Respiratory Flashcards
(197 cards)
1
Q
Asthma
A
Chronic, inflammatory condition causing episodes of REVERSIBLE airway OBSTRUCTION due to bronchoconstriction and excessive secretion production
2
Q
Aetiology of asthma
A
Hypersensitivity of the airways triggered by:
Cold air Exercise Cigarette smoke Air pollution Allergens e.g. pollen, animals, mould Time of day: early morning and night
3
Q
Presentation of asthma
A
Episodes of wheeze (widespread, polyphonic)
Breathlessness
Chest tightness
Dry cough (often nocturnal)
Hyper resonant percussion (too much air)
Atopy (family or personal history)
Diurnal variability
4
Q
Investigations for asthma
A
Spirometry:
- bronchodilator reversible testing (>5 years)
- obstructive pattern: FEV1 <80% predicted, FEV1/FVC ratio <0.7
Peak flow measurement (monitoring, not used for diagnosis)
Skin prick test + IgE
5
Q
FEV1
A
Forced expiratory volume in one second
Obstructive: DECREASED
Restrictive: minimally decreased or normal
6
Q
FVC
A
Forced vital capacity measures the amount of air you can breath out forcefully after taking a deep breath
Obstructive: decreased or normal
Restrictive: decreased
7
Q
FEV1/FVC
A
Amount of air a person can forcefully exhale in ONE SECOND compared to the TOTAL amount they can exhale
= FEV1%
Normal: 85%
Obstructive: <80% (DECREASED: EXHALE disorder)
Restrictive: 85% (EQUALLY REDUCED)
8
Q
Obstructive lung diseases
A
Difficulty EXHALING
Asthma
COPD
Wheezing, mucus production
9
Q
Restrictive lung diseases
A
Difficulty INHALING
Pulmonary fibrosis
10
Q
TLC
A
Total lung capacity = volume of air left in the lungs after exhalation (residual volume) + FVC
Obstructive: normal
Restrictive: DECREASED (INHALE disorder)
11
Q
FEV1% predicted
A
FEV1% of the patient divided by the average FEV1% in the population for any person of similar age, sex, and body composition
12
Q
Treatment of asthma
A
Avoid triggers
NICE guidelines: CHECK ADHERANCE AND INHALER TECHNIQUE BEFORE INCREASING DOSE OR ADDING NEW DRUG
1) SABA (salbutamol)
2) Add Low dose Inhaled corticosteroids (ICS; e.g. budesonide)
3) Add Leukotriene receptor antagonist (LRTA; e.g. montelukast)
4) Add LABA (salmeterol) (and stop LRTA)
5) Increase ICS dose
13
Q
Indication for localised wheeze
A
Foreign body (not asthma)
14
Q
COPD definition
A
NON-REVERSIBLE (i.e with bronchodilators) OBSTRUCTION in air flow through the lungs, caused by damage to lung tissue (almost always due to SMOKING)
15
Q
Two main types of COPD
A
Chronic bronchitis: chronic inflammation of the bronchial wall > mucus hypersecretion > progressive narrowing
Emphysema: loss of elastic recoil of alveoli > keeps airways open during expiration
16
Q
COPD presentation
A
Long term smoker Chronic shortness of breath Cough Sputum production (clear, white) Wheeze Recurrent respiratory infections (particularly in winter)
NO finger clubbing
17
Q
Differential diagnosis in COPD
A
Lung cancer
Fibrosis
Heart failure
COPD does NOT cause Finger clubbing
Unusual:
Haemoptysis
Chest pain
18
Q
MRC Dyspnoea scale
A
19
Q
COPD risk factors
A
SMOKING
Age (usually presents between 40-60)
Secondhand smoke exposure
Occupational therapy exposure (mining, dust, asbestos)
Pollution
Genetics (alpha-1-antitrypsin deficiency can lead to earlier onset and increased severity as A1AT is protective)
20
Q
COPD diagnosis
A
Clinical presentation and spirometry
LFT/Spirometry:
- FEV1/FVC ratio <0.7
- reversibility testing: no response
CXR: hyperinflated lungs
21
Q
Severity of airflow obstruction using FEV1
A
Stage 1: FEV1 >80% predicted
Stage 2: FEV1 50-79% predicted
Stage 3: FEV1 30-49% predicted
Stage 4: FEV1 <30% predicted
22
Q
Other investigations to support the diagnosis of COPD
A
Just know a few
Chest X-ray: exclude other pathology e.g. lung cancer
Full blood count: polycythaemia (high Hb; response to chronic hypoxia) or anaemia (low Hb)
BMI: weight monitoring for loss (cancer or severe COPD) or gain (steroids)
Sputum: chronic infection e.g. pseudomonas
ECG: cardiac function
Serum A1AT
23
Q
Emphysema symptoms
A
‘PINK PUFFERS’
Dyspnoea/tachypnoea Minimal cough Pink skin, pursed-lip breathing Accessory muscle use Cachexia (muscle wasting, weight loss) Hyperinflation (barrel chest)
Complication: pneumothorax (in bullous emphysema/vanishing lung syndrome)
24
Q
Chronic bronchitis symptoms
A
‘BLUE BLOATERS’
Chronic productive cough (purulent sputum)
Dyspnoea
Cyanosis (hypoxaemia): secondary polycythaemia, pulmonary HT (reactive vasoconstriction)
Peripheral oedema
Obesity
Haemoptysis
25
Management of COPD
General:
SMOKING CESSATION
Vaccine regime (pneumococcal, annual flu)
Step 1 (stable): SABA or SAMA
Step 2 (no asthmatic responsive features): LABA plus LAMA
Step 2: (asthmatic response): LABA plus ICS
Severe COPD: long term oxygen therapy (note: chronic COPD causes CO2 insensitivity so the system is dependent on hypoxia, 100% oxygen removes the respiratory drive)
26
SAMA
Short acting muscarinic antagonist
Ipratropium bromide
27
LAMA
Long acting muscarinic antagonist
Tiotropium
28
ICS
Inhaled corticosteroid
Budesonide
29
Management of exacerbated COPD (IE)
Usually triggered by infection (IE)
Acute worsening of symptoms i.e. SoB, sputum, wheeze
ABG:
- Co2 retention = acidosis
- normal pCO2 + low pO2 = T1RF
- high pCO2 + low pO2 = T2RF
CXR, sputum culture + sensitivities for AB therapy, FBC, U&Es
Steroids (hydrocortisone/prednisolone) + nebulised bronchodilators (salbutamol/ipratropium bromide) + ABs
30
Alpha 1 antitrypsin deficiency
A1AT is a protease inhibitor produced by the liver which acts protectively by inhibiting neutrophil elastase (an enzyme that digests connective tissue)
An autosomal recessive defect causes a deficiency in this enzyme causes:
- EARLY ONSET COPD (emphysema) and bronchiectasis (after 30 years old)
- cirrhosis of the liver (after 50 years old)
31
A1AT deficiency presentation (specific to liver pathology)
```
Fatigue
Loss of appetite
Weight loss
Oedema
Jaundice
Haematemesis/blood in stools
```
32
A1AT deficiency presentation (specific to lung pathology)
```
Shortness of breath
Excessive cough with sputum production
Wheeze
Decreased exercise capacity, persistent fatigue
Chest pain (worse on inhalation)
```
33
Diagnosis of A1AT deficiency
Gold standard: low serum A1AT
Liver biopsy: cirrhosis, acid-Schiff-positive staining globules (mutant A1AT proteins) in hepatocytes
Genetic testing: A1AT gene
CT thorax: diagnose bronchiectasis and emphysema
34
Management of A1AT deficiency
Smoking cessation
Supportive treatment: inhalers, oxygen therapy
Organ transplant for end stage liver/lung disease
Monitoring: hepatocellular carcinoma
35
Interstitial lung disease
Umbrella term to describe conditions that affect the lung parenchyma causing inflammation and fibrosis
36
Types of interstitial lung disease
Idiopathic pulmonary fibrosis (IPF)
Occupational: silicosis, asbestosis, hypersensitivity pneumonitis
Systemic: granulomatosis with polyangiitis, Goodpasture’s
37
Idiopathic pulmonary fibrosis
Formation of scar tissue in the lungs with no known cause
38
IPF epidemiology
The most common interstitial lung disease
2/3 of patients are >60 at presentation
M > F
39
Presentation of IPF
Ds!!
Dyspnoea
Dry cough (> 3 months)
Diffuse bibasal inspirations crackles
Digits (Finger clubbing)
40
Diagnosis of IPF
High resolution CT thorax: ground glass appearance
| Bloods: increased CRP
41
Treatment of IPF
No real cure
Pharmacological:
- Pirdenidone (antifibrotic)
- Nintedanib (monoclonal)
Non-pharmacological:
Smoking cessation, physiotherapy, vaccination schedule
Poor prognosis
42
Asbestosis presentation
Dyspnoea on exertion
Dry cough
Onset >10 years after initial exposure
Bibasal inspiration crackles
43
Investigations of asbestosis and silicosis
CXR
Spirometry (restrictive)
HRCT
44
Treatment of asbestosis and silicosis
Remove exposure
Smoking cessation
Symptom treatment
45
Complications of asbestosis
Mesothelioma
Adenocarcinoma
Pleural thickening
46
Symptoms: Acute renal failure and Haemoptysis
Differential diagnosis?
Goodpasture syndrome: anti-GBM antibodies
Granulomatosis with polyangiitis: c-ANCA antibodies, saddle-shaped nose
47
Goodpastures syndrome
Autoimmune anti-glomerular basement membrane (anti-GBM) disease
Anti-GMB antibodies attack glomerulus and alveoli basement membranes (Type IV collagen)
Glomerulonephritis and pulmonary haemorrhage
48
Presentation of Goodpasture syndrome
```
Haemoptysis
Haematuria
Dyspnoea
Glomerulonephritis
Oedema
Reduced urine output
Chest pain
Fever
Fatigue
```
49
Investigations for Goodpasture syndrome
Anti-GBM antibodies
Lung and kidney biopsy
50
Treatment for Goodpasture syndrome
Supportive
Corticosteroids (prednisolone)
Immunosuppressant (cyclophosphamide)
Plasmapheresis (removal of plasma)
51
Hypersensitivity pneumonitis
“Extrinsic allergic alveolitis”
Type 3 Hypersensitivity reaction to an inhaled allergen
Causes alveolar and bronchial inflammation
52
Examples of specific causes of hypersensitivity pneumonitis
Bird-fanciers lung: bird droppings
Farmers lung: mouldy spores in hay
Mushroom workers lung: specific mushroom antigens
53
Presentation of hypersensitivity pneumonitis
```
Dyspnoea
Cough
Fever
Malaise
Weight loss
```
54
Investigations for hypersensitivity pneumonitis
Bronchoalveolar lavage during bronchoscopy:
- raised lymphocytes
- mast cells
CXR
- acute: patchy reticulonodular infiltrates
- chronic: fibrosis
55
Treatment for hypersensitivity pneumonitis
Remove allergen
| Steroids
56
Granulomatosis with polyangiitis
Wegener’s granulomatosis
Systemic vasculitis involving small and medium vessels
ENT, lung and kidney involvement (ELK)
Associated with c-ANCA antibodies
57
Presentation of granulomatosis with polyangiitis
```
ENT:
Epistaxis
Crusty nasal secretions
Hearing loss
Sinusitis
Saddle shaped nose (perforated septum)
```
Lungs: Cough, wheeze, haemoptysis
Kidneys: Rapidly progressing glomerulonephritis (haematuria)
58
Investigations for granulomatosis polyangiitis
c-ANCA (anti-neutrophil cytoplasmic antibodies)
Urinalysis
CT chest
59
Treatment for granulomatosis polyangiitis
Corticosteroids (methylprednisolone, prednisolone)
Immunosuppression (rituximab, methotrexate)
Prophylactic ABx
60
Clinical presentation of lung cancer
```
Local disease:
Persistent cough
Shortness of breath
Haemoptysis
Weight loss
Chest pain, wheeze, recurrent infections
```
```
Metastatic disease:
Bone pain
Horners syndrome (ptosis, anhydrosis, miosis)
Headache, seizures, neurological deficit
Abdominal pain
```
```
Paraneoplastic changes:
Increased PTH (hyperparathyroidism)
Increased ADH (SIADH)
Increased ACTH (Cushing’s)
```
61
Two main types of lung cancer
Small cell lung carcinoma (SCLC) - 20%
| Non-small cell carcinoma - 80%
62
Types of non-small cell carcinoma
Adenocarcinoma (40%)
Squamous cell carcinoma (20%)
Large cell and differentiated carcinoma (10%)
Other including carcinoid tumours (10%)
63
Risk factors for lung cancer
```
Cigarette smoking (biggest cause)
Asbestos
Coal
Radon exposure
Pulmonary fibrosis
HIV
Genetic factors
```
64
Why is small cell lung cancer responsible for paraneoplastic syndromes
SCLC cells contain neurosecretory granules that can release neuroendocrine hormones
65
Investigations for lung cancer
First line: Chest X-ray (central mass, hilar lymphadenopathy, pleural effusion) but a negative CXR doesn’t rule out cancer
CT thorax: staging of cancer
Sputum cytology: malignant cells (high specificity, low sensitivity)
Diagnosis: biopsy + histology
66
SCLC
Strongly associated with cigarette smoking
Arises from ENDOCRINE cells (kulchitsky cells) typically in the central bronchus
Secretes polypeptide hormones which act as hormones and neurotransmitters
Treatment: chemotherapy
67
Squamous cell carcinoma
Most strongly associated with cigarette smoking
Arises from EPITHELIAL cells (cells that line the airways) typically in the central bronchus
68
Adenocarcinoma lung cancer
Most common cell type in non-smokers
Strongest association with asbestos exposure
Originate from mucus-secreting glandular cells
Metastasises to: pleura, lymph nodes, brain, bone, adrenal glands
69
Sites of metastatic spread TO lung
```
Breast
Colon
Prostate
Sarcoma
Bladder
```
Cancer metastasising from elsewhere is more common than a primary lung tumour!
70
Tuberculosis epidemiology
Majority of cases in Africa and Asia (India and China)
Cause of death for most people with HIV
71
Pathophysiology of TB
Mycobacterium TB spreads via respiratory droplets (airborne)
1) alveolar macrophages ingest bacteria and the rods proliferate inside
2) hilar lymph nodes > present antigen to T-cells > cellular immune response
3) delayed hypersensitivity reaction > tissue necrosis and CASEATING granuloma formation (central necrosis and cheese like) - primary TB
4) necrotic zone disintegrates (e.g. in immunocompromised) and TB spreads (secondary TB)
72
Systemic symptoms of TB
```
WEIGHT LOSS
Low grade fever
Anorexia
Drenching NIGHT SWEATS
Malaise
```
73
Pulmonary symptoms of TB
```
Productive cough
HAEMOPTYSIS
Cough >3 weeks (dry or productive)
Breathlessness
Chest pain (sometimes)
```
74
Signs of TB
```
Bronchial breathing
Dullness on percussion
Decreased breathing
FEVER
Cackles
```
RECENT TRAVEL
75
TB investigations
CXR:
- Ghon complex (primary TB lesion alongside ipsilateral mediastinal lymphadenopathy) - dense homogenous fibronodular opacities on upper lobes (caseating granuloma)
- hilar lymphadenopathy
Sputum culture (3 x samples): Ziehl-Neelsen stain on Lowenstein-Jensen agar = acid-fast bacilli
Lymph node aspiration or biopsy: caseating granuloma
76
Diagnosing latent TB
Mantoux skin test: TB injected intradermally; 72 hours later, positive test = induration of >5mm (offered to young people in close contact with TB and new entrants to UK from TB prevalent countries)
Positive Mantoux test but no features of active TB:
Interferon gamma release assay: sample of blood mixed with TB antigens; previous TB contact = WBCs will be sensitised and release IFN-y = positive for latent TB
77
Treatment for ACUTE active TB
RIPE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
78
Rifampicin
| Course, MOA, side effects
6 months
MOA: Bactericidal (blocks protein synthesis)
SE: red urine, sweats, hepatitis
79
Isoniazid
| Course, MOA, side effects
6 months
MOA: Bactericidal (blocks cell wall synthesis)
SE: neuropathy, hepatitis
Pyridoxine (Vit B6) is co-prescribed prophylactically for peripheral neuropathy SE
“I’m-so-numb-azid”
80
PYRAzinaMIDe
| Course, MOA, side effects
2 months
MOA: Bactericidal initially, less effective later
SE: hyperuricaemia resulting in GOUT, hepatitis
81
Ethambutol
| Course, MOA, side effects
2 months
MOA: Bacteriostatic (blocks cell wall synthesis)
SE: optic neuritis
“Eye-thambutol”
82
Miliary TB
immune system is unable to control the disease
| disseminated + severe disease
83
Extrapulmonary TB
Lymph nodes: “cold abscess” in neck without the inflammation, redness and pain from an acutely infected abscess
Cutaneous TB
CNS, GI, GU system
84
Pneumonia
Inflammation of the lung tissue
Acute lower respiratory tract infection (alveoli and terminal bronchioles)
Note: lower airways should always be sterile in a healthy person
85
Aetiology of pneumonia
Typically caused by a bacterial infection of the distal airways and alveoli
Two most common causes: Streptococcus pneumoniae (50%), Haemophilus influenzae (20%), mycoplasma pneumoniae
Can also be caused by viruses and fungi or atypical pneumonia e.g. Legionella pneumophila (AIR CONDITIONING IN A FOREIGN COUNTRY)
86
Types of pneumonia
```
Community acquired (CAP): develops outside of hospital
Hospital acquired (HAP): develops more than 48h after admission
```
Other:
Atypical: caused by atypical organisms not detected on gram stain
Pneumocystis jirovecii: fungi
87
Pathophysiology of pneumonia
Invasion and overgrowth of a pathogen in lung parenchyma
Overwhelming of host immune defences
Production of intra-alveolar exudates
88
Clinical presentation of pneumonia
```
Fever
Productive cough
Shortness of breath
Pleuritic chest pain
Delirium
```
Sepsis secondary to pneumonia:
Basic Observations - Increased RR and HR, Low BP, Hypoxia
89
Characteristic chest signs of pneumonia
Bronchial breath sounds (harsh sounds equally loud on inspiration and expiration)
Focal coarse crackles (air passing through sputum)
Dullness to percussion (lung tissue collapse and consolidation)
90
Severity assessment of pneumonia
```
CURB-65
Confusion
Urea >7
Respiratory rate >30
Blood pressure <90 systolic <60 diastolic
65 (Age)
```
91
Diagnosis of pneumonia
```
CXR: consolidation, multi-lobar (strep. pneumoniae, s. aureus), multiple abscesses (s. aureus)
FBC: raised WBC
CRP (useful for monitoring)
Sputum culture
U&Es (urea)
```
92
General management of pneumonia
Maintain O2 sats 94-98% (COPD: 88-92%)
Analgesia: paracetamol or NSAIDs
IV fluids
93
CURB-65 guided treatment for pneumonia
0-1: oral amoxicillin in the community
2: hospital: oral amoxicillin + macrolide (clarithromycin)
3+: consider ITU, IV co-amoxiclav + macrolide (clarithryomycin)
94
Complications of pneumonia
```
Sepsis
Pleural effusion
Emphysema
Lung abscess
Death
```
95
Community acquired pneumonia
Commoner in the age extremities
Commonest cause: Streptococcus pneumoniae
Other: Legionella, Haemophilus influenzae
Antibiotic: Amoxicillin and Clarithromycin
96
Type of sputum characteristic of strep pneumoniae
Rusty sputum
97
What organisms are hospital acquired pneumonia caused by?
Most cases caused by aerobic gram-negative bacilli:
After 4 days admission
- Staph aureus
- Strep pneumoniae
After 5 days admission
- Pseudomonas aeruginosa
- MRSA
98
Atypical pneumonia
Bacterial pneumonia caused by atypical organisms not detectable by standard methods e.g. legionella pneumophila
Characteristic symptoms: headache + low grade fever + cough
Legionnaires disease = pneumonia + hyponatraemia + recent hotel stay with poor air conditioning
99
Pleural effusion
Collection of fluid in the pleural cavity (between the parietal and visceral pleural surfaces)
100
Pathophysiology of pleural effusion
Rate of fluid formation > Rate of fluid removal
101
Exudative pleural effusion
Inflammation causes PROTEIN to leak out into the pleural space (ex = moving out)
Local factors
```
Causes: (think inflammation)
Lung cancer
Pneumonia
Rheumatoid arthritis
SLE
TB
```
102
Transudative pleural effusion
Fluid moving across into the pleural space (trans = moving across)
Systemic factors e.g. elevated pressure
Causes: (think fluid shifting)
Congestive HF
Hypoalbuminaemia
Hypothyroidism
103
Presentation of pleural effusion
DYSPNOEA (decreased lung volume)
Dullness to percussion over the fluid-filled effusion
Reduced breath sounds
Tracheal deviation if the effusion is massive
104
Investigations of pleural effusion
1st line: CXR
- blunting of the costophrenic angle
- fluid in the lung fissures
- meniscus
- tracheal deviation
Pleural ultrasound
Thoracocentesis identifies and diagnoses underlying cause
105
Treatment of pleural effusion
Dependent on cause:
Congestive HF: Loop diuretics
Infective: AB
Malignant: Thoracentesis (pleural aspiration)
106
What is a pulmonary embolism?
Type of venous thromboembolism
A thrombus (usually from DVT) passes through the IVC and RA/RV to reach the pulmonary circulation
Causes: FATBAT (fat, air (travel), thrombosis (venous), bacteria, amniotic fluid, tumour)
107
Risk factors for pulmonary embolism
```
Increased age
Immobility e.g. post surgery
Pregnancy
Active malignancy
DVT
Family history of VTE
Hormone therapy with oestrogen
```
108
Pathophysiology of venous thromboembolism formation
Virchow’s triad:
Vessel wall damage (e.g. surgery)
Venous stasis (e.g. long haul flight)
Hyper-coagulability
= Intrapulmonary dead space
= Decrease in CO
109
Clinical presentation of pulmonary embolism
Risk factors may give more of a clue than symptom presentation e.g. immobility/surgery
Acute onset dyspnoea
Pleuritic chest pain (increases on inhale, worse on lying down)
Cough or haemoptysis
Features of DVT e.g. unilateral leg swelling and tenderness
Hypoxia e.g. tachypnoea, tachycardia
Crepitations on auscultation
110
Wells score
Predicts the risk of a patient presenting with symptoms actually having a DVT or PE
Takes into account RF such as recent surgery and clinical findings such as tachycardia (>100) and haemoptysis
```
<4 = PE unlikely
>4 = PE likely
```
111
Pulmonary embolism investigations
Wells score >4 likely PE: immediate CT pulmonary angiogram
Wells score <4 unlikely PE: D-dimer and if positive, perform CTPA
Haemodynamically unstable: echocardiogram
112
PE investigation where CTPA is contraindicated
E.g. renal impairment, contract allergy or at risk from radiation
Ventilation-perfusion (VQ) scan
113
Two main causes of a respiratory ALKALOSIS
Pulmonary embolism
Hyperventilation syndrome
High respiratory rate causes CO2 to be expired
Differential: PE = low pO2, HS = high pO2
114
Initial management of PE
Anticoagulation: start immediately before confirming diagnosis
1) DOAC: Apixaban or Rivaroxaban
2) LMWH e.g. enoxaparin and dalteparin
115
Haemodynamic instability in PE
Patients presenting with hypotension + raised JVP + shock
Treatment: continuous unfractioned heparin and thrombolysis e.g. alteplase
Other options: surgical embolectomy, vena cava filter
116
Differential diagnosis in PE
```
Unstable angina
MI
Pneumonia
Acute bronchitis
Pneumothorax
```
117
Long term anti coagulation options for PE
Warfarin
DOAC e.g. apixaban, dabigatran, rivaroxaban
LMWH (1st line in pregnancy or cancer)
Continue for 3 months if there is an obvious reversible cause
Beyond 3 months if the cause is unclear
118
Pulmonary hypertension
>25mmHg
Increased resistance and pressure of blood in the small pulmonary arteries characterised by vasoconstriction, smooth muscle cell and endothelial cell proliferation and thrombosis
Progressive increase in pulmonary vascular resistance (PVR)
Causes strain on the right side of the heart and back pressure into the systemic venous system
119
Four causes of pulmonary hypertension
Increased PVR:
1) Primary pulmonary hypertension (pre-capillary)
2) LV failure (post-capillary)
3) COPD/emphysema (capillary)
4) PE (pre-capillary)
120
Main presenting symptoms of pulmonary hypertension
Exertional dyspnoea
Lethargy and fatigue
(Due to inability to increase CO)
121
Other signs and symptoms of pulmonary hypertension
As RV failure develops, there will be peripheral oedema, abdominal pain, and cyanosis
Raised JVP
Accentuated pulmonic component on 2nd heart sound
Tricuspid regurgitation murmur
122
Investigations pulmonary hypertension
```
Initial:
CXR: enlargement of pulmonary arteries, enlarged right atrium
ECG
trans-thoracic echocardiogram
raised NT-proBNP for RVF
```
Diagnostic: right heart catheterisation
123
ECG changes seen with right sided heart strain (in PHT)
Right ventricular hypertrophy (R waves on V1-V3 (right side) and S waves on V4-V6 (left side))
Right axis deviation
Right BBB
124
CXR changes seen in PHT
Dilated pulmonary arteries
| Right ventricular hypertrophy
125
Pulmonary hypertension management
General supportive therapy: oral anticoagulants, diuretics for fluid retention
Primary: IV prostanoids, endothelial receptor antagonists, phosphodiesterase-5 inhibitors
Secondary: treat underlying cause
126
Pneumothorax
Air in the pleural space
127
Causes of pneumothorax
Spontaneous
Traumatic
Iatrogenic
Lung pathology
128
Risk factors for pneumothorax
```
Smoking
Family history
Trauma
TALL, THIN, MALE (basketball player)
Young
Underlying lung disease
Previous PTX
```
129
Pathophysiology pneumothorax
Intrapleural pressure should be negative
Pneumothorax = Air enters the pleural space = Intrapleural pressure increases = lung volume decreases
130
Clinical presentation of pneumothorax
Stable patient
Sudden onset PLEURITIC CHEST PAIN, DYSPNOEA or cough
On examination:
Look for evidence of trauma
131
Diagnosis of pneumothorax
1st line: Erect CXR
| - reduced/absent lung markings between lung margin and chest wall + visible rim
132
Management of pneumothorax
Small primary spontaneous PTX (visible rim <2cm) and no SOB = will spontaneously resolve
Large primary spontaneous PTX (visible rim >2cm) and/or SOB = needle aspiration
Chest drain if >2cm on reassessment
133
Tension pneumothorax
MEDICAL EMERGENCY
Trauma to chest wall creates a one way valve mechanism: air enters pleural space but cannot exit (i.e. more air gets trapped with each breath causing increased positive pressure)
TRACHEAL DEVIATION: Pushes the mediastinum across, compressing the trachea, heart and other structures and causing cardiorespiratory arrest and collapse of the ipsilateral lung
134
Clinical presentation of tension pneumothorax
```
Cardiopulmonary deterioration:
Hypotension
Tachycardia
Low sats
Respiratory distress
```
Severe chest pain
135
Physical examination of tension pneumothorax
Tracheal deviation away from side of pneumothorax (contralateral)
Hypoxia
136
Management of tension pneumothorax
MEDICAL EMERGENCY
High flow oxygen
1st line: “Insert a large bore cannula into the second intercostal space in the midclavicular line” same side as the PTX
Chest drain
137
Whooping cough
UPPER respiratory tract infection caused by Bordetella pertussis (gram negative)
Whooping = loud inspiratory whoop when the coughing ends
Notifiable disease
138
Diagnostic test for whooping cough
<2 weeks: Nasopharyngeal PCR or bacterial culture
>2 weeks: Anti-pertussis toxin IgG
139
Mesothelioma summary
Cancer of the LINING of the lungs (pleura)
Main cause: asbestos (80%)
Gold standard diagnosis: pleural biopsy
CXR
Pleural aspiration
140
Bronchiectasis
Irreversible dilation of the bronchioles due to recurrent damage and inflammation (they become scarred, dilated, with loss of cilia)
Excess secretion of mucus but less clearance of it due to loss of cilia
Build up of mucus: stagnant bacteria cause increased chance of infection
141
Causes of bronchiectasis
Cystic fibrosis
COPD
Post-infectious bronchial damage: H. Influenzae, S. pneumoniae, S. aureus, TB
Immunodeficiency
Bronchiogenic carcinoma
142
Bronchiectasis investigations
Gold standard: HRCT: dilated bronchi (SIGNET RING sign = prominently dilated airway compared to accompanying vessel)
Sputum culture: look for infectious agents
CXR
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Treatment of bronchiectasis
Can’t be cured!
Symptom control:
Non-pharm: Stop smoking, healthy diet, exercise
Pharm: Bronchodilators, steroids, antibiotics (dependent on cause e.g. pseudomonas = ciprofloxacin)
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Cystic fibrosis
Autosomal recessive genetic condition
Defect in CFTR chloride channel protein on chromosome 7
- Transmembrane conductance regulator gene
- water follows salt = less water in mucus = thickened
Affects all ducts that produce mucus in the body (pancreas, airways, GI tract etc)
Presents in childhood
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Three key consequences of cystic fibrosis
Thick pancreatic and biliary secretions that cause blockage of the ducts resulting in a lack of digestive enzymes e.g. pancreatic lipase
Low volume thick airway secretions that reduce airway clearance, resulting in infection susceptibility
Congenital bilateral absence of the vas deferens in males
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Signs and symptoms of cystic fibrosis
Symptoms:
HEAVY MUCUS PRODUCTION
Chronic COUGH
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Signs:
Steatorrhea due to lack of lipase
Failure to thrive in children
Finger clubbing
Crackles and WHEEZE on aus
Rectal prolapse
Cyanosis
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Key diagnostic methods for CF
Gold standard: sweat test (NaCl) for chloride concentration
Genetic testing for CFTR gene during pregnant or after birth
Faecal elastase (pancreatic insufficiency)
Newborn blood spot testing
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First sign of CF in babies
Meconium ileus (not passing meconium within 24 hours, abdominal distention and vomiting)
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Two key bacteria that cause infections in CF
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Staphylococcus aureus
Pseudomonas aeruginosa (very difficult to get rid of and increases CF mortality)
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Patients take prophylactic Flucloxacillin to prevent S. aureus
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Management of CF
No cure, symptomatic management
Chest physiotherapy
Antibiotics, anti-mucinolytics, bronchodilators, enzymes, insulin, bisphosophonates
Lung transplantation in end stage respiratory failure
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Complications of CF
Respiratory tract infections
Bronchiectasis
Most males are infertile due to absent van deferens
90% develop pancreatic insufficiency
50% develop CF-related diabetes and require insulin
30% develop liver disease
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Sarcoidosis
Multi system inflammatory disorder
Mostly in the lungs and mediastinal lymph nodes
African American women <50
Non-caseating granulomas form due to CD4 interactions (Type 4 hypersensitivity)
Signs: bilateral hilar lymphadenopathy, erythema nodosum, polyarthritis, uvietis
Investigation: tissue biopsy for non-caseating granulomas; serum ACE levels (secreted from nodules)
Complications: interstitial lung disease
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Type 1 respiratory failure
V/Q mismatch/problem with gas exchange
Low Oxygen
Low or normal CO2
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Causes:
COPD
Pneumonia
Asthma
Pulmonary fibrosis
Pneumothorax
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Type 2 respiratory failure
Inadequate ventilation
Low oxygen
High CO2
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Increased resistance (COPD)
Respiratory centres (Drug overdose)
Neuromuscular problems (Guillain Barre/MND)
Reduced compliance (Pneumonia)
Severe asthma
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Respiratory centres
Medulla oblongata
Pons
Carotid bodies/Aortic arch
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Croup
Parainfluenza virus (HPIV)
Barking cough
157
Eosinophilic asthma
Allergic asthma
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Non-eosinophilic asthma
Exercise, cold air, stress, smoking, obesity
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Main cells involved in asthma
Eosinophils
| Mast cells
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Three characteristic pathological features of asthma
Airway obstruction (narrowing):
- Smooth muscle bronchial contraction leading to bronchoconstriction
- Mucosal inflammation (thickening of the airway) - mast cells + basophils
- Presence of mucosal secretions in the lumen
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Severity of acute asthma
PEFR:
>50% = moderate
33-50% = severe
<33% = life threatening (silent chest)
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Why does age matter in the history of asbestosis?
Many buildings built before the 80s contained asbestos
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Horners syndrome symptoms
Ptosis
Miosis
Anhydrosis
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Pancoast tumour
tumour of the apex of the lung
Invades the apical chest wall
Affects nearby structures including intercostal nerves, brachial plexus (shoulder pain, arm weakness), sympathetic chain (HORNERS SYNDROME)
Diagnosed based on clinical picture, imaging and biopsy
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Sites of metastatic spread FROM lung cancer
Bone
Brain
Adrenal glands
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Bilateral hilar lymphadenopathy on x-ray
Differential diagnoses
Sarcoidosis
Infection: TB
Malignancy: lymphoma (Hodgkin)
Occupational: silicosis
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Signs of bronchiectasis on examination
Coarse crackles in early inspiration and often in the lower zones
Large airway ronchi (low-pitched snore like sounds)
Wheeze
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Complications of bronchiectasis
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Repeated infection and deteriorating lung function
Empyema
Lung abscess
Pneumothorax (repeated coughing)
Respiratory failure
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Differential diagnosis of COPD
Asthma
A1AT deficiency
Bronchiectasis
Cystic fibrosis
170
COPD complications
Respiratory infections
Lung cancer
Cardiovascular
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Small gram-negative coccobacillus
Symptoms: malaise, coughing up green phlegm in the COMMUNITY
RF: elderly
Causative organism + Ab?
Causative organism: Haemophilus influenzae
Antibiotic: Co-amoxiclav
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Differential diagnoses for a COPD exacerbation
```
Pneumonia
Pneumothorax
Congestive HF
Pulmonary oedema
Pleural effusion
```
173
Groups of patients most at risk of respiratory infections
Extremities of age
COPD
Immunocompromised
174
D-dimer test
Pulmonary embolism
High sensitivity, low specificity
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Pneumothorax vs pleural effusion differentiated:
1) Respiratory examination
2) History
1)
Pleural effusion = dullness on percussion
PTX = hyper-resonant on percussion
2)
Pleural effusion = slower onset, PMH of CHF, cancer, pneumonia
PTX = rapid onset, history of trauma, PTX FH, smoking
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CT angiogram polo mint sign
Pulmonary embolism
Partial filling defect in blood vessel surrounded by a rim contrast material
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Hyperexpansion of the chest
Type of lung disease
Obstructive
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Patients most likely to develop a spontaneous PTX
Young males with low BMI
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Clinical features of bronchiectasis
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Persistent cough
Clubbing
Dyspnoea
No history of smoking + young age of onset
Haemoptysis
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Most commonly affected sinus in sinusitis
Maxillary: drains down to the bottom
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Beclomethasone inhaler MOA
```
STEROID ACTIONS e.g.
Decrease formation of cytokines
Inhibit influx of eosinophils
Reduce bronchial hyper responsiveness
Decrease microvascular permeability
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182
Walls of the bronchIOLEs lack
Hyaline cartilage
183
Kyphoscoliosis
Causes a restrictive lung disease
184
Respiratory symptoms are most likely caused by which bacteria
Haemophilus inFLUenzae
185
Aspiration pneumonia
Infection of the lungs caused by inhaling saliva, food, liquid, vomit and small foreign objects
More likely to go down right side in bottom two lobes
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Atypical pneumonia: Chlamydia psittaci
Contracted from infected birds - patient often owns a parrot
187
Atypical pneumonia: Coxiella burnetii
‘Q fever’ - associated with contact with animals
188
Mycobacterium avium complex
AIDS defining illness
| Presents similarly to pulmonary TB
189
Two most common causes of pneumonia
```
Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)
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190
Crepitations indication
Pneumothorax
191
Most likely cause for consolidation X-Ray
Lobar pneumonia
Consolidation = indicates filling of the alveoli and bronchioles in the lung with pus (pneumonia), fluid (pulmonary oedema), blood or neoplastic cells
192
Hyper-resonance indication
Hyperinflation with air i.e. COPD
193
Dullness on percussion indication
FLUID or solid replaces alveoli e.g. pneumonia or pleural effusion
194
Severe asthma Tx
Salbutamol on OXYGEN + steroids
195
Empyema
Infected pleural effusion (pus)
196
Prophylactic treatment for a pulmonary embolism
LMWH e.g. enoxaparin
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Which respiratory disease do you typically see high bicarbonate with respiratory acidosis?
COPD - chronically high CO2 causes the kidneys to COMPENSATE by releasing bicarbonate
