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MRS211 > Chest > Flashcards

Chest Flashcards

1
Q

What does the respiratory system do?

A
  • bring oxygen from the environment for the body to use

- expels CO2 from the body back to the atmosphere

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2
Q

What is the clinical presentation of both asthma and COPD?

A

Airflow obstruction indicated by:

  • SOB (dyspnea)
  • cough
  • chest tightness
  • wheezing
  • tachycardia
  • tachypnoea
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3
Q

Difference between asthma and COPD

A

Asthma:

  • usually present in childhood
  • stable disease with fluctuations
  • spirometry consistent
  • strong genetic link
  • allergens increase attacks
  • treatable
COPD: 
- presents in people over 40
Progressive disease
Spirometry decline
Environmental link ( smoking)
- treatment slows progression
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4
Q

What is asthma?

A
  • chronic inflammation of the airways
  • intermittent airflow obstruction
  • bronchial hypersensitivity
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5
Q

What is the cause/ aetiology of asthma?

A

Unknown cause but strong links with:

  • family history of asthma and allergies
  • smoking during pregnancy
  • premature birth
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6
Q

How do we prevent asthma?

A

Test to ensure diagnosis:

  • full medical history check
  • spirometry
  • Allergy testing
  • X-day to rule out other diseases
  • Blood tests
  • need action plan (severity differs)
  • avoid triggers
  • treat attack early
  • take prescribed medication
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7
Q

What can cause an acute asthma attack?

A 
Allergens
Airborne irritants
Medication 
Emotional triggers
Respiratory infections
Change to environment
Exercise
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8
Q

What medications are used to treat an acute asthma attack?

A

Preventers: corticosteroids to reduce airway inflammation

Relievers: fast acting bronchodilators

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9
Q

What imaging modalities are used for asthma?

A

Plain chest x-ray: 1st modality utilised

CT: usually hi-resolution CT chest (HRCT) if required

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10
Q

What imaging modalities are not utilised for asthma and why?

A

NM, MRI and US as they are not practical. Invasive

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11
Q

Chest x-ray features caused by asthma?

A
  • normal in 3/4 of patients
  • pulmonary hyperinflation
  • bronchial wall thickening
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12
Q

Complications seen on an x-ray caused by asthma

A
  • atelectasis/collapse (mucous plugging)
  • pneumonia
  • eosinophilic lung disease
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13
Q

What is COPD?

A

Chronic Obstructive Pulmonary Disease

  1. Pulmonary emphysema= abnormal, pathological, permanent enlargement of distal (distal to terminal bronchioles) airspaces + wall destruction without fibrosis
  2. Chronic bronchitis= defined clinically as a cough productive of sputum occurring on most days in 3 consecutive months over 2 consecutive years with enlargement of mucosal glands and inflammatory infiltration
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14
Q

Cause/ aetiology of COPD

A
  • cigarette smoke
  • exposure to dust and chemicals
  • alpha-1 antitrypsin deficiency
  • chronic IV use
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15
Q

COPD clinical diagnosis

A
  • dyspnea
  • chronic cough
  • chronic sputum production
  • history of exposure to risk factors
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16
Q

What are the clinical patterns associated with bronchitis?

A

Blue bloaters

  • patients may be obese
  • frequent cough and expectoration due to irritation by mucous
  • dyspnea
  • coarse cough and wheezing on auscultation
  • patients may have signs of right heart failure
  • cyanotic
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17
Q

Clinical indications of chronic bronchitis

A
  • productive cough for 3 months for 2 successive years where other chronic causes have been excluded
  • chronic inflammation of bronchi
  • bronchial narrowing
  • increased mucous production
  • hypertrophy of mucous glands
  • increased number of goblet cells
  • fibrosis and smooth muscle hypertrophy
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18
Q

What are the clinical patterns of emphysema?

A

Pink puffers

  • patients may be very thin with a barrel chest
  • loss of skeletal muscle and subcutaneous fat
  • patients typically have little or no cough or expectoration
  • dyspnea
  • the chest may be hyper-resonant, and wheezing may be heard in auscultation
  • non-cyanotic
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19
Q

Clinical indications for pulmonary emphysema

A
  • abnormal enlargement of distal airspaces (distal to terminal bronchioles)
  • wall distension and destruction with minimal or absent fibrosis
  • loss of alveolar capillaries
  • loss of elasticity in connective tissue
  • air becomes trapped in alveoli
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20
Q

What is the pathogenesis of COPD?

A
  • inflammatory response
  • damage to lung parenchyma
  • destruction of alveolar walls and septae
  • loss of elastic recoil
  • diminishes expiratory flow rate
  • air trapping
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21
Q

How is pulmonary emphysema classified?

A
  • centrilobular/ centriacinar (smoking/ upper zones)
  • panlobular/ panacinar (genetic disorder- alpha- 1 antitrypsin deficiency/ lower zones)
  • pRaseotal/ disralacinar (Bullae formation and spontaneous pneumothorax)
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22
Q

Describe how COPD is a progressive disease

A
  1. Decreased size and number of pulmonary vessels and branches
  2. Distorted vessels (stretched, straightened, curved) with increased branching angles
  3. Avascular regions
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23
Q

What features are displayed on a CXR when imaging chronic bronchitis?

A
  • bronchial wall thickening
  • prominent peripheral bronchovascular markings
  • pulmonary arterial hypertension
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24
Q

What features are displayed on a CXR when imaging emphysema?

A
  • normal or hyperinflation
  • increased lung fields
  • flattened hemidiaphragms
  • vertical, elongated cardiac silhouette
  • increased radiolucency
  • increased retrosternal airspace
  • increased AP chest diameter
  • splaying of Tina and sternal bowing
  • altered pulmonary vasculature
  • bullae formation
  • saber-sheath trachea
  • pulmonary arterial hypertension
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25
Q

What is the CXR appearance of bullae?

A
  • avascular regions of hyperlucency >10mm
  • demarcated by thin walls <1mm thickness
  • located commonly subpleural
  • Uni or multi-locula with thin septa
  • associated with pneumothorax formation, infection and haemorrhage
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26
Q

Advantages of high-resolution CT (HRCT) for COPD defection

A
  • greater sensitivity than standard chest radiography
  • high specificity for emphysema: detection and characterisation
  • quantity extent of emphysema: visual scoring system
  • potential for long term monitoring of emphysema progression
  • guide surgical intervention
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27
Q

What treatment is available for COPD?

A
  • no known cure
  • ease symptoms, prevent complications and slow disease progression
  • lifestyle changes: quit smoking, healthy diet
  • medication: bronchodilators and corticosteroids
  • oxygen therapy: bottled oxygen to compensate for low oxygen transfer
  • surgery: bullectomy, lung volume reduction, lung transplant
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28
Q

Name 4 types of upper/ middle respiratory infections

A

Rhinorrhea (runny nose), croup, epiglottitis, brochiolitis

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29
Q

Name 4 types of lower respiratory tract infections

A

Pneumonia, pulmonary tuberculosis, fungal disease, lung abscess

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30
Q

Name 5 clinical presentations of pneumonia

A
  • fever and/or chills
  • cough
  • tachypnoea and/ or dyspnea
  • tachycardia or bradycardia
  • wheezing
  • rhonchi
  • rales
  • sternal or intercostal retractions
  • dullness to percussion
  • pleurisy
  • cyanosis
  • rash
  • acute respiratory distress
31
Q

What is the pathogenesis of pneumonia?

A

Inhalation, aspiration and haematogenous

32
Q

pneumonia cause

A
  • classified by infecting organism
  • acute lung infection, cause: bacteria, viruses, fungi, parasites
  • inflammation within and around alveolar tissues
33
Q

What are the 4 sub- categories of pneumonia?

A
  • community- acquired
  • nosocomial
  • pneumonia in immunosuppressed patients
  • ventilator- associated
34
Q

What groups are at risk of pneumonia?

A
  • ATSI
  • elderly
  • infants
  • pre existing medical conditions
  • immunocompromised
  • smokers
35
Q

How is pneumonia clinically diagnosed?

A
  • suggestive signs and symptoms
  • microbiologic testing
  • CXR or other imaging modalities
  • bronchoscopy
36
Q

What is the etiology of streptococcus pneumoniae pneumonia?

A
  • gram positive bacterium
  • transmitted by physical contact or droplet
  • occurs at any age during winter/spring
  • most common community acquired bacterial pneumonia
  • often complicates influenza
37
Q

What are some symptoms of streptococcus pneumoniae pneumonia?

A
  • high fever
  • pleuritic pain
  • productive cough
  • sputum
38
Q

What are some predisposing factors for streptococcus pneumoniae pneumonia?

A
  • very young or old
  • chronic heart and/or lung disease
  • immunocompromised
  • influenza
39
Q

CXR radiographic features of streptococcus pneumoniae pneumonia

A 
Typically lobar consolidation 
Lower lobes or posterior segments of upper lobes
Limited volume loss
Frequent air bronchograms
Pleural effusion common
Cavitation rare
Consolidation may be spherical
40
Q

Role of CXR in pneumonia

A
  • establish presence of pneumonia
  • determine location and extent
  • May identify predisposing conditions
  • identify associated complications
  • satisfactory to follow response to treatment
41
Q

What are the basic radio graphic patterns of infective pneumonia?

A 
- consolidation
Classified according to appearances:
- lobar
- bronchopneumonia 
- interstitial
- spherical
- cavitary
42
Q

What are some limited differential diagnosis value for pneumonia?

A
  • same orgqnisms can produce several patterns
  • pattern partly dependent upon integrity of host’s defenses
  • patterns overlap in individual patients
43
Q

Pneumonia treatment

A

Based on the infective organism

  • bacterial infection treated with antibiotics
  • viral infections treated with antivirals, rest and hydration
  • physio useful in persistent cases
44
Q

What is the aetiology of pulmonary TB?

A

Lungs are a common site for infection

  • causative agent: typically Mycobacterium TB
  • classified as: primary, post primary, active, latent
  • testing: clinical history, sputum testing, imaging
45
Q

What are some characteristics of a primary TB infection?

A
  • located anywhere in the lung
  • large or small
  • cavitation is uncommon
  • possible lymph node enlargement
  • possible pleural effusions
46
Q

What are some characteristics of a post primary TB infection?

A
  • commonly located in upper lobe
  • large lesion with potential smaller ones
  • cavitation is more common
  • possible enlargement of hilar lymph nodes
47
Q

Name 5 predisposing factors for TB

A
  1. Contact with TB
  2. Infants
  3. Elderly
  4. Smokers
  5. Environmental/ socioeconomic
48
Q

Is TB symptomatic or asymptomatic?

A

Asymptomatic

49
Q

How can CT help with infective lung diseases?

A
  • to suggest causative pathogens
  • exclude non-infectious pneumonia
  • suspicious round opacification
  • severe or complex pneumonia
  • pneumonia in immunocompromised patients
  • recurrent/ non-resolving pneumonia
50
Q

How are NM, MRI and IS useful with infective lung diseases?

A

NM: VQ scans show defects with pneumonia
MRI: ventilation study
US: guided pleural drainage/aspiration

51
Q

What is the treatment for TB?

A
  • course of 4 oral drugs taken over at least 6 months
  • side effects: nausea/ vomiting, jaundice, unexplained fever/tiredness, tingling or numbness of hands or feet, joint pains, skin rash, itching skin or bruising, visual changes
52
Q

What is a pulmonary embolism?

A

PE comprises ‘stuff’ that enters the venous system and ends up in the pulmonary circulation

  • blockage will occur at the level where the vessel is too small to allow passage
53
Q

What are the different types of PE?

A

Air

Amniotic

Fat

Foreign body

Oil

Parasite eggs

Septic

Tumour

Thrombus

54
Q

What is the aetiology of PE?

A

DVT and PTE are the same disease at different stages and organs

VTE rarely originate in the pulmonary circulation but are transported there

95% of pulmonary thromboemboli originate in the lower extremity deep veins

Superficial and lower DVT rarely migrate to lung without first migrating above the knee

VTE originating from upper extremity or right side of the heart tend to be associated with IV catheters, pacing wires and IV drug use

55
Q

What causes venous stasis?

PE risk factor

A
  • bed rest
  • immobilisation (surgery, flights, drive)
  • low cardiac output (athletes)
  • pregnancy
  • obesity
  • hyperviscosity
  • vascular damage
  • central venous catheter
  • age (older)
  • IV drug use
56
Q

What causes coagulation?

PE risk factor

A
  • tissue injury (infarction, surgery, trauma)
  • malignancy
  • lupus antiocoagulant
  • nephrotic syndrome
  • oral contraceptive pull (oestrogen)
  • genetic coagulation disorders
57
Q

Epidemiology of PE

A
  • no exact epidemiological data available
  • acute PE third most common type of CVD
  • clinical data indicate that PE occurs most at 60-70 years but autopsy data suggest highest incidence at 70-80 years
  • if untreated, acute PE is associated with a 30% mortality rate
  • if treated, mortality rate is 8%
  • 10% of acute PE die suddenly
58
Q

What is the pathophysiology of PE?

A

Pulmonary embolism arise from thrombi in the deep venous of (mainly) the lower extremities. A blood clot dislodges and is swept into the pulmonary circulation and lodged in a pulmonary artery.

59
Q

What happens to the blood pressure when a PE occurs?

A

High pressure builds up in the pulmonary circulation proximal to the blockage, and acute strain is placed on the right side of the heart as it tries to pump blood past the obstruction

60
Q

What are the three deep vein thrombosis?

A
  • Acute
  • Subacute
  • Chronic
61
Q

What are some haemodynamic changes caused by PE?

A
  • effect of obstruction depends on % of pulmonary circulation obstructed + any pre- existing cardiopulmonary disease
  • right ventricular strain
  • death
  • fatal decrease in cardiac output
62
Q

Effect PE has on ventilation and perfusion

A
  • reduces perfusion distal to occlusion causing increased alveolar dead space
  • this impairs CO2 excretion= hyperventilation
  • leads to alveolar oedema, alveolar collapse and atelectasis
  • end result is arterial hypoxaemia
63
Q

What are some signs and symptoms of PE?

A
  • dyspnea, chest pain, haemoptysis, cough

Evidence of DVT:
- swollen, tender, warm red

Other:
- tachypnoea, cyanosis, fever

64
Q

ECG changes in PE

A 
- 75% of ECGs will be abnormal in PE
Non specific:
- sinus tachycardia 
- T wave inversion on precordial leads
- ST and T wave inversion
- deep S wave on lead l, Q wave and inverted T wave on lead III due to right ventricular strain
65
Q

What is D-dimer?

A
  • a fibrin degradation product
  • a protein that results after a clot is broken down by fibrinolysis
  • used for low pre-test likelihood of PE
  • negative D-diner in low pre-rest likelihood virtually excludes PE
  • elevated D-diner requires further evaluation
66
Q

What is BNP?

A
  • brain natriuretic peptide
  • indicator of ventricular stretch
  • often measure in PE but low sensitivity and specificity so not for diagnosis
  • a measure of the impact on cardiac strain
67
Q

How does DVT ultrasound work in detecting PE

A
  • 97% sensitivity for the proximal lower limb, 73% for calf
  • fail to compress
  • markedly distended veins
  • thrombus hypoechoic, homogenous
  • small flow streams around and through thrombus
  • free floating thrombus
68
Q

How does DVT CT Venography in detecting PE

A
  • filling defect in lumen
  • collateral veins
  • perivenous inflammation
  • May see compressing mass along veins
69
Q

What are some features of a CXR when detecting PE?

A

10-12% are normal
Enlarged central pulmonary artery
Focal oligemia
Necessary to exclude other lung disease

70
Q

What is the sensitivity and specificity of CTPA in PE detection?

A

Accurately identifies emboli
Misses some subsegmental emboli
Sensitivity: 66-93%
Specificity: 89-97%

71
Q

What are some indications to have a CTPA?

A 
Clinical suspicion of PE
cardiac or lung disease excludes VQ scan
Indeterminate VQ scan
CXR not clear to indicate VQ useful 
Pulmonary hypertension 
Immediate diagnosis needed
72
Q

Findings of PE on CTPA

A

Abrupt cut-off of artery

A filling defect within the pulmonary artery

73
Q

What are some limitations of CTPA?

A 
High radiation dose
Patient motion
Morbid obesity
Contrast bolus timing 
20% of CTPA are below quality standard

MRS211 (10 decks)

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