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PHYL2066 Content > PHARMACOLOGY NEED TO KNOW > Flashcards

PHARMACOLOGY NEED TO KNOW Flashcards

1
Q

Define Agonist

A

= binds to receptor and brings about physiological response

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2
Q

Define Receptor

A

= a molecular structure or site on the surface or interior of a cell that binds with substances

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3
Q

Define Antagonist

A

= bind to receptors, however, have no efficacy (don’t activate receptors)

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4
Q

4 Receptor Types

A
  1. Ligand-gated Receptors: Inotropic Receptors
  2. G-Protein Coupled Receptors: Beta-Adrenoreceptor
  3. Kinase-Linked Receptor
  4. Nuclear Receptors
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5
Q

Describe Inotropic Receptors: Nicotinic Receptors

A
  • 5 transmembrane units
  • endogenous agonist is Acetylcholine (Ach)
  • 2 molecules of Ach bind, opening Na channels
  • ions flow down concentration gradient
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6
Q

Describe Beta-Adrenoreceptors

A
  • 7 transmembrane units
  • endogenous agonist is adrenaline
  • agonist binding activates G-Protein
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7
Q

Define EC50

A

= Effective Concentration Value

  • the concentration of a drug that gives half-maximal response
  • used as a measure of potency
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8
Q

Define Potency

A

= amount of drug needed to produce a given effect

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9
Q

Define Efficacy

A

= maximal effect that a drug produces irrespective of dose/concentration

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10
Q

Define ADME

A 
A= Absorption
D= Distribution
M= Metabolism
E= Excretion
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11
Q

3 Pros & 3 Cons of Oral Administration

A

Pros:

  • convenient
  • 75% absorbed in 1-3 hours
  • slow release formulation

Cons:

  • some drugs not well absorbed
  • influence of foods on absorption
  • affected by first-pass metabolism in liver
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12
Q

3 Pros & 2 Cons of Rectal Administration

A

Pros:

  • avoids first pass metabolism
  • reduces vomiting/nausea
  • good when patient is unconsciousness

Cons:

  • inconvenient
  • absorption often incomplete
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13
Q

Metabolism by Liver Hepatocytes

A
  • drugs taken orally enter the liver via the hepatic portal vein
  • concentration of a drug is greatly reduced by the liver before it reaches systemic circulation
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14
Q

Injections to Avoid First Pass Metabolism

3 Pros & 3 Cons

A 
intramuscular = i.m. 
intravenous = i.v.
subcutaneous = s.c.
intradermal = i.d.

Pros:

  • rapid onset compared to oral (i.v. > i.m. > s.c.)
  • drugs are not broken down by acid/enzymes as in the gut
  • first pass metabolism in liver is less of a problem

Cons:

  • less convenient (needs skilled person)
  • risk of infection
  • more toxicities (higher peak blood levels)
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15
Q

Non-Needled Sublingual Administration

A
  • good vascularisation
  • avoids first pass metabolism
  • absorbed rapidly
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16
Q

Non-Needled Topical Administration

A
  • localised administration

- reduced systemic toxicity

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17
Q

Enzymatic Reactions

A

Phase 1 Reactions:

  • Oxidation (Cytochrome P450)
  • Hydrolysis (esterases)
  • Reduction (reductases)

Phase 11 Reactions: Add water soluble moiety to drug

  • sulfate
  • acetate
18
Q

Describe Phase 1 Reactions - Oxidation (Cytochrome P450)

A
  • enzymes that metabolise prescribed drugs

- cytochrome P450 can be inhibited or induced by drugs which affects distribution of drugs in the body

19
Q

List the 4 Drugs of Hypertensives

A
  1. Diuretics
  2. Vasodilators
  3. Calcium Channel Blockers
  4. Betablockers
20
Q

List the 4 Drugs of Heart Failure

A
  1. Positive Inotropic Agents: Digoxin/Digitalis
  2. Vasodilators: ACE Inhibitors, nitrates
  3. Diuretics
  4. Beta Blockers
21
Q

Describe Calcium Channel Blockers (Nifedipine and Verapamil)

A
  • inhibit Ca ion movement into vascular and cardiac muscle
  • causes peripheral and coronary vasodilation
  • decreases heart rate and contractility
22
Q

Describe Beta Blockers

A
  • act on heart tissue
  • reduce heart rate
  • reduce ventricular contractility
23
Q

Describe Positive Inotropic Agents: Digoxin/Digitalis

A
  • blocks Na/K pump which impairs Ca ion transfer OUT of membrane
  • this increased build up of Ca ions leads to a stronger, fuller, less-erratic heart beat
  • increased cardiac output
24
Q

Describe Vasodilators: ACE Inhibitors

A
  • dilated artery = lower blood pressure
  • coronary arteries open
  • ACE inhibitors stop angiotensin production
  • lower blood pressure and increased blood to heart
25
Q

Describe Diuretics

A
  • improve kidney function and relieve oedema
  • reducing swelling in the organs leads to reduced work of the heart
  • used in combination with all other heart failure treatments
26
Q

Stents

A

= small mesh tube that holds open narrowed blood vessels and allow blood flow to and from heart

  • best treatment if an emergency
  • however, facilities and personnel are needed
27
Q

Bypass Grafting

A

= arteries or veins from elsewhere in the body are grafted to coronary arteries to bypass atherosclerotic narrowing and improve blood supply to the coronary circulation to the myocardium

28
Q

Define Congestive Heart Failure

A

= a chronic condition in which the pumping power of the heart muscles is affected

29
Q

Triggers of Asthma

A
  1. Allergens: moulds, dusts, pollen, animal dander
  2. Irritants: secondhand smoke, odours, chemicals, perfume
  3. Exercise: cold and dry air
  4. Host: gender, obesity, predisposing genes
30
Q

Describe Delivery Method: Nebuliser

A
  • vaporises liquid medication
  • fast relief from inflammation, making breathing easier
  • medication goes directly into lungs
31
Q

Describe Delivery Method: Spacers

A
  • makes the use of inhalers easier
  • fast relief from inflammation, making breathing easier
  • medication goes directly into lungs
32
Q

List the 4 Pharmacological Interventions for Asthma: Relievers/Controllers (Bronchodilators)

A
  1. Beta-2 Adrenergic Agonists: Short Acting Beta-2 Agonists (SABAs)
  2. Beta-2 Adrenergic Agonists: Long Acting Beta-2 Agonists (LABAs)
  3. Methylxanthines
  4. Muscarinic Antagonists
33
Q

List the 3 Pharmacological Interventions for Asthma: Preventers (Anti-Inflammatory Agents)

A
  1. Leukotriene Receptor Antagonists
  2. Corticosteroids
  3. Anti-IgE Antibodies
34
Q

Describe Beta-2 Adrenergic Agonists: Short Acting Beta-2 Agonists (SABAs)

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Agonist
b) Short-term stimulation of beta-2 receptors on smooth muscle lining of the bronchioles. Effective in early phase asthma
c) 3-5 hours; with 1-5 minutes onset of action
d) Symptomatic relief of bronchospasm and constriction
e) Increased heart rate, muscle tremors, feeling light-headed or shaky, headache
f) Salbutamol

35
Q

Describe Beta-2 Adrenergic Agonists: Long Acting Beta-2 Agonists (LABAs)

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Agonist
b) Long-term stimulation of beta-2 receptors on smooth muscle lining of bronchioles
c) 12+ hours; with 30-45 minutes onset of action
d) Used prophylactically for asthma treatment
e) Increased heart rate, muscle tremors, feeling light-headed or shaky, headache
f) Salmeterol

36
Q

Describe Methylxanthines

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Antagonist
b) Inhibits phosphodiesterase (PDE), may reduce transcription of inflammatory genes. Stimulates the CNS and increases breathing rate
c) 12+ hours
d) Increases cAMP and promotes bronchodilation

e) Cardiac dysrhythmia, GI disturbances, seizures
Narrow therapeutic window, P450 metabolism

f) Theophylline

37
Q

Describe Muscarinic Antagonists

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Antagonist
b) Blocks M3 receptors, preventing parasympathetic contraction of smooth muscle. Used with Beta-2 agonists or steroids in acute severe asthma
c) 2-3 hours
d) Short acting bronchodilator inhibits bronchoconstriction and mucous secretion
e) Limited side effects, as not permeable into systemic circulation. Bitter in taste. Nebulised patients of age may develop glaucoma if using face mask
f) Ipratropium

38
Q

Describe Leukotriene Receptor Antagonists

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Antagonist
b) Taken orally to reduce leukotriene activity. Relaxation of smooth muscle. No effect on inflammation
c) 12+ hours
d) Relaxes airways
e) GI irritation
f) Montelukast

39
Q

Describe Corticosteroids

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Antagonist
b) Inhibition of release of immune mediators from macrophages, T-cells and eosinophils. Reduction of mucous secretion and reduced inflammation
c) 18-36 hours
d) Reduces mucous secretion and inflammation
e) Oral thrush, cataract risk, reduced bone density, glaucoma, reduced growth rate in children

f) Beclomethasone
Fluticasone
Prednisone

40
Q

Describe Anti-IgE Antibodies

a) Agonist vs. Antagonist
b) Mechanism of Action
c) Duration of Action
d) Outcome
e) Possible Side Effects
f) Active Drug Component

A

a) Antagonist
b) Reduces stimulation of mast cells and releases anti-inflammatory mediators
c) 2-4 weeks
d) Controls/reduces inflammation
e) Rash, itching, joint pain, nausea, dizziness, cold-like symptoms
f) Omalizumab

PHYL2066 Content (8 decks)

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