Top 100 drugs Flashcards

1
Q

what is activated charcoal used for?

A

Emergancy treatment of poisoning

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2
Q

what are important adverse effects of activated charcoal?

A

pneumonitis, bronchospasm and airway obstruction
black stools
vomiting

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3
Q

what are warnings of activated charcoal use?

A
  • patients with reduced level of consciousness unless the airway is protected
  • persistant vomiting due to aspiration
  • reduced GI motility
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4
Q

what is the mechanism of action for activated charcoal?

A

using van de waals forces molecules are adsorbed onto the surface of the charcoal as it moves through the gut but is only helpful for poisons that are likely to be adsorbed

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5
Q

what are angiotensin converting inhibitors typically used for?

A
  • hypertension
  • chronic heart failure
  • ischaemic heart disease
  • diabetic nephropathy and CKD with proteinurea
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6
Q

what is the mechanism of action for ACE inhibitors?

A

Block the action of angiotensin converting enzyme, meaning angiotensin I to angiotensin II.

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7
Q

ACE inhibitors stop the formation of angiotensin II, what are the actions of angiotensin II?

A
  • vasoconstriction
  • stimulates aldosterone secretion
    Blocking angiotensin II reduces afterload helping reduce hypertension
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8
Q

why are ACE inhibitors helpful in heart failure?

A

reduces blood pressure because it reduces afterload

reduces aldosterone levels meaning it promotes sodium and water excretion helping reduce preload

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9
Q

why are ACE inhibitors helpful in CKD?

A

blocking angiotensin II means dilation of the efferent glomerular arteriole which reduces intraglomerular pressure which slows progression

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10
Q

what are the adverse effects of ACE inhibitors?

A

hypotension, persistant dry cough, hyperkalaemia, renal failure, angiodema

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11
Q

why can ACE inhibitors cause a dry cough?

A

normally bradykinin is inactivated by ACE but it’s inactivated so levels will build up

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12
Q

why can ACE inhibitors cause hyperkalaemia?

A

no AGII means lower aldosterone levels, this promotes potassium retention.

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13
Q

what patients should avoid ACE inhibitors?

A

Renal artery stenosis, acute kidney injury, pregnant women and breastfeeding.
Lower doses in patients with chronic kidney disease.

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14
Q

what are examples of ACE inhibitors?

A

Ramipril, Lisinopril, perindopril

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15
Q

What are the common indications for aspirin?

A
  • treat acute coronary syndrome
  • treat ischaemic stroke
  • long term secondary prevention of arterial events
  • reduce the risk of intracardiac thrombus and embolic stroke in atrial fibirillation when warfaring is contraindications
  • control mild to moderate pain and fever.
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16
Q

in brief what is the mechanism of action for aspirin?

A

Irreversibly inhibits COX to reduce production of thromboxane from arachidonic acid which reduces platelet aggregation and risk of arterial occlusion

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17
Q

what are the important adverse effects of aspirin?

A
  • GI irritation
  • GI ulcers
  • hypersensitivity reactions like bronchospasm
  • tinnitus
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18
Q

what are the warnings of aspirin?

A

Shouldn’t be given to Children under 16
Shouldnt be given to people with aspirin sensitivity
Avoided in 3rd trimester

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19
Q

why should aspirin not be given to children?

A

A risk of reyes syndrome which affects the liver and brain

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20
Q

why should aspirin not be given in the 3rd trimester?

A

Prostaglandin inhibit can lead to premature closure of the ductus arteriousus

21
Q

what are the indications for acetyl cysteine?

A

Antidote for paracetomal poisoning
prevent renal injury due to contrast radiography
reduce the viscosity of respiratory secretions

22
Q

What is the mechanism of action for acetyl cysteine?

A

It works by replenishing the bodies stores of glutathione this is important in paracetomal overdose as it detoxifies NAPQI
Antioxidant effect protects the body against contrast agents

23
Q

How is paracetomal metabolised and why is acetyl cysteine important in overdose?

A

Normally paracetomal is conjugated with glucuronic acid and sulfate. Some is converted to toxic NAPQI but this is converted by conjugation with glutathione. Acetylcysteine replenishes the bodies glutathione supply.

24
Q

what are the important adverse effects of acetylcysteine?

A
  • when given in a large dose for paracetomal poisoning causes an anaphylactoid reaction.
  • in nebulised form can cause bronchospasm
25
Q

why should salbutamol be given before giving acetylcysteine in nebulised form?

A

Acetylcysteine can cause bronchospasm

Salbutomal is a bronchodilator so prevents this

26
Q

what are the common indications for calcium and vitamin D?

A
  • osteoporosis (along with bisphosphonates)
  • chronic kidney disease
  • in the form of calcium gluconate for hyperkalaemia
  • hypocalcaemia
  • vit D deficiency
27
Q

why is calcium gluconate given for severe hyperkalaemia?

A

to prevent life threatening arrhythmias

28
Q

what is the mechanism of action for calcium?

A

calcium homeostasis is controlled by PTH and vitamin D which increase plasma calcium levels, calcitonin decreases plasma calcium.
In osteoporosis there is loss of bone mass so you are restoring this.

29
Q

what are important adverse effects of calcium?

A

dyspepsia, constipation.

30
Q

what are the indications for oxygen?

A
  • To increase tissue oxygen delivery in hypoxaemia
  • to increase reabsorption of plural gas in pneumothorax
  • to reduce the half life of carboxyhaemoglobin in carbon monoxide poisoning.
31
Q

what is the mechanism of action of supplemental oxygen?

A

Increases partial pressure of oxygen in the alveoli will increase diffusion of oxygen into the blood for hypoxaemia
In pneumothorax it reduces the fraction of nitrogen in the alveoli increases the diffusion of nitrate out of the body.

32
Q

what are warnings of supplemental oxygen?

A

Patients with COPD can get high carbon dioxide levels

33
Q

what type of drug is salbutomal?

A

A beta 2 agonist

34
Q

What are beta 2 agonists given for?

A
  1. Ashtma
  2. COPD
  3. hyperkalaemia
35
Q

When are beta 2 agonists given for ashtma?

A

Short acting are used to relieve breathlessness. Long acting are used as step 3 treatment for chronic ashtma with inhaled corticosteroids

36
Q

what is the mechanism of action for beta 2 agonists?

A

beta 2 receptors are found in the smooth muscle of the bronchi, GI, uterus and blood vessels. It’s a G protein coupled receptor and stimulation leads to smooth muscle relaxation improving airflow.
Like insulin is stimulates the Sodium/potassium ATPase pump causing a potassium shift.

37
Q

What are shrt acting beta 2 agonists?

A

Salbutomal, terbutaline

38
Q

what are long acting beta 2 agonists?

A

Salmeterol, formoterol

39
Q

What are important adverse effects of beta 2 agonists?

A

tachycardia, palpitations, anxiety, tremor.

they promote glycogenolysis

40
Q

what should be given with long acting beta 2 agonists when used for ashtma?

A

An inhaled corticosteroid

41
Q

what are the indications for corticosteroids (glucocorticoids)?

A
  1. treat allergic or inflammatory disorders like anaphylaxis and ashtma
  2. suppress autoimmune disease
  3. given for some cancers
  4. adrenal insufficiency and hypopituitarism
42
Q

what is the mechanism of action for corticosteroids?

A

Bind to cytosolic glucocorticoid receptors which translocate to the nucleus and bind to regulate gene expression, mainly upregulating anti-inflammatory genes and down regulatory pro-inflammatory genes

  • suppress circulating monocytes and eosinophils
  • stimulate sodium and water retention and potassium excretion
43
Q

what are examples of pro-inflammatory genes that corticosteroids downregulate?

A

TNF alpha, cytokines

44
Q

what are important adverse effects of glucocorticoids?

A
  • immunosuppression
  • diabetes mellitus
  • osteoporosis
  • hypertension, hypokalaemia and oedema due to their mineralocorticoid like actions
45
Q

why should you be careful when giving NSAIDS with corticosteroids?

A

increase the risk of peptic ulceration and GI bleeding

46
Q

what type of drug is prednisolone?

A

A corticosteroids

47
Q

what are examples of corticosteroids?

A

Prednisolone, hydrocortisone and dexamethasone

48
Q

what is the most potent corticossteroid in terms of anti inflammatory?

A

Dexamethasone