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Pharmacy Year 2 Semester 2 > Drugs > Flashcards

Drugs Flashcards

1
Q

B2 agonists act by

A

relaxation of smooth muscle and enhance mucociliary clearance

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2
Q

Salbutamol

A

SABA

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3
Q

SABA

A

Short-acting Beta-agonist

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4
Q

Terbutaline

A

SABA

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5
Q

LABA

A

Long-acting Beta-agonist

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6
Q

Salmeterol

A

LABA

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7
Q

Formoterol

A

LABA

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8
Q

Name 6 Beta-2 agonists ADRs

A
  • fine tremor
  • nervous tension
  • headache
  • peripheral vasodilation
  • tachycardia
  • hypokalaemia
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9
Q

Corticosteroids - place in treatment?

A

2nd line preventers

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10
Q

How do corticosteroids work?

A

Anti-inflammatory, reducing bronchial hyper-response

Suppress inflammatory process

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11
Q

ICS are available in combination with..

A

LABA

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12
Q

Beclomethasone

A

ICS

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13
Q

Budesonide

A

ICS

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14
Q

Ciclesonide

A

ICS

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15
Q 
Prednisolone
class
dose
A

Oral corticosteroid

dose: 40-50mg of 5/7 for acute attack

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16
Q

When are corticosteroids indicated? (4)

A
  • exacerbation of asthma in last 2 years
  • using inhaled B2-agonist >3 times/week
  • symptomatic >3 times/week
  • waking 1 night per week
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17
Q 
ICS ADRs (3)
and how to help with them
A
  • hoarseness or dysphonia (use spacer/dry powder)
  • oral candidiasis (rinse mouth after use/spacer)
  • adrenal suppression BUT only in sustained doses >1500mcg of bethlamethosone daily
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18
Q

Oral corticosteroids ADRs (7)

Guidance on when to take

A

-Hypertension
-osteoporosis
-skin thinning
-hyperglycaemia
-adrenal suppression
-moon face
-acne
For oral corticosteroids: use lowest dose that will control symptoms for the shortest time possible

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19
Q

How do leukotriene antagonists work?

Where is their place in therapy?

A

anatagonise bronchoconstriction, airway oedema and mucous production
3rd/4th line controller/preventer therapy

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20
Q

oral montelukast

A

leukotriene antagonist

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21
Q

oral zafirlukast

A

leukotriene antagonist

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22
Q

ADRs of leukotriene antagonists(5)

A
  • abdominal pain
  • headache
  • thirst
  • rash
  • sleep distrubance/CNS effects
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23
Q

Cromones mechanism of action

A

mast cell stabilisers, inhibits mediator (histamine) release from mast cells

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24
Q

Nedocromil

A

Cromone

Preventer in 5-12 year olds

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25
Q

ADRs of cromones (3)

A
  • N&V (nausea and vomiting)
  • bitter taste
  • dyspepsia
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26
Q

Immunosuppresants for asthma treatment

A

Steroid-sparing agents

specialist use- rare

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27
Q

Gold for asthma

A

immunosuppresant

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28
Q

Methotrexate for asthma

A

immunosuppresant

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29
Q

Ciclosporin for asthma

A

immunosuppresant

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30
Q

how do methylxanthines work?

Where is their place in treatment of asthma?

A

phosphodiesterase inhibitors that inhibit leukotriene synthesis and thus inhibit inflammation and bronchodilation
3rd/4th line controller/preventer therapy

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31
Q

oral theophylline for asthma

A

methylxanthine

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32
Q

IV/oral aminophylline

A

methylxanthine

aminophylline is a salt of theophylline

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33
Q

Downside of methylxanthines (3)

How can you reduce these downsides (2)

A 
Narrow therapeutic index
ADRs
Interactions
reduce downsides by
-using slow release preparations to give a more predictable effect
-brand of drug must be kept constant
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34
Q

Methylxanthine therapeutic range

A

10-20mg/L

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35
Q

ADRs of methylanthines according to blood levels:

A
  • <20mg/L - nausea, diarrhoea, nervousness, headache
  • > 20mg/L - vomiting, insomnia, arrthymias
  • > 35mg/L - hyperglycaemia, arrthymias, convulsions, death
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36
Q

what is clearance of methylxanthines affected by?

A

CYP450 metabolism

37
Q

Effects of decrease clearance of methylxanthines

A

-Decreased clearance means increased plasma levels
-CCF (congestive heart failure)
-liver disease
-obesity
Note: dose is by ideal body weight (IBW)

38
Q

drug interactions with methylxanthines that can lead to toxicity due to decreased clearance

A

enzyme inhibitors e.g.

  • cimetidine
  • erythromycin
  • allopurinol
  • ciprofloxacin
39
Q

drug interactions with methylxanthines that can lead to reduced clearance and hence a sub-therapeutic effect

A

enzyme induction e.g.

  • carbamazipine
  • rifampicin
  • phenytoin
  • smoking
40
Q 
Omalizumab 
drug class and how it works
A

Anti-IgE monoclonal antibodies

inhibits binding of IgE to mast cell receptors therefore preventing inflammatory response to trigger

41
Q

what is Omalizumab licensed for?

A

Add-on therapy in adults and children over 12 years for severe persistent asthma

42
Q

how is omalizumab given?

Who can initiate omalizumab treatment?

A

S/C injection every 2-4 weeks
only initiated by specialist centres
patients must fulfill specific criteria (NICE)

43
Q

when is omalizumab treatment discontinued?

A

Discontinued after 16 weeks if inadequate response

44
Q

How is magnesium sulphate used in the treatment of ashtma?

How does the drug work?

A
  • considered in acute asthma if PEF>50%
  • given as single dose IV
  • smooth muscle relaxant, t cell and mast cell stabiliser
45
Q

Dapaglifozin

A

SGLT2 Inhibitor drug

Licensed to treat type 2 diabetes

46
Q

Antacids are for
are available how
advantages

A
  • Neutralise acid – first choice for dyspepsia and mild symptoms of GORD (also alginates)
  • sodium bicarbonate containing
  • OTC in liquid and tablet formulations
  • simple, cheap, effective
  • liquid is better but less convenient and portable
47
Q

Antacids dose

A 
As required (PRN)
QDS or more daily
48
Q

Antacids side effects

A
  • if contain magnesium - laxative effect
  • if contain aluminium - constipation
  • If contain calcium- rebound acid secretion and hypercalcaemia
49
Q

When to avoid antacids?

A 
-if on salt-restrictive diet
Avoid drugs with sodium in when:
-renal and cardiac conditions 
-pregnant
-hypertension
50
Q

Low Na+ definition

A

The words “low Na” after some preparations indicate less than 1mmol per tablet or 10mL dose

51
Q

Antacids interactions

A

-may impair absorption of other drugs taken at the same time
-may damage enteric coating by raising the pH
Rarely:
-may affect pH-dependent renal excretion e.g. increase excretion with possible reduction in serum levels (aspirin and lithium for example)

52
Q

H2 antagonists
(Histamine2 antagonists)
suffix and 4 examples
Where are they available

A

-tidine
-Cimetidine
-Ranitidine
-Nizatidine
-Famotidine
All available OTC in low doses

53
Q

H2 antagonists
What do they do?
What conditions are they licensed for?

A 
All heal duodenal and gastric ulcers at higher doses than available OTC 
Licensed for:
-maintenance treatment 
-NSAID prophylaxis (stop them causing 
-reflux (less effective than PPIs)
-GORD (but less effective than PPIs)
54
Q

H2 antagonists interactions

A

CYTP450 systwm
Cimetidine (oldest) interacts with
-warfarin - inhibits metabolism ↑INR - potential to bleed
-phenytoin, carbamazpine, valporate - inhibits metabolism, ↑plasma concentrations
-theophylline - inhibits metabolism, ↑plasma concentrations
-sidenafil - ↑plasma concentrations

Rantidine less interactions

55
Q

Side effects of H2 antagonists

A

but usually

  • headache
  • diarrhoea
  • dizziness
  • occasionally rashes
  • altered LFTs

Ranitidine less side effects

56
Q

Helicobacter pylori does what?

A
  • causes persistent infection in gastroduodenal mucosa
  • infection always causes gastritis
  • patient may not be aware of infection
  • Host cofactors are critical to the development of ulcers
  • 73% of gastric cancers MAY be caused by H.pylori
57
Q

How does H.pylori do it’s damage

A
  • buries itself in epithelia/mucosa
  • produces urease
  • produces good environment to itself
  • mucosal cell death can expose them to pepsin and stomach acid
58
Q

H.pylori tests

A

-H.pylori produces and antibody response detectable in serum, saliva or urine (antigens in the stool)
-Urea breath test kits whereby patient swallows 13C-labelled urea solution.
Urease activity by the enzyme produces labelled CO2

-Mucosal biopsies taken at gastroscopy
Urease test, histopathology or culture

-High antibody titre in patient generally indicates active infection

59
Q

Testing parameters

do nots

A

-Antibody tests cannot be used for follow up after eradication therapy
-These tests should not be performed within 4 weeks of treatment with antimicrobials
or
2 weeks with PPIs or anti-secretory drugs

60
Q

H.pylori treatment aims

A

Treatments should be

  • Simple
  • Well-tolerated
  • easy to comply with
  • cost effective
61
Q

Triple therapy to eradicate H.pylori

A 
High eradication rates
7 days
-Clarithromycin
-PPI
-metronidazole or amoxicillin
62
Q

doses of antibiotics used in triple therapy

A
  • Clarithromycin (always used) 500mg BD or if with metronidazole then 250mg BD
  • Amoxicillin 1mg BD (not if penicillin sensitive)
  • Metronidazole 400mg BD
63
Q

Anti-secretory agents (gold standard is PPIs)

Name 5 PPIs and their doses

A
  • Omeprazole 20mg BD
  • Esomeprazole 20mg BD
  • Lansoprazole
  • Pantoprazole 40mg BD
  • Rabeprazole 20mg BD
64
Q

Omeprazole side effects

A
  • Rash

- Diarrhoea

65
Q

Counselling for H.pylori

A

-emphasise importance of completing the course
Interactions:
-clarithromycin and statins (stop taking statin)
-metronidazole and alcohol - nausea if taken with it
-penicillin allergic or not?

66
Q

Eradication of H.pylori

A
  • In cases of complicated ulceration, continue the antisecretory agent alone for a further 3 weeks to achieve healing
  • symptoms after eradication suggest GORD (reflux problems) or ulcer
67
Q

Key treatment recommendations for GORD

A
  • Full dose PPI for 1-2 months
  • If symptoms reoccur than lowest dose PPI with alginate to control symptoms
  • Patients should be advised to step down PPI (dose reduction plus alginate) or Step-off PPI (stop treatment)
  • Intermittent treatment may work
  • Symptomatic relief continues with antacids and/or alginate therapy alone
68
Q

GORD in pregnancy

A
  • dietary and lifestyle changes - clothing, small meals frequently, not a lot of fluid
  • antacid or alginate
  • Ranitidine
  • Omeprazole in severe or complicated conditions
69
Q

GORD in infancy

A
  • usually resolves by 12-18 months
  • change frequency and volume of feed
  • feed thickener or thicker formulation feed
  • use an alginate instead of thickened feeds
  • Lifestyle changes and alginate for older children
70
Q

GORD in older children

A
  • alginate and lifestyle changes

- H2-receptor antagonists then PPI

71
Q

NSAID-associated ulcers

High risk

A
  • 2nd major cause of PUD

- High risk if over 65 and/or patients with a history of PUD

72
Q

PUD is

A

Peptic ulcer disease

73
Q

NSAID-associated ulcers prevention/protection drug classes

A

PPI
H2-antagonists (duodenal) .e.g Ranitidine at twice the normal dose
Misoprostol

74
Q

Why are NSAIDs a problem in PUD?

A

NSAIDS are gastric irritants
NSAIDs are prostaglandin inhibitors
Prostaglandins is important for maintenance of mucosal blood supply, production of ,mucus and bicarbonate by cells

75
Q

What is Misoprostol

A
  • A prostaglandin analogue

- PGE1 has antisecretory and cytoprotective effects

76
Q

Uses of mioprostol

A
  • promote ulcer healing

- prevent NSAID-induced ulcers

77
Q

Misoprostol is used in combination with

A

-Diclofenac
-Naproxen
These are both NSAIDs

78
Q

Misoprostol side effects

Contraindications

A

Diarrhoea
DO NOT USE IN PREGNANCY
avoid in ladies of child-bearing age

79
Q

treatment of NSAID-associated ulcers

A

Assume H.pylori negative

  • stop NSAID if possible - Ibuprofen has lowest effects
  • PPIs
  • H2 antagonists
  • Misoprostol
80
Q

Treatment of NSAID-associated ulcers if the NSAID is needed to continue
Combo preps

A

Options

  • Treat with PPI and continue long term at same dose
  • Treat with PPI and on healing switch to misoprostol
  • Treat with PPI and switch NSAID to selective COX-2 inhibitor
  • Combination preparations:
  • naproxen/esomeprazole 500/20
  • ketoprofen/omeprazole - 100/20 and 200/20
81
Q

Lifestyle advice for PUD

A
  • smoking cessation
  • avoid foods that cause dispepsia ie
  • -fatty, acidic, fried foods and chocolate
  • -reduction or exclusion of alcohol and caffeine
  • avoid eating late in the evening
  • don’t go hungry as this stimulates gastric acid secretion
  • reduce stress
  • weight reduction
  • raising the head of the bed (GORD) with block, not pillows
  • wear loose clothing
82
Q

GORD is

A

Gastro-oesphageal reflux disease

83
Q

What is long-term PPI therapy associated with

A

increased risk of adverse effects:

  • Achlorhydria - low gastric acid production is associated with increased risk of…
  • gastric cancer
  • H.pylori infection (especially the elderly)
  • pneumonia
  • Clostridium difficle infection
  • bacterial overgrowth
  • reduced calcium absorption leading to hip fracture
84
Q

PPI OTC

A

Esomeprazole
GSL medicine
use for up to 2 weeks

85
Q

Potential interaction between omeprazole/esomeprazole with clopidogrel

A

Clopidogrel prevents blood clots
-The potential interaction between omeprazole and clopidogrel involving effects on its metabolism via the CYP2C19 enzyme has received much attention; however the evidence that it results in any clinically significant changes in outcomes is minimal

Recommendations include using an alternative PPI or an H2 Antagonist

86
Q

Fatty foods…

A

delay gastric emptying

irritant effect on mucosa

87
Q

Spironolactone for liver

A

treatment of ascites
100-600mg OD
Aldosterone antagonist

88
Q

Furosemide for liver

A

Ascites treatment
40-160mg OD
diuretic

89
Q

Metolazone

A

diuretic used in cases of ascites that are unresponsive to 1st/2nd line treatment
Rare

Pharmacy Year 2 Semester 2 (33 decks)

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