Pharmacology -Part 2 Flashcards Preview

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Flashcards in Pharmacology -Part 2 Deck (124)
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1
Q

Give examples of patient risk factors that increase their chance of drug interactions

A
Poly-pharmacy
Old age
Genetics e.g. slow/fast metabolism
Hepatic disease
Renal disease
2
Q

What is the therapeutic index of a drug?

A

A comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity

3
Q

Give examples of drug related risk factors that increase their chance of drug interactions

A

NARROW Therapeutic index
Steep dose/response curve
Saturable metabolism

4
Q

Give example of saturable metabolism

A

Paracetamol and alcohol are metabolised at a SET RATE

5
Q

What 4 factors make up the pharmacokinetics of a drug

A

Absorption
Distribution
Metabolism
Elimination

6
Q

What factors can be influenced Absorption in pharmacokinetics of drug metabolism?

A
Motility
Acidity
Solubility
Non-absorbed complex formation
Direct action on enterocytes
7
Q

How does Erythromycin influence Motility in absorption in pharmacokinetics

A

Increases Gut Motility

8
Q

What 2 drugs have the commonest interaction causing motility changes?

A

Oral contraceptive pill

Antibiotics

9
Q

What drugs can influence the pH/acidity of the stomach and thus affect absorption in pharmacokinetics

A

Antacids and Proton Pump Inhibitors

These change pH of the stomach so if take with another medication, the absorption of the drug can be altered

10
Q

Give example of solubility being affected in drug metabolism due to interaction.

A

Eating avocado (high in fat) and taking a fat soluble drug e.g. anti-coagulant

Drug will dissolve meaning there will be less or no drug absorption

11
Q

Give example of a fat soluble drug

A

Anti-coagulant

12
Q

What would be effect on drug absorption if took a fat soluble drug with high fat food such as avocado

A

Drug will dissolve meaning there will be less or no drug absorption

13
Q

Give example of drug not being absorbed due to formation of a large complex in body

A

Cholestyramine +
Thyroxin, Warfarin or Digoxin

(large complexes formed in intestinal lumen)

14
Q

What are enterocytes

A

Intestinal absorptive cells

15
Q

What is effect of Grapefruit juice on uptake of certain drugs?

A

Grapefruit juice inhibits P-glycoprotein resulting in increased uptake of certain drugs

16
Q

What can cause a decrease in distribution of drug concentration in plasma (not including being use by target cells)

A

Drug can bind to proteins in plasma, thus reducing distribution and meaning effect is lowered.

17
Q

What drugs can have a reduced distribution due to protein binding in the plasma

A

Sulphonamide antibiotics

Warfarin

18
Q

What wavelength of light is absorbed by CYP450?

A

450nm

19
Q

What can be metabolised by CYP450?

A

Haemoproteins

Many other substrates, including Endogenous (body products) and Exogenous (durugs, toxins and food) products

20
Q

What classes of CYP450 are found in humans

A

Classes 1, 2, 3

21
Q

When would you give drug to inhibit CYP450

A

To block metabolism of drug (that would usually be metabolised by CYP450), leaving more of the drug free in plasma and Increasing its effects.

22
Q

When would you not inhibit CYP450, even if drug is metabolised by CYP450

A

If pro-drug

If block metabolism then effects of it will be decreased

23
Q

What is effect of drug of CYP450 induction?

A

Increased metabolism of drug causing decreased therapeutic effects

24
Q

When would CYP450 induction increase effects of a drug?

A

Pro-drug

Increase in metabolism leads to more of active form so increased effects

25
Q

What CYP is affected by grapefruit juice?

A

Grapefruit juice affects CYP3A4

Results in increased bioavailability and can therefore make a drug more effective.

26
Q

What makes up the majority and minority of drug excretion

A

Renal excretion is majority

Biliary excretion is minority

27
Q

True or False:

Renal excretion is not pH dependent

A

False

Renal excretion is pH dependent

28
Q

In what circumstance would a weak base be excreted faster?

A

If the urine is acidic

29
Q

In what circumstance would a weak acid be excreted faster?

A

If urine is alkaline

30
Q

How can you alter the excretion of a weak acid or weak base

A

By altering pH of urine

31
Q

Give examples of weak acids that are drugs

A

Aspirin
Ibuprofen
Paracetamol
Warfarin

32
Q

What can be done to increase excretion of aspirin if given an overdose?

A

Alkalinise urine as aspirin is a weak acid

33
Q

Give examples of weak bases that are drugs

A

Amphetamine
Atropine
Propranolol
Salbutamol

34
Q

Give general examples of pharmacodynamic mechanisms of drug interaction

A

Receptor based
Signal Transduction
Physiological systems

35
Q

Give example of agonist receptor based drug interaction

A

Alcohol and Benzodiazepine at GABA A receptor

drugs bind to receptor

36
Q

Give example of a partial agonist receptor based drug interaction

A

(Partial binding/activation at receptor)

Buprenorphine for Opioid Addiction

37
Q

Give example of a antagonist receptor based drug interaction

A

(blocks receptor -can be competitive or non-competitive)

Beta-blockers and Asthma (competitive)

38
Q

Why should you never give Beta-Blockers to Asthmatic

A

Asthmatics will be on B-agonists to help with bronchodilation
If using beta-blockers then will cause bronchoconstriction and increase risk of asthma attack

39
Q

Why do you not give Beta-blockers to a diabetic

A

Beta-blockers in a diabetic:
Results in action at B3 receptor (in adipose tissue) which normally detect and alter blood glucose.
However action at B2 receptor can suppress hypoglycaemic awareness so they will not detect fall in glucose.

40
Q

Why do you not give ACE inhibitors with NSAIDs?

A

High degree of nephrotoxicity

41
Q

Can you give Ca channel antagonist and Beta-blocker?

A

No
Symptoms of heart failure may worsen because these drugs reduce the ability of the heart to pump blood.
(Also sexual function can be impaired)

42
Q

*What is effect of giving Digoxin and Furosemide?

A
  • Digoxin works on cardiac fibres and its effect is increased if there are low levels of potassium in blood plasma
  • Furosemide is a diuretic that lowers arterial pressure but favours the loss of potassium
  • This could lead to hypokalaemia, which could increase the toxicity of digoxin
43
Q

How can you avoid prescribing drugs causing interactions

A

Prescribe rationally
BNF
Medicines infroamtion service

44
Q

Effect of avocado and warfarin

A

Avocado reduces effectiveness of warfarin - could increase risk of blood clots

45
Q

Effect of Grapefruit juice on Calcium channel blockers

A

Increases effectiveness of calcium channel blockers

46
Q

Effect of Grapefruit juice on Anti-rejection medication

A

Increases effectiveness of anti-rejection medication

47
Q

Effect of Garlic on Anti-platelet activity

A

Garlic increases anti-platelet activity so can increase risk of bleeding

48
Q

Effect of Soya on NSAIDs or Warfarin

A

Soya increases effectiveness of NSAIDs and warfarin so can increase risk of bleeding

49
Q

Effect of Ginger on Anticoagulants

A

Ginger reduces effectiveness of anticoagulants so increases risk of bleeding

50
Q

What is a major interaction of antiarrhythmic agents

A

Amiodarone

51
Q

What is major interaction of antihistamines

A

Terfenadine,

Diphenhydramine

52
Q

Name some minor interctions of Ca Channel Antagonists

A

Felodipine
Nifedipine
Nimodipine
Nicardipine

53
Q

Give a major interaction of Statins

A

Simvastatin

54
Q

Give a minor interaction of Statins

A

Atorvastatin

55
Q

Give examples of minor interctions of immunosurpressants

A

Cyclosporin,

Tacrolimus

56
Q

What is side effect of Simvastatin

A

Rhabdomyolysis

muscle pain/breakdown

57
Q

What is side effect of Warfarin

A

Bleeding

58
Q

What is side effect of SSRIs

A

Serotonin syndrome

59
Q

What is side effect of Simvastatin + Warfarin + SSRIs

A

Renal failure

60
Q

What is required for a safe prescription

A
Patient Name
Dose
Route
Frequency
Duration
Total number of tablets
Drug Name
Date and Signature
61
Q

What needs to be kept in mind when deciding on a safe prescription

A

Diagnosis
Drug treatment
Indication and Contraindications
Others: does it require plasma monitoring or is there a risk of drug interaction?

62
Q

Where can errors arise that affect prescription given

A

Home: Drug history & Pharmacy printout

Hospital admission: In patient prescription chart

In patient: Multi disciplinary prescribing

Discharge from hospital: Take home medication or not & discharge summary to GP

63
Q

What are potential causes of prescribing error

A
  • The number of different times the same information is translated or transposed
  • Inadequate information on admission
  • Duplication; paper, different teams
  • Clerical/legibility/ administration errors
  • Emergency situations
64
Q

True or False:

Prescribing errors are avoidable and thus a form of neglect

A

True

65
Q

If drug name has prefix co- and suffix -amol, what does this mean

A

Drug contains paracetamol

66
Q

Why is it important to specify route of administration of morphine

A

Since only a 1/3 of this dose will actually be absorbed due to high liver metabolism if administering orally - thus will be less effective

67
Q

What is intrathecal

A

Via spinal cord

careful not to confuse with IV, to prevent unnecessary spinal cord damage

68
Q

What drugs can have withdrawal reactions if stopped after long term use

A

Analgesics
Anti-hypertensives
Anti-depressants

(but only stop if important reason or complaint)

69
Q

What is policy of fluid use before surgery

A

Nil by mouth for fluid is 2 hours
This is due to fear of aspiration under anaesthesia

(sip of water with tablet OK tho)

70
Q

What drugs should be discontinued prior to surgery

A

Ace inhibitors, Losartan (Angiotensin receptor blocker)
Warfarin (since should be rbidged to heparin -easier to manage dosage since injected)
Diabetes drugs

71
Q

What drugs would you find at Step 1 on WHO analgesic ladder

A

Non-opioid analgesics

NSAIDs

72
Q

What drugs would you find at Step 2 on WHO analgesic ladder

A

Weak Opioids

73
Q

What drugs would you find at Step 3 on WHO analgesic ladder

A

Strong opioids
Methadone (PO administration)
Transdermal patches

74
Q

What drugs would you find at Step 4 on WHO analgesic ladder

A
Nerve block
Epidurals
PCA pump 
Neurolytic therapy
Spinal stimulators
75
Q

When would you use drugs higher on the analgesic ladder (e.g. step 3 or 4)

A

Chronic pain
Some Non-malignant pain
Cancer pain

76
Q

When would you use drugs lower on the analgesic ladder (e.g. step 1 or 2)

A

Acute pain
Chronic pain without control
Acute crises of chronic pain

77
Q

Where is tramadol on analgesic ladder

A

Weak opioid so Step 2

do other examples

78
Q

Where is diamorphine on analgesic ladder

A

Step 3

Strong opioid

79
Q

Why are intravenous IV infusions used>

A
  • Enables steady state plasma (where drug intake is in equilibrium with its elimination) levels to be maintained for as long as possible
  • Enables highly accurate drug delivery
  • Useful for drugs that are ineffective administered by other routes or those who cannot absorb oral medication
  • Is the quickest administration route
  • Guarantees 100% bioavailability (the gold standard)
80
Q

Describe chemicals that lead to synthesis of adrenaline

A

Tyrosine > DOPA > dopamine > noradrenaline >adrenaline

81
Q

What type of chemical is DOPA, dopamine, noradrenaline or adrenaline?

A

Catecholamines

82
Q

Give examples of chemicals that can metabolise/inactive adrenaline by metabolising it and thus reducing its stimulant effect

A
MonoAmine Oxidase (MAO)
Catechol-O-Methyl Transferase (COMT)
83
Q

Describe characteristics of C fibres (pain transmission)

A

Unmyelinated

Diffuse dull intense pain

84
Q

Describe characteristics of A delta fibres (pain transmission)

A

Small and myelinated

Conduct localised sharp sensation

85
Q

Describe gate control theory

A

There is a balance of activity between large (A beta fibres) and small (A delta fibres & C fibres) fibres
Interneurons of the substansia gelatinosa regulate the input in Lamina V (dorsal horn of spinal cord)
If A beta fibres are NOT stimulated by nociceptive stimulus then the pain signal goes through to the brain and is perceived
If A beta fibres ARE stimulated then the pain signal is halted and does not reach the brain and is thus not perceived
This means that low intensity stimulation of the skin or peripheral nerves or vibration in order to stimulate the A beta fibres will generate analgesia

86
Q

Applying gate control theory, how can you relieve pain?

A

Rubbing site of injury
Application of heat
Spinal cord stimulaiton
TENS - trans cutaneous nerve stimulation of A beta fibres

87
Q

What is effect of prosaglandins

A

Act directly on the nociceptors and reduce their threshold meaning normal stimuli can activate them resulting in a sensation of pain (peripheral sensitisation)
(used by NSAIDs and paracetamol possibly) - add flashcard

88
Q

What is main inhibitory neurotransmitter?

A

GABA

89
Q

What is role of peri-aqueductal grey and locus cerulus in endogenous pain system

A

They inhibit the firing of the dorsal horn neutron that responds to noxious stimulus (gate control theory).
This can be done by changing the levels of neurotransmitters at the level of synapses meaning less pain is transmitted.

90
Q

What happens in peri-aqueductal grey after modulation of afferent noxious transmission from extreme stress (as example)?

A

Once activated, opioid receptors are activated resulting in a reduction in PRE-SYNAPTIC neuronal sensitivity (thereby reducing Substance P release) which in turn results in reduced pain sensation

91
Q

Give examples of Endogenous opioid peptides

A

Enkephalin
Dynorphine
Beta endorphine: effect similar to morphine

92
Q

*How do opioids work

A

Bind to opioid receptors in periaqueductal grey, thereby conferring profound analgesia

93
Q

Give examples of opioids

A

Morphine
Methadone
Codeine
Oxycodone

94
Q

Give example of excitatory neurotransmitter

A

Glutamate

95
Q

What are the 2 types of basis for pain treatment/transmission?

A

Reducing excitatory neurotransmitters (glutamate) and excitation of the nerve.
Enhancing inhibitory neurotransmitters.

96
Q

What is the basis for anti-epileptics

A

Reducing excitatory neurotransmitters (glutamate) and excitation of the nerve (with respect to pain transmission)

97
Q

Other than GABA, give examples of inhibitory neurotransmitters

A

Noradrenaline
Serotonin
(used as basis for anti-depressants)

98
Q

*How do local anaesthetics work?

A

Na+ channel blockers

Prevent depolarisation of nerve and propagation of an action potential

99
Q

What is effect of prostaglandins in pain snesation

A

Prostaglandins act directly on the nociceptors and reduce their threshold meaning normal stimuli can activate them resulting in a sensation of pain (peripheral sensitisation)

Ultisied by NSAIDs and possibly paracetamol

100
Q

Define chronic pain

A

Ongoing persistent pain greater than 3-6 months

101
Q

What are principles of treating chronic pain

A
Improve pain perception
Improve function/mobility
Improve sleep
Improve emotional and psychological consequences of pain
Improve quality of life
102
Q

What % of the population can not metabolise morphine?

A

10%

103
Q

Give examples of naturally occurring opioids

A

Morphine
Codeine
(from opium)

104
Q

Is codeine a strong or weak opioid?

A

Weak

105
Q

Give examples of simple chemical modified opioids

A

Diamorphine (heroin)
Oxycodone
Dihydrocodeine (more predictable than codiene)

106
Q

Give examples of synthetic opioids

A

Pethidine
Fentanyl (v potent)
Alfentanil (v potent)
Remifentanil (v potent)

107
Q

Give example of opioid antagonist

A

Naloxone

give to reverse overdose

108
Q

You start a patient on a new commonly used medication. Unfortunately they develop an unusual adverse drug reaction (ADR) that you have never seen before which results in their hospitalisation. Which of the following is the correct course of action after stopping the drug and informing the patient?
Report the adverse drug event on a ‘yellow card’

Contact the pharmaceutical company that makes the drug to inform them of the ADR

Write the case up as a case report to ensure that other doctors are educated

Contact the local pharmacist to inform them of the ADR

Stop prescribing the drug for all patients

A

Report the adverse drug event on a ‘yellow card’

As the patient has been hospitalised due to the ADR you should fill in a ‘yellow card’.

109
Q
A 53-year old woman presents to her G.P. with symptoms of an over-active bladder, she is given an anti-cholinergic drug to help with her symptoms. Which of these symptoms is NOT a side effect of the anti-cholinergic drug she has been prescribed.
Constipation
Constricted pupils
Dry mouth
Reduction in sweating
Tachycardia
A

Constricted pupils

Anticholinergics will cause dilated pupils and all the rest are common side effects of anticholinergics

110
Q
A 65-year old man has lower urinary tract symptoms and also suffers from narrow angle glaucoma. Which of the following drugs may help his lower urinary tract symptoms but would be contra-indicated due to his narrow angle glaucoma?
5-alpha-reductase inhibitor
Alpha-1 receptor antagonist
Anticholinergic
Beta-3 receptor agonist
Intra-vesical botulinum toxin
A

Anticholinergic

Contra-indiated in narrow angle glaucoma
none of others are contraindicated

111
Q
An 18-year old man who is known to be an iv drug abuser is admitted to the emergency department unconscious with reduced respiratory rate and pin-point pupils. Which one of the following drugs is most appropriate to reverse his opioid overdose?
intravenous flumazenil
intravenous fentanyl
intravenous glucagon
intravenous naloxone
intravenous neostigmine
A

intravenous naloxone

Flumazenil will reverse a benzodiazepine overdose,
fentanyl is an opioid and so would compound the situation,
glucagon is used in hypoglycaemia,
neostigmine will reverse the effects of non-depolarizing muscle relaxants

112
Q

What can be used to reverse a benzodiazepine overdose?

A

Flumazenil

113
Q
Which of the following drugs does NOT have a narrow therapeutic index?
Digoxin
Gentamicin
Lithium
Simvastatin
Warfarin
A

Simvastatin

has a wide therapeutic index

114
Q

Define therapeutic index

A

Comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity

115
Q
An 80-year old lady with metastatic cancer has been taking oral morphine for pain at home. She is admitted to hospital as an emergency as she has accidentally taken a large overdose and is confused and hypoxic. Which of the following is the side effect that may be contributing to her hypoxia.
Constipation
Cough
Neuromuscular paralysis
Respiratory depression
Tachypnoea
A

Respiratory depression

116
Q

A 22-year old woman is prescribed oral penicillin, an hour later she develops a rash, facial swelling and difficulty breathing. A diagnosis of anaphylaxis is made and she is treated appropriately.
Which type of adverse drug reaction is an anaphylactic reaction to penicillin?

Type A
Type B
Type C
Type D
Type E
A

Type B

Bizarre or Idiosyncratic

117
Q

A 50 year old male patient found to be at increased risk of cardiovascular disease mentions at a routine GP check-up that he has not been taking the statin prescribed at his last visit. He comments that he is “not anti-medication” but he “feels fine without it”. Which of the following seems to be the most pertinent reason for his non adherence?

	Capacity and resources
	Concerns about medication
	Necessity beliefs about medication
	Practical barriers to adherence 
	Specific beliefs about medication
A

Necessity beliefs about medication

The answers relate to various potential reasons for non adherence

a. Capacity and resources – a practical rather than perceptual barrier
b. Concerns about medication – perceptual barrier to adherence that relates to worries about a potential adverse consequences
c. Necessity beliefs about medication - relates to perceptions of personal need for treatment, in this case to reduce risk rather than make him feel better
d. Practical barriers to adherence - capacity and resource to adhere to treatment
e. Specific beliefs about medication – relates to beliefs about the specific treatment (statin), in this example it is implied that the patient doesn’t fully understand that this is not a treatment to make him ‘feel better’ at present.

118
Q

A 44 year old man receives penicillin V from his general practitioner for tonsillitis. He becomes very unwell with a rash, flushing, wheezing and he collapses. He is told that he has had an anaphylactic reaction to penicillin. This type of allergic reaction is mediated by which one of the following antibodies?

	IgA antibodies
	IgD antibodies
	IgE antibodies
	IgG antibodies
	IgM antibodies
A

IgE

IgA is found in mucosal areas, such as the gut, respiratory tract and urogenital tract, and prevents colonization by pathogens, it is also found in saliva, tears, and breast milk.
IgD is found on B cells that have not been exposed to antigens.
IgG is the most abundant antibody and responsible for the secondary response.
IgM is the most primitive antibody and eliminates pathogens in the early stages of B cell-mediated (humoral) immunity (primary response) before there are sufficient IgG.
IgE is in response to parasites and is responsible for anaphylaxis.

119
Q

Where are IgA antibodies found and what is there function?

A

IgA is found in mucosal areas, such as the gut, respiratory tract and urogenital tract, and prevents colonization by pathogens, it is also found in saliva, tears, and breast milk.

120
Q

Where would you find IgD antibodies?

A

IgD is found on B cells that have not been exposed to antigens.

121
Q

What is purpose of IgG?

A

IgG is the most abundant antibody and responsible for the secondary response.

122
Q

What is purpose of IgM?

A

IgM is the most primitive antibody and eliminates pathogens in the early stages of B cell-mediated (humoral) immunity (primary response) before there are sufficient IgG.

123
Q

What is purpose of IgE?

A

IgE is in response to parasites and is responsible for anaphylaxis.

124
Q

A 70 kg woman is prescribed digoxin for atrial fibrillation . The digoxin has a half life of 42 hours.

The half life is:

  • the time taken for the plasma drug concentration to fall to half its original value
  • the time to metabolise half the drug into its active metabolite
  • the time to absorb half the drug
  • the time to bind half the drug to plasma proteins
  • the time to maximum plasma levels after a dose of the drug
A

the time taken for the plasma drug concentration to fall to half its original value