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PHASE 2A (Mine) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacology?

A

The study of the effects of drugs

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2
Q

What is pharmacokinetics?

A

How the body affects drugs

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3
Q

What are pharmacodynamics?

A

He drug affects the body

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4
Q

What are the different ways the body can affect a drug?

A

Absorption
Distribution
Metabolism
Excretion

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5
Q

What are receptor ligands?

A

Anything that acts at a receptor

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6
Q

What is potency?

A

Meaure of how well a drug works

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7
Q

What is an agonist?

A

A compound that binds to a receptor and activates it

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8
Q

What is an EC50?

A

Drug concentration that gives half the maximal response

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9
Q

What does efficacious mean?

A

More successful in producing a desired result (e.g. Drug A is more efficacious than drug B)- higher Emax

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10
Q

What is a partial agonist?

A

A drug that binds to and activates a receptor, but is not able to elicit the maximum response produced by full agonists

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11
Q

What does it mean if one drug is more potent than another?

A

Lower concentrations of it will produce a greater response

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12
Q

What is an antagonist?

A

Compound that reduce the effect of an agonist

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13
Q

What are the different mechanisms of antagonist action?

A

Competitive: Compete with agonists to bing to receptors

Non-competitive: Binds near a receptor and prevents activation.

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14
Q

What are cholinergic receptors and what are they activated by?

A

Involved in signal transduction of the somatic and autonomic nervous system.
Acetylcholine neurotransmitter

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15
Q

What are the cholinergic receptor agonists?

A

Muscarine

Nicotine

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16
Q

What are cholingeric receptor antagonists?

A

Atropine

Curare

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17
Q

What does affinity mean?

A

How well a ligand binds to a receptor

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18
Q

What does efficacy mean?

A

How well a ligand activates a receptor.

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19
Q

What are the actions of NSAIDs?

A

Analgesia
Anti-pyretics (reduce fever)
Anti-inflammatory

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20
Q

What are some NSAID examples?

A

Aspirin

Ibuprofen

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21
Q

How do NSAIDs work?

A

Inhibit COX (enzyme responsible for the breakdown of arachidonic acid to prostaglandin H2) via competitive inhibition

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22
Q

What are prostaglandins/ their action?

A

Group of lipids made at sites of tissue damage or infection that control inflammation, blood flow and clotting.

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23
Q

What are the two forms of COX?

A

COX-1 : Found normally and widely around the body

COX-2: Induced in inflammation

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24
Q

Is aspirin COX selective?

A

No- Works on COX-1 and 2.

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25
Q

What are examples of ACE inhibitors?

A

Ramipril, captopril

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26
Q

What is the action of ACE inhibitors?

A

Anti-hypertensives:
Work by inhibiting ACE so prevent the conversion of Angiotensin 1 to Angiotensin 2, resulting in reduced vasoconstriction and less aldosterone release.

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27
Q

What are B-lactam antibiotics + examples?

A

Antibiotics that work by inhibiting cell wall biosynthesis of bacterial cell walls by inhibiting enzymes.
E.g. Penicillins, amoxicillin, cephalosporins.

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28
Q

What are CYP450’s used for?

A

Enzymes required to introduce a hydroxyl group to some drugs to enable them to be excreted from the kidneys.

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29
Q

What are examples of proton pump inhibitors?

A

Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole

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30
Q

What is the action of proton pump inhibitors?

A

Act to inhibit acid secretion,

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31
Q

What are the different types of diuretics?

A

Loop
Thiazide
Potassium sparing

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32
Q

Where do loop diuretics work?

A

Inhibit sodium-potassium co-transporter in the thick ascending loop of Henle

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33
Q

Where to thiazide diuretics work?

A

Inhibit sodium reabsorption in the distal convoluted tubule

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34
Q

Where to potassium sparing diuretics work?

A

Interfere with the sodium-potassium exchange in the distal convoluted tubule.

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35
Q

What is the action of neuronal uptake inhibitors?

A

Result in increased concentration of neurotransmitter in the synapse by preventing re-uptake

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36
Q

What neurotransmitters are subject to reuptake?

A

Dopamine
Noradrenaline
Serotonin
GABA

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37
Q

What are SSRI’s?

A

Selective serotonin reuptake inhibitors

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38
Q

What is the action of cocaine?

A

Inhibits the reuptake of dopamine

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39
Q

What are some examples of calcium channel blockers?

A

Amlodipine
Verapamil
Diltiazem

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40
Q

What is the action of calcium channel blockers?

A

Anti-hypertensives: Block the voltage dependent calcium channels found in cariac and vascular smooth msuscle, resulting in reduced vasoconstriction

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41
Q

How do local anaesthetics work?

A

By interrupting axonal neurotransmission in sensory nerves

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42
Q

What is a first order drug reaction?

A

The rate of diffusion is directly proportional to the concentration of the drug

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43
Q

What is a second order drug reaction?

A

Rate is directly proportional to the square of the concentration of the drug

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44
Q

What is a third order drug reaction?

A

Rate is directly proportional to the cube of the drug concentration

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45
Q

What is a zero order drug reaction?

A

The rate of diffusion is unrelated to the concentration of the drug

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46
Q

What is the most commonly used graph in pharmacokinetic theory>

A

Concentration time curve

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47
Q

How many litres of fluid is in the:

  • Plasa
  • Interstitium
  • Intracellular?
A 
Plasma= 5 litres
Interstitial= 15 L
Intracellular= 45 L
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48
Q

What are the 5 ways a drug can move from its site of administration to its target?

A 
Simple diffusion
Facilitated diffusion
Active transport
Through extracellular space (through pores) 
Non ionic diffusion
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49
Q

What is bioavailability?

A

The amount of drug taken up as a proportion of the amount administered

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50
Q

What are the different routes of drug administration?

A 
Oral
Intramuscular
Intravenous
Transcutaneous
Intrathecal (into CSF)
Sublingual
Inhalation
Topical 
Rectal
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51
Q

What route of administration has the lowest bioavailability?

A

Oral

52
Q

What is the volume of drug distribution?

A

The total amount of drug in the body divided by concentration of drug in the plasma

53
Q

Where are proteins/ large molecules active?

A

In the plasma compartment

54
Q

Where are water soluble molecules active?

A

In the plasma and interstitial compartment

55
Q

Where are lipid soluble molecules active?

A

In the intracellular fluid

56
Q

Where is the elimination of a drug from?

A

The plasma compartment via the renal or hepatic route

57
Q

What is clearance?

A

The volume of plasma that can be completely cleared of drug per unit time OR the rate at which plasma drug is eliminated per unit plasma concentration

58
Q

What is the unit for clearance?

A

ml/ min

59
Q

How are drugs cleared?

A

Either by the kidney or the liver

60
Q

How can renal clearance be measured?

A

Rate of appearance in urine divided by plasma concentration

61
Q

What kind of drugs are eliminated by the kidneys?

A

Water soluble small molecules

62
Q

What is the hepatic extraction ratio?

A

The proportion of drug removed by one passage through the liver

63
Q

What is phase 1 of hepatic drug metabolism?

A

Make the drug more hyrophilic so it can be excreted by the kidneys (add hyrdoxyl group)

64
Q

What enzyme is involved in Phase 1 reactions?

A

CYP450

65
Q

What is phase 2 of hepatic drug metabolism?

A

Glucocordination: Add a glucuronic acid group to make very hydrophobic drugs more hydrophilic

66
Q

What happens to the drugs once they have been metabolised by the liver?

A

They enter the bile and then the gut via the cystic duct.

67
Q

What happens to the phase 2 glucuronides once they enter the gut?

A

They are metabolised by large bowel flora and can then reenter the blood to have greater effects, before going back to the liver to be re-conjugated and excreted again

68
Q

What is steady state?

A

When the infusion dosage= the rate of elimination from the plasma

69
Q

What is the ideal drug for IV infusion?

A

One with small volume of distribution so it is easy to reach steady state
One which is broken down by tissue/ plasma enzymes irrespective of liver and renal function
One with low risk of toxicity and easy to determine concentration in plasma

70
Q

What neurotransmitter is used by the parasympathetic nervous system?

A

ACh

71
Q

What neurotransmitter is used by the sympathetic nervous system?

A

Noradrenaline

72
Q

What are the side effects of muscarinic agonists?

A 
Diarrhoea
Urination
Miosis
Bradycardia
Emesis (vomiting)
Lacrimation (tears)
Salivation
Sweating
73
Q

What are the different classes of adrenoreceptors?

A 
Alpha-1
Alpha-2
Beta-1
Beta-2
Beta-3
74
Q

What is the action of alpha-1 adrenoreceptors?

A

Vasoconstriction
Pupil dilation
Bladder contraction

75
Q

What is the action of alpha-2 adrenoreceptors?

A

Presynaptic inhibition of noradrenaline

76
Q

What is the action of Beta-1 adrenoreceptors?

A 
Increased force of contraction
Increased heart rate
Increased electrical conduction
Increased renin release
Increased blood pressure
77
Q

What is the action of Beta-2 adrenoreceptors?

A

Bronchodilation
Vasodilation
Reduced GI motility

78
Q

What is the action of Beta-3 adrenoreceptors?

A

Increased lipolysis

Relaxation of bladder

79
Q

What are the 3 components to pain?

A

Sensory
Emotional
Actual/ potential tssue damage

80
Q

What are the different classifications of pain?

A 
Acute pain
Cancer pain
Chronic non-cancer pain
Nociceptive pain
Neuropathic
81
Q

What is nociceptive pain?

A

Pain caused by structural dysfunction (e.g. fracture or IBS)

82
Q

Where does acute pain arise from>

A

Nociceptors

83
Q

What are nociceptors?

A

Nerve endings of the peripheral nervous system (myelinated A delta fibres and unmyelinated C afferent fibres)

84
Q

What is the pain pathway?

A
  1. Noxious stimulus
  2. Nociceptors
  3. Spinal cord via ascending pathway
  4. Spinal cord modulation
  5. Thalamus
  6. Cortical areas + somatosensory cortex + prefrontal cortex
  7. Pain experience/ memory
85
Q

What are the different types of noxious stimulus?

A

Mechanical
Thermal
Chemical

86
Q

Which nerve fibres transmit pain and what type?

A 
C fibres (unmyelinated): characterised by diffuse, dull pain
A delta fibres (myelinated): Localised sharp pain
87
Q

What is the action of A beta and A alpha fibres?

A

A-alpha: Carry information related to proprioception

A-Beta: Carry information related to touch

88
Q

Why does rubbing the site of injury/ Tens machine work to reduce pain?

A

If A-Beta fibres are stimulated at the same time as A delta or C fibres, the pain signal is halted and doesn’t reach the brain

89
Q

What excitatory neurotransmitter is responsible for pain?

A

Glutamate

90
Q

What are the basis of pharmacological treatments for pain?

A

Reducing glutamate and therefore excitation of nerve

Enhancing inhibitory neurotransmitters (GABA, Noradrenaline, Serotonin)

91
Q

What neurotransmitter is the main CNS inhibitory transitter?

A

GABA

92
Q

What is chronic pain>

A

Persistent pain for longer than 3-6 months

93
Q

What does noxious mean?

A

Harmful or poisonous

94
Q

How many patients do adverse drug reactions occur in?

A

10-20% of hospital patients

95
Q

What are the different types of adverse drug reaction?

A 
Augmented
Bizarre
Chronic
Delayed
End of use
96
Q

What are augmented ADR’s?

A

Commonest type. An exaggeration of the clinical effect. Predictable and dose related

97
Q

What are some examples of augmented ADR’s

A

Diuretic causing dehydration
Anticoagulant causing bleeding
Anti-hypertensive causing hypotension

98
Q

What patients are more at risk of augmented drug reactions and why?

A

Elderly- have decreased glomerular filtration

Those with renal or hepatic impairment: elimination difficulties

99
Q

What are type B drug reactions?

A

Bizarre;
Unexpected/ unpredictable and unrelated to dosage.
May be history of allerfy

100
Q

What is an example of a chronic drug reaction?

A

Long term steroids predisposing to hypoglycaemia which may result in diabetes

101
Q

What is an example of a delayed drug reaction?

A

Teratogenesis (congenital malformations) after taking thalidomide
Neoplasia

102
Q

What is an end of use ADR?

A

Withdrawal reactions after stopping a relatively long-term used drugs

103
Q

What are the different types of hypersensitivity and how can drugs cause ADR’s with each type?

A

T1=IgE mediated drug hypersensitivity (Anaphylaxis)
T2= IgG-mediated cytotoxicity (some drugs can cause renal failure)
T3= Immune complex deposition ( reacts with antibiotics)
T4= T-cel mediated (usually substance containing metals)

104
Q

What are the different types of drug interactions?

A

Synergy

Antagonism

105
Q

What is synergy?

A

Where the actions of 2 drugs combine

106
Q

What are the risk factors for drug interactions?

A

Polypharmacy
Old age
Genetics (fast/ slow metabolism)
Hepatic or renal disease

107
Q

What are the risk factors for a drug having a drug interaction?

A

Narrow therapeutic index
Steep dose/ response curve
Saturable metabolism

108
Q

What are the pharmacokinetic mechanisms of drug interaction?

A

Absorption
Distribution
Metabolism
Excretion

109
Q

What are the ways drug interactions can affect absorption of drugs?

A 
Motility changes 
Acidity changes
Solubility 
Non-absorbed complex formation
Direct action on enterocytes
110
Q

How can drug interactions affect the distribution of certain drugs?

A

Protein binging affects drugs concentration in plasma and therefore reduces its distribution

111
Q

How can drug interactions affect the metabolism of drugs?

A

CY450 metabolises many drugs: Inhibition or induction.

112
Q

What effect can grapefuit have on certain drugs?

A

Can increase their uptake (increased bioavailability)

113
Q

How can drug interactions affect the excretion of drugs?

A

Renal excretion is pH dependant. Therefore drugs that change the pH can affect the excretion of other drugs.

114
Q

What are the pharmacodynamic mechanisms of drug interaction?

A 
Receptor based: 
Agonists
Partial agonists
Antagonists
Signal transduction
Physiological system- drugs that affect different receptors in the same system.
115
Q

What is required for a prescription?

A 
Patient name
Dose
Route
Frequency
Duration
Total no. tablets
Drug name
Date & signature
116
Q

What is the oral bioavailability of morphine?

A

50%

0 in 10% of population

117
Q

What is given to reverse a morphine overdose?

A

Naloxone- antagonist

118
Q

What percentage of the dose of morphine should you give if giving IM or IV instead of orally?

A

50%

e.g. 5mg instead of 10mg

119
Q

What is the main side effect of opioid use?

A

Respiratory depression

addiction

120
Q

What are the two systemic routes of drug administration?

A

Enteral

Par-enteral

121
Q

What does enteral mean?

A

Through the GI tract

122
Q

What are the enteral routes of drug administration?

A

Oral (PO)
Rectal (PR)
Sublingual

123
Q

What are the par-enteral routes of drug administration?

A 
IV
IM
SC
Inhalation (can be systemic or local)
Transdermal
124
Q

What are the local routes of drug administration?

A 
Topical
Intranasal
Eye drops
Inhalation
Transdermal
125
Q

What will an inducer do?

A

Increase Cytochrome P450 and speed up the metabolism of other drufs, may result in sub-therapeutic dose

126
Q

What will an inhibitor do?

A

Decrease CP450 activity reducing the metabolism of other drugs which may result in toxicity

127
Q

What happens in a paracetamol overdose?

A

The Phase II metabolic pathways become saturated, and more paracetamol is shunted to the CPY450 system to produce NAPQI which is toxic.

PHASE 2A (Mine) (15 decks)

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