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BDS2: Oral Medicine > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

What is meant by an idiosyncratic side effect?

A

A side effect that only happens to you i.e. uncommon

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1
Q

What is a drug?

A

An external substance that acts on living tissue to produce a measurable change in the function of that tissue.
Generally act to stimulate or interrupt normal body communications.
They also act on non-host organisms to aid body defences.

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2
Q

What drug types are commonly used in dentistry?

A

Local anaesthetics - prevent pain
Antimicrobials - treat and prevent infection
Anxiolytics - reduce anxiety
Analgesics - reduce post op pain

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3
Q

Compare hormone and neural messages.

A

Hormone - slow, general info to all tissues

Neural - fast, target info for specific tissues

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4
Q

What nervous system involves adrenaline release?

A

Autonomic nervous system

- Sympathetic

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5
Q

What are the different branches of the body’s nervous system?

A

Central Nervous System/CNS

Peripheral Nervous System/PNS

  • Autonomic (involuntary)
    • > Sympathetic
    • > Parasympathetic
  • Somatic (voluntary)
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6
Q

What is the effect of the sympathetic NS on heart rate?

A 
Adrenergic stimulation (adrenaline)
Speeds up heart rate via Beta-receptors
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7
Q

What is the effect of the parasympathetic NS on heart rate?

A 
Cholinergic stimulation (acetyl choline)
Slows the heart via cholinergic receptors
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8
Q

What are the effects of adrenaline?

A 
Beta agonist
Increases h.r.
Increases b.p.
Increases force of contraction
Bronchodilation
Enlarges pupils
*Part of the body's fight or flight response, released in response to stress
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9
Q

Where is adrenaline produced?

A

Medulla of the adrenal glands

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10
Q

What is atenolol?

A

Beta blocker - slows heart rate

Used to treat angina, hypertension and in preventing heart attacks.

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11
Q

What is pilocarpin and what are its actions?

A

Cholinergic agonist
Mimics the actions of acetyl choline
Vasodilation, decreased heart rate, bronchiole constriction

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12
Q

What is atropine and what is it used for?

A

Cholinergic blocker - blocks ACh receptors

Used for asthma, diarrhoea and nausea

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13
Q

How do drugs interact with tissues?

A 
Receptors
Enzymes
Ion channels
G-proteins
Gene transcription
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14
Q

What is an agonist?

A

A drug which stimulates a receptor in turn producing the full response of that receptor

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15
Q

What is an antagonist?

A

A drug which binds to a receptor but has no effect i.e. blocks the action of that receptor

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16
Q

What factors affect drug-receptor interaction?

A

Affinity - the attraction of the drug to receptor affects the likeliness to bind
Occupancy - response of body is directly proportional to the amount of drug bound (occupied receptors)

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17
Q

What factor affects the drug induced response?

A

Efficacy - how much effect a specific drug has on the body system
*the more drugs/receptors, the more chance of the drug being effective

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18
Q

What is a partial agonist?

A

Compounds that can activate receptors but are unable to elicit the maximal response of the receptor system.

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19
Q

What is a competitive antagonist?

A

Binds to receptors in a reversible way without activating the effector system for that receptor. It’s effect can be overcome by increasing the conc of the agonist.
e.g. atenolol

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20
Q

What is a non-competitive antagonist?

A

Binds to receptors and reduces the available receptors for the agonist - irreversible. It’s effects cannot be overcome.
e.g. phenoxybenzamine

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21
Q

What is the path of drugs?

A 
Gut - oral
(via HPV)
Liver
Vein - intravenous
(via IVC)
Heart
(via PA)
Lungs - inhalation
(via PV)
Heart
(via aorta)
Arteries
Sytemic circulation - subcutaneous
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22
Q

What are the different routes of drug administration?

A 
Enteral
- oral
Parenteral
- intravenous
- intramuscular
- subcutaneous
- inhalation
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23
Q

What are the phases of drugs in the body?

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
    ADME
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24
Q

What are the pros and cons of enteral drug administration?

A

Socially acceptable, easier for patients

Slow onset, variable absorption (unpredictable), gastric acid of stomach may destroy drug, first pass metabolism

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25
Q

What is first pass metabolism?

A

Drugs in the gut will pass to the liver via the hepatic portal vein. It is metabolised in the liver before it reaches the systemic circulation where it can have an effect. This means only a portion of the drug consumed becomes active in the bloodstream. First pass metabolism can either activate or deactivate the drug.
*Consider patients liver function when creating doses (age, liver failure etc)

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26
Q

What is the pathway of drugs absorbed in the mouth/rectum?

A

They are not part of the GI tract so do not undergo first pass metabolism. Instead they pass straight into the systemic circulation, meaning all of the drug will be active in the bloodstream.

27
Q

What are the pros and cons of parenteral administration?

A

Predictable plasma levels, no first pass metabolism.

Allergic reactions more severe, access difficulties with self medication, drug cost higher as it must have v low levels of impurities

28
Q

What are the factors affecting oral absorption?

A

Lipid solubility and ionisation - drug must be partially ionised to pass through lipid membrane
Drug formulation - e.g. rapid action, slow release
Gastrointestinal motility - slow at post op, diarrhoea
GIT disease - decreased absorption e.g. Crohn’s

29
Q

What is bioavailability in terms of drugs?

A

The proportion of an ingested drug that is available for clinical effect.

30
Q

What factors determine drug distribution?

A

Blood flow
Tissue solubility
Metabolism in the area

31
Q

What are phase 1 reactions of drug metabolism?

A

Oxidation, reduction, hydrolysis

32
Q

What are phase 2 reactions of drug metabolism?

A

Conjugation - the addition of an ionised group in order to make the metabolite more water soluble
(glucuronidation, sulphation, methylation, acetylation, glutathione)

33
Q

How can drugs be excreted?

A

Renal - urine
Liver - bile, faeces
Lungs - exhalation

34
Q

When should you be wary of drug excretion?

A

Patients with renal disease (leads to excretion problems) or liver disease (leads to metabolism problems).
In both these cases drug dose must be reduced to avoid overdose.

35
Q

What is meant by drug distribution?

A

The dispersion of a drug throughout your body.

Drug going from vascular (bloodstream) to extravascular space (e.g. muscle, fat)

36
Q

What are the four major body compartments in terms of drug distribution?

A

Blood (plasma)
Extracellular fluid
Fat
Intracellular fluid

37
Q

What are the two different models for drug distribution in the body?

A

One compartment model - equal distribution

Two compartment model - more concentrated in certain areas, then equal distribution

38
Q

What is first order kinetics?

A

Drug elimination by passive diffusion - no ATP required, down a conc gradient.
The more drug you have in your system, the higher the excretion rate.
Drug removal is proportionate to the drug concentration (logarithmic graph).

39
Q

What is zero order kinetics?

A

Drug elimination is an active process and can be saturated by high drug concentrations.
Linear graph of drug elimination.
Rate of excretion is fixed - doesn’t change with increased/decreased intake of the drug.
e.g. alcohol, paracetamol

40
Q

What is drug clearance?

A

The volume of plasma cleared of a drug per unit time,

Elimination rate divided by plasma concentration.

41
Q

What are NSAIDs?

A

Non-steroidal anti-inflammatory drugs

Used to reduce inflammatory mediators

42
Q

What are corticosteroids?

A

Drugs used to reduce the inflammation process

NOT direct painkillers - reduce inflammation, therefore reduce pain

43
Q

What are examples of inflammatory mediators?

A

histamine
eichosanoids - arachadonic acid, cyclo-oxygenase products, prostaglandins, leukotrienes
kinins - cause painful reaction

44
Q

What cells are involved in the cellular response of inflammation?

A

Neutrophils

Lymphocytes

45
Q

What are prostaglandins?

A

Hormone like substance made by a chemical reaction at the site they are needed. Derived from arachadonic acid. Involved in the body’s response to inflammation, pain and swelling.

46
Q

What are leukotrienes?

A

The leukotrienes are a family of biologically active molecules, formed by leukocytes, mastocytoma cells, macrophages, and other tissues and cells in response to immunological and nonimmunological stimuli.
Cause bronchoconstriction, airway obstruction and cell infiltration (more leukotrienes).

47
Q

What type of anti-inflammatory drug are COX inhibitors?

A

NSAIDs
Inhibit prostaglandin synthesis
e.g. aspirin, ibuprofen

48
Q

What is aspirin?

A

an effective painkiller that can be purchased over the counter
dose = 300-600mg up to 4 times daily

49
Q

What are the pharmacokinetics of aspirin?

A

Taken enterally.
Rapid absorption from GIT
Eliminated by first order kinetics
Toxic effects lead to acidosis

50
Q

What are the actions of aspirin?

A

Inhibits COX 1

  • decreased synthesis of prostaglandins
  • decreased production of inflammatory mediators
  • anti-pyrexic
  • Same as ibuprofen
51
Q

How long does it take for aspirin to take effect?

A

20/30 minutes

can be taken as a pre-emptive analgesia

52
Q

What are the side effects of aspirin?

A 
Gastric irritations (worse with alcohol)
Inhibition of platelet function - inc. bleeding
Bronchospasm - exacerbates asthma
Allergic reactions - rash
Drug interactions - warfarin
*Same as ibuprofen but more problematic
53
Q

What is ibuprofen?

A

NSAID
Painkiller
Dose = 200-600mg 3 times daily
Sold without restriction

54
Q

What are the actions of ibuprofen?

A

Inhibits COX 1

  • decreased synthesis of prostaglandins
  • decreased production of inflammatory mediators
  • anti-pyrexic
  • Same as aspirin
55
Q

What are the side effects of ibuprofen?

A

Gastric irritations (worse with alcohol)
Inhibition of platelet function - inc. bleeding
Bronchospasm - exacerbates asthma
Allergic reactions - rash
Drug interactions - warfarin
*Same as aspirin but less problematic and less common

56
Q

What is diclofenac?

A 
Prescription drug
NSAID
Similar action to ibuprofen and aspirin
Similar effects but more effective, however there is a higher chance of gastric bleeding & asthma triggering.
Dose = 50mg 3 times daily
57
Q

What are COX2 inhibitors?

A

NSAIDs better for long term used with reduced gastric side effects.
More expensive.
Increased incidence of cardiac death.

58
Q

Give examples of COX2 inhibitors?

A

Celecoxib

Etoricoxib

59
Q

What are the actions of corticosteroids?

A

Decrease inflammation by inhibiting - capillary permeability, formation of bradykinin, migration of WBCs, reduce eicosanoid synthesis.
Suppress the features of inflammation but do not address the cause.

60
Q

What are examples of topical corticosteroids?

A

Steroid inhalers in asthma e.g. beclomethasone
Hydrocortisone cream for eczema
Steroid pastes for mouth ulcers e.g. triamcinolone

61
Q

What are examples of systemic corticosteroids?

A

Prednisolone - prevent transplant rejection or treat autoimmune diseases
Dexamethasone - to reduce swelling after surgery

62
Q

What is prednisolone?

A

Prescription only medicine
Dose varies
Reduces inflammation
Corticosteroid

63
Q

What are the side effects of prednisolone?

A 
High b.p.
Weight gain
Fat distribution change - centripital obesity, buffalo hump
Gastric ulceration
Adrenal suppression
Osteoporosis
Diabetes
64
Q

What is paracetamol?

A

Antipyretic and analgesic
Purchased without restriction
Dose = 1g 4 times daily

65
Q

What are the actions of paracetamol?

A

Used as a painkiller and for controlling fever
Mechanism uncertain
Few side effects
Often combined with co-codamol or co-dydramol

BDS2: Oral Medicine (7 decks)

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