Drug reactions and interactions Flashcards

1
Q

How are Adverse drug reactions investigated

A
ABCDE
Augmented? - is reaction predicted
Bizarre? -is there Hx of allergy
Chronic? - Has Px used it for a long time
Delayed? -Has Px used drug before
End of use? - Has Px stopped drug use
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2
Q

Where should adverse drug reactions be reported to

A

MHRA Yellow card scheme

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3
Q

What patient factors affect drug interactions

A

Age
Polypharmacy
Genetics
Hepato/renal disease

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4
Q

What drug factors affect interaction

A

Narrow therapeutic index

Solubility

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5
Q

What is poly pharmacy

A

Use of Concurrent medication

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6
Q

What drug has a very narrow therapeutic index

A

Digoxin

-Slight overdose = bad news

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7
Q

What Pharmacokinetic influences affect drug action (ADME)

A

Admin - Affected by acidity, Motility and solubility
Distribution - Affected by protein binding
Metabolism
-CYP450 Induction = lowers therapeutic effect
-CYP450 Inhibition = Increase therapeutic effect
Excretion - affected by Urine pH
-Acid cleared fast in weak basic urine
-Base cleared fast in weak acidic urine

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8
Q

Whats the difference between CYP450 Induction and inhibition for drug metabolism

A
Induction = Lowers therapuetic effect (Alcohol)
Inhibition = Increase therapeutic effect (Isoniazid and grape juice)
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9
Q

What three absorption influences affect drug interaction

A

Acidity
Motility
Solubility

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10
Q

What are naturally occurring Opiods

A

Morphine

Codeine

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11
Q

What are modified Opioids

A

Diamorphine (Heroin)

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12
Q

What is the oral bioavailability of Opiods

A

50%

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13
Q

Where are opiod receptors found and what are they targeted by

A

CNS
GIT
Pontine resp centers
Target of analgesia

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14
Q

What are the SE of opiod use

A

Addiction and depression
Constipation, N+V
Resp distress

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15
Q

What is meant by tolerance

A

Overstimulated opioid receptor causes desensitisation

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16
Q

What is meant by dependance

A

Craving euphoria

17
Q

How is opiod induced resp depression treated

18
Q

When is Naloxone used

A

Opioid causing resp depression

19
Q

What are Antiplatelets

A

Aspirin and Clopidogrel

20
Q

How does Aspirin work

A

Inhibit Cox1 so less Thromboxane 2 so less platelet activation

21
Q

How does Clopidogrel work

A

Inhibit P2Y12

22
Q

What are the main Anticoagulants

A

Heparin
Warfarin
DOACs
Thrombolysis

23
Q

How does Heparin work

A

Activate antithrombin 3 and inhibit factor X

24
Q

How does warfarin work

A

Inhibits Vit K epoxide reductase

25
How do DOACs work
Anti Factor Xa
26
What are some examples of DOACs
Rivoroxaban | Apixaban
27
How does Alteplase thrombolysis work
Activate plasmin to degrade fibrin = less coagulation
28
How do NSAIDs work
Inhibit Cox 1+2 = prevent prostaglandin production Cox1 inhibition = less gastric mucosal protection, Raised Gastric acid = GI ulcers Cox 2 inhibition = Anti inflammatory
29
How do NSAIDs cause GI Ulcers
Inhibit Cox 1 Less gastric mucosal protection Gasric acid wears away lining GI Ulcers
30
What is a SE of NSAIDs
Peptic ulcer disease
31
What is a SE for ACE-i
bradykinin increase = dry cough Afferent arteriole dilation = low GFR = AKI hyperkalemia
32
What is a SE of PPI
Increase fracture risk
33
What is a SE of Opioids
Resp distress (Give naloxone) Tolerance and dependance and addiction N+V and Constipation
34
What is the SE of loop diuretic and thiazides
Hypokalemia
35
What is the SE of Spiranolactone
Hyperkalemia because potassium sparring
36
How do loop diuretics work
Inhibit NKCC2 in ascending Loop of Henle | NA, K, CL and water excretion
37
How do thiazides work
Inhibit NaCl in DCT | NaCl and water excretion
38
How does spironolactone work
Inhibit ENaC Channel = aldosterone antagonist | Na and water excretion w/ K retention