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Second Year > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Definition: Pharmacodynamics

A

How the drug affects the body

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2
Q

Definition: Pharmacokinetics

A

How the body affects the drug

Describes the disposition of a compound within an organism (absorption, distribution, metabolism, excretion)

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3
Q

Definition: Drug

A

A medicine or other substance which has a physiological effect when ingested or otherwise introduced to the body

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4
Q

Name three things that activate receptors

A

1) Neurotransmitters
2) Autocoids (cytokines, histamine)
3) Hormones

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5
Q

Name the 4 main types of receptor

A

1) Ligand-gated ion channel
2) G-protein coupled receptors
3) Kinase-linked receptors (tend to be growth factors)
4) Nuclear receptors

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6
Q

Imbalance of chemicals/receptors can lead to pathology; give an example of a disease caused by a chemical imbalance

A

Parkinson’s Disease: reduced dopamine

Allergy: reduced histamine

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7
Q

Imbalance of chemicals/receptors can lead to pathology; give an example of a disease caused by a receptor imbalance

A

Myasthenia gravis: loss of ACh receptors

Mastocytosis: increased c-kit receptor

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8
Q

Definition: ligand

A

A molecule that binds to another molecule

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9
Q

Definition: agonist

A

A compound that binds to a receptor and activates it

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10
Q

Definition: antagonist

A

A compound that reduces the effect of an agonist

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11
Q

Definition: efficacy (Emax)

A

Maximum response achievable from a dose, describes how well a ligand activates the receptor (agonist only)

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12
Q

What are the 4 factors governing drug action?

A

RECEPTOR RELATED:

1) Affinity
2) Efficacy

TISSUE RELATED:

1) Receptor number
2) Signal amplification (signal cascade increases response)

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13
Q

Definition: affinity

A

Describes how well a ligand binds to the receptor (agonists and antagonists)

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14
Q

Give two examples of enzyme inhibitors

A

1) ACE inhibitors- reduces BP by inhibiting component of RAAS system
2) Statins- lower cholesterol by blocking rate limiting step in cholesterol pathway

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15
Q

What are the 3 protein ports in ion transport?

A

1) Uniporters: molecules into cell
2) Symporters: two or more molecules move into cell
3) Antiporters: inward and outward movement in cell

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16
Q

What are the 4 main ion channels?

A

1) Epithelium (e.g. sodium)
2) Voltage-gated (e.g. calcium, sodium)
3) Metabolic (e.g. potassium)
4) Receptor-mediated (e.g. chloride)

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17
Q

Definition: absorption (with regards to pharmacokinetics)

A

The process of transfer from the site of administration into the general or systemic circulation

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18
Q

What are the 4 main ways in which drugs can cross a membrane?

A

1) Passive diffusion
2) Diffusion through pores or ion channels
3) Carrier mediated processes
4) Pinocytosis

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19
Q

Where are weak acid drugs best absorbed?

Where are weak base drugs best absorbed?

A

Weak acids- stomach

Weak bases- intestines

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20
Q

What affects the rate of oral absorption of a drug?

A

1) STRUCTURE- must be lipid soluble to be absorbed from gut
2) DRUG FORMULATION- the drug must disintegrate and dissolve rapidly to be absorbed
3) GASTRIC EMPTYING- determines how quickly drug is delivered to small intestine
4) FIRST PASS METABOLISM- drugs taken orally must ‘first pass’ 4 metabolic barriers to reach circulation (mainly liver) which will greatly reduce the concentration of a drug before it reaches circulation

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21
Q

What are the other routes of absorption besides orally?

A
  • Transcutaneous
  • Intradermal and subcutaneous
  • Intramuscular
  • Intranasal
  • Inhalational
  • IV (fastest)
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22
Q

Definition: distribution (with regards to pharmacokinetics)

A

The process by which a drug is reversibly transferred from general circulation to tissues as the blood concentration increases and then returns to the blood from tissues once the concentration falls

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23
Q

What is elimination in pharmacokinetics and what are its two routes?

A

Removal of drugs from the body

1) Metabolism (lipid soluble)
2) Excretion (solids, liquids, gases)

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24
Q

What is zero order kinetics?

A

The change in concentration per time is a fixed amount of drug per time, independent of concentration (straight line graph)

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25
Q

What is first order kinetics?

A

Change in concentration at any time is proportional to the concentration (e.g. 10% of a drug is eliminated by unit time)

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26
Q

Definition: half-life

A

The time taken for a concentration to reduce by one half

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27
Q

Definition: bioavailability

A

The fraction of the administered drug that reaches the systemic circulation

I.V 100%
Oral will be a fraction as some may be incompletely absorbed or undergo first pass metabolism

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28
Q

How do you measure the bioavailability of a drug?

A

Plot a concentration/time graph for IV and oral administration
Area under curve (oral)/ Area under curve (IV) = F
F= Bioavailability

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29
Q

How is the extent of distribution calculated?

A

‘Volume of distribution’- Vd
Vd= total amount of drug in body (dose)/plasma concentration
If Vd is low it suggests drug is mainly confined to circulation
If Vd is high it suggests it is in tissues

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30
Q

What is clearance and how is it calculated?

A

The volume of blood or plasma cleared of drug per unit of time

Cl= Dose/ AUC for IV drug
Cl= Dose x F/AUC for oral (F<1)
31
Q

What is steady state?

A

The balance between drug input and elimination

important during repeat drug administration when concentration aims to be constant

32
Q

What is the path of the parasympathetic nervous system? (receptors and neurotransmitters)

A

Preganglionic fibre— ACh—Nicotinic receptors—Postganglionic fibre—ACh—Muscarinic receptors

33
Q

What is the path of the sympathetic nervous system? (receptors and neurotransmitters)

A

Preganglionic fibre— ACh—Nicotinic receptors—Postganglionic fibre—NAd—Alpha/Beta receptors

34
Q

What do the muscarinic receptors do?

A

M1: Mainly in brain

M2: Mainly in heart- activation slows down heart

M3: Smooth muscle contraction (bronchoconstriction, pupil secretion), stimulates gland secretion (salivary)

M4-5: mainly in CNS

35
Q

Give an example of a muscarinic agonist

A

Pilocarpine- stimulates salivary secretion, constricts pupil (treats glaucoma)

36
Q

Give some examples of muscarinic antagonists (anticholinergics)

A

Atropine- speeds up heart
Hyoscine- antagonises secretions (dry mouth)

They can be used to treat bradycardia in cardiac arrest
They can treat an overactive bladder
They can treat bronchoconstriction

37
Q

Anticholinergic side effects

A
  • Anticholinergics worsen memory and may cause confusion

- Constipation, drying of mouth, blurring of vision, worsening of glaucoma

38
Q

Cholinergic side effects

A

Muscle paralysis, twitching, salivtion, confusion

39
Q

What is the precursor of Adrenaline/Noradrenaline?

A

Dopamine

40
Q

Where is noradrenaline released from?

A

Sympathetic nerve fibre ends (also adrenal glands)

41
Q

Where is adrenaline released from?

A

Adrenal glands

42
Q

What do Alpha 1 agonists cause?

A

Smooth muscle contraction (vasoconstriction, pupils etc.) Increases BP (vasoconstriction)

43
Q

What do Alpha 2 agonists cause?

A

Mixed effects on smooth muscle

44
Q

What do Beta 1 agonists cause?

A

Act upon heart, inotropic and chronotropic effects

45
Q

What do Beta 2 agonists cause?

A

Relaxes smooth muscle (premature labour, asthma)

46
Q

What do Beta 3 agonists cause?

A

Enhances lipolysis, relaxes bladder detrusor

47
Q

What can alpha antagonists treat?

A 
Prostatic hypertrophy
Lower BP (doxazosin)
48
Q

Give some examples of Beta blockers:

A 
B1 and B2 blocker (propanolol) slows HR, reduces tremor (but may cause wheeze)
B1 blocker (atenolol) slows HR
Bisoprolol, metoprolol may not be safe in asthma and COPD due to bronchconstriction
49
Q

What can Beta blockers treat?

A 
Angina
Prevent MIs
High BP
Anxiety
Arrhythmias
Heart failure
50
Q

What are side effects of beta blockers?

A 
Tirednesss
Cold extremities
Bronchoconstriction
Bradycardia
Hypoglycaemia
Cardiac Depression
51
Q

What are the 3 main types of drug interaction?

A

Synergy (work together- positive)
Antagonism (work against each other- negative)
Other (bit of both?)

52
Q

What are risk factors regarding drugs?

A

Narrow therapeutic index (fine line between therapeutic and toxic effect)

Steep dose/response curve (easy to overdose)

Saturable metabolism (takes a long time to break down e.g. alcohol)

53
Q

Definition: Adverse Drug Reaction (ADR)

A

Unwanted or harmful reaction following administration of a drug or combination of drugs, under normal conditions of use, and is suspected to be related to the drug

54
Q

Give an example of an ADR

A

Beta blockers can cause bradycardia and bronchospasm

55
Q

ADR: Rawlins Thompson Classification

What is type A?

A

AUGMENTED PHARMACOLOGICAL
Predictable, dose dependent, common
(morphine and constipation, hypotension and antihypertensive- common side effects?)

56
Q

ADR: Rawlins Thompson Classification

What is type B?

A

BIZARRE OR IDIOSYNCRATIC
not predictable and not dose dependent, unique
(anaphylaxis and penicillin, can be allergy or hypersensitivity)

57
Q

ADR: Rawlins Thompson Classification

What is type C?

A

CONTINUOUS

e.g. osteoporosis when taking steroids

58
Q

ADR: Rawlins Thompson Classification

What is type D?

A

DELAYED

e.g. malignancies after immunosuppression

59
Q

ADR: Rawlins Thompson Classification

What is type E?

A

END OF TREATMENT
Occur after abrupt drug withdrawal
e.g. withdrawal seizures when anti-convulsants are stopped

60
Q

When should an ADR be suspected?

A
  • Symptoms soon after new drug is started
  • Symptoms after a dosage increase
  • Symptoms disappear when the drug is stopped
  • Symptoms reappear when the drug is restarted
61
Q

What is the yellow card scheme?

A

A voluntary reporting scheme that collects reports on ADRs

Allows identification of new ADRs, namely in ‘black triangle drugs’ (drugs that are undergoing additional monitoring)

62
Q

What is included on a yellow card?

A
  • Suspected drug
  • Suspected reaction
  • Patient details
  • Reporter details
63
Q

What is type 1 hypersensitivity?

A

Acute anaphylaxis

64
Q

What is type 2 hypersensitivity?

A

Antibody dependent cytotoxicity

body treats protein as foreign after is combines with thee drug

65
Q

What is type 3 hypersensitivity?

A

Immune complex mediated

antigen and antibody form large complexes and activate compliment

66
Q

What is type 4 hypersensitivity?

A

Lymphocyte mediated

67
Q

Main features of anaphylaxis

A 
Rash
Wheeze/SOB
Hypotension (shock)
Cardiac arrest
Swelling of lips, face; cyanosis and oedema
Rapid onset
68
Q

How is anaphylaxis treated?

A
  • IM adrenaline (Vasoconstriction, increase heart rate, bronchodilation)
  • IV adrenaline if in shock
  • Stop giving causative drug
  • High flow oxygen
  • IV hydrocortisone
  • IV fluids
  • IV anti-histamine
69
Q

What is the clinical criteria for allergy to a drug?

A
  • Response does not correlate with drug properties
  • Reaction disappearance when drug stops
  • Reappears on re-exposure
  • Occurs in a minority of patients on drug
  • Incubation period of primary exposure
  • Reaction similar to those produced by other allergens
  • No linear relation with dose (tine dose can cause severe effects)
70
Q

Definition: potency

A

How powerful a drug is (affinity)

71
Q

What can be used to treat opioid overdose?

A

Naxolone

72
Q

How do opioids work?

A

Inhibit release of pain transmitters at spinal cord and midbrain-
Modulate pain perception in higher areas- euphoria (changes emotional perception of pain)

73
Q

What are the different opioid receptors?

A

MOP- all drugs currently used are agonists of this
KOP- agonists cause depression instead of euphoria
DOP
NOP

Second Year (5 decks)

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