Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Body Systems > Respiratory strand: Lecture 12 - Respiratory Pharmacology > Flashcards

Respiratory strand: Lecture 12 - Respiratory Pharmacology Flashcards

1
Q

Why do we cough?

A

Its a protective reflex that prevents lungs from aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What will happen if we don’t have the cough reflect?

A

Lungs will aspirate into the lung

and we will die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does aspirate mean?

A

To withdraw fluid by negative pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the two types of cough?

A

Useless and useful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 3 features of a useless cough?

A

persistent, unproductive, dry cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In what conditions do we see a useless cough?

A

asthma, oesophageal reflex, sinusitis, psychogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Should a useless cough be suppressed?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are antitussives called?

A

Cough suppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are 3 features of a useful cough?

A

when you inhale something and you want to expel it out

  • expels secretions i.e produces sputum
  • productive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In what condition would you see a useful cough?

A

chest infection (as they’re accumulating infective sputum that needs to be expelled)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Should a useful cough be suppressed?

A

No

yes if exhausting and dangerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the 3 step mechanism of a cough?

A
  1. Cough receptors or lung irritant receptors
  2. Cough centre in medulla
  3. Vagal stimulation leading to cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where can linctuses serve?

A

Above the larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can we stop dry coughs on the afferent side?

A

-reduce stimuli e.g by stopping smoking, using linctuses (e.g strepsils cover the mucus membrane with a protective layer) or inhale steam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does inhaling steam stop coughing?

A
  • works below the larynx
  • makes the environment warmer
  • more mucus is secreted
  • mucus provides protective layer to the inflamed larngyl membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do nebulised local anaesthetics do?

A
  • work on the afferent side
  • completely numb the afferent receptors that are present in the larynx or the trachea
  • allows us to insert tube whilst patient is awake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where do antitussives work?

A

the medullary cough centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 3 categories of antitussives for dry coughs?

A
  1. Opiods (codeine, methadone, phocodeine)
  2. Non-opoids (dextromethorphan, noscapine)
  3. Sedatives (diohenhydramine, chlorphreniramine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two categories of treatment for productive coughs?

A
  1. expectorants
  2. mucolytics
    These are substances that make secretions thinner so they can be expelled
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What do expectorants do?

A

Increase the volume of secretion

They don’t add any value but they are increasing the required respiratory effort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What do mucolytics do? give examples

A
  • decrease the viscosity
  • used in conditions like cystic fibrosis
  • acetyl cysteine, carbocystine, mecystein, recombinant human DNAse break the disulphide bonds in sputum to make sputum thinner
  • expensive
  • used for specific conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 3 most common causes of chronic cough?

A
  • upper airways cough syndrome (post nasal drip)
  • bronchial asthma
  • chronic obstructive pulmonary disease
  • gastroesophageal reflux disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the difference between restrictive and obstructive lung conditions?

A

In restrictive, the total lung volume is decreased

In obstructive, the total lung volume Is normal to start with then increases?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does inflammation cause?

A

Swelling of the epithelium mucosa which leads to narrowing of the lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What type of disease is asthma?

A

chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 4 types of bronchial asthma?

A
  1. Asthma associated with allergic reactions - IgE mediated
  2. Asthma not associated with specific allergen - intrinsic asthma
  3. Exercise induced asthma
  4. Asthma associated with chronic obstructive pulmonary disease due to obstruction of elastic tissue in airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Explain the process in allergen mediated asthma that causes bronchoconstriction

A
  1. Exposure to antigen causes lymphocyte system to be activated
  2. T cells stimulate your B cells to make IgEs
  3. IgE antibodies combine with mast cells and activate them
  4. Mast cells release histamine and other mediators which activate the arachidonic acid pathway leading to secretion of leukotrienes which cause inflammation of the mucous, and constriction of the smooth muscle
  5. This leads to brochoconstriction
28
Q

What are the treatments available for asthma?

A
  1. Prevention of Ag:Ab reaction - avoidance of antigen
  2. Non-specific reduction of bronchial hyperactivity:
    - non pharmacological: stop smoking, weight reduction
    - pharmacological: corticosteroids
  3. Dilation of narrowed bronchi:
    - mimicking dilator neurotransmitter: sympathomimetics
    - direct acting bronchodilators: methylxanthines
    - blockage of constrictor transmitter: anticholinergics
  4. Prevention of release of transmitter
    - mast cell stabilisers
  5. Antagonism of released transmitter
    - leukotriene receptor antagonist
29
Q

What are the 5 actions of corticosteroids?

A

-anti inflammatory
-inhibition of influx of inflammatory cells after exposure
-reduced micro vascular leakage: decreased oedema
-inhibition of release of mediators i.e cytokines
-inhibition of cycloxygenase enzyme
overall, they are causing reduced bronchial reactivity

30
Q

What are the limitations of corticosteroids?

A
  • They take a long time to have effect
  • reduce asthma exacerbations but do not relax bronchial smooth muscle
  • can’t be used during asthma attack / not useful in acute severe asthma
31
Q

How are corticosteroids used by patients?

A
  • As brown inhalers

- first line of regular therapy (mild to mod asthma)

32
Q

What can be used for severe asthma?

A

Oral corticosteroids

33
Q

What are the adverse side effects of corticosteroids?

A
  • iatrogenic cushing’s syndrome
  • inhibition of hypothalamic pituitary axis
  • oropharyngeal candiasis
  • hoarseness: direct effect vocsl chords
34
Q

How can you prevent the adverse side effects?

A
  • by administering early in the morning
  • inhalation route: 4 puffs
  • gargle and spit after every treatment
  • use newer drugs e.g cyclesonide
35
Q

what do mast cell stabilisers do?

A
  • no longer combine with IgE

- Inhibit release of mast cell mediators

36
Q

What are examples of mast cell stabilisers and how are they administered?

A
  • Cromolyn sodium, nedocromil sodium

- administered by inhalation and very poorly absorbed

37
Q

Do mast cell stabilisers have an effect on bronchial smooth muscle?

A
  • no
  • no use in acute bronchospasm
  • only valuable if taken prophylactically
38
Q

What are the main uses of mast cell stabilisers now?

A

Allergic rhinitis, allergic conjunctivitis

39
Q

What are the side effects of mast cell stabilisers?

A

Throat irritation, cough, dermatitis, myositis, gastroenteritis

40
Q

When a patient is having an asthma attack - what does arachidonic acid synthesise?

A

leukotriene and prostaglandins

41
Q

What does leukotriene do?

A

Act on a receptor to cause a bronchospasm

42
Q

Which enzyme converts arachidonic acid to leukotriene?

A

5 lipoxygenase

43
Q

What are the two ways we can prevent a bronchospasm?

A

Use leukotriene synthesis inhibitors or leukotriene receptor antagonists to reduce the production of leukotriene or block the receptors respectively

44
Q

Why do we no longer use drugs that inhibit 5-lipoxygenase?

A

They caused liver toxicity

45
Q

What types of asthma are leukotriene receptor antagonists used for?

A
  • allergen induced asthma
  • exercise induced asthma
  • no effect for acute asthma as they need time to work on receptor and block them
46
Q

Why are leukotriene receptor antagonists given orally?

A

Better for children

47
Q

What does montelukast do?

A

Blocks receptors and reduces frequency of exacerbations

48
Q

How do we control bronchial tone?

A

slide ….

49
Q

What colour inhaler is the sympathomimetic agents? How does it act?

A

Blue inhaler

Acts via B2 adrenoceptors

50
Q

What are the 2 types of selective B2 agonist agents? give examples

A
  1. Short acting (SABA) e.g salbutamol

2. Long acting (LABA) e.g salmetrol

51
Q

What is the non-selective B2 agonist?

A

Adrenaline

52
Q

When is adrenaline used?

A
  • used in emergency

- as subcutaneous injection or micro-aerosol

53
Q

Give 3 features of selective B2 agonists?

A
  • metered dose inhalers or nebulisation
  • onset is immediate
  • 1st line of therapy
54
Q

What are the side effects of B2 agonists?

A
  1. Heart - palpitation, tachycardia, cardiac arrhythmias
  2. Muscles - tremor
  3. Other - restlessness, nervousness, hypokalemia
55
Q

What are the side effects of methylxanthines?

A

palpitations, cardiac arrhythmia, hypotension, GI irritation (increased acid production), diuresis, hypokalemia, anxiety, headache, seizures

56
Q

What are the two forms of methylxanthines and how are they different?

A
  1. theophylline - taken orally

2. aminophylline - intravenous

57
Q

Where do anticholinergic agents act?

A

Via inhibiting muscarinic receptors (M3)

They inhibit effects of vagus nerve stimulation

58
Q

What colour inhalers are anticholinergics?

A

Green

59
Q

How are green inhalers administered?

A

Inhalation

60
Q

What is an example of a selective muscarinic antagonist agent?

A

Tiotropium

61
Q

What do anti IgE monoclonal antibodies do? give example of one

A

Inhibits binding of IgE to mast cells

e.g omalizumab (v expensive)

62
Q

What are other drugs we can use to treat asthma?

A
  • anti IgE monoclonal antibodies
  • ketotifen
  • magnesium
  • ketamine
63
Q

When do we use magnesium and ketamine?

A
  • in ICU - when all else fails

- patients who fail to respond to inhaled bronchodilators

64
Q

How are mast cells activated?

A

by the attachment of the Fc portion of immunoglobulin IgE and other complement fractions

65
Q

What does activation of mast cells lead to?

A

Synthesis of arachidonic acid derivatives such as the leukotriene C4 that cause a slow but sustained contraction of bronchial smooth muscle

Body Systems (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions