receptors?

A

contraindicated - see both occurring

22
Q

specific characteristics of epinephrine + what is added to it and what are those implications?

A

as the acid salt it is highly soluble in water
*addition of sodium bisulfite is added to delay deterioration (if allergic rxn occurs it is usually due to this aspect of the drug)

synthetic + secreted from adrenal medulla

acts DIRECTLY on alpha and beta receptors

23
Q

which receptors predominate with administration of epinephrine?

A

Beta predominates - which is vasodilation HOWEVER AT HIGH CONCENTRATIONS THE ALPHA predominate – which causes vasoconstriction and why we use it for this with administration of LA (high concentration in area we inject)

but at lower concentrations - beta receptors will dominate

24
Q

marked increase in systolic pressure when?

A

epinephrine with alpha receptors

25
Q

myocardial oxygen consumption?

A

increases when heart is working more

a systemic effect of epinephrine - increases cardiac output with HR and SV so more oxygen is needed to the heart

26
Q

epinephrine effect on respiratory

A

is a potent dilator B2 effect of the smooth muscle of the bronchioles

27
Q

termination of action of epinephrine

A
  1. reuptake by the adrenergic nerves
  2. inactivation in the blood by the enzyme catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO), both which are present in the liver
28
Q

COMT and MAO

A

enzymes that are present in the LIVER - and these break down and elimate the action of epinephrine

29
Q

max dosage of epinephrine in normal healthy pt.

A

.2mg per appointment

10 ml per 1:50,000 dilutoin - 5 cartridges

30
Q

max dosage of epinephrine in ASA III or IV

A

0.04 mg per appointment

31
Q

side effects and overdose of epinephrine

A

CNS stimulation - increases fear, anxiety, tension, resltessness, headache, tremor, weakness

cardiac dysrhythmias
increased systolic
angina

32
Q

norepinephrine - specific +aka

A

AKA - levarterenol

relatively stable in acid solution, deteriorating on exposure to light and air

acetone-sodium bisulfite added to retard deterioration

natural and syntehtic forms

actions are 90% alpha and 10% beta

33
Q

systemic effects of norepinephrine

A

DECREASED HR - because we increased systolic and diastolic pressures so maintain

*increased total peripheral resistance

most noteable are the increases in systolic (greatest variation) and diastolic and mean arterial pressure with compensatory effect of decreased HR

34
Q

norepinephrine on respiratory system

A

does NOT relax bronchial smooth muscle as does epinephrine

35
Q

termination of norepinephrine

A

reuptake and its oxidation by MOA

+ exogenous norepinphrine is inactivated by COMT

36
Q

clinical applications of norepinephrine

A

in LA as vasoconstrictor + helps with management of hypotension because increases peripheral resistance

37
Q

max dose of norepi in healthy patient

A

0.34 mg / appointment

38
Q

max dose of norepi in ASA III or IV patient

A

0.14 mg / appointment

39
Q

Levonodefrin

A

synthetic vasoconstrictor

direct alpha receptor - stimulation is 75% with some beta activity (25%)

systemic effects are similar to epinephrine but to a lesser degree

40
Q

weakest vasoconstrictor used in dentistry?

A

Phenylephrine Hydrochloride

  • soluble in water
  • direct alpha receptor
  • exerts little or no B action on the heart
41
Q

Felypressin

A

Synthetic analogue of the antidiuretic hormone vassopressin

acts as a direct stimulant of vascular smooth muscle

*no direct effect on the myocardium - which could be of benefit

42
Q

relative contraindications

A

patients with more significant cardiac disease
patients with certain noncardiovascular diseases (thyroid dysfunction, diabetes, sulfite sensativity)

patients receiving MAO inhibitors(drug would not be eliminated in normal fashion), tricyclic antidepresants and phenothiazines

Pain Control (12 decks)

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