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Clinical Pharmacology, Therapeutics & Principles of Prescribing > Session 11 > Flashcards

Session 11 Flashcards

1
Q

What is a vagotomy and when is it commonly used?

A

a surgical operation in which one or more branches of the vagus nerve are cut, typically to reduce the rate of gastric secretion (e.g. in treating peptic ulcers)

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2
Q

What is a highly selective vagotomy?

A

refers to denervation of only those branches supplying the lower esophagus and stomach (leaving the nerve of Latarjet in place to ensure the emptying function of the stomach remains intact). It is one of the treatments of peptic ulcer.

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3
Q

Why is a vagotomy less commonly used for PUD?

A
  • acid secretion control with H2 receptor antagonists, such as cimetidine, ranitidine, and famotidine
  • proton pump inhibitors (PPIs), such as pantoprazole, rabeprazole, omeprazole
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4
Q

Highly selective vagotomy includes:

A
  • denervation of only the fundus and body (parietal cell-containing areas) of the stomach (also called parietal cell vagotomy)
  • preserves the nerve supply of the antrum and pylorus; a pyloric drainage procedure is not needed. It does not denervate the liver, biliary tree, pancreas, or small and large bowel. This procedure is also called proximal gastric vagotomy.
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5
Q
  1. What is Gastro-oesophageal reflux disease (GORD)?
  2. Symptoms include:
  3. Complications include:
  4. Risk factors include:
  5. Cause:
  6. Treatment
A
  1. Long-term condition where stomach contents come back up into the esophagus
    • the taste of acid in the back of the mouth, heartburn, bad breath, chest pain, vomiting, breathing problems, and wearing away of the teeth.
  3. esophagitis, esophageal strictures, and Barrett’s esophagus
  4. obesity, pregnancy, smoking, hiatus hernia, and taking certain medicines (antihistamines, calcium channel blockers, antidepressants, and sleeping medication)
  5. poor closure of the lower esophageal sphincter
  6. Lifestyle changes - not lying down for three hours after eating, losing weight, avoiding certain foods, and stopping smoking

Medications - antacids, H2receptor blockers, proton pump inhibitors, and prokinetics

Surgery - Anti-reflux surgery

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6
Q

Gastric mucosa

  1. Defensive factors:
  2. Aggressive factors:
A
    • Epithelial integrity
      - Cell replication & restitution
      - Mucous membrane barrier
      - Vascular supply
    • Acid
      - Helicobacter pylori
      - Drugs
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7
Q

What does hyperemia mean?

A

an excess of blood in the vessels supplying an organ or other part of the body.

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8
Q

Parietal [oxyntic] cell

  1. Targets: Stimulatory receptors of the baso-lateral membrane

Medication which binds to this target?

  1. Target: Baso-lateral membrane receptors

Medication which binds to this target?

A
  1. Proton pump [canalicular membrane]
  2. Acetylcholine, Cholecystokinine B [CCK-B], Histamine 2 receptor [H2]
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9
Q

What is this image showing?

A

HK ATPase exchanges H for K

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10
Q

PPI action?

A
  • Delayed as not all pumps active all of the time
  • Max efficacy after 2-3 days
  • Restoration of acid secretion requires de novo synthesis
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11
Q

H2 receptor antagonists

A
  • Short half life
  • bd dosage
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12
Q

State the targets for Neuro-endocrine regulation for acid control

A
  • Cholecstokinine B [CCK B]
  • Enterochromaffine like cells [ECL]
  • Gastrin [G]
  • Gastrin releasing protein [GRP]
  • Somatostatin 2 receptor [SSTR2]
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13
Q

Which bacteria causes peptic ulcer disease & state its pathology

A
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14
Q

State the no. Of patients with a duodenal & gastric ulcer infected with H.pylori

A
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15
Q
  1. Describe the Helicobacter pylori pathogen
  2. Symptoms
  3. Causes
  4. Diagnostic method
  5. Medication:
A
    • gram-negative
      - microaerophilic (low o2 conc)
      - helix
      - contains a hydrogenase that can produce energy by oxidizing molecular hydrogen (H2) made by intestinal bacteria. It produces oxidase, catalase, and urease.
  2. Asymptomatic
  3. Helicobacter pylorispread by fecal oral route
  4. Urea breath test, fecal antigen assay, tissue biopsy
  5. Proton pump inhibitor, clarithromycin, amoxicillin, metronidazole (triple therapy)
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16
Q

‘Drugs for peptic disorders’

Antacids

Alginates (mops up excess acid and forms a pH-neutral barrier that reduces reflux episodes)

  1. H2RA e.g.
  2. PPI e.g.
A
    • Cimetidine, Ranitidine,
      - Nizatidine, Famotidine [‘safe, interactions and SE minimal]
    • Omeprazole,Lansoprazole,
      - Rabeprazole,Pantoprazole,
      - Esomeprazole [possibly safe (intermittend scares), diarrhoea]
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17
Q

GORD treatment [principles]

A
  • Symptom control
  • Healing of oesophagitis
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18
Q

GORD symptom control

  1. Step up:
  2. Step down:​
A
    • Lifestyle
      - Antacids? Alginates
      - H2 RA
      - PPI
    • PPI
      - H2RA
      - Anacids/ alginates
      - lifestyle
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19
Q

Subtypes of oesophagitis

A
  • reflux
  • infectious ( Candida (Esophageal candidiasis), Herpes simplex (Herpes esophagitis), CMV)
  • drug induced (NSAIDs, quinidine)
  • chrons
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20
Q

Treatment for oesophagitis

A

reflux esophagitis - H-2 receptor blockers, proton pump inhibitors, and prokinetics, which help with the emptying of the stomach

infectious esophagitis - antibiotics

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21
Q

Peptic ulceration treatment:

A
  • Stop NSAIDS
  • H2RA/ PPI 6/52
  • H pylori eradication -> 2 antibiotics and full acid blockade with PPI e.g. Clarithromycin 500 mg bd, Amoxycillin 1g bd, lansoprazole 30mg bd
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22
Q

Asthma Pathophysiology

A
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23
Q

Treatment for asthma

A
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24
Q

Why is asthma a heterogeneous disease

A
  • Pathologically e.g. eosinophilic versus neutrophilic inflammation
  • Symptom patterns and triggers of exacerbations
  • Response to treatment
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25
Q

Stepwise management of asthma in adults

A
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26
Q

Asthma control

  1. Asthma control means:
  2. Before initiating a new drug therapy:
A
  1. • minimal symptoms during day and night
  • minimal need for reliever medication
  • no exacerbations
  • no limitation of physical activity
  • normal lung function (FEV1 and/or PEF >80% predicted or best)

Aim for early control, with stepping up or down as required

  1. • check compliance with existing therapies
  • check inhaler technique
  • eliminate trigger factors
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27
Q

Give a summary of asthma management in adults

A
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28
Q

Step 1

Mild intermittent asthma

  1. Treatment given?
  2. Mechanism of action?
  3. Used?
  4. B2 -agonist site of action when considering symptom relief
A
  1. Short-acting B2- agonist (salbutamol, terbutaline)
  2. Used for symptom relief through reversal of bronchoconstriction
    * *Prevention of bronchoconstriction i.e. on exercise**
  3. Agonists should only be used on an as-required basis
    If used regularly, they reduce asthma control
  4. • Predominant action is on airway smooth muscle
    • Potentially inhibit mast cell degranulation if only used intermittently
    • On regular use of B2 degranulation in response to allergen increases
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29
Q

What is the B2 receptor function in airway smooth muscle?

A
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30
Q
A
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31
Q

Using the graph state which lines are likely to be

Formoterol 12 µg

Formoterol 6 µg

Salbutamol 200 µg

Salbutamol 100 µg

Placebo

Salmeterol*

A
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32
Q

State which line is Formoterol Turbuhaler® 6 mg and Terbutaline Turbuhaler® 0.5 mg

A
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33
Q

B2-agonist side-effects?

A

Adrenergic i.e. tachycardia, palpitations, tremor……

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34
Q

Step 2

Regular preventer therapy

Medication given?

Start when?

A

Inhaled corticosteroids

  1. Using B2 agonist ≥3 times/week
  2. Symptoms ≥3 times/week
  3. Waking ≥1 time/week
  4. Exacerbation requiring oral steroids in last 2 years (consider)
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35
Q
  1. How does corticosteroids affect the asthma pathophysiology?
  2. Other than it’s effects on the bronchioles what are the benefits of inhaled corticosteroids
A
  1. Image
  2. • Improve symptoms
  • Improve lung function
  • Reduce exacerbations
  • Prevent death
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36
Q

What cell do inhaled corticosteriods target?

What is the effect?

37
Q

Molecular actions of steroids (2)

38
Q

Chemical basis for potency and topical selectivity of inhaled GCS

39
Q

Lipophilic substiuents on D-ring lead to a combination of three key properties:

A
  • a very high affinity for the GCS receptor
  • increased uptake and dwell time in tissue on local application
  • rapid inactivation by hepatic biotransformation following systemic absorption

​

40
Q

How to work systemic availability of inhaled drugs

41
Q

Systemic absorption of ICS

  1. ? absorbed through gut and lungs
  2. ? undergo extensive first-pass metabolism
  3. Lung absorption is still relevant and at high doses all ICS have the potential to produce ?
A
  1. Beclomethasone
  2. Budesonide & fluticasone
  3. systemic side-effects
42
Q

Which asthmatic patients have a better response to inhaled corticosteroids

A

Eosinophilic asthmatics

43
Q

Step 3 – Add on therapy

Before initiating a new drug therapy we must?

A

• Re-check patient’s medication compliance

• Check inhaler technique
- Is it the right inhaler? - Are they still using it correctly?

• Eliminate trigger factors

44
Q

Step 3 Add-on therapy

  1. Medication given?
A

First choice – long-acting B2- agonists (formoterol, salmeterol)

Add-in LABA when patients not controlled on 400 mcg/day ICS (flat ICS dose-response curve)

45
Q

Pharmacological properties of salmeterol and formoterol

46
Q

Which B2- agonist has the greatest potency

A

Formoterol

47
Q

Out of Formoterol & Salmeterol which one has a better efficacy

48
Q

What is this showing?

49
Q

What is this showing?

50
Q

What are the benefits of Long-acting B2-agonists

A
  • Reduce asthma exacerbations
  • Improve asthma symptoms
  • Improve lung function
  • Not anti-inflammatory on their own, and must always be prescribed in conjunction with an inhaled steroid
51
Q

Give examples of Combined inhalers containing both an ICS and long-acting B2-agonist & frequency of use.

A

Twice daily:

  • Budesonide/formoterol
  • Beclomethasone/formoterol
  • Fluticasone/formoterol
  • Fluticasone/salmeterol

Once daily:

• Fluticasone furoate/vilanterol

52
Q

Rationale for combining LABA and ICS in single inhaler (5)

A
  • Ease of use*
  • Compliance
  • 1 versus 2 prescriptions to worry about
  • Potentially cheaper than 2 individual inhalers
  • Safety
53
Q

What is the SMILE study?

54
Q

Outcome of the SMILE study on exacerbations

55
Q

Effect of SMILE study of PEF

56
Q

Alternative step 3/step 4 add-ons: (4)

A
  • High dose ICS
  • Leukotriene receptor antagonists
  • Theophylline
  • Tiotropium
57
Q
  1. Give examples of Leukotriene Receptor Antagonists (?)
  2. Leukotriene is released by mast cells and eosinophils, what is it’s effect? What leukotriene does it release?
  3. Mechanism of LRAs
  4. Some anti-asthma activity but only useful in about ?% patients as add-on therapy
A
  1. Montelukast, Zafirlukast
  2. can induce bronchoconstriction, mucus secretion. mucosal oedema & promote inflammatory cell recruitment

LTC4

  1. Block the effect of cysteinyl leukotrienes in the airways at the CysLT1 receptor
  2. 15
58
Q

Leukotriene Receptor Antagonists

Side effects:

A
  • Angioedema
  • Dry mouth
  • Anaphylaxis
  • Arthralgia
  • Fever
  • Gastric disturbances
  • Nightmares

Rarely a problem in clinical practice

No important drug interactions

59
Q
  1. Give examples of Methylxanthines
  2. Mechanism of action:
  3. Efficacy?
  4. Broad or narrow therapeutic window?
  5. Frequent side-effects:
  6. Potentially life-threatening toxic complications:
  7. Important drug interactions –
A
  1. theophylline, aminophylline
  2. -Antagonise adenosine receptors
    - Inhibit phosphodiesterase – increase cAMP – unlikely to be relevant in vivo
  3. As with LTRAs, often poorly efficacious
  4. Narrow therapeutic window (10-20 mmol/L)
  5. nausea, headache, reflux
  6. arrhythmias, fits
  7. levels increased by cytochrome p450 inhibitors eg erythromycin, ciprofloxacin
60
Q
  1. Give an example of a Long acting anticholinergics (LAMAs)
  2. Frequency
  3. Used for?
  4. Benefit?
  5. Receptor it acts upon?
  6. Side effects
A
  1. Tiotropium bromide (SPIRIVA)
  2. long-acting once daily anti-cholinergic
  3. COPD and severe asthma (step 4/5)
  4. reduces exacerbations in both COPD and asthma, small improvements in lung function and symptoms
  5. Relative selectivity for M3 muscarinic receptor
  6. dry mouth, urinary retention, glaucoma (more of a risk with nebulisation of ipratropium)
61
Q

Long acting anticholinergics (LAMAs)

  1. Other LAMAs licensed for COPD only:
  2. LABA/LAMA combinations licensed for COPD only:
A
  1. • Aclidinium (twice daily)
  • Umeclidinium
  • Glycopyrronium
  1. • Tiotropium/Olodaterol
  • Aclidinium/formoterol (twice daily)
  • Umeclidinium/vilanterol
  • Glycopyrronium/indacaterol
62
Q

Step 5

  • Oral steroids (usually need 10 mg o.d. or more for maintenance therapy)
  • Biological therapies

Give two examples, effects on asthmatic patients

A

1) dAnti-IgE (Omalizumab)

– Strict criteria for use (atopy, IgE within strict range). Potentially reduces exacerbation rates in patients not controlled on oral steroids, may allow oral steroid tapering

– Works by preventing IgE binding to high affinity IgE receptor (FceRI)

– Cannot bind to IgE already bound to receptor, so cannot cross-link IgE and activate mast cells

2) Anti-IL-5 (Mepolizumab, Reslizumab)
- Reduce peripheral blood and airway eosinophil numbers
- Most effective at reducing rate of severe asthma exacerbations
- More effective if >3 exacerbations/year with blood eos >0.3x109/L in last year
- Also allow steroid tapering (on average 10 mg → 5 mg)

63
Q

What causes exacerbations in asthma

64
Q

Self-management plans (Asthma action plans)

  • Every asthmatic should have a self-management plan with written instructions on when & how to step-up and step down treatment
  • Leads to better outcomes in terms of day-to-day control, frequency & severity of exacerbations

What do we mean by step down?

A

Stepping down

• Once asthma is controlled stepping down is recommended

• If stepping down does not take place these patients may receive a higher dose than is
necessary

• Patients should be maintained at the lowest possible dose of inhaled steroid

65
Q

Drug delivery via inhaler devices

Where do these different sized particles deoposited?

10 micron particles –

1-5 micron particles –

0.5 microns –

A

10 micron particles – deposited in the mouth and oropharynx

1-5 micron particles – most effective as they settle in small airways

0.5 microns – too small. Inhaled to alveoli and exhaled without being deposited in the lungs

66
Q

Deposition of GCS in Healthy Volunteers

Looking at the image determine which one is CFC-BDP MDI & HFA-BDP MDI

67
Q

Inhaler devices

  1. What should be done if a patient is unable to use a device satisfactorily?
  2. The patient should have their ability to use an inhaler device assessed by a ?
  3. The medication needs to be titrated against clinical response to ensure optimum efficacy
  4. Re-assess inhaler technique as part of a structured clinical review
A
  1. alternative should be found
  2. competent healthcare professional

3.

68
Q

Acute severe asthma in adults

Severe- any one of:

A
  1. Unable to complete sentences
  2. Pulse ≥ 110 beats / min
  3. Respiration ≥ 25 / min
  4. Peak Flow 33-50% of best or predicted
69
Q

(1. Unable to complete sentences
2. Pulse ≥ 110 beats / min
3. Respiration ≥ 25 / min
4. Peak Flow 33-50% of best or predicted)

Life-threatening features. Previous plus any one of:

Near-fatal: PaCO2 >6 kPa, mechanical ventilation

A
  • PEF <33%
  • sPO2 <92
  • PaO2 <8 kPa
  • PaCO2 >4.5 kPa
  • Silent chest
  • Cyanosis
  • Feeble respiratory effort
  • Hypotension, bradycardia, arrhythmia
  • Exhaustion, confusion, coma
70
Q

Treatment of acute severe asthma:

A
  1. Oxygen, high flow – aim to keep O2 94-98% sat
  2. Nebulised salbutamol – continuous if necessary, oxygen driven
  3. Oral prednisolone ~40 mg daily for 10-14 days
  4. If moderate exacerbation not responding, or acute - can be stopped without tailing down severe/life threatening, add nebulised ipratropium bromide
  5. Consider IV aminophylline if no improvement and life threatening features not responding to above treatment (BEWARE if taking oral theophylline).
71
Q

Anticholinergic

  1. Give an example
  2. Difference between an adrenergic agonist ?
  3. When used?
A
  1. Iprotrapium bromide ( ATROVENT ). A quaternary anticholinergic agent
  2. Bronchodilation develops more slowly and less intense than adrenergic agonists. Response may last up to 6 hours.
  3. Useful add-on in acute severe/life-threatening asthma, or moderate exacerbation with poor response to initial therapy
72
Q

What are the five tasks in managing patients with COPD

A
  1. Confirm COPD
  2. Stop smoking
  3. Record MRC dyspnoea score
  4. Offer vaccinations
  5. Medications
73
Q

State what you must do before changing an asthmatics prescription

A
  • adherance
  • inhaler technique
  • update plan
74
Q

What medications should you give for persistent breathlessness

75
Q

What medications should you give for frequent exacerbations

76
Q

What should you do if the patient has a chronic productive cough in COPD

77
Q

GORD – Gastroesophageal Reflux Disease

  1. What is GORD?
  2. Causing: ?
  3. How do we manage these symptoms?
A
  1. Stomach contents come back up into the oesophagus (through lower oesophageal sphincter)
  2. heart burn, acid taste in mouth, nausea/vomiting - these symptoms grouped as “dyspepsia” GORD is one cause of dyspepsia, but may also be related to a GI cancer/ more serious pathology.
    • Give appropriate lifestyle advice
      - Can trial management with PPI to see if symptoms improve if no red flags
      - Consider test for helicobacter.pylori
      - Stop any aggravating drugs e.g. NSAIDs which disrupt mucosal lining
  • If red flag symptoms hematemesis, meleana, weight loss, abdominal mass, age of onset age >55 then need ENDOSCOPY
    NOTE: epigastric pain/vomiting and other dyspepsia symptoms can be as a result of an myocardial infarction
78
Q

GORD MANAGEMENT

Step one

Step two

Step three

79
Q

H.pylori

  1. H.pylori is?
  2. How do we test for H.pylori? (note: only those with reflux are tested)
  3. How do we get rid of h.pylori?
  4. Note: over 50% of the worlds population are colonised with h.pylori, but of those with it – around 80% are ?
A
  1. gram negative bacteria found in the GI tract, which can cause gastric and duodenal inflammation/ulceration – toxic to epithelial cells/degrades mucosal lining
    • Carbon-13 urea breath test
      - Stool antigen test
      ensure the person has not taken a PPI in the past 2 weeks, or antibiotics in the past 4 weeks
  3. = triple therapy for 1 week

Clarithromycin 500mg BD
Amoxycillin1g BD
Lansoprazole 30mg BD

  1. asymptomatic
80
Q

Describe the Autonomic innervation of airway smooth muscle

A
  • Parasympathetic (dominant) – bronchoconstriction, vascular dilatation, increased
    secretion from mucus glands
  • Sympathetic (non dominant) – only innervate vascular smooth muscle + glands so
    doesn’t affect airway however B-Adrenoreceptors found in airway smooth muscle
81
Q

Benefits of…

  1. Beta agonists – ?
  2. Inhaled steroids:
A
  1. relieve symptoms
    • Improve symptoms
      - Improve lung function
      - Reduce exacerbations
      - Prevent death
82
Q

Asthma Treatment – Stepwise Approach:

83
Q
  1. Examples ICS: ?
  2. Combined LABA + steroid = ?
A
  1. budesonide, Beclomethasone, fluticasone
  2. symbicort
84
Q

Beta-2-Agonists

  1. SHORT ACTING BETA AGONISTS (SABA)
    a. Examples: ?
    b. Mechanism: ?
    c. ADRs:
  2. LONG ACTING BETA AGONISTS (LABA)
    a. Examples:
    b. Mechanism and ADRs
A
  1. a. salbutamol, terbutaline
    b. used for immediate symptom relief as prevent bronchoconstriction by relaxing airway smooth muscle – bind to B2 adrenoceptors
    c. adrenergic: tachycardia, palpitations, tremor
  2. a. formoterol (quick onset), salmeterol (slow onset)
    b. as above
85
Q

Leukotriene Receptor Antagonists

  1. Examples:
  2. Mechanism:
  3. ADRs:
  4. Note: some anti-asthma activity but only useful in about 15% patients as add-on therapy
A
  1. montelukast
  2. leukotrienes are released by mast cells/eosinophils and induce
    bronchoconstriction, mucus secretion and mucosal oedema, and promote
    inflammatory cell recruitment. LTRAs block the effect of cysteinyl leukotrienes in the
    airways at the CysLT1 receptor.
  3. Angioedema, Dry mouth, Anaphylaxis, Arthralgia, Fever, Gastric disturbances,
    Nightmares
86
Q

Methylxanthines

  1. Examples:
  2. Mechanism:
  3. ADRs: a. Common - ?
    b. Potentially life-threatening toxic complications – ?
  4. Interactions: ?
  5. Efficacy, therapeutic window & use?
A
  1. theophylline, aminophylline (can be given orally or IV)
  2. antagonise adenosine receptors - inhibit phosphodiesterase – increase cAMP.
    3a. nausea, headache, reflux
    b. arrhythmias, fits
  3. levels increased by cytochrome p450)inhibitors e.g. erythromycin, ciprofloxacin
  4. often poorly efficacious with narrow therapeutic window. Used more IV in severe/life threatening asthma as additional therapy
87
Q

Long acting anticholinergics (LAMAs)

  1. Examples: ?
  2. Indication: ?
  3. Mechanism: ?
  4. ADRs: ?
A
  1. tiotropium bromide, glycopyrronium
  2. COPD & severe asthma
  3. Bind to M3 muscarinic receptor and block it’s action (prevent bronchoconstriction – see diagram)
  4. think anticholinergic - dry mouth, urinary retention, glaucoma
88
Q

Biological Therapies

  1. Omalizumab (anti- IgE)
    a. Strict criteria for use (atopy, IgE within strict range). Potentially reduces exacerbation rates in patients not controlled on oral steroids, may allow oral steroid tapering
    b. Mechanism: ?
  2. Reslizumab (Anti IL-5)
    a. How does it work?
    b. More effective if ?
    - Also allow steroid tapering (on average 10 mg → 5 mg)
A

1b. Works by preventing IgE binding to high affinity IgE receptor. Cannot bind to IgE already bound to receptor, so cannot cross-link IgE and activate mast cells
2a. Reduce peripheral blood and airway eosinophil numbers. Most effective at reducing rate of severe asthma exacerbations
b. >3 exacerbations/year with blood eos 0.3x109/L in last year

Clinical Pharmacology, Therapeutics & Principles of Prescribing (19 decks)

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