Pathologies Flashcards

1
Q

Define atelectasis

A

Complete or partial collapse of lung or lobe of lung

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2
Q

What happens to the alveoli in atelectasis?

What does this mean in terms of ventilation?

A

Become deflated or filled with fluid

There is no ventilation in these areas - gas exchange cannot occur

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3
Q

Physiological process leading to atelectasis

A

Not deep breathing due to post op pain –> secretion retention
Anaesthesia paralyses cilia during surgery
No mucociliary clearance of sputum
Leads to mucus plug
No ventilation to lung areas distal to plug, but perfusion maintained
No gas exchange
Lack of O2 and hypoxaemia

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4
Q

How does atelectasis occur in relation to functional residual capacity (FRC) and closing capacity (CC)?

A

FRC reduced during and filling surgery
When FRC becomes less than CC smaller airways close and stick together due to not enough air holding them open
Alveoli below this level don’t receive any new air
Closure of small distal airways leads to closure of large lung areas
Leads to lack of O2 and hypoxaemia

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5
Q

Clinical features of atelectasis

A
SOB
Increased respiratory rate - rapid shallow breathing
Wheezing
Cough
Chest pain
Increased HR
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6
Q

Physiotherapy interventions for atelectasis

A

Postural drainage
Chest wall percussion/vibration
FET

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7
Q

Postoperative atelectasis occurs within how many hours post surgery?

A

72 hrs post general anaesthesia

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8
Q

What V/Q mismatch occurs in atelectasis? Why?

A

“shunt” mismatch - no ventilation distal to blockage of airway but perfusion maintained

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9
Q

Patients more at risk for post-op atelectasis

A
Longer anaesthesia duration
Smoker
Chronic lung disease
Inadequate post-op pain medication
Poor pre-op pulmonary education
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10
Q

Complications of atelectasis

A

Type I respiratory failure
Lung infections from retained secretions - Pneumonia
Lung scarring

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11
Q

Values of PaO2 and PaCO2 respectively, in an atelectasis patient

A

Low PaO2 and normal PaCO2

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12
Q

What does COPD stand for?

A

Chronic Obstructive Pulmonary Disease

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13
Q

What 2 conditions cover COPD?

A

Chronic bronchitis and emphysema

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14
Q

Is COPD reversible?

A

No, it is a progressive disease

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15
Q

What clinical feature defines chronic bronchitis?

A

Cough and sputum expectoration for at least 3 months over 2 successive years

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16
Q

Symptoms of chronic bronchitis

A
Chronic sputum production
Chronic cough
Wheeze
Dyspnoea/SOB at rest
Fatigue
Difficulty with ADLs and exercise 
Depression/anxiety
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17
Q

In chronic bronchitis, there is an overproduction of mucus due to what?

A

inflammation

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18
Q

Pathophysiology of chronic bronchitis

A
  • Inhalation of noxious particles > release of inflammatory mediators by epithelial cells > activation of macrophages & neutrophils > proteases released and protease/anti-protease imbalance > causes inflammation
  • Increased swelling and blood flow in bronchial mucous membranes
  • Increase size and number of goblet cells – hyperplasia > increased mucus production
  • Cilia damage and dysfunction > Diminished mucociliary escalator
  • Airflow limitation, reduced sputum clearance > further irritation, fibrotic changes and increased risk of infection
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19
Q

Emphysema is disease of…

A

the alveoli

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20
Q

Define emphysema

A

Enlargement of air spaces distal to the terminal bronchiole with destruction of their walls

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21
Q

What 2 things are destroyed in emphysema?

A

Alveolar septa and capillary bed

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22
Q

Main result of emphysema

A

gas trapping leading to hyperinflation

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23
Q

Pathophysiology of emphysema

A
  • Inhalation of noxious particles > release of inflammatory mediators by alveolar epithelial cells > activation of alveolar macrophages & neutrophils > proteases released and protease/anti-protease imbalance
  • Inflammation, degradation and destruction of alveolar walls and elastic fibres
  • Erosion of alveolar septa > enlarged airspaces (potential bullae formation) > decreased surface area
  • Loss of elastic recoil > collapse of respiratory bronchioles and small airways > gas trapping
  • Hyperinflation
24
Q

Symptoms of emphysema

A

Dyspnoea/SOB at rest
Fatigue
Difficulty with ADLs and exercise
Depression/anxiety

25
What are the clinical features of COPD?
``` Barrel chest due to hyperinflation Accessory muscle use Decreased breath sounds - course crackles if sputum present Reduced functional exercise capacity O2 desaturation during exercise ```
26
Risk factors for COPD
``` Cigarette smoking Passive smoking Occupational - dusts, fumes, chemicals Outdoor air pollution Genetic - eg. Alpha-1 antitrypsin deficiency Low socio-economic status ^risk with age ^risk if female ```
27
Why should you be cautious giving O2 to a COPD patient?
Decreases hypoxic drive to breath
28
Is COPD more common in men or women?
Women
29
Acute exacerbation of COPD defined by...
a sustained worsening of patients condition that is acute in onset
30
What may occur in an acute exacerbation of COPD?
Change in baseline dyspnoea, cough, sputum production that is beyond normal day-to-day variability
31
Physiotherapy interventions for COPD
``` early mobilisation - prevent deconditioning sputum clearance control of dyspnoea self-management pulmonary rehab smoking cessation ```
32
Describe the cycle of inactivity
feels breathless fear of activity increasing breathlessness avoids activities which increase breathlessness less active muscles become weaker weak muscles use more oxygen and are less efficient feeling breathless
33
Describe the dyspnoea spiral
``` Respiratory impairment dyspnoea during moderate exercise avoidance of exercise physical deconditioning dyspnoea during mild exercise further avoidance of exercise further deconditioning dyspnoea during ADLs ```
34
What does STEMI stand for?
ST elevation myocardial infarction
35
Significant Ischaemia leads to...
significant necrosis of cardiac muscle
36
What causes an MI?
prolonged or permanent occlusion of coronary arteries due to atherosclerosis
37
What does CABG stand for?
Coronary artery bypass graft
38
Pathophysiology of MI
• Atherosclerosis of coronary arteries o Foam cells are too big and become trapped in intima – plaque builds up o Plaque continues to grow • Occlusion of one/more coronary arteries due to an unstable atherosclerotic plaque that ruptures • Fatty plaque materials highly thrombogenic • Leads to large thrombus in the coronary artery • Reduced/complete loss of blood flow distal to the blockage • Not sufficient O2 • Ischaemia leading to necrosis of cardiac muscle
39
Modifiable risk factors for MI
``` hypertension smoking obesity sedentary lifestyle hypercholesterolemia poor oral health alcohol drug use ```
40
Non-modifiable risk factors for MI
``` Sex - more M>F age family history male pattern baldness previous MI ```
41
Are women or men more at risk of an MI
men
42
Purpose of CABG procedure
bypass atheromatous blockages in coronary arteries with harvested veins (long saphenous vein) revascularise ischaemic myocardium
43
Aims of CABG
restore blood flow to cardiac muscle alleviate SOB and angina improve exercise tolerance
44
Post-op complications - cardiac surgery following STEMI
``` infection - mediastinitis wound instability postoperative pulmonary complications (PPCs) arrhythmias haemorrhage pain reduced exercise capacity 'Post-pump syndrome' ```
45
Clinical presentation of STEMI
``` intense pain - chest, left arm, left side neck nausea/vomiting sweating acute SOB syncope/collapse substernal heaviness ```
46
Physiotherapy goals post STEMI
``` reduce myocardial demand mobility enhance QoL increase CV fitness reduced dyspnoea on exertion assist return to employment ```
47
Physio interventions post-cardiac surgery following STEMI
``` Pre-op assessment and education cardiac rehab early post-op mobilisation wound supported FET and cough LTEE foot/ankle circulatory exercises posture - thoracic extension needed thoracic/shoulder mobility ```
48
Examples of shoulder/thoracic exercises post cardiac surgery
``` shoulder shrugs - elevation/depression ball around body theraband abductions/flexions pendulum shoulder retraction thoracic rotations - hands on hips, hands on head ```
49
Drugs used in medical management post-cardiac surgery
``` ACE inhibitors Beta blockers GNT spray Anticoagulants Antiplatelets Calcium channel blockers ```
50
What are ACE inhibitors
vasodilators - lower BP
51
What do beta blockers do?
lower BP and HR
52
What is GNT spray?
vasodilator - reduces angina symptoms
53
What do anticoagulants do?
inhibit thrombus formation
54
What do anti platelets do?
inhibit thrombus formation
55
What do calcium channel blockers do?
reduce myocardial contractility and propagation of electrical impulses