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Yr 3 - Pharmacology > Drug Interactions > Flashcards

Drug Interactions Flashcards

(56 cards)

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1
Q

Define pharmacodynamics

A

What the drug does to the body

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2
Q

Define pharmacokinetics

A

What the body does to the drug

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3
Q

What is a pharmacodynamic interaction?

A

When two drugs work via different pathways (receptor vs enzyme) to produce a different outcome.

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3
Q

What is a pharmacodynamic interaction?

A

When two drugs work via different pathways (receptor vs enzyme) to produce a different outcome.

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4
Q

Which speciality are pharmacodynamic interactions more commonly seen?

A

Cardiology:

  • Aspirin & clopidogrel
  • Diuretics & ACE inhibitors
  • Digoxin & beta blockers
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5
Q

What are bendroflumethiazide and indapamide examples of?

A

Thiazide diuretics

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6
Q

What class of drug is doxazocin?

A

Alpha blocker

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7
Q

What class of drug is diltiazem?

A

Calcium channel blocker

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8
Q

Patient has history of LVF with pulmonary oedema and RVF with ankle oedema.

The patient is given furosemide to get rid of excess fluid and ramipiril to prevent the HF from getting worse.

The patient collapses, why?

A

Furosemide and ramipril both have a BP lowering effect → hypotension

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9
Q

Patient has AF and hypertension. Patient given digoxin (cardiac glycoside) in order to lower HR and atenolol (beta blocker) to treat hypertension. The patient collapses, why? What would be a better solution?

A

Digoxin and atenolol both lower HR → bradycardia

Better solution → give beta blocker on its own to treat AF and hypertension simultaneously

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10
Q

In patients with existing hypotension or bradycardia, what can the effects of being prescribed a calcium channel blocker and a beta blocker be?

A

Both dilate the coronary arteries, reduce BP and HR.

Can lead to severe hypotension or bradycardia → patient collapses.

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11
Q

What are the 4 stages of pharmacokinetics?

A

Absorption/administration

Distribution

Metabolism

Elimination

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12
Q

What is first pass metabolism?

A

A phenomenon of drug metabolism whereby the concentration of a drug, specifically when administered orally, is greatly reduced before it reaches the systemic circulation.

  1. Taken via mouth and swallowed
  2. Passes to stomach
  3. Absorbed by the splanchnic circulation (which takes blood from the gut to the liver)
  4. Liver then metabolises drug
    1. Some drugs are not metabolised very much and the rest passes into the blood to give desired effect
    2. Some drugs are substantially metabolised by the liver in the first-pass metabolism that no effective drug enters the blood e.g. GTN (hence GTN spray)
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13
Q

Why is GTN spray given sublingually instead of orally?

A

As first pass metabolism would substantially reduce the amount of effective drug that enters the blood

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14
Q

Which phenomenon explains why some drugs cannot be given orally?

A

First pass metabolism

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15
Q

Where does first pass metabolism occur?

A

Liver

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16
Q

Which circulation takes the drug from the gut to the liver for first pass metabolism?

A

Splanchnic

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17
Q

Where does the drug pass after first pass metabolism?

A

Bloodstream

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18
Q

Drugs can be hydrophilic or lipophilic. What does this mean for their distribution?

A

Lipophilic - distributes through membranes with preference for adipose tissue and muscle (greater volume of distribution)

Hydrophilic - remains mostly in blood compartment until the drug is eliminated

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19
Q

Do hydrophilic or lipophilic drugs have a greater volume of distribution?

A

Lipophilic

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20
Q

What is the most important enzyme system in drug metabolism?

A

P450 system in the liver

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21
Q

What is the major site for drug metabolism?

A

Liver

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22
Q

Are lipophilic or hydrophilic drugs more likely to be metabolised by the liver? Why?

Study These Flashcards
A

Lipophilic - can be converted into products that more water soluble so can be more easily excreted

23
Q

Are lipophilic or hydrophilic drugs more likely to be excreted unchanged by the kidneys?

24
Describe the steps in the metabolism of lipophilic drugs
Phase 1 → Converts lipophilic molecules into more polar molecules (hydrolysis, oxidation, reduction) Phase 2 → Further convert lipophilic molecules into more polar molecular through conjugation with glucuronic acid, sulfuric acid, acetic acid or amino acid
25
What does it mean if a drug has a narrow therapeutic window?
There is only a small difference between the **minimum effective concentrations** and the **minimum toxic concentrations** in the blood.
26
Give 5 important examples of drugs that are metabolised by the P450 system that have a **narrow therapeutic window**
1. Warfarin 2. Phenytoin 3. Carbamazepine 4. Theophylline 5. Oral contraceptive pill
27
How do **inhibitors** of the P450 system affect the serum level of a drug?
Inhibitors **slow down** the metabolism of drugs, meaning the drug level will be higher with the potential to cause toxicity
28
How do induces of the P450 system affect the serum level of a drug?
Inducers **speed up** the metabolism of drugs, meaning the drug level will be lower with the potential to become ineffective
29
What are the 6 main **inducers** of the P450 system?
1. Carbamazepine 2. Phenytoin 3. Rifampicin 4. Chroni alcohol intake 5. Barbecued meat 6. St John's Wort
30
What are the 6 main **inhibitors** of the P450 system?
1. Erythromycin 2. Ciprofloxacin 3. Miconazole 4. Sodium valproate 5. Grapefruit juice 6. Cranberry juice
31
How do **carbamazepine** and **phenytoin** affect the P450 system? Why are they unique?
They are **inducers** of the P450 system BUT they also induce their own metabolism
32
How should phenytoin and carbamazepine be prescribed?
* Start on low dose as they will be very susceptible to toxic effects * As more starts to enter system, carbamazepine starts to induce its own metabolism and the body becomes more tolerable of it (can increase dose)
33
What is Rifampicin? What is it typically used for?
Antibiotic - typically used for treatment of TB and prophylaxis of meningitis
34
Which drug turns all bodily fluids bright orange?
Rifampicin
35
What is St John's Wort typically used for?
* Commonly used by people for mild-moderate depression * Herbal remedy → ensure to ask about it!
36
Who may be prescribed erythromycin or ciprofloxacin?
In chest infections, patients who are allergic to penicillin
37
How would erythromycin affect the effects of warfarin?
Erythromycin is an inhibitor → can lead to high levels of warfarin in body → huge bleeds (warfarin toxicity)
38
A patient is on warfarin due to a previous PE. They are prescribed carbamazepine. What effect may this have?
Carbamazepine is an inducer → serum levels of warfarin drop → patient may have a PE
39
A patient is on warfarin due to a previous PE. They develop a chest infection and are prescribed clarithromycin as they are penicillin allergic. What effect may this have?
Clarithromycin is an inhibitor → serum levels of warfarin rise → patient may have a bleed
40
What does an increased INR mean?
Increased clotting time
41
A patient is on phenytoin due to seizures. They develop TB and are prescribed rifampicin. What effect may this have?
Rifampicin is an inducer → levels of phenytoin drop → patient may have a seizure
42
A patient is on phenytoin due to seizures. They develop a chest infection and are prescribed ciprofloxacin. What effect may this have?
Ciprofloxacin is an inhibitor → phenytoin levels rise → phenytoin toxicity (ataxia)
43
How may phenytoin toxicity present?
Ataxia etc - patient may complain of feeling drunk
44
What are the 2 main routes of drug eliminated?
a) kidneys (urine) b) biliary tract (faeces)
45
How are most hydrophilic drugs excreted?
**Hydrophilic drugs** (to start with) do _not_ need to undergo metabolism in the liver → are excreted **unchanged** by the kidneys
46
How is digoxin excreted?
By the kidneys
47
Why should digoxin NOT be prescribed in renal failure?
If there is kidney failure, the body is unable to eliminate digoxin, causing levels to accumulate. This can cause digoxin toxicity (as it is still an **active drug** as has not been metabolised by the liver)
48
Some lipophilic drugs are metabolised into **active metabolites** when they are turned into hydrophilic drugs (i.e. drug _stays_ active or _becomes_ active). Give a prime example of this
Opioids
49
Why should opioids not be prescribed in renal failure?
Are metabolised into **active metabolites** when they are turned into hydrophilic drugs (i.e. drug _stays_ active or _becomes_ active) → accumulate in kidney failure
50
A 72-year-old hypertensive man is started on an alpha-blocker for prostatic hypertrophy. He collapses whilst in the pub. Why? A. He is drunk B. He is straining to pass urine C. He has developed postural hypotension D. He has had a seizure E. He has had a ventricular dysrhythmia
**_He has developed postural hypotension_** ## Footnote He is hypertensive and presumably on medication to treat this. He has now been prescribed an **alpha blocker** for BPH. However, this group of drugs is also used to treat hypertension so his blood pressure may have dropped too low (hypotension), causing him to pass out.
51
A 66-year-old man on **warfarin** for AF is admitted with PR bleeding. He was recently treated for a chest infection. Which antibiotic was he most likely given? A. Amoxicillin B. Ciprofloxacin C. Doxycycline D. Trimethoprim
**_Ciprofloxacin_** Ciprofloxacin is an **P450 enzyme inhibitor**, potentiating the effect of warfarin.
52
A 19-year-old woman presents with 2 seizures in a month. There is a family history of epilepsy. She is on the oral contraceptive pill**.** Which is an appropriate anti-epileptic? A. Carbamazepine **B. Levetiracetam** C. Phenytoin D. Sodium Valproate
**_Levetiracetam_** ## Footnote Carbamazepine & phenytoin are **P450 system inducers** which would increase the risk of the patient become pregnant. Sodium valproate is contraindicated in women of child-bearing age as it can cause neural tube defects.
53
A 60-year-old alcoholic smoker on carbamazepine is admitted to hospital with an exacerbation of COPD, for which he is given nebulizers, steroids and clarithromycin**.** What would you expect? A. Fewer fits B. More fits **C. Nausea and ataxia** D. No effect
**_Nausea & ataxia_** ## Footnote Clarithromycin is a **P450 enzyme inhibitor** which will increase the effects of carbamazepine, leading potential toxicity. The side effects of carbamazepine toxicity include nausea & ataxia.
54
A 78-year-old woman takes **digoxin** for atrial fibrillation. She is started on a **diuretic** for heart failure. She develops increasing confusion over the following month. Her U+E are as follows (normal ranges in brackets) * Na+ 142 (135-145) * K+ 4.4 (3.5 – 5.1) * Urea 31 (3-7) * Creat 251 (60-110) Why is she confused? A. Alzheimer’s dementia B. Dehydration C. Digoxin toxicity D. Hypoxia due to heart failure
**_Digoxin toxicity_** ## Footnote Digoxin is excreted via the kidneys **without being metabolised**, so if a patient develops AKI it can build to toxic levels, causing **delirium**. She is unlikely to have heart failure as she is significantly dehydrated. To make a diagnosis of dementia you need to elicit a longer history and exclude reversible causes for cognitive decline.
55
What are some symptoms of digoxin toxicity?
* Confusion. * Irregular pulse. * Loss of appetite. * Nausea, vomiting, diarrhoea. * Fast heartbeat. * Vision changes (unusual), including blind spots, blurred vision, changes in how colours look, or seeing spots.

Yr 3 - Pharmacology (18 decks)

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