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Pase 2a Notes > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define pharmacodynamics

A

The biochemical, physiological and molecular effects of a drug on the body
= What the body does to the drug

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2
Q

Define pharmokinetics

A

The fate of a chemical substance administered to a living organism
= what the body does to the drug

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3
Q

Why is pharmacology important?

A

Knowledge to support safe, legal and efficient prescribing

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4
Q

4 pharmokinetic processes

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
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5
Q

Which types of administration gives 100% dose?

A

IV
IA (intra-arterial)

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6
Q

4 mechanisms for drugs to permeate across cell membrane

A

Diffusion through pores or channels
Passive diffusion (lipid soluble)
Carrier protein mediated
Pinocytosis

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7
Q

3 factors affecting drug absorption

A

Drug structure
Ionised drugs give poor lipid solubility
Large or hydrophilic poorly absorbed

Medicine formulation
Coating or modified release slows rate
Oral drugs must cross many barriers

Weak acids or bases
Acids - best absorbed in stomach
Bases - best absorbed in intestine

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8
Q

What is first pass metabolism?

A

Metabolism of drugs preventing them from reaching the systemic circulation

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9
Q

2 sites of first pass metabolism

A
  1. Degradation of enzymes in the intestinal wall
  2. Absorption into hepatic portal vein and then metabolism via liver enzymes
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10
Q

Define bioavailability

A

Proportion of administered dose which reaches the systemic circulation

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11
Q

Does bioavailability rely on rate of absorption?

A

No!
Extent of absorption and first pass metabolism

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12
Q

Inhaled absorption pro and cons

A

Well perfumed, large SA and blood flow

Limited by risk of toxicity to alveoli so restricted to volatiles

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13
Q

Pros and cons of intramuscular absorption

A

Can make slow release drug by incorporating lipophilic

Increase in blood flow or water solubility removes drug quicker

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14
Q

4 factors affecting drug distribution

A

Size of the molecule
Lipid solubility
Protein binding
Volume of distribution

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15
Q

3 ways for drugs to reach CNS

A

High lipid solubility
Intrathecal administration
Inflammation causes leaky barrier

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16
Q

What is Vd?

A

Volume if distribution (higher if drugs are well distributed)

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17
Q

Why is caution required for drugs in elderly?

A

Leads to smaller Vd, higher plasma concentration and more likely to cross BBB

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18
Q

Should we dose smaller or larger in obese patients?

A

Smaller !
Drugs not distributed to fat so dose based on ideal body weight not actual

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19
Q

2 processes of drug elimination

A

Metabolism - modification of chemical structure for lipid soluble drugs
Excretion - of unchanged drug

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20
Q

How does sepsis affect pharmokinetics

A

Leaky blood vessels increases distribution and greater penetration of BBB

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21
Q

How does liver impairment affect pharmokinetics

A

Hypoalbuminaemia leads to more drug crossing BBB

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22
Q

2 phases of drug metabolism

A

Phase 1 - oxidation/reduction/hydrolysis by CP450 adds reactive group to make drug polar

Phase 2 - conjugation of functional group to produce hydrophilic inert molecule for excretion

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23
Q

4 types of metabolisers

A

Poor - minimal therapeutic effect
Intermediate - reduced effect
Extensive- converted to morphine
Ultra-rapid - risk of toxicity

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24
Q

Excretion types

A

Liquids - urine, bile, sweat
Solids - faeces
Gases - expired air

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25
Q

3 processes accounting for renal excretion of drugs

A
  1. Glomerular filtration
  2. Active Tubular secretion
  3. Passive reabsorption
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26
Q

What happens in reduced kidney function?

A

Accumulation and toxicity of renally cleared drugs e.g. gentamicin

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27
Q

Define first order kinetics

A

Rate of elimination is proportional to the plasma drug concentration
(Constant % is eliminated)

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28
Q

Define zero order kinetics

A

Rate of elimination is NOT proportional to the plasma drug concentration
(Constant and unaffected by conc so caution when adjusting doses)

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29
Q

Differences between first and zero order kinetics

A

First - process do not become saturated
Zero - processes become saturated

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30
Q

What is clearance?

A

CL = removal of drug by all eliminating organs per unit time

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31
Q

Cmax vs Tmax

A

C - maximum plasma concentration
T - time taken to reach Cmax

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32
Q

How does a prolonged release oral does affect Tmax?

A

Slower absorption so increases Tmax and reduces Cmax

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33
Q

Define half life

A

t 1/2 - time taken for plasma drug concentration to fall 50%

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34
Q

Half life equation

A

T 1/2 = 0.693k = ln2

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35
Q

Half life depends on

A

Clearance
Volume of distribution - large Vd cleared more slowly

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36
Q

What needs to be taken into account with a short half life?

A

Frequent dosing
Increases risk of withdrawal symptoms

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37
Q

After how many half lives is a drug considered cleared?

A

5

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38
Q

What happens to half life in organ dysfunction

A

Is increased
= dose reduction required

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39
Q

Define steady state

A

When rate of drug input is equal to rate of drug elimination

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40
Q

What is Css?

A

Drug plasma concentration at steady state
Time to Css = 5 x t 1/2

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41
Q

Why is steady state important?

A

Repeated dosing causes peaks and troughs around mean plasma concentr

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42
Q

When is a loading dose required?

A

When urgently need to reach steady state e.g. antibiiotics

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43
Q

Water soluble vs lipid soluble drugs rate of distribution depends on…

A

Water - rate of passage across membranes

Lipid - blood flow to tissues

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44
Q

Rate of elimination is inversely proportional to..

A

Vd

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45
Q

Define pharmacogenetics

A

The use of genetic and genomic information to tailor pharmaceutical treatment to an individual

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46
Q

How can genomics affect pharmacodynamics

A

Variations in drug receptor varies efficacy and increased incidence of adverse drug reactions

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47
Q

How can genomics affect pharmokinetics

A

Variations in drug metabolism

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48
Q

4 drug targets

A

Receptors
Enzymes
Transporters
Ion Charles

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49
Q

Define enzyme inhibitor

A

A molecule that binds to an enzyme and decreases its activity

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50
Q

2 types of enzyme inhibitors

A

Irreversible- changes enzyme chemically

Reversible - binds non-covalently

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51
Q

Describe how statins work

A

Blocking the rate limiting step HMG-CoA reductase in the cholesterol pathway
= reduces cholesterol and Cardiovascular diseases

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52
Q

What happens when ACE is inhibited?

A

Reduction of Angiotensin 2 production reduced blood pressure

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53
Q

3 types of protein ports (active transport)

A

Uniporter - Uses energy from ATP
Symporter - Use movement of one molecule to pull in another
Antiporter - once substance moves against its gradient using energy from another moving gown the gradient

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54
Q

Example of a symporter

A

Na-K-Cl Co transporter (NKCC) all in the same direction
= Furosemide in oedema inhibits so allows for Na, K, Cl loss in urine

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55
Q

Types of ion channels and examples

A

Metabolic (K) - diabetes
Receptor activated (Cl) - epilepsy
Epithelial (Na) - heart failure
Voltage gated (Ca, Na) - nerve, arrhythmia
Active ion transporter (3Na, 2K)

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56
Q

Example of irreversible enzyme inhibitor

A

Organophosphate inhibit cholisterase
E.g. insecticides, nerve gases

Muscarinic, Nicotinic and CNS symptoms

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57
Q

Define xenobiotics

A

Foreign compounds to the organisms normal biochemistry

58
Q

Describe xenobiotic metabolism

A

Metabolic breakdown occurs through specialised enzymatic systems and generates readily excreted compounds

Most undergo deactivation by CYP enzymes

59
Q

What does rate of metabolism determine?

A

A drugs duration and intensity

60
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects

61
Q

Exogenous v endogenous receptors

A

Exo - drugs
Endo - hormones, neurotransmitters

62
Q

3 chemical for communication

A

Neurotransmitters (Ach, serotonin)
Hormones (hydrocortisone, testosterone)
Autacoids (local infections - cytokines, histamine)

63
Q

Examples of an imbalance in chemicals and receptors

A

Allergy - increased histamine
Parkinson’s - reduced dopamine

Myasthenia gravis - loss of Ach receptors

64
Q

4 types of receptors

A

Ligand gated ion channels - conformational change generates and electrical charge e.g. Ach

G protein coupled - largest group of molecular switches activated by many different ligands eg. Beta -adrenoreceptor

Kinase linked - enzymes of phosphorylation (growth factors)

Cytosolic / nuclear -specific domains on DNA e.g. steroid

65
Q

How do G proteins work?

A

Guanine nucleotide binding proteins involved in transmitting signals from GPCRs and downstream signalling

66
Q

Agonists vs Antagonists

A

Agonist - high affinity, high efficacy
Antagonist - high affinity, low efficacy

67
Q

Potency vs efficacy

A

P - concentration that elicits a response

E - how great of a response is elicited

68
Q

Competitive vs non-competitive antagonists

A

C - binds to same site
NC - binds to allosteric site

69
Q

2 categories of cholinergic receptors

A

Agonist - Antagonist
Muscarine - Atropine
Nicotine - Curare

70
Q

Define signal transduction

A

Process converting a signal from outside the cell to a different functional change within the cell

71
Q

What is a receptor reserve?

A

Some agonists only need to activate a small fraction of receptors for a maximum response which allows for a second wave (not possible for partial agonist)

72
Q

Tolerance vs desensitisation

A

T - slow reduction in effect over time due to repeated, continuous high

D - rapid internalised degraded ligands uncouples whole system

73
Q

Specificity vs sensitivity

A

Sp - no compound is truly ever specific

Se - describes enhanced activity

74
Q

What is allosteric modulation?

A

Agonist binds to site and allosteric ligand binds to different site for a combined therapeutic response

75
Q

What is inverse agonism

A

Interacts with the same receptor as the agonist but reduces the response

76
Q

Current steps of drug development

A

Lead compound identification
Pre-clinical research
Doing for regulatory status
Clinical trials on humans
Marketing the drug

77
Q

Define drug ability

A

The ability of a protein target o bind to small molecules with high affinity

78
Q

Drugs are developed from:

A

Plants - digitalis foxis
Inorganic elements
Organic molecules - chloroform, phenol
Bacteria/ fungi/ molds
Sterioisomers
Immunotherapy antibodies
From animals
Gene therapy

79
Q

Recombinant proteins in clinical use

A

Insulin
Erythropoietin
Growth hormone
Interleukin 2
Gamma interferom
Interleukin 1 receptor

80
Q

3 mechanisms of gene therapy

A
  1. Synthesis
  2. Replication of DNA e.g. cisplatin
  3. Incorporation e.g. purines into DNA
81
Q

Define gene therapy

A

An experimental technique which repairs or replaces a mutated gene

82
Q

What is rational drug design?

A

The process of finding we educations based on the knowledge of a biological target

83
Q

Pharmokinetics issues for immunotherapy

A
  1. Immunoglobulin not filtered by kidney
  2. FcRn receptor absorb IgG
  3. Mouse antibodies not suitable for humans
84
Q

What is tumour necrosis factor a?

A

Cytotoxic factor released by activated macrophages, stimulates acute phase proteins

85
Q

Routes of opioid administration

A

Oral
Bioavailability
First pass metabolism - 50% of oral morphine is metabolised, halve dose if IV / IM

86
Q

What is the controlled drug (CDs) legislation?

A

Misuse of drugs act 1971
Opioids - class A drugs
Practical issues is secure storage and CD books (2 signatures needed)

87
Q

How do opioids work?

A

Inhibition of descending pathways of pain to euphoria
Natural endorphins activate G protein coupled receptors for secondary messengers

88
Q

Down regulation with prolonged use leads to

A

Tolerance

89
Q

Side effects of opioids

A

Respiratory distress
Sedation
Nausea and vomiting
Constipation
Itching
Immune suppression
Endocrine effects

90
Q

Treatment of Opioid induced respiratory distress

A

Call for help ABC
Naloxone (IV)
Titrate to effect - 1ml to 10ml saline
Beware of short half life

91
Q

Opioids for non cancer pain

A

Opioids are marketed aggressively
But loses effectiveness quickly and causes addiction

92
Q

Metabolism of morphine in renal failure

A

Morphine is metabolised to morphine 6 glucuronide which is more potent and renally excreted
In renal failure, builds up and causes respiratory distress

93
Q

Parasympathetic vs sympathetic ganglia

A

Both preganglionic release Ach acting on Nicotinic receptors

P - Ganglia near targets with short post-ganglionic neurone, Ach acts on Muscarinic receptors

S - Ganglia near spinal chord with long post-ganglionic neurone, NAd acts on A/B adrenergic receptors

94
Q

Cholinergic and adrenergic pharmacology controls

A

Blood pressure
Heart rate and contractility
Anaesthetic agents
Airways
Pressure in eyes
Control of GI
Muscle contraction

95
Q

5 types of adrenergic receptors

A

A1 - postsynaptic vasoconstriction
A2 - presynaptic negative feedback
B1 - increase HR and contractility
B2 - bronchodilation
B3 - reduces over active bladder

96
Q

Alpha agonists vs blockers

A

Agonist - Adrenaline raises blood pressure

Antagonist - doxazosin lowers blood pressure for hypertension

97
Q

Drug side effects of Beta

A

Too much beta 1 can affect beta 2 (bronchoconstriction) and vice versa (tremors)

98
Q

Which nerve supplies parasympathetic to all organs?

A

CN 10 - vagus

99
Q

5 Muscarinic receptors located in

A

M1 - CNS, brain
M2 - heart
M3 - glands and smooth muscle
M4 + 5 - CNS

100
Q

Anti-cholinergic side effects

A

Worsen memory and cause confusion

101
Q

Atropine function

A

Blocks parasympathetic by competing with acetylcholine
But:
Cross BBB and causes confusion in elderly
Only used in life threatening bradycardia

102
Q

Reversal of muscle relaxants

A

Neostigimine blocks breakdown of acetylcholine so muscles work again

103
Q

What kind of receptors are nicotinic?

A

Ligand gated ion channels

104
Q

Beta blockers function

A

Lowers blood pressure

105
Q

Nicotinic antagonist

A

Trimetaphan

106
Q

M1 receptor function and antagonist

A

Increases motility, secretions in gut and CNS effect

= Atropine (crosses BBB) + Glycopyrrolate (doesn’t cross BBB)

107
Q

M2 receptor function and antagonist

A

Bradychardia, reduced contractility

= Hyoscine

108
Q

M3 receptor function and antagonist

A

Vasodilation, bronchoconstriction, pupil dilation

= Ipratropium

109
Q

A drug interaction occurs when:

A

Pharmacodynamics - drugs have an effect on the same target or system
Pharmokinetics - a drug affects the expected performance of another

110
Q

4 types of pharmacodynamic drug interactions

A

Synergy - interaction of drugs with same effect totals greater effect

Antagonism - substance acts and blocks action of another

Summation - different drugs used together has the same effect as a single drug

Potentiation - enhancement of one drug by another so effect is greater than total

111
Q

Examples of synergetic interactions

A

Morphine for pain relief and lorazepam for anxiety both agonists
= Increased risk of sedation

Amlodipine and ramipril for hypotension both reduce vasoconstriction
= Some drug interaction are beneficial!

112
Q

Example of antagonism interaction

A

Atenolol for hypertension and Salbutamol for asthma both compete at B2 receptors
= reduced bronchodilation

113
Q

4 Mechanisms by which one drug can affect the absorption of another (Pharmokinetics)

A
  1. Alters pH and pKa
  2. Formation of insoluble drug complex
  3. Slowing gut motility
  4. P-glycoprotein drug transporters inhibited or induced
114
Q

How can a drug affect the distribution of another?

A

If both drugs compete for protein binding plasma albumin, more drug is free and therapeutic effect increases

115
Q

How may a drug affect metabolism of another?

A

CYP450 enzyme metabolise molecules via phase 1 reactions to create hydrophilic molecules for kidney excretion

Inhibition of CYP450 blocks metabolism and excretion of drug, so increased effect and vice versa

116
Q

How may a drug affect excretion of another?

A

Renal
- pH dependent ( weak bases cleared faster if urine is acidic and vice versa)
- Competing for transporters in kidney tubules reduces elimination

117
Q

Drug interactions to be wary of

A

Codeine + Morphine = double opioid agonists

NSAIDs + ACEi = acute kidney injury

Warfarin + many vitamin K food / drugs = enzyme induction

118
Q

Define an adverse drug reaction

A

Unwanted or harmful response to a drug or combination of drugs under normal conditions

119
Q

Define side effects

A

An unintended effect of a drug including unexpected benefits

120
Q

What types of Adverse Drug Reactions are there? (Rawlin’s Thompson)

A

A. Augmented - exaggerated effect at therapeutic dose, common + reversible
B. Bizarre - not predictable and not drug or dose related
C. Chronic - continue after the drug has been stopped
D. Delayed - becomes apparent time after stopping drug
E. End of use - occurs abruptly after drug withdrawal
F. Failure of treatment - unexpected due to interaction
G. Genetic - drug causes irreversible damage to genome

121
Q

Alternate way of classing ADRs (DOTs)

A

Dose
- hyper susceptibility (at low doses)
- Collateral (side effects)
- toxic effects (at high doses)
Timing
- Time dependent or independent
Susceptibility
- Certain groups (ages, gender, disease)

122
Q

What stages are ADRs identified?

A

Preclinical - toxicity in animals
Clinical - efficacy and safety
Post market surveillance (black triangle) - to find susceptibility
Pharmacovigilance - everyday reports for safe prescribing

123
Q

What is a yellow card and when to report?

A

=A system to record every day ADRs
(Confidential, quick, accessible)

Report when
- serious ADR
- Unlicensed use (herbal, illicit)
- Any ADR with black triangle

124
Q

When should we suspect ADRs?

A

Symptoms:
- after new drug started
- after dosage increase
- disappears when drug stopped
- reappear when drug restarted

125
Q

4 important information to record on a yellow card

A

Suspected drug
Suspect reaction
Patient details
Reporter qualifications

126
Q

Who may have an ADR?

A

= Anyone taking drugs

127
Q

Who is at increased risk of ADRs?

A

Polypharmacy
Multimorbidity
Extreme weight
Liver or kidney impairment
Children, neonatal, elderly
Genetic variants
Atopic (increased allergies)

128
Q

Common ADRs

A

Confusion
Nausea
Balance problems
Diarrhoea
Constipation
Hypotension

129
Q

What to do if there is an ADR?

A

Assess if treatment required
Take history
Review profile of suspected drug
Modify dose, swap or stop
Document ADR in patient record
If criteria met, report

130
Q

Define hypersensitivity

A

Objectively reproducible symptoms or sign caused by exposure to a stimulus at a dose tolerated by normal people. May be caused by immunologic (allergic) and non-immunologic (no prior exposure, direct mast cell degranulation) mechanisms

131
Q

Define anaphylaxis

A

An acute allergic reaction to an antigen which the of has become hypersensitive
(First exposure may not be medical e.g. penicillin in dairy)

132
Q

Does anaphylaxis have a linear reaction to dose?

A

No! Small dose may cause severe reaction

133
Q

Describe type 1 hypersensitivity

A

Acute anaphylaxis:
Prior exposure to antigen
IgE is expressed as cell surface receptors on mast and leukocytes
Re-exposure causes mast cell degranulation

134
Q

Describe type 2 hypersensitivity

A

Antibody dependent cytotoxicity:
Drug or metabolite combines with a protein. Body treats as foreign and forms antibodies which activates

135
Q

Describe type 3 hypersensitivity

A

Immune complex deposition:
Small blood vessels are damaged or blocked so leukocytes are attracted to site and inflammatory response

136
Q

Describe type 4 hypersensitivity

A

T-lymphocytes develop antigen specific receptors and subsequent administration leads to local or tissue allergic reactions

137
Q

Main symptoms of anaphylaxis

A

Immediate rash - vasodilation
Hypotension
Cardiac arrest
Swelling of lips, oedema, central cyanosis
Wheeze - Bronchoconstriction

138
Q

Management of anaphylaxis

A

Basic life support - ABCDE
Remove trigger, position flat, legs up
Adrenaline - IM 500ug
High flow oxygen, IV fluids

Antihistamines and steroids

139
Q

Action of adrenaline

A

Vasoconstriction:
A1 = increased vascular resistance
A2 = Inhibition of transmitter release

B1 = Increased HR and contractility
B2 = bronchodilation, reduces oedema

140
Q

Clinical criteria for allergy to drug

A

Doe not correlate with drug pharmacological properties
Reaction similar to those with allergens
Induction period of primary exposure
Disappearance on cessation

141
Q

Risk factors for hypersensitivity

A

Host - females more, uncontrolled asthma, prev drug reactions, EBV, HIV

Genetic factors

Medicine factors - protein or polysaccharide based macromolecules

Pase 2a Notes (6 decks)

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