Week 3 (parts 1 and 2) Flashcards

1
Q

WEEK 3 - pt1

A

pathology symptoms, subjective Ax + auscultation intro

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2
Q

what are the main cardinal signs and symptoms

A
  • Cough
  • Sputum
  • Dyspnoea
  • Wheeze
  • Chest pain
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3
Q

what are the other cardinal signs and symptoms

A
  • Tachycardia and Tachypnoea
  • Blood in Sputum (haemoptysis)
  • Frequent infections
  • Cyanosis
  • Peripheral Oedema
  • Fatigue
  • Insomnia
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4
Q

What do OD, BD, TDS, QDS, PRN stand for in terms of drug history

A

 OD – once a day
 BD – twice a day
 TDS – three times a day
 QDS – four times a day
 PRN – patient required needs

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5
Q

how many lobes does the right lung have

A

3 - upper, middle, lower

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6
Q

how many lobes does the left lung have

A

2 - upper and lower

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7
Q

what are the 4 auscultation points on the right lung

A

1 - Apex, palpate and mark 2.5cm above medial 1/3 of clavicle
2 - palpate and mark rib 4 (just above and to the right of the nipple)
3 - palpate and mark rib 6 (bra line)
4 - palpate and mark rib 7 (laterally)

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8
Q

what are the 3 auscultation points of the left lung

A

1 - apex, palpate and mark 2.5cm above medial 1/3 of clavicle
2 - palpate and mark rib 6 (bra line)
3 - palpate and mark rib 7 (laterally)

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9
Q

what are the 4 auscultation points (both sides) on the back

A
  • apices (upper curve of scapula)
  • superior lobes (medial curve of scapula)
  • Inferior/ lower lobes (slightly lateral and lower to superior lobe point)
  • lung bases (lateral and lower to inferior lobe point)
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10
Q

WEEK 3 - pt 2

A

Pulmonary Pathology notes

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11
Q

What are the 3 classifications of lung disease

A
  • Tissue or vessel affected
  • Obstructive or Restrictive Lung Disease
  • Other Classifications
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12
Q

What is Tissue or vessel affected lung disease

A
  • Airways: asthma, COPD etc
  • Lung tissue: pulmonary fibrosis, sarcoidosis etc
  • Lung circulation: Pulmonary embolism, pulmonary hypertension
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13
Q

what is obstructive or restrictive lung disease

A
  • Obstructive: COPD, bronchitis etc
  • Restrictive: sarcoidosis, interstitial lung disease etc
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14
Q

what are the other classifications of lung disease

A
  • Acute
  • Chronic
  • Occupational
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15
Q

what are the 5 cardinal signs of respiratory disease

A
  1. Cough
  2. Sputum
  3. Dyspnoea (breathlessness)
  4. Wheeze
  5. Chest pain
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16
Q

what is COPD (Chronic Obstructive Pulmonary Disease)

A

 ’a common preventable and treatable disease, is characterised by persistent air flow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases..’
 Progressive lung disease
 Airflow obstruction with little or no reversibility

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17
Q

what are the causes of COPD

A
  • Smoking
  • Industrial pollutants
  • Mining
  • Bacterial infection
  • Viral infection
  • Wood, fires, biomass fuels
  • Vehicle exhaust pollution
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18
Q

what is emphysema

A

 Permanent enlargement of the alveoli
 Destruction of alveolar walls
 Lungs lose their elasticity
 Walls of terminal bronchioles and alveoli are destroyed by inflammation
 Airway collapse
 Air trapping
 Enlarged alveoli sacs-dead space
 Air trapping
 Bronchioles open on inspiration but
 collapse on expiration
 Air trapped within alveoli
 Hyperinflation-barrel chest
 Diaphragm flattens
 Ventilation capacity decreased
 Usually co-exists with chronic bronchitis
 Primarily a disease of the alveoli
 Caused by smoking or Congenital

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19
Q

what are the accessory muscles of inspiration

A

 Sternocleidomastoid
 Scalene (anterior, middle and posterior)
 Serratus anterior
 Serratus posterior
 Pectoralis major
 Pectoralis minor
 Trapezius
 Latissimus dorsi

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20
Q

what are the accessory muscles of expiration

A

 Abdominals
 Rectus Abdominis
 External Obliques
 Internal Oblique
 Transversus Abdominis

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21
Q

what is a barreled chest

A

 Enlarged chest
 Rounded cross section
 Fixed horizontal position of ribs

22
Q

what happens during emphysema

A

 Alveolar walls disintegrate
 Increases resistance in pulmonary circulation
 Right ventricle has to work harder
 Enlarged right ventricle
 Cor pulmonale

23
Q

what is cor pulmonale

A

 Cor pulmonale is a condition that causes the right side of the heart to enlarge and fail. It’s also known as pulmonary heart disease caused by long term high pressure in the pulmonary arteries of the lungs and right ventricle of the heart

24
Q

what are the symptoms of Cor Pulmonale

A

 SOB
 Syncope
 Tachycardia
 Chest pain
 Foot and ankle swelling
 Cyanosis

25
Q

what are the symptoms of COPD

A

 Cough
 Dyspnoea-difficult or laboured breathing
 Excessive sputum production
 Chest tightness or wheeze
 Oedema
 Heart Failure
 Recurrent chest infections
 Hyperinflated lungs
 Fatigue
 Chest pain/discomfort

26
Q

risk factors associated with COPD and smoking

A

 smoking history
 occupational exposure to harmful fumes, dust or chemicals
 exposure to fumes, such as biomass fuels

27
Q

what is bronchitis

A

an inflammation of the lining of the bronchial tubes

28
Q

what is chronic bronchitis

A

 Chronic bronchitis is defined as a cough that occurs every day with sputum production that lasts for at least 3 months, 2 years in a row.
 The major cause of chronic bronchitis is cigarette smoking; other causes are bronchial irritants, usually inhaled repeatedly by the affected person
 Over 90% of patients with chronic bronchitis have a history of smoking
 The lining of the bronchial tubes repeatedly becomes irritated and inflamed.
 The continuous irritation and swelling can damage the airways and cause a buildup of sticky mucus, making it difficult for air to move through the lungs.
 This leads to breathing difficulties that gradually get worse.
 The inflammation can also damage the cilia
 When the cilia don’t work properly, the airways often become a breeding ground for bacterial and viral infections.
 Infections typically trigger the initial irritation and swelling that lead to acute bronchitis.
 Chronic production of excessive mucus
 Lower respiratory airways becomme inflammed and fibrosed causing airway obstruction
 Gaseous exchange is impaired
 Frequent chest infections
 More mucus doesn’t lead to disability
 The subsequent fibrosis and inflammation does as it progresses to larger airways

29
Q

what effect does short term smoking have on the cilia

A
  • In acute (short term) cases of exposure to smoke, coughing is induced and cilial beating increases to clear the smoke out of the lungs.
30
Q

what effect does long term smoking have on the cilia

A
  • In long term exposure, smokers’ cilia beat slower than normal, and continue to slow down the longer the person smokes.
30
Q

what is alpha 1 anti-trypsin deficiency

A

 a rare, inherited condition, which can cause lung and liver problems
 lack a protective enzyme inhibitor called alpha-1-antitrypsin
 more vulnerable to the effects of inhaling smoke or other toxic materials like dust, fumes or chemicals.
 More likely to develop chronic obstructive pulmonary disease (COPD).

31
Q

why do you perform spirometry on diagnosis

A

 At diagnosis
 To reconsider the diagnosis, for people who show an exceptionally good response to treatment
 To monitor disease progression

32
Q

when is diagnosis of COPD confrimed in terms of post-bronchodilator

A

 FEV1/FVC < 0.7 (i.e. <70%) &
 FEV1 < 80% of predicted
 FEV1 = forced expiratory volume in 1 second
 FVC = forced vital capacity

33
Q

what are the stages of the GOLD (2008) and NICE (2010) grades 1-4 (severity of airflow obstruction)

A

1- mild, below 80% predicted for post bronchodilator FEV, 0.7 PB FEV
2- moderate, 50-79% predicted % for PB FEV,
3- severe, 30-49% PB FEV predicted
4- very severe, <30% PB FEV

34
Q

what further investigations could patients have on diagnosis

A

 A chest x-ray
 A full blood count (FBC) to identify anaemia or polycythaemia
 Body mass index (BMI) calculated
 Additional investigations may include:
 Sputum culture
 Home peak flow measurements (to exclude asthma if doubt remains)
 Electrocardiogram (ECG)
 Echocardiogram
 CT thorax
 Serum alpha-1 antitrypsin

35
Q

what is the BODE index used for prognosis

A

 Assessment of the prognosis of COPD
 BMI
 Airflow Obstruction (FEV₁ % predicted)
 Dyspnoea (MRC dyspnoea scale)
 Exercise capacity (6 minute walk test)
 Approx. 4 year survival rate
 0-2 points 80%
 3-4 points 67%
 5-6 points 57%
 7-10 points 18%

36
Q

what are the differences between COPD and asthma

A

smoker/ ex-smoker - Nearly all/possibly
Symptoms under 35
- Rare/ often
Chronic productive cough
-common/uncommon
breathlessness
- persistent and aggressive/ variable
night-time waking with breathlessness
- uncommon/ common
Significant varying of symptoms
- uncommon/ common

37
Q

why do airflow obstructions occur

A

 Airflow obstruction due to a combination of damage to the airways and also to lung parenchyma (e.g. alveoli)
 The damage is the result of chronic inflammation that differs to that seen in asthma
 Significant airflow obstruction may be present before the individual is aware of it

38
Q

what are the main symptoms of COPD

A

cough, sputum, dyspnoea, wheeze, chest pains, swollen ankles, haemoptysis, weight loss/ anorexia, muscle weakness and wasting

39
Q

what happens in lung areas with chronic under-ventilation

A

there is a local shutdown of vessels which forces blood to the better ventilated regions
This is achieved by the pulmonary blood vessels vasoconstricting therefore increasing pulmonary vascular resistance

40
Q

what does pulmonary vascular resistance over a long period of time have as a consequence

A

 Re-modelling of the pulmonary circulation and hypertrophy of the small pulmonary arteries
 Narrower, thicker and more muscular pulmonary arteries provide higher resistance to blood flow, this = pulmonary hypertension

41
Q

what is cor pulmonale

A

alteration in the structure and function of the R ventricle
 Dilation and hypertrophy of the right ventricle in response to diseases of the pulmonary vasculature and/or lung parenchyma (pulmonary heart disease)
 Chronic obstructive lung disease and chronic bronchitis are responsible for approx. 50% of cases of cor pulmonale in the developed countries
 Aka right sided heart failure

42
Q

what is pulmonary hypertension

A

↑ afterload on the right ventricle
 Right ventricle hypertrophy
 ↓R ventricular ejection fraction (pump failure)
 Back pressure into venous circulation
 ↑ pressure at venous end of capillary bed
 Interrupts normal capillary dynamics
 Peripheral oedema

43
Q

what is peripheral oedema

A

 Palpable swelling produced by the expansion of interstitial tissue
 Starling’s law tells us that forces dictate the movement of fluid between the capillary and the interstitial space
 ↑ pressure at venous end of capillary bed = increased capillary hydrostatic pressure = net efflux of fluid into the interstitial tissue

44
Q

what is exacerbation of COPD

A

an acute worsening of respiratory symptoms that result in additional therapy

45
Q

how is exacerbation of COPD classified

A

 Mild – treated with short acting bronchodilators (SABD) only
 Moderate – treated with SABDs plus antibiotics and/or oral corticosteroids
 Severe – patient requires hospitalisation or visits to the emergency department. Severe exacerbations may also be associated with acute respiratory failure
 COPD patients experience 1-4 exacerbations per year

46
Q

what are the symptoms of exacerbation of COPD

A

 Dyspnoea (84%)
 Fatigue (81%)
 Cold symptoms e.g. runny nose (59%)
 Sputum colour changes (53%)
 Sputum volume changes (47%)
 Cough (44%) (Costi et al., 2006)

47
Q

what causes exacerbation

A

 Viral – most common cause (especially rhinovirus) associated with more symptoms and slower recovery
 Bacterial infections – less common however airways of COPD patients often colonised with bacteria which can lead to secondary bacterial infection (up to 60% of cases)
 Environmental pollution
 1/3 of severe exacerbations have unknown cause

48
Q

what are the symptoms of both infective and non-infective exacerbation of COPD

A

 Increased dyspnoea
 Upper airway symptoms (eg, colds and sore throats)
 Increased wheeze and chest tightness
 Fatigue and reduced ex tolerance
 Marked respiratory distress with dyspnoea and tachypnoea
 Possibly acute confusion, increased cyanosis, peripheral oedema
 Respiratory failure - may develop

49
Q

what is infective exacerbation of COPD

A

 Added symptoms of infective exacerbation only:
 Increased cough
 Increased sputum purulence (change in colour and viscocity)
 Increased sputum volume
 Pyrexia (fever)

50
Q

what is the process of exacerbation

A

 Exposure to trigger (viral, bacterial or environmental) causes worsening airway inflammation
 Increased inflammation = increased airway oedema and mucus hypersecretion
 Also have worsening:
 airway obstruction
 dynamic hyperinflation
 dyspnoea
 cough
 Increased WOB
 Sometimes leads to respiratory failure

51
Q

what are the long term effects of exacerbation

A

 Inflammatory cascade that occurs during acute exacerbation thought to contribute to structural lung damage responsible for the progression of COPD over time
 Exacerbations associated with:
 A more rapid decline in lung function
 Sustained reduction in health related QOL
 Increased risk of future exacerbation