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Paramedic Revision > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

What are benzodiazepines?

A

a class of drug that are used for their sedative effect. In large doses they produce unconsciousness and amnesia

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2
Q

what type of drug is midazolam?

A

a benzodiazepine

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3
Q

what is midazolam used for on road?

A

primarily it is used for seizure management but it can also be used for its sedative effects in some mental health cases

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4
Q

What are some of the side effects if midazolam that it is important to be aware of?

A

the main side effect to be aware of is respiratory depression, if not addressed this can lead to respiratory and cardiac arrest

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5
Q

What does GABA stand for and what is it?

A

gamma-aminobutyric acid
- an inhibitory neurotransmitter found throughout the CNS

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6
Q

what is the mechanism of action of midazolam?

A

Benzodiazepines work by binding to GABA receptor-chloride channel complex and increasing the neurons affinity for GABA.
When GABA binds to it’s receptor on the complex it causes chloride channels to open and in turn there is an influx of negatively charged Cl ions into the cell.
This causes it to become hyperpolarized (makes cell highly negative) and decreases the cells ability to fire by bringing the membrane potential of the cell farther away from the threshold potential

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7
Q

What is the dose and route of midazolam given to manage a seizure (in SAAS)?

A

route: intramuscular (IM)
dose: 0.1mg/kg up to 10mg, repeat once to max 10mg per dose (consult for further clinical support)

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8
Q

what needs to be done if midazolam is required for a mental health transfer?

A

consult with a higher level clinician

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9
Q

What is the befit of using a spacer when administering inhaled medication?

A

A spacer impacts the distribution of the medication. When a spacer is used roughly 22% of the medication stays in the mouth and throat and 21% enters the lungs, compared to 81% staying in the mouth and only 9% entering the lungs without a spacer

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10
Q

What type of drug is salbutamol?

A

an inhaled beta-2 adrenergic agonist

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11
Q

what is the mechanism of action of salbutamol and other beta-2 adrenergic agonist?

A

beta-2 adrenergic agonists work by selectively activating beta-2 receptors found in the smooth muscle of the lungs. this binding promotes the relaxation of smooth muscle and therefore bronchodilator. In turn reducing bronchospasm. B-2 agonists also suppress histamine release in the lungs, reducing inflammation and increasing ciliary movement.

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12
Q

what is the dose of salbutamol given (doses and route for each severity, and different conditions)?

A

ASTHMA
mild - moderate: via spacer, 1200microg (12 puffs, 4 breaths between)

moderate: 5mg via neb (every 20 mins up to 3 doses)
severe: 15mg via neb, repeat if required

life threatening: 15mg continuous

COPD
5mg via NEB, repeat every 20 mins up to 3 doses for severe exacerbations

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13
Q

are there any side effects that can be expected when salbutamol is administered? What are they?

A

mild interaction with b1 receptors in the heart may cause increased heart rate, tremors/shaking, headache, palpitations, etc.

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14
Q

What type of drug is ipratroprium bromide?

A

an inhaled anticholinergic, also classified as a bronchodilator

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15
Q

what is the mechanism of action of ipratropium bromide?

A

Impratroprium bromide is a muscarinic antagonist. It works by blocking muscarinic cholinergic receptors and therefore the parasympathetic response that is promoted by the activation of these binding sites. It reduces production of mucus and promotes bronchodilation.

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16
Q

how long does it take for ipratroprium bromide to start working?

A

only 30 seconds, it reaches 50% of it’s maximum effect within 3 minutes, and the effect lasts for up to 6 hours

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17
Q

why is it beneficial to use ipratroprium bromide in addition to salbutamol even though it is considered less effective the beta-2 agonists?

A

because beta-2 agonists, like salbutamol, and ipratroprium bromide achieve their bronchodilator effects through different means, therefore improving effectiveness when used together

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18
Q

what is ipratroprium bromide used for within SAAS?

A

treatment of asthma and COPD

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19
Q

what is the dose of ipratroprium bromide given (doses and route for each severity, and different conditions)?

A

MDI and Spacer: 168microg (8 puffs with 4 breaths between), once only

Neb: 500microg (once only)

In cases of severe or life threatening asthma or COPD only
Neb: 500microg, repeat every 20 mins to 3 doses

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20
Q

What does GTN stand for

A

glyceryl trinitrate

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21
Q

What is the mechanism of action of GTN (even just briefly becuase this is a hard one)?

A
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22
Q

How does GTN work in the treatment of angina and chest pain?

A

by dilating the veins GTN reduces decreases venous return to the heart and therefore decreases ventricular filling. This results in a decreased pre-load (wall tension in the ventricles) and a decreased oxygen demand from the heart. In prinzmetal angina GTN works by relaxing and preventing spasm in coronary arteries and therefore increasing oxygen supply to the heart rather than decreasing oxygen demand.

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23
Q

What is GTN used for on road?

A

treatment of cardiac chest pain and ACPO

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24
Q

How does GTN help in the treatment of ACPO?

A
  • *NEED TO CHECK**
  • As GTN causes vasodilation and reduces preload it helps both in reducing blood pressure and reducing the ‘back-logging’ that can occur in ACPO.*
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25
Q

What are the contraindications of GTN?

A
  • systolic blood pressure below 100mmHg
  • in a preload dependant rhythm or have a condition making them preload dependant (e.g. severe aortic stenosis)
  • had a PDE-5 within the last 48 hours (e.g. viagra, cialis, levitra)
  • exercise casution if on hypotensive drugs such as beta-blockers, calcium channel blockers, diuretics, etc.
26
Q

what are the expected side effects of GTN?

A

a decrease in blood pressure, headache, dizziness, orthostatic hypotension, tachycardia

27
Q

What class of drug is adrenaline?

A

alpha- and beta- adrenergic agonsist

28
Q

What are the clinical concequenses of alpha 1 activation?

A

vasoconstriction (of vessels in the skin viscera and mucous membrane) - most common use, and mydriasis (dialation of the pupil of the eye)

29
Q

what are the potential adverse effects of alpha-1 activation?

A
  • hypertension, caused by widespread vasoconstriction
  • necrosis, resulting from leakage of alpha-1 agonist into the tissue from a pooly places IV line
  • bradycardia, reflex slowing of the heart from increased BP
30
Q

What are the clinical consequences of alpha-2 activation?

A

peripherlly - little clinical significance

within the CNS - reduction of sympathetic outflow to the heart and blood vessels and relief of severe pain

31
Q

What are the clinical consequences of beta-1 activation?

A

clincally relevant effects of beta-1 activation occur in the heart.

  • Activation causes increases in contractility
  • increase in heart rate
  • enhanced impulse conduction through the AV node
32
Q

what are some of the clinical applications of beta-1 agonsists, both within and outside of SAAS?

A

Heart failure - this disease is characterised by a reduction in the force of contraction, therefore activation causing increased contractility can help with caridac performance

shock - by increasing HR and force of contration beta-1 agoinists can help maintain blood flow to vital organs (shock causes profound hypotension and reduced tissue perfusion)

AV heart block - enhanced impulse conduction through the AV node

Cardiac arrest (specifically in asystole) - can encourange the initiation of contraction in the heart

33
Q
A
34
Q

what are the clinical consequences of beta-2 activation?

A
  • primarily bronchodilation
  • can be used to delay preterm labour
35
Q

what are the potential adverse effects of beta-2 agonists?

A
  • hyperglycaemia (generally only in patients with daibetes, b2 activation in the liver and skeletal muscle promote the breakdown of glycogen into glucose)
  • tremor (activation of b2 agonists in skeletal muslce causes enhanced contraction)
36
Q

what is the dosage of GTN given on road to treat ACS or ACPO?

A

400 microg (1 spray) every 5 mins with adequate BP

(dosage may have changed now that GTN is in tablet form)

37
Q

What is adrenaline used to treat on road?

A
  • anaphylaxis
  • asthma
  • severe croup
  • cardiac arrest
38
Q

what dose and route of adrenaline is given in the treatment of asthma?

A

intramuscluar - 10 microg/kg to max 500 microg, every 5 mins as needed

39
Q

what dose and route of adrenaline is administered in the treatment of anaphylaxis?

A

intramuscluar - 10 microg/kg to max 500 microg, every 5 mins as needed

40
Q

what dose and route of adrenaline is administered in the treatment of severe croup?

A

nubuliser - 5mg

41
Q

what dose and route of adrenaline is administered in the treatment of cardiac arrest?

A

intravenous or intraosseous - 1mg every 4 minutes as needed (double interval if temp 30 - 35 degrees, withold if below 30 degrees)

42
Q

what class of drug is fentanyl?

A

narcotic opiate analgesic

43
Q

what is the mechanism of action of fentanyl?

A

Essentially binding of fentanyl to mu receptors (mostly foundin the amygdala, thalamus, mesencephalon, and some of the brain stem) causes hyperpolerisation of cells and inhibition of nerve activity

*more detailed but above anser is fine

binds to opioid receptors (specifically mu wich is a G-coupled protein receptor) > causes a series of effects on proteins > leads to reduced concentrations of cAMP, reduced cAMP results in decreased cAMP dependant influx of calcium > causes hyperpolarisation of cell

44
Q

what is fentanyl used for on road?

A

pain management

45
Q

in what doses and by what routes is fentanyl administered on road?

A

intravenous - 25-50 microg every 5 minutes as needed to max cumulative dose of 300 microg

intranasal - up to 200 microg repeat every 5 mins as needed to a max cumulative dose of 400 microg

46
Q

what are the potential adverse effects of fentanyl?

A
  • respiratory depression
  • euhoria and confusion
  • nausea
  • visual disturbances/ hallucinations
  • constipation
  • muscle rigidity
  • LOC/ coma/ death
47
Q

what are the contraindications of fentanyl administration?

A
  • recent operations in the biliary tract
  • respiratory depression or obstructive airway diseases (asthma, COPD, hyperventilaiton, obesity)
  • liver failure
  • known intolerance or hypersensitivy
48
Q

what class of drug is amiodarone?

A

antiarrhythmic

49
Q

what is the mechanism of action of amiodarone?

A

amiodarone works primarily by blocking potassium rectifier currents responsible for the repolarization of the heart during phase 3 of the cardiac action potential. This potassium channel-blocking effect results in increased action potential duration and a prolonged effective refractory period in cardiac myocytes. Myocyte excitability is decreased, preventing reentry mechanisms and ectopic foci from perpetuating tachyarrhythmias.

50
Q

when is amiodarone given on road?

A

during cardiac arrest

the first dose should be given after the 3rd shock is delivered during cardiac arrest management. A second half dose can be administered under higher clinical direction after the 5th shock.

51
Q

what is the dose and route of amiodarone?

A

300mg IV after the 3rd shock, 150mg IV after the 5th shock (under higher clinical direction)

52
Q

You are faced with a cardiac arrest. You established IV access after the 4th round of charge and checks, the rhythm analysis has been as follows for these C+Cs - VF, VF, VF, PEA. you have administered your first dose of adrenaline and have amiodarone drawn up. Your next rhythm analysis is asystole. Do you administer the amiodarone?

A

No, as the patient is currently in a non-shockable rhythm. It can be administered if the patient goes back into a VF or VT rhythm.

53
Q

what class of drug is aspirin?

A

antiplatelet

54
Q

when is aspirin administered on road?

A

in the treatment of angina or suspected MI (cardiac chest pain)

55
Q

what is the dosage and route of administration of aspirin in road?

A

300mg orally, usually a chewable tablet.

56
Q

what is the mechanism of action of aspirin in relation to cardiac chest pain?

A

Aspirin supresses platelet aggregation by causing irreversible inhibition of COX-1. COX-1 is the enzyme involved in the formation of TXA-2, the synthesis of which in platelets promotes aggregation. Hence, aspirin supresses aggregation. This does not reduce the size of a clot but will prevent further platelet aggregation from increasing it’s size.

57
Q

are there any contraindications of administering aspirin?

A
  • known allergy to NSAIDS
  • not a contraindication but it should be monotered in people with asthma as it can cause bronchospasm and lanygeal odema
58
Q

What class of drug is naloxone?

A

opiod receptor antagonist

59
Q

what is naloxone used for on road?

A

in the treatment of opiod overdose

60
Q

what is the dosage and route of administration of naloxone on road?

A

intranasal: 120 microg every 30-60 secs PRN

Intramuscular: 400microg every 1-2 min PRN

intravascular: 100microg every 30-60 secs PRN

*can be useful to do a slow push or titrate to allow the patient to wake enough to suport their own breathing but be drowsy enough that they are not combative

61
Q

what is the mechanism of action of naloxone?

A

acts as a competitive antagonist at opiod receptors, thereby blocking opiod action (in simple terms it ‘knocks’ opiods off of the receptor and bind with a stronger affinity blocking the binding of narcotics to the site)

62
Q

what are some important things to consider when adminstering naloxone to a patient?

A
  • it has a shorter half life than opiods, this means that opiods can take effect again once naloxone has worn off

Paramedic Revision (22 decks)

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