Case study: Mary (COPD) Flashcards

1
Q

Who is Mary?

A

A 74 year old retired government office worker with severe COPD.

In the past month her COPD has worsened to the point in which she became breathless when getting out of bed, dressing or showering.

She has also experienced a decreased appetite and has lost 2 kg in the past month.

This has significantly impacted on her ability to engage in everyday activities, prompting admission to hospital.

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2
Q

What caused mary’s recent hospital admission?

A

Breathlessness.

She’s fine sitting but as soon as she tries to walk has issues.

Has to “feel” like going out. Struggles with groceries; has to hold onto trolley.

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3
Q

What are the effects of Mary’s condition on her family?

A

Husband: Where they shop depends on whether Mary can enter the store or not. (If you have to go upstairs or if they cannot find a park closer means he will do it by himself).

Hubby gets worried- Watches her, and is alert. If she takes too long on the toilet. thinks “why is she taking so long”. “Big drain on the family”. “Still love her”.

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4
Q

What are mary’s previous hospital admissions?

A

Mary has been admitted to hospital three times in the past two years for exacerbations of her COPD.

“Been in hospital a few times. They have managed to get me stable enough to go back home”

Hospital admission october last year “Was really ill. Didn’t think I was going to come out”. Was bring up a lot of “muck”. “Lots of congestion in the lungs”. Septum was all colours- green, yellow… no blood.

Dr said to breath out fully, then cough. This technique helped mary get the mucous out.

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5
Q

What are the general risk factors for COPD?

A

Main risk factor is smoking.

Other risk factors include
- Environmental irritants/ pollution
- Asthma
- Family hx/ Genetics
- Frequent resp infections as a child
- Age

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6
Q

What COPD risk factors did Mary specifically have?

A
  • Smoking 10 cigarettes per day for 40 years.
  • Family hx. 3 people have passed away in her family due to COPD.
  • Social welfare work: Being exposed to environmental irritants. “Dropping muck”.
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7
Q

What is the genetic risk factor for COPD?

A

Alpha-1 anti-trypsin (AAT) deficiency

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8
Q

How does smoking contribute to the development of COPD?

A

Long term exposure to irritants associated with smoking leads to an inflammatory response in the resp tract.

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9
Q

What does smoking do to the alveoli?

A

Smoking causes an increase in oxidants and a protease-antiprotease imbalance. This causes tissue/protein breakdown, which leads to enlarged air spaces and decreased surface area for gas exchange.

Protease- Enzymes that break down protein.
Antiproteases- Inhibit protease/ protein breakdown and modulate immune responses in the lung.

COPD protease outweighs antiproteases.

Smoking leaves carbon deposits in the air spaces

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10
Q

What does smoking do to the bronchioles?

A

Inflammation from smoking causes bronchial edema, impaired cilia function, and increase mucus production.

Therefore causing narrowed airways and a greater airway resistance.

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11
Q

What are general signs of COPD?

A
  • Barrel chest
  • Blue tinged lips
  • Chronic cough
  • Pursing lips with breathing
  • SOB on exertion
  • Use of accessory muscles
  • Laboured breathing
  • Finger clubbing
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12
Q

What signs of COPD did mary have?

A
  • Breathlessness
  • SOB
  • Dyspnea/laboured breathing
  • Pursed lips breathing
  • Barrel shaped chest
  • Increased expiratory effort
  • Use of accessory muscles
  • Slightly blueish tinged lips
  • Wheezing
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13
Q

What are the two main kinds of COPD?

A

Emphysema & bronchitis

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14
Q

What is emphysema?

A

Inflammation that causes destruction in the alveoli and capillaries.

Causes a decrease in alveolar surface area for gas exchange.

The destruction of alveoli tissue also includes the breakdown of elastin; Which decreases expiratory airflow leading to trapping and a further reduction in the volume of exchangeable air.

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15
Q

What is chronic bronchitis?

A

Inflammation of the bronchioles leading to bronchial edema, increasec mucous production and decreased ciliary action.

Causing an increase of airway resistance, therefore decreasing the volume of of air flowing in/out of the lungs for gas exchange.

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16
Q

What kind of COPD does mary have?

A

Emphysema and chronic bronchitis

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17
Q

What are the conclsuions of Marys COPD?

A

Principle symptom and complaint is SOB on effort. Progressive over the period of 8 to 10 years.

Shes thin.

Grosley increased WOB.

When she gets a winter chest infection- She decompensates and tips into respiratory failure. At risk of losing her life due to hypoxia, or retention of carbon dioxide (Hypercapnia).

Once in a while will get ankle swelling. Secondary to R) sided heart problems; complication of her COPD.

Lifestyle severely impacted by SOB.

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18
Q

What does alveolar tissue damage result in?

A

As a consequence of alveolar tissue damage, air spaces enlarge and air is trapped in the lungs at the end of expiration. Gradually the residual volume (RV) increases, causing hyperinflation.

This causes a further reduction in the volume of exchangeable air.

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19
Q

What are consequences of hyperinflation?

A

Hyperinflation of the lungs flattens the diaphragm, causing it to become less effective at regulating the pleural pressures necessary for efficient breathing.

Therefore, the chest and neck muscles must work harder to assist with breathing.

This increases the work of breathing significantly, and thus patients suffer from dyspnoea.

Patients often breathe faster in an effort to ventilate their lungs normally.

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20
Q

During pulmonary function tests, what does hyperinflation show up as?

A

Hyperinflation of the lungs is also demonstrated by an increase in functional residual capacity (FRC).

Characteristically, expiration becomes prolonged relative to inspiration.

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21
Q

What do you see in Marys chest xray that is different to a normal persons chest xray

A
  • Marys lungs take up more space in the chest cavity.
  • Marys heart is pushed out of position by her over-inflated lungs
  • Marys clavicles are pulled up superiorly (Due to increased action of accessory muscles to breathe)
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22
Q

How does Marys expanded ribcage make breathing harder?

A

The expanded rib cage makes it more difficult to reduce intrathoracic pressure during inspiration

23
Q

How does increased airway resistance make it harder to breathe?

A

Increased airway resistance means that higher pressures must be generated to force air out of the lungs during expiration.

24
Q

As the COPD worsens, what happens at the end of expiration?

A

There is an increase in PCO2 (partial pressure of carbon dioxide), and a decrease in PO2 (partial pressure of oxygen) in the alveolar air at the end of expiration.

25
Q

What issues are associated with an increase of PCO2 and a decrease in PO2

A
  • respiratory acidosis
  • metabolic acidosis
  • cyanosis
  • tissue wasting/emaciation
  • pulmonary hypertension & cor pulmonale
  • respiratory failure
26
Q

What are some complication of marys COPD?

A
  • Bluish lips (sign of cyanosis)
  • Thin
  • Occasional ankle edema (sign of R) HF)
  • Episodes of acute respiratory failure
27
Q

What was noted on Marys Physical examination

A

Her breathing was quiet, but labored, and she exhibited a barrel chest.

Her respiratory rate was 20 breaths/min.

  • Her chest movements were poor, but symmetrical
  • Accessory inspiratory muscles, and increased expiratory effort.

Listening to her chest revealed very quiet breath sounds.

There were occasional crepitations and scattered rhonchi (also known as fine and coarse crackles).

Crepitations: A rattling or crackling sound like that made by rubbing hair between the fingers

Rhonchi: A rattling sound similar to snoring that can be heard when listening to the chest on breathing. Rhonchi are caused by an airway obstruction due to inflammation, mucous secretions or bronchial muscle spasms.

28
Q

Which laboratory tests would you expect for a routine COPD admission?

A
  • Blood gasses and PH
  • Septum sample
29
Q

Which investigations would you expect for a routine COPD admission?

A
  • Pulmonary function tests
  • Chest x-ray
  • ECG
30
Q

What is a arterial blood gas for?

A

Checks oxygen status and acid balance

31
Q

What is peak expiratory flow for? (PEF)

A

Measures how quickly you can exhale

32
Q

What is body plethysmography?

A

Measures thoracic volume and airway resistance

33
Q

What is forced expiratory volume? (FEV)

A

Tests how much air you can exhale in 1 second

34
Q

What is diffusing capacity?

A

Tests oxygen transfer from the alveoli to circulation

35
Q

What is sputum sample?

A

Used to diagnose bacterial lung infection

36
Q

Why in COPD patients will you often see a raised hemoglobin level, red blood cell count and hematocrit?

A

The body’s attempt to compensate for the lower PO2 by increasing the O2 carrying capacity of the blood.

37
Q

What does raised PCO2 lead to?

A

Chronic respiratory acidosis

These patients are prone to acute respiratory infections which may precipitate them into acute respiratory failure.

38
Q

What is the most common pulmonary function test?

A

Spirometry

39
Q

What is the purpose of Spirometry?

A

The spirometer records inspiratory and expiratory lung volumes, and how fast a patient can inhale/exhale.

Spirometry is used to help diagnose or monitor conditions such as COPD, asthma and cystic fibrosis.

40
Q

What is a the pneumotachometer?

A

A pneumotachometer is an alternative to using a spirometer.

It uses flow rate to measure volume. This is achieved by a fine mesh in the flowhead – as air is breathed through the mesh, it creates a pressure difference across the mesh and this difference is proportional to flow rat

41
Q

In respiratory tests what volumes are generally increased?

A

Residual volume and total lung capacity

42
Q

What indicators on Mary M’s pulmonary function test suggest COPD.

A

Increased residual volume (RV)

Increased functional residual capacity (FRC)

Increased total lung capacity (TLC)

Reduced vital capacity (VC)

Reduced forced vital capacity (FVC) and forced expired volume in 1 second (FEV1)

43
Q

Why is lung elasticity important?

A

Mary M’s emphysema is associated with a loss of lung elasticity.

Elasticity plays an important role in expiration. Elastic recoil compresses air in the lungs, generating pressures that force air out.

Without this elastic recoil, it is harder for Mary M to generate the pressures required to drive expiration.

Elastic tissue also helps maintain airway structure, preventing involuntary airway closure during expiration.

Loss of this elastic tissue means that Mary M’s airways are prone to collapse during expiration.

This also results in expiration ending prematurely, and air becoming trapped in the lungs.

This trapped air increased Mary M’s residual volume, which is correlated with a decrease in vital capacity.

44
Q

What are Common medications for COPD?

A
  • Beta-agonists (bronchodilator)
  • Anticholinergics (bronchodilator & mucus reduction)
  • Corticosteroids
  • Oxygen
45
Q

What are Beta-agonists?

A

Bind to beta2 adrenergic receptors on bronchiole smooth muscle, stimulating bronchodilation.

There are various forms, including short acting and long acting.

46
Q

What are Anticholinergics?

A

Block muscarinic acetylcholine receptors on bronchiole smooth muscle, preventing bronchoconstriction and therefore allowing bronchodilation.

47
Q

What are Corticosteroids?

A

Anti-inflammatory agents used to decrease the inflammatory response

48
Q

What is Oxygen used for?

A

Low-level oxygen therapy may be used to maintain adequate oxygen saturation.

49
Q

Why was medication via nebuliser not optimal for mary

A

Used a variety of medications via inhaler and nebulizer.

Problem with nebuliser was she had to use it every 4 hourly. This is difficult are nebulisers are transmissible. which bounds people to their house.

50
Q

What medication is mary now on?

A
  • Salbutamol (Ventolin, short-acting β₂ adrenergic receptor agonist)
  • Seretide (Corticosteroid long-acting bronchodilator)
  • Spiriva (Anticholinergic long-acting bronchodilator)
  • Domiciliary oxygen therapy
51
Q

What is Salbutamol (Ventolin)?

A

This is a short acting beta-agonist bronchodilator

52
Q

What is Seretide?

A

This is a combined medication that includes a long acting beta-agonist bronchodilater & corticosteroid.

53
Q

What is Spiriva?

A

This is an anticholinergic used for bronchodilation

54
Q

How to use a spacer?

A

One way valve (When you breath out doesn’t go into the spacer)

Leave it to drip dry when washed.

Shake medication

Hold breath for 10 second after inhaling medication.

If you cant hold breath- one puff and four normal tidal breathes would work.

Never multi load. Medication will clump together and cannot get down into the small areas of your airway.