1
Q
AMI
A
blood flow to the heart is cut off due to a blockage in the coronary artery
2
Q
Bronchiectasis;
A
irreversible dilation of the bronchi due to structural airway injury.
3
Q
CF:
A
caused my mutations to the CFTR gene. Causing abnormalities to salt and fluid clearance across the epithelium
4
Q
Lobar pneumonia;
A
inflammatory exudate within the alveolar space
5
Q
Pleural effusion;
A
excess fluid in the pleural space
6
Q
Pneumothorax;
A
air in the pleural space between the visceral and parietal pleura
7
Q
Chronic bronchitis;
A
expectoration (sputum) on most days for 3/12 for 2 years
8
Q
emphysema
A
enlargement of air spaces and destruction of alveolar walls
9
Q
bronchopneumonia
A
inflammation of the bronchi and lungs
10
Q
ILD
A
lung disorder that produces similar inflammatory and fibrotic changes in the interstitum or intra-alveolar septa of the lung
11
Q
pathology of emphysema
A
Thin atrophied airway walls, and loss of alveolar walls and capillary beds
12
Q
pathology of chronic bronchitis
A
Mucous gland hypertrophy & goblet cell hyperplasia → ↑ mucus production.
Ciliary dysfunction → impaired clearance of mucus.
Chronic inflammation in small airways →
* Narrowing of lumen
* Cellular infiltrates (inflammatory cells),
* Oedema of airway walls.
13
Q
pathology of pneumothorax
A
Loss of negative intrapleural pressure causes the lung to collapse inwards.
14
Q
Pathology of pleural effusion
A
Fluid compresses the lung underneath and restricts expansion.
15
Q
pathology of lobar pneumonia
A
Alveolar spaces are filled partially or completely with fluid and blood cells (infectious debris & exudate)
16
Q
Pathology of CF
A
Defective CFTR protein causes impaired chloride secretion and increased sodium absorption.
Leads to dehydrated, thick mucus on epithelial surfaces.
Lungs’ airway obstruction leads to infections, inflammation and bronchiectasis.
17
Q
pathology of bronchiectasis
A
Loss of cilia, mucous gland hyperplasia, airway wall destruction, and permanent dilation of the bronchi
18
Q
pathology of ILD
A
Inflammation and fibrosis develops in the interstitial and alveolar tissues.
This makes the lungs stiffer (↓ compliance) → harder to expand with each breath.
The alveolar–capillary membrane thickens, impairing diffusion of gases, especially oxygen.
19
Q
pathology of bronchopneumonia
A
Alveolar spaces are filled partially or completely with fluid and blood cells (infectious debris & exudate)
20
Q
pathology of AMI
A
- a plaque in the heart artery breaks open forming a thrombus
- this blocks O2 from reaching part of the heart muscle
- without O2 the muscle gets injured and starts to die (necrosis) starting in the inner layer and going out
- dead tissue is replaced by scar tissue
21
Q
describe the differences in presentation between a person with angina vs myocardial infarction
A
ANGINA:
- Chest pain that’s triggered by exercise and stress
- pain eases with rest
-temporary decreased blood flow
- no permanent heart damage
MYOCARDIAL INFACTION:
- chest pain is more severe and long-lasting
- pain doesn’t go away
- leads to permanent damage (death of the heart muscle)
22
Q
What does NSTEMI stand for
A
Non-ST elevation myocardial infarction
23
Q
What STEMI stand for
A
ST Elevated myocardial infarction
24
Q
What is STEMI
A
complete artery blockage causing necrosis, characterized by elevated Troponins
25
Whats NSTEMI
Partial artery blockage with some necrosis. Has lower Troponins then STEMI
26
symptoms of chronic bronchitis
- chronic productive cough
- mucus production
- shortness of breath
- check tightness
- wheezing
27
symptoms of emphysema
- pursed lip breathing
- minimal cough
- little sputum
- use of accessory muscles for breathing
28
symptoms of CF
- thick sticky mucus
- wheezing
- shortness of breath
- crackles
29
Symptoms of bronchiectasis
- chronic productive cough
- SOB
- crackles
- wheezing
30
symptoms of ILD
- dry cough
- fatigue
- check discomfort
- SOB
31
symptoms of AMI
- SOB
- chest pain
- palpitations
32
symptoms of bronchopneumonia
- cough
- SOB
- crackles
- sputum
33
symptoms of lobar pneumonia
- SOB
- productive cough
- sputum
-crackles
34
symptoms of pneomothorax
- one sided chest pain
- SOB
- rapid HR
35
symptoms of pleural effusion
- SOB
- dry cough
- chest pain
36
Ask me two (2) questions, in the way you would ask a patient, to help you differentiate between chest pain that was angina vs. oesophageal reflux?
“Can you describe what your chest pain feels like and when it usually happens?”
- angina: Pressure, squeezing, or heaviness, often triggered by exertion or stress, relieved by rest or nitrates.
- Oesophageal reflux: Burning sensation (heartburn), often after meals or when lying down, may improve with antacids.
“Does the pain ever radiate to your arm, jaw, neck, or back, or is it just in your chest?”
-Cardiac: Often radiates to left arm, jaw, neck, or back.
- Reflux: Usually localized to the chest or upper abdomen, rarely radiates.
37
what might you hear if you ausultated a person with chronic bronchitis
- wheeze
- crackle
- ronchi
- prolonger expiration
38
what might you hear if you ausultated a person with emphysema
- quiet lungs
- distant breath sounds
- wheeze
- decreased diaphragmatic movement
39
what might you hear if you ausultated a person with bronchiectasis
- coarse crackles
- wheezes
- ronchi
40
what might you hear if you ausultated a person with CF
- wheezes
- crackles
41
what might you hear if you ausultated a person with ILD
- no wheeze
- velcro inspiration crackles
42
what might you hear if you ausultated a person with pneumothorax
- decreased or absent breath sounds
- no crackles
- rhonchi
43
what might you hear if you auscultated a person with pleural effusion
- absent breath sounds due to the fluid
44
what might you hear if you ausultated a person with lobar pneumonia
- bronchial breath sounds over affected lobe
- coarse crackles
45
what might you hear if you ausultated a person with bronchopneumonia
- coarse crackles
- scattered wheeze
- rhonchi
46
what might you hear if you ausultated a person with ACM
- normal breath sounds
47
describe a CXR for someone with emphysema
- hyperinflated lungs
- increased blackness in the tissues
- striated lucencies in the tissues that may outline muscles
48
describe a CXR for someone with chronic bronchitis
- increased bronchial markings
- enlarged pulmonary arteries
- mild hyperinflation
49
describe a CXR for someone with CF
- hyperinflated lungs
- bronchiectasis
- areas of collapse
- mucus plugging (patchy opacities)
50
describe a CXR for someone with bronchiectasis
- patchy opacities
- consolidation
- hyperinflation
51
describe a CXR for someone with ILD
- blunted costophrenic angles
- ground glass opacities
- honeycombing
52
describe a CXR for someone with bronchopneumonia
- patchy opacities
- no clear lobe boarders
- air bronchograms
- atelectasis
53
describe a CXR for someone with lobar pneumonia
- well defined lobe boarders
- no patchiness
**may cause silhouette sign; the boarder of the heart is obscured if the affected lobe is next to them
54
describe a CXR for someone with pleural effusion
- blunted costophrenic angles
- homogenous opacity
- shift of mediastinum
55
describe a CXR for someone with pneumothorax
- depressed diaphragm on affected side
- visible pleural line
- no lung markings
56
pathophysiology of emphysema
- There is a loss of elastic recoil in the lungs due to the destruction of alveolar walls
- Enlargement of air spaces decreases the surface area available for gas exchange
57
pathophysiology of chronic bronchitis
Smoking or irritation makes mucus glands bigger → too much mucus.
Cilia don’t clear mucus well → secretions build up → constant cough with sputum.
Inflammation narrows and swells airways → blocks airflow.
Long-term damage reduces lung stretch (elastic recoil) → gas trapping and trouble breathing.
58
pathophysiology of ILD
The lungs become thick and stiff, making it hard for oxygen to pass into the blood and forcing the breathing muscles to work harder. If the muscles tire out, carbon dioxide can build up as a secondary problem.
59
pathophysiology of pneumothorax
occurs when air enters the pleural space between the lung and chest wall, disrupting the negative pressure needed to keep the lung inflated. This causes the elastic lung to recoil and collapse, reducing its volume and impairing gas exchange.
60
pleural effusion pathophys
Effusion= disruption or alteration to the pleural pressure and a lung compression underneath the effusion.
61
lobar pneumonia pathophys
1. infection starts - organisms enter the alveoli and trigger inflammation
2. alveolar fills with consolidation
3. impaired gas exchange leading to hypoxemia
62
pathophys bronchopneumonia
1. bacterial spreads from the bronchi into the alveoli
2. the infection spreads in scattered patched across multiple lobes
3. alveoli fills with pus
4. airways become obstructed
5. creating a gas exchange deficiency
63
pathophys bronchiectasis
1. recurrent lung infections
2. repeated infections cause persistent inflammation of the bronchi
3. this destructs smooth muscle and elastic tissue in the bronchial walls
4. damaged cilia - mucus cant be cleared
5. gas exchange problems
64
pathophys CF
1. mutation in the CFTR gene
2. creates impairment in Cl and sodium movement
3. causes less water in secretions - mucus = sticky and thick
4. mucus blocks the airway leading to resp fail
65
pathophys AMI
1. rupture of atherosclerotic plaque
2. blood flow to the myocardium is reduced
3. O2 cant get to the heart muscle
4. cell death occurs (necrosis)
5. macrophages and neutrophils go to the site and remove the dead tissue
66
how would you distinguish between collapse and consolidation on a CXR
consolidation = opacity without volume loss
collapse= opacity with volume loss
67
how would you distinguish between collapse and consolidation on auscultation
Consolidation = bronchial breathing + increased vocal resonance.
Collapse = usually reduced/absent breath sounds + reduced vocal resonance
68
list PFT findings for obstructive disorders
decrease FEV1
decrease FEV1/FVC
increase TLC
Increase rv
69
list PFT findings for restrictive pattern
decrease FEV1
decrease FVC
high FEV1/FVC
decrease TLC
decrease RV
70
what would ECG findings for AMI be
ST elevation
T wave inversion
Q waves
71
what would ECG findings for AMI represent
acute ishaemia
acute infarction
72
ECG findings for pleural effusion
low voltage QRS
axis shift
electrical alternans
73
what would ECG findings for pleural effusion represent
- fluid compressing on the heart
- dampening of electrical signals
74
what findings on a blood test would suggest myocardial infarction
- increase troponins
- CK-MB
75
what causes blunted costophrenic angles on a CXR
in pleural effusion; fluid that accumulates at base blunts the angles
76
which condition has silhouette sign
lobar pneumonia; RML can obscure the right heart border, LLL can obscure left hemidiaphragm
77
what is a silhouette sign on a CXR
when 2 structures on a CXR touch each other causing the boarder between them to disappear
78
impairments of emphysema
decrease lung compliance due to destruction of alveoli walls leading to gas movement problem of CO2
79
impairments of chronic bronchitis
MCC, decrease cilia clearance to structure of the airways being effected thus gas movement
80
impairments of asthmatic component
- mucus production and clearance
- structure of the airways
81
impairments of bronchiectasis
- impaired MCC
- decreased lung compliance
82
impairments CF
- decrease MCC
decrease cough effectiveness
decrease gas movement
83
impairment of pneumothorax
84
impairment of ILD
- decrease gas movement problem
85
pathology of chronic asthma
Hypertrophied smooth muscle– Hypertrophy of mucous glands– Oedema of the bronchial wall– Infiltration by eosinophils and lymphocytes– Thick tenacious sputum
85
chronic asthma
Asthma is a chronic lung disease affecting people of all ages. It is caused by inflammation and muscle tightening around the airways, which makes it harder to breathe.
86
What does PEP stand for
positive expiratory pressure
87
what does OPEP stand for
oscillatory positive expiratory pressure
88
PEP
therapy is delivered on the breath out, the device creates the positive pressure and splits the airways open, allowing for more air behind secretions, increasing number of alveoli open creating better expiratory flow
89
OPEP
delivered on the breath out, device creates positive pressure and splits open the airways via a percussion noise, allowing for more air behind the secretions
90
rationale for deep breathing excersises
- reopens closed airways that will then facilitate MCC and allow for gas exchange
- can cause fatigue
- can facilitate more effective cough
91
rationale for GAD
- uses gravity to assist movement/drainage of secretions
- moves secretions from peripheral airways to central airways
- does this via placing the bronchus of the lung segment being drained uppermost and perpendicular to the horizontal
92
rationale for percussion
- increases expiratory flow rate (EFR)
- loosens secretions
- makes mucus less sticky
93
rationale for vibration
- increases EFR
- makes secretions less sticky
- increases mechanical energy
94
rationale for shaking
- increases EFR
- makes secretions less sticky
- increases mechanical energy
95
rationale for huff
MID TO LOW HUFF:
- moves secretions from peripheral airways to central airways
HIGH TO IMD HUFF:
- aims to move secretions from central airways out the mouth
96
FET rationale
breathing control:
- aims to reduce bronchospasm and desaturation
huffs:
- move secretions
97
what is a relevant finding
any piece of information, observation, or result that is directly related to the condition, problem, or goal you are assessing.
98
describe the pathophysiology of dyspnoea
perception of uncomfortable/unpleasant respiratory sensations/ respiratory systems version of pain.
- Work required to breath
- ‘Air hunger’
- Chest tightness
99
short term outcome measures
* Do they feel their chest is now ‘clear’?
* Do they feel it’s easier to bring up the sputum? (ease of
expectoration)
* Do they feel less breathless (if secretions were a cause of ↑
airway resistance → SOB)
100
Objective assessment for short term outcome measures
* Change in sputum: volume, color, rheology (thickness)
* Cough: sounds drier
* Auscultation: reduced coarse crackles, reduced upper
respiratory tract noises, ?wheeze
101
long-term outcome measures for cough
– Pulmonary function tests (reduced deterioration)
– Improved quality of life
102
what is dynamic hyperinflation
reversible. can occur during:
Acute exacerbation; when there is an increase airflow resistance (from swelling, secretions or spasms)
Exercise; when there is an increase ventilatory demand (TV and RR increase to supply O2)
103
structure of respiratory system
1. visceral structures:
- upper tract
- lower tract
- conducting airways
- gas exchange areas: alveoli
- mucociliary apparatus: mucus and cilia for clearing particles
104
How is a CXR performed
solid tissue absorbs radiation and appears white on diagnostic imaging
air filled spaces dont absorb radiation and thus appear dark
105
6 approaches to CXR
1. Technical details
2. Quality of film
3. Extra-thoracic structures
4. Thoracic cage
5. Intra-thoracic structures
6. Attachments
106
CT scan
movement science
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