Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Obstructive Airways Disease > Flashcards

Obstructive Airways Disease Flashcards

1
Q

Locations affected in obstructive disease and in restrictive disease?

A

Airways - obstructive disease

Lungs - restrictive disease

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

Divisions of obstructive airway syndrome?

A

Asthma
Chronic bronchitis
Emphysema

However, OVERLAP can occur, e.g: ACOS (asthma/COPD overlap syndrome) where smokers can have both asthma and COPD features

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

Aetiology of airway obstruction in COPD?

A

Lumen surrounded by epithelium and then mucosa, (has a lamina propria) and then a sub-mucosa

In mucosa and sub-mucosa is where inflammation occurs in COPD and asthma
Inflammation causes infolding/invagination, so lumen narrows creating turbulent air flow and wheezing
In COPD and asthma, smooth muscle tone can increase, causing constriction and reducing lumenal diameter

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

Inflammatory responses in asthma and COPD?

A

Main inflammatory cells:
Asthma - eosinophils
COPD - neutrophils

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

What happens in emphysema?

A

Alveolar walls give bronchial tree some structural integrity; breaking these walls means bronchial tree will collapse when intra-thoracic pressure rises
Occurs in emphysema, not asthma, which is smoking-induced

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

Describe the asthma triad

A

3 aspects:
Reversible airflow obstruction - unlike COPD, which is irreversible
Airway inflammation - mostly due to eosinophils
Airway hyper-responsiveness - excessively twitchy smooth muscle

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

Describe the dynamic evolution of asthma (what each change causes)

A

Bronchoconstriction - produced brief symptoms
Chronic airway inflammation - exacerbations and airway hyper-responsiveness
Airway remodeling - fixed airway obstruction

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

What occurs in uncontrolled asthma?

A

Uncontrolled eosinophilic inflammation and collagen/scar tissue is laid down in mucosa/sub-mucosa - known as AIRWAY REMODELING
The obstruction is now fixed/irreversible

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

What occurs during airway remodeling in asthma?

A

THICKENING of basement membrane
Collagen sheet deposition in sub-mucosa
Smooth muscle hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Briefly state the steps in the asthma inflammatory cascade

A

Genetic predisposition + triggers cause:
Eosinophilic inflammation

Release of mediators and TH2 cytokines

Twitchiness (AKA hyper-reactivity)

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

Describe the genetic predisposition + trigger step of the asthma inflammatory cascade and interventions for this stage

A

No. of genes that interact, e.g: can be inherited from parents with asthma, allergic eczema, allergic rhinitis, etc

+

Trigger factors (dust mites, virus, allergens, chemicals - chlorine -, nutrition - lack of vitamin D)

Nothing can be done about genetic predisposition but triggers can be avoided sometimes

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

Describe the eosinophilic inflamamtion step of the asthma inflammatory cascade and interventions for this stage

A

Sensitive to corticosteroids (body produces cortisol so a synthetic analogue can be given)
Cromones can be used to melt away mast cells - not used as often now

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the mediator/TH2 cytokine release step of the asthma inflammatory cascade and interventions for this stage

A

Mediators release include histamine, leukotriene 4 (LT-4)
Anti-histamines can be given

Antibody released is IgE, so can give Anti-IgE

TH2 cytokines are also released, like interleukin 5 (IL-5) - can be blocked by mepolizumab (monoclonal antibodies)

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

Describe the hyper-reactivity step of the asthma inflammatory cascade and interventions for this stage

A

Mediators and TH2 cytokines sensitise airway smooth muscle - causing twitchiness (hyper-reactivity)

Treated using bronchodilators, which relax smooth muscle (β2-agonists and muscarinic antagonsists)

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

Difference between β2-agonists and muscarinic antagonists?

A

β2-agonists mimic sympathetic pathway to cause bronchodilation

Muscarinic antagonists block parasympathetic receptors (muscarinic receptors - M1, M3) to prevent constriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe how asthma can be recognised

A

Symptoms/exacerbations - typically, occur at night (diurnal) as eosinophilic activation occurs
Airflow obstruction - can be measured using simple pulmonary function tests
Bronchial hyper-responsiveness - difficult to measure
Airway inflammation

Bronchoscope + biopsy is only used for research purposes as too invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Compare a histological image of normal airway and asthma airway (inflammation)

A

Normal - orderly with a pseudostratified columnar epithelium, sharp basement membrane and few eosinophils
Asthma - desquamation, thicker basement membrane and more eosinophils

18
Q

Describe corticosteroids and their importance

A 
ONLY class of drugs proven to convert disorganised airway to organised is inhaled corticosteroid
Reduced inflammation, airway remodelling and mortality 
Thus, it is the mainstay of first-line treatment for inflammation
19
Q

How to assess symptoms?

A

ASK ABOUT TRIGGERS
Symptoms can occur/worsen in presence of:
Allergens - animal dander, dust mites, pollen, fungi
Others - exercise, viral infection, smoke, cold, chemicals (like chlorine) and drugs (most important are NSAIDs and β-blockers)

Always consider drug therapy as a possible cause of symptoms

20
Q

Clinical presentation/characteristics of asthma?

A

EPISODIC symptoms and signs
DIURNAL variability - nocturnal/early morning
NON-PRODUCTIVE cough
TRIGGERS
ASSOCIATED atopy (other allergic problems like rhinitis, conjunctivitis and eczema)
FAMILY HISTORY of asthma
WHEEZING - turbulent air flow

21
Q

Methods of diagnosing asthma?

A

History and examination
DIURNAL variation of peak flow rate - prescribe peak flow monitor and ask patient to keep a record
Reduced forced expiratory ratio (FEV1/FVC 15%)
Provocation testing to induce bronchospasm by:
Exercise
Histamine/metacholine/mannitol exposure

22
Q

Describe the COPD disease process

A

Noxious particles/gases, SMOKERS
causes NEUTROPHILIC inflammation leading to:
Damage of mucociliary escalator (paralysed cilia)
Tissue damage in bronchial and alveolar walls

Causes development of OBSTRUCTION and ongoing disease progression, that is only PARTIALLY REVERSIBLE SOMETIMES

23
Q

Characteristics of COPD?

A

Exacerbations

Reduced pulmonary function

24
Q

Symptoms of COPD?

A

Breathlessness

Worsening/progressing quality of life

25
Q

Normal airway compared to one affected by COPD?

A

Normal - airway held open by alveolar attachments, normal mucous secretion and no inflammation
COPD - disrupted alveolar attachments (emphysema)
Mucus hypersecretion (luminal obstruction) - due to hyperplasia of goblet cells
Mucosal & peribronchial inflammation and fibrosis (obliterative bronchiolitis)

26
Q

Disease processes in COPD?

A

Exposure to cigarette smoke causes lung inflammation, leading to COPD if normal protective/repair mechanisms are overwhelmed/defective
Activate alveolar macrophages and airway epithelial cells - release neutrophil chemotactic factors, like IL-8 and LT-B4
Neutrophils and macrophages release proteases that breakdown connective tissues in lung parynchema and also stimulate mucus hypersecretion

Cytotoxic T cells (CD8+ lymphocytes) - may be involved in inflammatory cascade (perhaps, in destruction of alveolar walls epithelial cells

27
Q

Physiological mechanisms that combat COPD and how this can present in COPD?

A

Proteases released by macrophages and neutrophils are normally counteracted by PROTEASE INHIBITORS, like α1-antitrypsin, secretory leukoprotease inhibitor (SLPI) and tissue inhibitors of matrix metalloproteinases

In COPD, appears to be an IMBALANCE between PROTEASES and ANTI-PROTEASES (either increase in proteases or a deficiency of anti-proteases) leading to inflammatory changes in airways, including respiratory mucosa damage

28
Q

Two disease processes of COPD?

A

Chronic bronchitis

Emphysema

29
Q

Chronic bronchitis features in COPD?

A 
Chronic neutrophilic inflammation
Mucus hyper-secretion
Mucociliary dysfunction
Altered lung microbiome (different flora from normal)
Smooth muscle spasm and hypertrophy
PARTIALLY REVERSIBLE
30
Q

Emphysema features in COPD?

A

Alveolar destruction
Impaired gas exchange
Loss of bronchial support
IRREVERSIBLE

31
Q

Describe the protease imbalance in emphysema?

A

Genes coding for antiproteases

Smoking causes protease production which causes alveolar destruction and emphysema, when they overwhelm the anti-proteases

32
Q

Assessment of COPD?

A

Assess symptoms
Assess degree of airflow limitation using spirometry
Assess risk of exacerbations
Assess co-morbidities, as smoking can contribute to ischaemic heart disease and heart failure

33
Q

Indicators of high risk?

A

2+ exacerbations within the past year

FEV1

34
Q

Clinical presentation/characteristics of COPD?

A 
Chronic symptoms - not episodic
Smoking is big indicator
Non-atopic (not in response to allergen)
Daily productive cough 
PROGRESSIVE breathlessness
Frequent infective exacerbations
Chronic bronchitis - WHEEZING
Emphysema - REDUCED BREATH SOUNDS, when listening with stethoscope
35
Q

Describe the chronic cascade in COPD?

A

Progressive fixed airflow obstruction
Impaired alveolar gas exchange
Respiratory failure - decreased PaO2 and increase PaCO2
Pulmonary hypertension
Right ventricular hypertrophy and failure (right ventricle must work harder) - COR PULMONALE and has a high mortality
Death

36
Q

How to prevent COPD progression?

A

Stopping smoking arrests further decline in lung volume

37
Q

How is the severity of COPD determined?

A

GOLD stages

38
Q

Non-pharmacological management of COPD?

A

Smoking cessation
Immunisation against influenza and pneumococcal
Physical activity
Oxygen - domiciliary
Venesection (removal of increased rbcs caused by polycythaemia in hypoxia)
Stenting - replaced lung volume reduction surgery

39
Q

Pharmacological management of COPD?

A

LAMAs - Tiotropium or Aclidinium
LABAs - Salmeterol or Formoterol
LAMA-LABA combination - Aclidinium and Formoterol together
LABA-ICS combination - Beclometasone and Formoterol together
PDE4I - Roflumilast
Mucolytic - Carbocisteine
Antibiotics - azithromycin

40
Q

EXAMS

Compare asthma to COPD with asthma on left and COPD on right?

A

Non-smokers vs smokers
Allergic vs non-allergic
Early/late onset vs late onset
Intermittent symptoms vs chronic symptoms
Non-productive cough vs productive cough
Non-progressive vs progressive decline
Eosinophilic inflammation vs neutrophilic inflammation
Diurnal variability vs no diurnal variability
Good corticosteroid response vs poor corticosteroid response
Good bronchodilator response vs poor bronchodilator response
Preserved FVC and TLCO vs reduced FVS and TLCO
Normal gas exchange vs impaired gas exchange

41
Q

What is TLCO?

A

Diffusing capacity/transfer factor of lungs for carbon monoxide (CO)
Extent to which oxygen passes from the air sacs of the lungs into the blood

Pharmacology (17 decks)

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