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YEAR 1 MED > Pharmacology and prescribing > Flashcards

Pharmacology and prescribing Flashcards

1
Q

how can you find out what drugs a patient takes?

A
  • from patient or relatives
  • from medical notes
  • from clinic letters / discharge summaries
  • from the GP (shared care records)
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2
Q

what are the 2 mechanisms in which NSAIDs can damage the stomach?

A
  • direct: erosion of gastric lining
  • indirect: blocks COX enzymes so decreased lvls of prostaglandins, therefore unable to make protective gastric mucus barrier against acid
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3
Q

what can be given to reduce the risk of a GI bleed in a patient who takes drugs which increases their risk (eg. patient takes NSAID+aspirin+prednisolone)

A

Give a gastroprotective agent:

  • Proton pump inhibitor (PPI) or H2 antagonist to reduce gastric acid
  • Misoprostol: prostaglandin analogue that increases gastric mucus to protect stomach
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4
Q

what are the 2 main drugs used to treat osteoporosis?

A
  • bisphosphonates
  • denosumab
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5
Q

what is gout and what causes crystals to form, and what class of drugs are a risk factor for gout?

A
  • gout is monosodium urate crystals
  • can also get gouty tophi in soft tissues

Crystals form with rise in uric acid concentrations…
- Overproduction (diet, genetic factors)
- Reduced ability of kidney to get rid of uric acid
- Influence of drugs (eg. Thiazide diuretics used in treatment of high BP)

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6
Q

what are some side effects of NSAIDs?

A

short term OK, longer term and higher doses…
- peptic ulcers, cause GI bleeding
- renal failure
- heart failure

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7
Q

what are some side effects of colchicine?

A
  • common: nausea, diarrhoea, abdo pain
  • longer term: bone marrow suppression
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8
Q

how does allopurinol work to reduce uric acid production?

A
  • inhibits xanthine oxidase which reduces serum levels of uric acid
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9
Q

how do bisphosphonates work? (and give 2 examples)

A
  • attach to bone crystals, inhibit osteoclast activity
  • eg. alendronic acid, zolendronic acid (once a year IV injection)
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10
Q

how does denosumab work?

A
  • monoclonal antibody: RANKL inhibitor
  • therefore reduces osteoclast activity
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11
Q

what are some side effects of methotrexate?

A
  • immunosuppression (can make patient susceptible to infections)
  • liver toxicity
  • lung damage
  • teratogenicity
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12
Q

what drug should not be taken with methotrexate (hint: the drug is commonly used to treat UTIs)

A
  • trimethoprim
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13
Q

what corticosteroids are taken as oral tablets and what corticosteroids are given intravenously?

A
  • oral tablets: prednisolone
  • IV: hydrocortisone, methylprednisolone, dexamethasone
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14
Q

What is Cushing’s disease?

A

Too much steroids (caused by tapering of steroids being too slow)
- symptoms: osteoporosis, obesity, hypertension, hyperglycemia

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15
Q

What is Addison’s disease and what is the emergency condition that can occur?

A

Too little steroids ( (body doesn’t have enough cortisol): caused by tapering of steroids being too fast
- symptoms: nausea, headaches, fever, hypotension, hypoglycaemia

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16
Q

what is the chemical name for heroin?

A
  • 3, 6-diacetylmorphine or diamorphine
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17
Q

What is the chemical name for codeine?

A
  • 3-methylmorphine
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18
Q

Is the half-life of morphine short or long, how does this affect how often it is needed to be taken?

A
  • short (3-6 hrs usually)
  • therefore most morphine derivatives have to be given multiple times a day (or synthetic patches given which is slow release)
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19
Q

Where is morphine metabolised and excreted?

A
  • metabolised in liver
  • excreted in urine
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20
Q

If giving a morphine derivative IV or IM, should you choose a lower or higher dose compared to oral?

A
  • lower dose
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21
Q

What is the main opioid receptor antagonist? (eg. you would give this if somebody overdosed on morphine or another opioid)

A
  • Naloxone
  • given IV/SC in acute opioid toxicity (eg. drowsy patient with small pupils and poor respiration)
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22
Q

What is the most important opioid for severe pain?

A
  • Morphine
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23
Q

What drugs are often given alongside morphine?

A
  • anti-emetics (for the vomiting): eg. metoclopramide, ondansetron
  • laxatives (if long term use): eg. lactulose
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24
Q

When is diamorphine typically used?

A
  • palliative care
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25
Q

What is a prodrug?

A
  • a medication that after intake is metabolised into a pharmacologically active drug
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26
Q

Codeine is a prodrug, what is it metabolised into in the liver?

A
  • morphine
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27
Q

Which drug is used in substitution therapy to reduce IV drug use?

A
  • methadone (orally)
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28
Q

Would you prescribe opioids for neuropathic pain?

A
  • no
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29
Q

Would you prescribe opioids for migraine or tension-headaches?

A
  • no
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30
Q

How would you deal with opioid tolerance?

A
  • starting dose of morphine (5-10mg in most patients, higher if no response)
  • with regular use, review dose every few days, and increase by 30-50% if pain recurs
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31
Q

What is meant by pharmacodynamics?

A
  • pharmacodynamics = drug action in humans
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32
Q

What are the 4 important sites of drug action?

A
  • receptors
  • enzymes
  • ion channels
  • transporters
33
Q

What is the difference between an agonist and an antagonist regarding drugs?

A
  • agonist (right key for right lock): drug that binds to receptor site and elicits a response (eg. morphine)
  • antagonist (right key for right lock, but doesn’t work/blocks it): drug that binds to receptor site and does not elicit a response/blocks agonist from working (eg. naloxone)
34
Q

What is meant by the term pharmacokinetics?

A
  • pharmacokinetics = what the body does to the drug
35
Q

What are some factors that affect drug concentrations (ie. how the drug passes through the body)?

A
  • bioavailability: proportion of drug that passes into systemic circulation (eg. absorption from stomach affects this)
  • then first-pass metabolism (eg. activation or breakdown by liver enzymes)
  • clearance/excretion (metabolism and elimination through urine)
36
Q

What is meant by the term half-life?

A
  • half-life = time taken for drug concentration to fall to half its initial value (tells us how long the drug is in body)
37
Q

Name 4 ways in which a drug can be administrated.

A
  • oral
  • injection
  • rectal
  • topical
  • sub-lingual (under tongue)
  • inhaled
38
Q

What is meant by the term receptor?

A
  • receptor = protein molecule in or on cells whose function is to interact with the bodies endogenous chemical messengers and initiate a physiological response
  • (basically when a “drug” binds to receptor, it initiates a physiological response)
39
Q

What are the 4 types of receptors?

A
  • ligand gates (ion channels)
  • G protein coupled receptors
  • kinase linked receptors
  • nuclear receptors
40
Q

What is meant by the term affinity and why is it important?

A
  • affinity = how well a drug binds to a receptor
  • if we know how much drug we need to occupy our receptor site we begin to understand how much drug we need for therapeutic response
41
Q

Describe how paracetamol helps to reduce fever

A
  • Paracetamol is a COX enzyme inhibitor (thought to be selective for COX-3)
  • (COX enzymes stimulate the production of prostaglandins)
  • In fever, the temperature set point is elevated by the production of PGE2
  • Paracetamol helps to prevent PGE2 synthesis, PGE2 is the main compound that alters the homeostatic temperature set point in the hypothalamic neurons that regulate body temperature
  • PGE2 synthesis is stimulated by cytokines (IL-1, TNF-alpha) which are produced by the action of bacteria/viruses on the immune system
  • By blocking PGE2 synthesis, paracetamol brings down the temperature set point to normal
42
Q

During his last few months of life the patient was prescribed morphine. Describe how morphine works

A
  • Morphine attaches to opioid receptors (Mu)
  • Morphine reduces membrane excitability and hence action potential firing frequency
  • (Opioids act on the dorsal horn as well as the peripheral terminals of nociceptive afferents neurons)
  • Thus preventing pain signals travelling up the spinal column
  • Morphine also increases release of enkephalins and 5-HT (serotonin) onto dorsal horn neurons via stimulation of the periaqueductal grey matter (PAG) and the raphe nucleus
43
Q

How might the side effects of morphine undermine the quality of life in end stage cancer treatment?

A
  • Undermines physical wellbeing
  • side effects: constipation, nausea, confusion, sedation
44
Q

What class of hormone is cortisol?

A
  • Steroid hormone
45
Q

In which anatomical structure is cortisol synthesised and what is the precursor molecule from which it is made?

A
  • Synthesised in the zona fasciculata (ZF) of adrenal cortex/gland
  • Precursor molecule is cholesterol
46
Q

Hormones act by binding to receptors to transduce their signal into cells, describe how cortisol transduces its signal

A
  • It is a lipid soluble hormone which diffuses into cells
  • binds to its receptor inside the cell in the cytoplasm
  • receptor/hormone complex moves into the nucleus to bind to DNA and activates or repress gene expression
47
Q

Name two other important issues, other than drug interactions, which need to be addressed for patients prescribed methotrexate

A
  • Need for folic acid to reduce side effects and regular bloods to monitor
  • Common side effects: nausea, increased risk of infection
  • Avoid pregnancy / alcohol
48
Q

Name four routes of administration or forms of drug, apart from oral, which should be considered in a full drug history

A
  • Rectal (eg. Suppositories)
  • Sublingual (eg. Spray, dissolvable tablet)
  • Topical (eg. Spray, cream)
  • Inhaled/nebuliser
  • Eye drops
49
Q

what are the effects of old age on prescribing?

A
  • metabolism slower (liver enzymes slower)
  • kidneys: excretion of medications slower (drugs spend more time in the body)
  • medications have different effects (eg. need lower dose of diazepam in elderly)
  • polypharmacy due to multiple diseases / interactions of medications
50
Q

where are glucocorticoids secreted from?

A
  • from the cortex within adrenal glands (ZF)
51
Q

what are the 3 main types of opioid receptors and their functions?

A
  • Mu (for morphine): analgesia, euphoria (but also constipation, respiratory depression)
  • Kappa (for ketcyclazocine): analgesic at periphery (but also dysphoria, hallucinations)
  • Delta for vas Deferens: analgesic effects at spinal cord
52
Q

what are the effects and side effects of morphine, and then what are 2 things that you need to be aware of with long-term opioid use?

A

EFFECTS:
- analgesia, euphoria, sedation, pupil constriction

SIDE EFFECTS:
- nausea and vomiting (chemoreceptor trigger zone in medulla)
- constipation (from reduced motility and muscle tightening)
- respiratory depression (inhibits respiratory centres in brainstem)
- suppressed cough reflex
- tolerance: with recurrent use: desensitisation of Mu receptors, dose has to be increased
- dependence: physical (restless, aggression, runny nose, shivering) and psychological (cravings may persist for months and years)

53
Q

where are opioids metabolised and excreted?

A
  • metabolised in liver
  • excreted in urine
54
Q

what are some considerations to take into account when prescribing morphine?

A
  • most morphine derivatives have a short half-life so have to be given several times a day
  • IV/IM morphine: choose lower dose as compared to oral
  • synthetic opioid patches go on releasing the drug for days and days so check and remove if toxicity is suspected, or if change in drug/dose is needed
55
Q

what pathways do NSAIDs and aspirin block?

A
  • cyclooxygenase (COX enzymes)
  • COX 1, COX 2, COX 3
56
Q

what pathways do corticosteroids block?

A
  • they block the conversion of phospholipids to arachidonic acid
57
Q

why do NSAIDs have anti-inflammatory, analgesic, and antipyretic effects?

A
  • Anti-inflammatory: decreases lvls of prostaglandin E2 and prostacyclin
  • Analgesic: decreases lvls of prostaglandins which makes nerves less sensitive to inflammatory mediators (eg. bradykinin)
  • Anti-pyretic: decreases lvls of IL-1
58
Q

what drugs can be given to reduce the risk of GI problems?

A
  • Proton pump inhibitor (PPI) or H2 antagonist: to reduce gastric acid
  • Misoprostol: prostaglandin analogue that increases gastric mucus to protect stomach
59
Q

what pathway does methotrexate target and mechanism of methotrexate?

A
  • folate pathway
  • methotrexate is an antimetabolite that inhibits dihydrofolate reductase
60
Q

what drug should be taken with methotrexate, when should you not give methotrexate, and what drug should you not give methotrexate with?

A
  • folic acid should be given (on another day) to reduce toxicity
  • avoid if patient has liver problems, avoid in pregnancy
  • do not give methotrexate and trimethoprim together
61
Q

how much and when should methotrexate be prescribed, and folic acid, and what should be monitored?

A
  • methotrexate 7.5mg once a week (oral or subcutaneous injection)
  • folic acid 5mg once a week (on a different day to methotrexate)
  • do FBC, renal, and liver function tests regularly
62
Q

what are the main anti-TNF biologics?

A
  • Infliximab
  • Entanercept
  • Adalimumab
63
Q

when should anti-TNF biologics be prescribed according to NICE guidance and what is the issue with anti-TNFs?

A
  • patient has active RA disease activity
  • tried at least 2 DMARDs (including methotrexate) for >6 months
  • anti-TNFs should usually be used together with methotrexate
  • problem with anti-TNFs: expensive, have to be given by injection or infusion
64
Q

what should be prescribed if anti-TNF biologics do not work?

A
  • Rituximab: targets CD20
  • Tocilizumab: targets IL-6
65
Q

which corticosteroids are given in what forms?

A
  • oral tablets: prednisolone (eg. 30mg daily for 2 weeks in acute flares)
  • IV: hydrocortisone, methylprednisolone, dexamethasone (eg. 1g a day for 3 days)
66
Q

what drugs are prescribed for acute gout flare-ups?

A
  • NSAIDs (ibuprofen, naproxen)
  • colchicine
  • corticosteroid (local injection or oral)
67
Q

what drugs are prescribed for chronic gout (prevention)?

A
  • allopurinol
  • (or febuxostat)
68
Q

what is the mechanism by which colchicine works?

A
  • inhibits granulocyte migration
  • this causes depolarisation of microtubules
  • this causes inhibition of lymphocyte migration and division
  • results in decrease in inflammation
69
Q

when should corticosteroids be given in gout?

A
  • local injection should be given if only single joint affected
  • (this is better than patient taking naproxen for eg. for 2 weeks)
70
Q

what is the mechanism by which bisphosphonates work?

A
  • pyrophopshate analogue
  • attach to bone crystals and inhibit osteoclast breakdown of bone
71
Q

what are the main side effects of bisphosphonates and what should the patient be told to do regarding taking the medication to help reduce side effects?

A
  • oesophageal problems (eg. dyspahgia), upper GI problems
  • rarer: osteonecrosis of the jaw, hypocalcaemia
  • take on an empty stomach at least 30 minutes before breakfast or any other oral medicines
  • after taking, patients should remain sat or stood upright for at least 30 minutes
72
Q

how does Denosumab work?

A
  • monoclonal antibody: RANK ligand inhibitor
  • reduces osteoclast activation, differentiation, and survival
  • used if patients cannot have bisphosphonates, 1 injection every 6 months
73
Q

What enzyme is required to generate arachidonic acid from membrane phospholipids and what drug class can stop this reaction?

A
  • Phospholipase A2
  • steroids
74
Q

What enzymes are required to generate Prostaglandins from Arachidonic acid and name 2 drugs which can block these enzymes?

A
  • Cyclooxygenase 1+2 (COX 1+2)
  • Aspirin/Non-steroidal anti-inflammatory drugs
75
Q

Mechanism of action of NSAIDs.

A
  • NSAIDs inhibit cyclooxygenase/COX (which is responsible for converting the arachidonic acid into endoperoxidase)
  • Reduction of COX enzymes decreases prostaglandin production, therefore reducing inflammation and pain sensation (as well as decreasing thromboxane A2 and prostacyclin production)
76
Q

Side effects of corticosteroids.

A
  • central obesity, moon face
  • acne, thinned skin
  • immunosuppression
77
Q

WHO analgesic ladder…

A
78
Q

A patient is taking methotrexate for RA, they are planning on being pregnant in the next year, what should be done for this patient?

A
  • a washout at least 3 months before conception
  • methotrexate should be avoided during pregnancy due to the risk of teratogenicity
79
Q

What are the side effects of hydroxychloroquine?

A
  • retinopathy, rash

YEAR 1 MED (49 decks)

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