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CSI > COPD > Flashcards

COPD Flashcards

1
Q

Dyspnoea

A

Difficulty breathing (breathlessness)

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2
Q

What is breathlessness

A

And acute or chronic onset of shortness of breath and difficulty breathing (dyspnoea)

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3
Q

Why does breathlessness occur

A

The body needs more oxygen than it is getting

So you breathe faster to try and increase the flow of oxygen rich air into the lungs where it can exchange to the bloodstream

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4
Q

Who is affected by breathlessness

A

Everyone when they exercise especially if overweight or unfit

Or due to a serious underlying medical condition
E.g. pneumonia, asthma, lung and heart disease (smokers)

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5
Q

How can breathlessness be measured

A

MRC scale (1-6)

1- no breathlessness
6- too breathless to leave the house

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6
Q

What is a pulmonary embolus

A

Clot originating in the vein in the leg which moves to the lung -> coughing blood, shortness of breath and stabbing pain in chest when breathing

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7
Q

Causes of short term or acute breathlessness

A

Asthma
Pneumonia
COVID
COPD
Heart disease
PE
Anxiety
Some medicines
Anaemia

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8
Q

Causes of long term or chronic breathlessness

A

Obesity
Asthma (not well controlled)
COPD
Heart failure
Heart rhythm problems (af)
Anaemia

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9
Q

Investigations to breathlessness questions

A

Acute or chronic onset
Any triggers
How far can patient walk
Ill, high temp, weight loss or cough, pain in chest
Cough in phlegm or blood
In contact w anyone with tb
Ne bound or on a long flight
Smoke?

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10
Q

Investigations

A

CXR
check heart and bp
Lung function test
Blood tests (anaemia, under active thyroid, heart failure)

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11
Q

Respiratory differential diagnoses for shortness of breath

A

Asthma
COPS
Pulmonary fibrosis
Lung cancer
PE
Pneumothorax
Lower respiratory tract infection

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12
Q

Cardiovascular/ systemic differential diagnosis for shortness of breath

A

Congestive heart failure
Pulmonary oedema
Vascular defects
Acute coronary syndrome
Anaemia
Renal or liver failure
Deconditioning

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13
Q

Decondition

A

Change following a period of inactivity, bed rest, sedentary lifestyle

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14
Q

Is there chest pain?

A

Indicative of cardiac causes - lung doesn’t have many pain fibres

Except for lung pleura w.g. Pleural effusion or pneumonia

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15
Q

Pleural effusion

A

Collection of fluid in pleural space

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16
Q

Have you travelled overseas recently?

A

Rule out TB

Long haul travel- PE

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17
Q

What is orthopnea

A

Breathlessness lying flat

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18
Q

Do you have breathlessness lying flat?

A

Orthopnea

Can indicate heart failure

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19
Q

Being immobilised, long haul travel?

A

PE

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20
Q

Question coughing

A

Productive
Colour, consistency
Frequency
Anything making better or worse

COVID, COPD, lower respiratory infections, pulmonary fibrosis, pneumonia, lung cancer

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21
Q

Systemic symptoms?

A

Fever
Weight loss
Night sweats

Indicate infections nad malignancies

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22
Q

How to OBTAIN fev1 and fvc results

A

Patient inhales as much as possible then exhales forcefully into spirometer as hard and fast as possible

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23
Q

FVC

A

Forced vital capacity- maximum air that can be forcefully exhaled from the lungs

Est. 4.1L

24
Q

FEV1

A

Forced expiratory volume in 1 second- amount of air that can be forcefully exhaled in one second

Est. 3.7L

25
Q

FEV1/FVC below 0.7

A

Obstructive

26
Q

Obstructive disease

A

Difficult getting air OUT of the lungs

Air expelled more slowly- FEV1 is lower

Filling of lungs is less affected so FVC closer to normal

FEV1FVC ratio is therefore decreased (less than 0.7)

27
Q

Restrictive disease

A

Difficulty filling lungs completely

FVC lower

FEV1 affected proportionately

Therefore fev1/fvc roughly same

28
Q

Examples of restrictive lung disease

A

Pulmonary fibrosis
Neuromuscular disorders
Congestive cardiac failure
Sarcoidosis
Obesity

29
Q

Examples of obstructive lung disease

A

COPD
Asthma
CF

30
Q

What is pulmonary fibrosis

A

Lung tissue scarring

Healthy tissue replaced by thick scarred tissue (difficult for lungs to inflate)

31
Q

Sarcoidosis

A

Inflammatory cells form clumps called granulomas

Healthy tissue replace by damaged - difficult to inflate

32
Q

Neuromuscular disorders

A

Nervous innervations of muscles needed for inhalation - problems expanding chest wall and so lungs can’t inflate fully

33
Q

Obesity

A

Inhaling against excess weight requires extra effort - difficulty filling

34
Q

Congestive cardiac failure

A

Inability of the heart to pump blood efficiently
Unable to meet oxygen demand
Increasing force of contractions
Heart becomes bigger (cardiomegaly)

Lungs have less space to inflate so cannot fill fully

35
Q

Chronic bronchitis

A

Increase in number of goblet cells
Mucous gland hypertrophy
Mucous hyper-secretion and chronic inflammation

Airway narrowing

Persistent coughing with SPUTUM to try and remove mucus

36
Q

Emphysema

A

Alveolar walls are broken down
Formation of large airspaces (less SA for gas exchange)

Elastin fibres that hold the airways open during exhalation are lost
Airways collapse early in exhalation (due to loss of elastic recoil)
Excess air retained in lungs instead of being fully exhaled- hyperinflation

37
Q

Two Pathophysiological processes in COPD

A

Chronic bronchitis and emphysema

38
Q

Hyperinflated CXR

A

More than 7 anterior ribs visible

Flattening of diaphragm

Heart small and narrow (floating heart sometimes)

Seen with COPD

Flattened diaphragm pulls mediastinum down making heart look narrower and smaller
Extreme hyperinflation indicated by air under heart (floating)

39
Q

Counting anterior ribs

A

Count the ribs visible at mid clavicular line until final rib intersects the diaphragm

Should be 5-7,, more than 7 indicated hyperinflation

40
Q

Cigarette induced lung damage

A

Components of cig smoke activate macrophages in lungs which recruit neutrophils and release proteases, neutrophils release proteases and oxidants, smoke also contains oxidants

These are required in the lung but need to be balanced with anti-proteases and anti-oxidants

In excess these damage lung parenchyma leading to emphysema and induce inflammation (bronchitis)

41
Q

Nicotine replacement

A

Has negative effects in cardiovascular system but does not damage the lungs and so will remove the damage on lungs

42
Q

Smoking cessation on pathophysiological processes of COPD

A

Bronchitis can be reversed
Emphysema cannot

43
Q

Smoking cessation methods

A

Non drugs:
- nicotine replacement therapy (nrt)
-behavioural changes
-counselling
-GP support

Drugs
- varenicline
- bupropion
Interfere with dopamiegic-induced reward to lessen reward after smoking

44
Q

Nutrition with COPD

A

Low carb diet (less co2 generated)

Fruit and veg contain anti oxidants

Anti inflammatory components (vitD, omega3)

45
Q

Avoiding lower respiratory tract infections

A

Vaccinations
Wearing masks
Washing hands
Home environment (damp)

46
Q

Sympathetic influence on airway

A

No sympathetic nerve

Sympathetic influence occurs via circulating adrenaline and noradrenaline which penetrate the lung and act on beta 2 receptors

Dilates the airway smooth muscle - widening the airway

47
Q

Parasympathetic influence on airway

A

Parasympathetic nerve innervates the lung, NT involved is Ach

Contracts airway smooth muscle- narrowing airways

48
Q

Beta agonists on airway

A

Mimics the sympapatheric nervous system activating beta 2 receptors to dilate the airways

Class of bronchodilator

49
Q

Muscarinic antagonists on airway

A

Antagonises the parasympathetic nervous system blocking muscarinic m3 receptors to dilate the airways

SAMA- ipratropium bromide
LAMA- tiotropium, gkycopyrronium

50
Q

Rescue vs maintenance therapy

A

Rescue - reliever: taken during an episode of breathlessness. Short acting e.g. bronchodilator SABA (salbutamol)

Maintenance- longer lasting e.g. long acting bronchodilator LABA (salmeterol, formoterol)

51
Q

If a patient is breathless even on maintenance therapy

A

Combine drugs e,g, LABA & LAMA

Results in an added effect

52
Q

Inhaled corticosteroids

A

Steroids are anti-inflammatory (good for COPD)
Powerful immunosuppressants (bad for COPD)

Used in asthmatic traits or combined with beta agonists to restore sensitivity of ASM

53
Q

Long term beta agonists

A

ASM cells reduce number of beta 2 receptors

ICS restore this sensitivity

54
Q

Inhalation as a delivery method benefits

A

Drug gets sent exactly where it needs to go

55
Q

Inhalation as a delivery method drawbacks

A

Only about 10% gets deep enough into lung for effect
Patient needs to be trained
Drug can get into systemic circulation as lung tissue is heavily perfused with blood

CSI (4 decks)

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