Brainscape's Knowledge GenomeTM

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


See full index

(ZUZ) Respiratory MED > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD?

A

COPD is a progressive obstructive airway disease that is not fully reversible and encompasses chronic bronchitis and emphysema.

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

What is chronic bronchitis ?

A

Chronic inflammation of the airways.
Clinical term relating to a chronic productive cough for at least 3 months over two consecutive years.

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

What is emphysema?

A

Typically refers to abnormal airspace enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis.

Emphysema is characteristically panlobular with a lower zone predominance. This is compared to emphysema from smoking, which is characteristically centriacinar.

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

Causes of COPD?

A
  • Smoking
  • alpha- 1 anti-trypsin deficiency
  • Recurrent childhood infections
  • Occupational exposure
  • Household exposure to burning coal or biomass fuel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does Chronic bronchitis lead to in the airways?

A
  • Goblet cell hyperplasia
  • Mucus hypersecretion
  • Chronic inflammation and fibrosis of small airways
  • Narrowing of small airways
  • Loss of cilial function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology?

A

Inflammatory processes lead to the production of proteases by inflammatory cells such as macrophages and neutrophils.
The protease elastase causes the destruction of elastin, a protein important to the structural integrity of the alveoli.
Loss of elastin has two effects:

  • Collapse: the alveoli are prone to collapse.
  • Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring alveoli forming bullae.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can you get cor pulmonale in COPD?

A

Chronic hypoxia → vasoconstriction of pulmonary arteries → elevated pulmonary arterial pressure → chronic elevation of pulmonary arterial pressure → right heart failure

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

Differentials?

A
  • lung cancer
    -asthma
  • fibrosis
  • heart failure
  • pulmonary embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Symptoms

A
  • Chronic Shortness of breath
  • Chronic Productive cough
  • White sputum
  • Frequent episodes of ‘bronchitis’
  • Wheeze
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Signs?

A
  • Barrel chest
  • Dyspnoea
  • Pursed lip breathing
  • Wheeze
  • Coarse crackles
  • Loss of cardiac dullness
    -Downward displacement of liver
  • Signs of CO2 retention
  • signs of cor pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MRC dyspnoea score ? 1-5

A

1- I only get breathless with strenuous exercise
2- I get short of breath when hurrying on level ground or walking up a slight hill
3- On level ground, I walk slower than people of my age because of breathlessness, or I have to stop for breath when walking at my own pace on the level
4- I stop for breath after walking about 100 yards or after a few minutes on level ground
5- I am too breathless to leave the house or I am breathless when dressing/undressing

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

How to diagnose COPD?

A

Clinical picture + spirometry

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

What will Spirometry show ?

A
  • Obstructive picture on spirometry
    • FVC:may be normal but often reduced due to air trapping.
    • FEV1:reduced
    • FEV1/FVC:< 70% (<75%?)
  • Spirometry does not show reversibility with salbutamol (bronchodilator)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bedside investigations

A
  • Obs- pulse oximetry
  • ECG
  • Sputum culture- infection
  • BMI
  • ABG- if hypercapnia or hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bloods investigations

A
  • FBC - anaemia and polycythaemia
    -Alpha-1 antitrypsin levels
  • U&Es
  • CRP
  • TLCO-Transfer factor for carbon monoxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Imaging investigations? what findings

A

CXR- hyperexpanded, flattened hemidiaphragm,- Hypodense, Saber-sheath trachea

CT scan- only if:
- Symptoms disproportionate to spirometric assessment
- Alternative diagnosis suspected (e.g. bronchiectasis, fibrosis)
- Lung cancer suspected or to investigate abnormalities on chest x-ray

Echo- only if:
cor pulmonale suspected.

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

Grading of COPD using FEV1

A

Using predicted FEV1- average FEV1 in a population of similar age, sex and body composition

  • stage 1: FEV above 80% of predicted
  • stage 2: FEV1 50-79% of predicted
  • stage 3: FEV1 30-49% of predicted
  • stage 4: FEV1 less than 30% of predicted
18
Q

Overview of COPD care

A
  • Education: about their condition and check inhaler technique
  • Smoking cessation
  • Vaccination: seasonal influenza vaccine and the pneumococcal vaccine
  • Pulmonary rehabilitation
  • Self-management plans
  • Management of co-morbidities
  • Pharmacotherapy
19
Q

Pharmacological management

A

Inhaled therapy:
Step 1- SABA or SAMA
Step 2- LABA +LAMA or if steroid responsive= LABA+ ICS
Step 3- Triple therapy- LABA+LAMA+ICS
If ongoing symptoms or acute exacerbations despite optimal treatment try ORAL treatment options, nebulisers and consider assessment for LTOT

20
Q

Evidence of steroid responsiveness or asthmatic features? for ICS treatment

A
  • previous diagnosis of asthma or atopy
  • a higher blood eosinophil count
  • substantial variation in FEV1 over time (at least 400 ml)
  • substantial diurnal variation in peak expiratory flow (at least 20%)
21
Q

For triple therapy in what cases would you try this?

A

Already on LABA + LAMA:
- 3 month trial of triple therapy if clinical features impact quality of life. If no improvement, revert back to LABA + LAMA only
- offer triple therapy if 1 severe or 2 moderate acute exacerbations within one year.

Already on LABA + ICS:
offer triple therapy if clinical features impact quality of life or 1 severe or 2 moderate acute exacerbations within one year

22
Q

Severe long term management

A
  • salbutamol (SABA) or ipratropium (SAMA) nebs
    -oral theophylline: Many interactions and requires monitoring levels. At risk of toxicity.
  • oral mucolytics
  • long term prophylactic Abx (eg. azithromycin)
  • LTOT
23
Q

What surgical interventions can you have in COPD?

A
  • Lung reduction surgery
  • Bullectomy
  • Lung transplantation
24
Q

COPD discharge CARE BUNDLE- 5 points

A
  1. Assessment of inhaler technique
  2. Self-management action plan and an emergency drug pack
  3. Smoking cessation
  4. Access to a treatment programme that can help people with a lung condition stay active (pulmonary rehabilitation)
  5. Follow-up arrangements
25
Q

Outpatient COPD management

A
  • COPD Care bundle
  • Smoking cessation
  • Pulmonary rehab
    -Diet

Pharmacological:
- Bronchodilators
- Antimuscarinics
- Steroids
- Oral mucolytics
- LTOT

Surgery
- LUNG VOLUME Reduction

26
Q

What is the role of pulmonary rehabilitation in COPD treatment?

A

-aims to optimise thephysical and social performance of patients suffering from long-term chronic lung conditions like COPD.
- Break the cycle of avoiding exercise and physical activity due to SOB which leads to weakened muscles and doing less
- This vicious cycle leads to increasing social isolation, depression and worsening of symptoms

27
Q

What do they do in Pulmonary rehabilitation? Who is it used for and who not?

A

an MDT 6-12 week programme of
supervised exercise,
unsupervised home exercise,
nutritional advice
disease education
Breathing techniques

Pulmonary rehabilitation is offered to any patient with COPD who feels disabled by their condition.

It isnotsuitable:
- cant walk
- Recent MI
- unstable angina

28
Q

LTOT -When are patients considered

A
  • very severe airflow obstruction (FEV1 < 30% predicted)
  • cyanosis
  • polycythaemia
  • peripheral oedema
  • raised jugular venous pressure
  • oxygen saturations less than or equal to 92% on room air
29
Q

LTOT- Criteria

A

Long-term oxygen therapy(LTOT) is reserved for patients who meet the following criteria:

  • Arterial Pa02< 7.3 kPa,OR
  • Arterial Pa02< 8 kPawith any of:
    • Pulmonary hypertension
    • Peripheral oedema
    • Secondary polycythaemia
30
Q

How many hours a day is LTOT used?

A

LTOT to be used at least 16 hours/day for a survival benefit

31
Q

Why may uncontrolled oxygen be potentially dangerous in someone with COPD?

A

CO2 retention can occur as administering oxygen reverses Hypoxic pul vasoconstriction
This allows blood flow to non ventilated alveoli which increases the V/Q mismatch
This leads to CO2 not having enough ventilated alveoli to allow diffusion out of the blood stream
Hypercapnia caused = Resp acidosis

32
Q

What is the oxygen in LTOT treating

A

oxygen is not a treatment for breathlessness; it is a treatment to help prevent organ hypoxia

33
Q

Complications of COPD

A
  • Respiratory failure
  • Pneumonia: often recurrent
  • Pneumothorax: rupture of bullous disease
  • Polycythaemia or anaemia
  • Depression
34
Q

What interventions alter prognosis (Mortality) of patients in COPD

A
  • LTOT
  • Pul rehab
  • Smoking cessation
35
Q

What are the 2 types of COPD exacerbations?

A

Infective
- Change in sputum volume / colour
- Fever
- Raised WCC +/- CRP

Non-infective
- PE

36
Q

Clinical features of acute exacerbation

A
  • Worsening breathlessness
  • Worsening cough
  • Increased sputum production
  • Change in sputum colour
37
Q

Investigations:acute exacerbation

A
  • Arterial blood gas(ABG)
  • Cultures: Blood (if pyrexial- ?sepsis), sputum
  • Electrocardiogram(ECG): arrhythmias or evidence of heart strain
  • Bloods: FBC, U&E, CRP
  • Chest x-ray: look for pneumonia, PE
  • Theophylline levels(if part of admission medications)
37
Q

Management : acute exacerbations

A
  • A-E approach
  • Give O2 via fixed performance face mask (Venturi masks if non-rebreathe causing retention) due to risk of CO2 retention
  • Nebs of salbutamol and ipratropium
  • Steroids- Oral prednisolone
  • ABx- if raised CRP/WCC or purulent sputum
  • CXR
  • consider IV aminophylline
  • if pH below 7.25 consider referral to ITU
38
Q

Why is there respiratory acidosis in COPD?

A
  • PaO2< 8 kPa andraised PaCO2 >6.5 KPa
  • retained CO2 decreases the pH of the blood, usually seen in acute exacerbation of COPD when the kidney can’t release bicarbonate quick enough in response to the increased CO2
39
Q

What does raised bicarbonate in COPD suggest?

A

CO2 is chronically retained causing bicarbonate to be released by the kidneys in response to the acidosis over an extended period of time causing compensation and therefore a normal pH

40
Q

Describe type 1 respiratory failure

A

PaO2< 8 kPa or <90% o2 sats on air
low/normal pCO2 (only one affected)

41
Q

Describe type 2 respiratory failure

A

PaO2< 8 kPa and raised PaCO2 >6.5 KPa (two affected)

(ZUZ) Respiratory MED (21 decks)

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