Respiratory Flashcards
What type of hypersensitivity reaction is asthma?
Type I (IgE)
What type of hypersensitivity reaction is Goodpasture’s disease?
Type II (IgG)
What type of hypersensitivity reaction is SLE?
Type III (immune complex formation)
What type of hypersensitivity reaction is TB?
Type 4 (cell mediated)
What is a type I hypersensitivity reaction?
Reaction mediated by IgE antibodies.
(Allergy) ie anaphylaxis
What is type II hypersensitivity?
Cytotoxic reaction mediated by IgG or IgM antibodies.
(antibody binds to host cell which is perceived to be foreign destruction)
Goodpastures, Graves, Myasthenia Gravis
What is type III hypersensitivity?
Reaction mediated by immune complexes – deposited in vessel walls.
RA, post-strep glomerulonephritis, reactive arthritis, SLE
What is type IV hypersensitivity?
Delayed reaction mediated by cellular response.
Cytotoxic, cell-mediated.
T helper cell activated by antigen presenting cells.
Antigen presented again in the future causes inflammatory response.
Contact dermatitis, Mantoux test, MS, coeliac
What happens in type I hypersensitivity?
IgE mediated, mast cell degranulation, antibody binding to antigen eg asthma, allergy
What happens in type II hypersensitivity?
IgG reaction – cytotoxic – IgG binds to cell and kills its – Rhesus haemolytic disease, Goodpastures,
What happens in type III hypersensitivity
Immune complex forms (soluble but saturates) – SLE, EAA
What happens in type IV hypersensitivity?
Cell mediated delayed (CD-4 cells are sensitized to infection but cant clear it - granuloma) – TB, sarcoid, Wegeners,
What is total lung capacity?
(5900ml): max volume of air/gas the lungs can contain/accommodate
What is vital capacity?
(4700ml): amount of effort that can be exhaled with max effort after max inspiration
What is tidal volume?
(500ml): Volume of air inspired (inhaled) and expired (exhaled) in a normal breath
What is inspiratory capacity?
(3500ml): max volume of air that can be inhaled after normal tidal expiration
What is expiratory reserve volume?
(1200ml): Volume of air exceeding tidal expiration that can be exhaled with max effort
What is inspiratory reserve volume?
(3000ml): Volume of air exceeding tidal inspiration that can be inhaled with max effort
What is functional residual capacity?
(2400ml): Volume of air remaining in the lungs after a normal tidal expiration
What is residual volume?
(1200ml): Volume of air that remains in lungs after expiration (keeps alveoli inflated)
What is FEV?
How much air a person can exhale during a forced breath
What is FEV1?
FEV in 1 second
What is FVC?
Total volume of air forcefully exhaled during FEV test
What is peak expiratory flow rate (PEFR)?
The peak flow rate during expiration
How do you calculate total ventilation per minute?
Tidal volume x resp rate
What is COPD?
Irreversible progressive disorder of airway obstruction
What does COPD include?
Chronic bronchitis and emphysema
What causes COPD?
Smoking, fumes and dust, air pollution, genetics
How does COPD present?
Dyspnoea, tachypnoea, barrel chest
SOB, chronic cough, recurring chest infections, wheeze
What measurement classifies COPD?
FEV1/ FVC <70%
How is COPD managed?
- SABA/ SAMA
- LABA +LAMA OR LABA and ICS (if asthmatic features/ steroid responsive)
- triple therapy. + smoking cessation, regular physical activity
Other tx options: oxygen, abx in exacerbation, mucolytics, theophylline.
What might you want to rule out if no smoking history in COPD?
Alpha-antitrypsin deficiency
What vaccinations are given to someone with newly diagnosed COPD?
Pneumococcal and influenza
How are COPD exacerbations treated?
Oral pred. 30mg for 7-14 days
What is spirometry?
Post-bronchodilator measurement.
Why might you aim for sats of 88-92% in a patient with COPD?
For most COPD patients, a target saturation range of 88%–92% will avoid the risks of hypoxia and hypercapnia
What are the stages of COPD?
1: FEV1 >80%
2: FEV1 50-79%
3: FEV1 30-49%
4: FEV1 <30% of predicted value
What are chronic bronchitis patients nicknamed?
Blue bloaters
What are emphysema patients nicknamed?
Pink puffers
What is chronic bronchitis?
Airway inflammation and narrowing
Increased mucous production
What is emphysema?
Destruction and dilation of air spaces
Can’t recoil and expel air
What is required to be diagnosed with chronic bronchitis?
Inflammation of bronchi with a productive cough for 3/12 for at least 2 years
How does chronic bronchitis present?
Hypoxemia, hypercapnia, cyanosis, wheeze, rales/ crackles, infection
How do you investigate chronic bronchitis?
Spirometry, Reid index
How is chronic bronchitis diagnosed?
FEV1/ FVC <0.7, Reid index >40%
How is chronic bronchitis managed?
Supplemental O2, abx + as with COPD
What is the pathophysiology of emphysema?
Alveoli permanently enlarge and lose elasticity
Inflammatory: proteases break down structural collagen/ elastin in the alveoli
How does emphysema present?
Pink puffer: exhaling slowly through pursed lips to increase pressure in bronchi, dyspnoea, weight loss, cough, “barrel chest”
How is emphysema diagnosed?
Spirometry, CXR: increase ant-post diameter, flattened diaphragm, increased lung-field lucency (more black)
How is emphysema treated?
As with chronic bronchitis/ COPD
What is obstructive lung disease?
Narrowed airways – normal lung volume (FVC), long time to exhale (wheeze) ie FEV is low
FEV1/FVC <0.7
Shallow spirometry graph
Asthma (variable) + COPD (fixed)
What is restrictive lung disease?
Tissue damage results in reduced lung volume
Low FVC, low FEV1
FEV1/FVC >0.8 - normal ratio
What is the difference between obstructive and restrictive lung disease?
If it’s obstructed ie a peanut - the air can eventually all get out it just takes ages to get it out. Whereas in restricted there is some dead tissue that can never be ventilated so can never be fully exhaled.
What is type 1 respiratory failure?
Type 1 Respiratory failure (1 thing wrong)
PO2 low (hypoxia), PCO2 normal
Damage of lung tissue preventing adequate oxygenation of the blood. The remaining normal lung is still sufficient to excrete co2.
Ventilation (V), Perfusion (Q) mismatch
ie COPD, pneumonia, pulmonary oedema, asthma, pneumothorax, ARDS
What is type 2 respiratory failure?
Type 2 Respiratory failure (2 things wrong)
PO2 low (hypoxia), PCO2 high (hypercapnia)
Alveolar ventilation insufficient to excrete co2 produced. Either due to reduced ventilatory effort or inability to overcome increased resistance to ventilation- affects lungs as a whole- co2 accumulates
Ie COPD, severe asthma, myasthenia gravis.
What is PaO2 in hypoxia?
↓ PaO2 (<8kPa), ↓ / ↔ PaCO2
What is PaCO2 in hypercapnia?
↓ PaO2 (<8kPa), ↑ PaCO2 (>6kPa)
What is respiratory failure?
Failure to maintain adequate gas exchange and characterised by abnormalities of arterial blood gas tension” = failure to oxygenate blood adequately
How is respiratory failure treated?
ABC
Treat underlying cause (COPD/Asthma/Pneumonia etc)
Oxygen
Continuous Positive Airway Pressure (CPAP) – Type 1
Non-Invasive Ventilation (NIV) – Type 2
What are the respiratory centres?
Respiratory stimulus
Act via effects on the brainstem respiratory centres in medulla oblongata and pons
What is asthma?
Paroxysmal and reversible airway obstruction.
What is the pathophysiology of asthma?
Airflow limitation
Hypersensitivity
What type?
Inflammation and Airway Remodelling
Hypertrophy of smooth muscle
Increased number of goblet cells
What causes asthma?
Allergic: Allergen (environmental stimuli), genetics, hygiene hypothesis
Non-Allergic: exercise, cold air, b-blockers (WHY?), infection
What exacerbates asthma?
Infection, trauma, allergens, pollution, smoking, stress, some medications
How does asthma present?
Diurnal variation (worse in morning), triggers, worse after NSAIDs/ B-blockers, wheeze, chest tightness, SOBOE, Unproductive cough
How is asthma investigated?
PEFR- peak flow diary, reversibility testing, asthma control questionnaire, FEV1/FVC <70%
How is asthma treated?
- SABA PRN - salbutamol
- Regular ICS - beclometasone
- LTRA - montelukast
- LABA - salmeterol
+/- Theophylline. If severe IgE mediated ?Omalizumab.
How is a severe asthma exacerbation managed?
O xygen
S albutamol nebs back to back
H ydrocortisone
I pratropium bromide
T heophylline
M agnesium sulphate
E escalate ie intubate/ ventilate
Theophylline, magnesium, escalate : will not be starting without a senior present
What is hypersensitivity pneumonitis?
Inflammation of the alveoli within the lung caused by type 3/ 4 hypersensitivity to inhaled organic dusts
How does hypersensitivity pneumonitis present?
Acute: fever, chills, malaise, cough, SOB, poorly formed granulomas; chronic: cough, progressive SOB, fatigue, weight loss, clubbing, tachypnoea, respiratory distress
How is hypersensitivity pneumonitis diagnosed?
Hx of symptoms after exposure to allergen, spirometry, lung biopsy- expansion of interstitium
How is hypersensitivity pneumonitis treated?
Avoid antigen, corticosteroids- prednisolone
What is cystic fibrosis?
Autosomal recessive mutation of the CFTR gene causing a misfolded CFTR protein. CFTR gene- Cl- channel chromosome 7. Thickens any secretions.
How does cystic fibrosis present?
Newborns: meconium ileus; childhood: failure to thrive, rectal prolapse. Young Adult: Chronic resp symptoms and infection test it. Pancreatic insufficiency (insulin dependent diabetes or steatorrhoea). Male infertility. Ileus.Lungs: cough, recurrent infection, clubbing, bronchiectasis, course bilateral crackles.
How is cystic fibrosis diagnosed?
Newborn screening (immunoreative trypsinogen due to damaged pancreas), sweat test: high Cl-
Sweat test Cl- >60mmol.
Faecal elastase for exocrine pancreatic dysfunction
Genetics for common CFTR mutations
Vitamin A, D,E levels - what are the fat soluble vitamins? A d e k
FBC, UANDE, LFT, Clotting factors, annual glucose tolerance test
CXR- hyperinflation, bronchiectasis signs,
Fatty liver, cirrhosis, chronic pancreatitis.
Faecal fat analysis
Aspergilis serology- 20% develop ABPA (FUNGAL)
How is cystic fibrosis treated?
Nutrition (fat soluble vitamins), chest physio, mucolytics: DNAase, SABAs, N-acetylcysteine, lung transplant
Physiotherapy (postural drainage)
Antibiotics for acute exacerbations or prophylactically
Mucolytics Dnase
Bronchodilators
Pancreatic enzyme supplements
Fat soluble vitamins supplements
Ursodeoxycholic acid
Median survival around 40 years
What are the problematic bacteria associated with cystic fibrosis?
Problematic bacteria include staph. aureus and pseudomonas aeruginosa
What is pneumothorax?
Abnormal collection of air in the pleural space leading to partial lung collapse
‘Sudden onset, sharp one sided pleuritic chest pain and SOB’
Air should not be found in the pleural space – there is no pathway for the air for to get in and the air in the lungs and bloodstream are of too low pressure to leak through into it.
The only way for air to enter the pleural space therefore is if there is damage to either the chest wall or the lungs allowing air to leak in, or if there is a micro-organism in the pleural space that is producing gas.
It is a build up of air in the pleural space (the area between the lungs and the chest wall). It causes the lung on the affected side to collapse and unable to inflate, leading to problems with breathing.
What causes pneumothorax?
Trauma (tension pneumothorax if one-way valve formed), spontaneous - air can move in and out- can heal on its own
Primary: damage to lungs with no underlying lung pathology
Secondary: underlying lung pathology that’s caused it
- Primary: no underlying lung disease, but risk factors include MALE, SMOKING, FAMILY HISTORY, CONNECTIVE TISSUE DISEASE (Marfans, Ehlers Danlos)
- Secondary: underlying lung pathology that has caused it.
- Trauma: injury inside the body (fractured ribs), injury outside the body (stab wound, gunshot, etc), medical procedure (catheter, biopsy, etc).
What are the symptoms of pneumothorax?
Pleuritic chest pain, SOB, tiredness, tachycardia
Signs: low blood pressure, low oxygen levels, diminished breath sounds on the affected side
•Symptoms: SOB, sharp, ONE SIDED chest pain, altered consciousness
In exam: sudden onset, one sided sharp chest pain, worse when breathing in, and becoming short of breath – lead you to think of pneumothorax.
How is pneumothorax investigated?
CXR (standing) - Gold standard
Gold standard: CXR
Absent lung markings
Collapsed lung
Tracheal deviation towards the pneumothorax
How is pneumothorax treated?
Observation, simple aspiration, intercostal tube drainage; tension: Bore needle in MCL 2nd space
Small spontaneous ones can heal on their own (no SOB, underlying lung disease)
- Treat the underlying cause, e.g. close the hole if there is an open wound causing it
- Chest drain
- Can also have surgery if its really bad
How does tension pneumothorax present?
Sudden onset breathlessness, pleural pain, reduced chest expansion, hyperresonant to percussion, reduced breath sounds. MEDICAL EMERGENCY
What is tension pneumothorax?
In a pneumothorax in which the hole in the pleura allows air in and out of it, whereas in a tension pneumothorax the hole acts as a one way valve; i.e. air can come into the pleural space but not out. This means that there amount of air in the pleural space increases rapidly – less space for air to come into the lung means the resp rate increases, which actually makes things worse as
Trachea deviated on CXR AWAY from tension pneumothroax – increased pressure on this side.
How is tension pneumothorax treated?
EMERGENCY > immediately insert a chest drain (insert a needle in the 2nd intercostal space mid clavicular line and drain out the extra air )
Emergency needle thoracotomy
What are the different types of lung cancer?
Small cell- paraneoplastic syndromes
non-small cell most common (80%)
Adenocarcinoma cell- most common + most common in non smokers
Squamous cell- most common in smokers
Large cell
How does lung cancer present?
Cough, weight-loss, haemoptysis, dyspnoea, chest pain, anaemia, clubbing,
What cancers can metastasise to the lungs?
Brain, bone, prostate, breast, thyroid, kidney
What can small cell lung cancer cause?
Paraneoplastic syndromes - ectopic Cushing’s syndrome, hypertrophic osteoarthroparthy (clubbing), SIADH
How is lung cancer investigated?
CXR: hilum enlargement, pulmonary opacity, rib bone lesions, pleural effusion, lung collapse. Chest CT. Bronchoscopy. Needle or surgical biopsy
How is lung cancer treated?
Stage 1/2: surgery, radical DXRT, stage 3/4: chemo/ RT, laser therapy and stenting palliative care
What is mesothelioma?
What: Cancer of the mesothelium (most commonly; pleura: lining covering the outer surface of the lungs - between that and the chest wall)
- Associations: Asbestos exposure, occupational link with delayed onset after exposure
- Symptoms: SOB, swollen abdomen, chest wall pain, fatigue, weight loss, fever, persistent cough, clubbing
- Dx: CXR and CT, confirmed by tissue biopsy
- Tx: Surgery, RT, Chemo (cisplatin and pemetrexed), pleurodesis. Often palliative
Why might a lung cancer patient present with a hoarse voice?
Laryngeal nerve palsy caused by tumour compression usually in L lung.
What is a pancoast tumour?
Tumour in apex of lung invades into sympathetic plexus in the neck causing compression of plexus resulting in Horner’s syndrome (ptosis, miosis, anhidrosis)
Where do lung cancers most commonly metastasise to outside of the lungs?
How does the prognosis vary between SCLC and NSCLC?
Poorer prognosis for SCLC
Neuroendocrine Tumours
Arise from APUD cells (type of neuroendo cells)
Rapid growing, highly malignant, early mets
Can cause –SIADH – secrete ADH
What is Wegener’s granulomatosis?
Systemic disorder that involves granulomatosis and polyangitis (autoimmune)
Autoimmune condition (small vessel vasculitis) with granulomas
Affecting the respiratory system and the kidneys
Associated with Cytoplasmic anti-neutrophil cytoplasmic antibodies (cANCAs)- responsible for the inflammation.
How does Wegener’s granulomatosis present?
Haemoptysis, cough, wheeze, SOB, glomerulonephritis, saddle nose deformity, nosebleeds, hearing loss, sinusitis
How is Wegener’s granulomatosis investigated?
Test for cANCA, CXR, renal biopsy
How is Wegener’s granulomatosis treated?
Immunosuppressant drugs:
Cyclophosphamide
Steroids ie prednisolone
plasma exchange
kidney transplant
What is pneumonia?
Inflammation of the lung parenchyma: lung tissue. Acute LRTI
What causes pneumonia?
Bacteria- strep. Pneumoniae, staph. aureus, haemophilus influenzae
Atypical: fungal- histoplasmosis, legionella, mycoplasma pneumoniae, viral: Influenza A
Aspiration pneumonia: poor swallow. RF?
Hospital acquired pneumonia: >48 hours after hospital admission
How does pneumonia present?
SOB, chest pain, productive cough (pus/ bloody sputum), fatigue, fever,
Signs: -Pyrexia -Cyanosis -Confusion, Tachycardia -Tachypnea, Consolidation- diminished expansion dull percussion, tactile vocal fremitus, bronchial breathing, pleural rub.
How is pneumonia managed?
Amoxicillin +/- clarithromycin (for atypical pneumonia cover)
Co-amoxiclav + clarithromycin for severe
How is pneumonia investigated?
CXR, bronchopneumonia: patchy areas/ lobar: localised fluid/ atypical: concentrated in peri-hilar region lobar/multilobar infiltration/cavitation/pleural effusion.
Late inspiratory crackles, bronchial breath sounds. bLood cultures. Obs. ABG. Bloods FBC, U&E, CRP, Pulse oximetry, sputum culture and microscopy.
What are the risk factors for pneumonia?
Stroke, Myasthenia gravis, reduced consciousness, oesophageal disease/ reflux
What are the complications of pneumonia?
Pleural effusion
Empyema – pus
Lung abscess
Respiratory failure
Septicaemia
Pericarditis
What is given to groups at risk of pneumonia?
Pneumococcal vaccine given to at risk groups
>65yrs old, Chronic disease, Diabetes mellitus, Immunosuppressed
What are the differentials for pneumonia?
If it doesn’t get better/ the question sounds weird
Old and just back from holiday?- Legionella disease- water tanks will be involved in the question
HIV/AIDS- PCP pneumocystis jiroveci – need bronchoalveolar lavage for diagnosis
Pseudomonas aeruginosa- green sputum
Bronchiectasis/ Cystic fibrosis patient get it
What is CURB-65?
Mortality risk assessment for pneumonia
Confusion (abbreviated Mental Test score 8 or less, or new disorientation in person, place or time).
Urea over 7 mmol/litre
Respiratory rate : 30 breaths per minute or more
Blood pressure <90/60mmHg
age 65 years or more.
What is TB?
Mycobacterium tuberculosis with caseating granulomas that eventually calcify within the lungs. Type 4 hypersensitivty.
How does TB present?
Systemic: Kidneys- sterile pyuria, brain- meningitis, lumbar vertebrae- Pott’s disease, adrenal glands- Addison’s, liver- hepatitis
Symptoms: Fever, night sweats, weight loss, haemoptysis, productive cough
How is TB investigated?
Man-toux test, Interferon GammaReleaseAssay, 3 sputum samples with Ziehl- Neelsen stain
How is TB treated?
Rifampicin: red secretions, isoniazid: peripheral neuropathy, pyrazinamide: gout and rash, ethambutol: optic neuritis (All 4 for 2 months, R and I for 6 months) Latent: Isoniazid ONLY 6 months
NOTIFIABLE DISEASE, contact tracing
What is a granuloma?
an aggregation of epithelioid histiocytes
TB
Secret ACE marker for systemic granulomatosis
TB, leprosy, Sarcoidosis, Crohns
Rifampicin: orange/ red discolouration of urine/ tears. Liver failure
Isoniazid- LFT, decreased WCC
Pyrozinomide- hepatitis, arthralgia
Ethambutol: optic neuritis always check ishara test before initiation
Risk factors
Poverty
Alcohol
Tobacco
Contact with TB
Immunosuppression
Biggest killer of HIV patients
Miliary TB
Haematogenous dissemination of TB all over.
Ix
Latent TB: Mantoux test if positive Tspot TB test
Tuberculin skin test- identifies immunity
Active TB: CXR- typically upper lobe consolidation+cavitation
3x sputum sample. 1 early in morning. MC+S Zeihl Neilsen stain - Acid Fast Bacilli
Extrapulmonary TB
Get a sample where you can. Lownstein Jenson medium 12 weeks.
Can go anywhere- meningitis big one.
Bone- collapse
Histology of sample: Caseating granuloma
What does A1AT cause?
Causes 2% of emphysema – RARE
inherited
What is A1AT deficiency?
A1AT regulates elastase activity
No A1AT = uncontrolled elastase activity
Elastase builds up in liver, causing cirrhosis
Elastase destroys alveoli leading to emphysema
Always consider in young patients with COPD and deranged LFTs
What is PE?
Emboli in lungs, usually from DVT below knees
What are the risk factors for PE?
Recent Immobility - >3 days
Previous DVT/ PE
Pregnancy
Thrombophilic syndromes – antiphospholipid, Factor V Leidens
Malignancy
Hormone Therapy – HRT, COCP
Smoking
How does PE present?
sudden onset dyspnoea, pleuritic chest pain, ?red swollen leg, haemoptysis, tachycardia, tachypnoea
How is PE investigated?
CT pulmonary angiogram (GOLD STANDARD), V/Q scan: mis-match, D-dimer (sensitive not specific)
How is PE managed?
Large clots: Oral anticoagulation (DOAC/ Warfarin), Fondaparinux, Unfractionated Heparin, LMWH then oral anticoagulation.
PE
Causes of Emboli: thrombosis, fat, amniotic fluid, air
Can get a low grade fever (Doesn’t always mean infection!!)
What score? Well’s >4pts CTPA, <4pts D-dimer.
Well’s Score
<2 – PE unlikely
2-6 – moderate possiblity – do a D-Dimer
6+ - CTPA
What do you need to investigate if unprovoked PE? Cancer
D-Dimer – what does it measure?
Is it accurate? negative excludes PE but positive doe not prove it. If positive, need to do imaging
What is the length of anti-coagulation therapy?
At least 3 months
If risk factors (and cause) have gone then stop
If unknown cause/ prolonged risk then at least 6 months+ - warfarin
SUDDEN ONSET OF SOB + CHEST PAIN WITH PAST HISTORY OF PAINFUL CALVES (DVT) AND RECENT LONG HAUL FLIGHT/IMMOBILISATION = PE.
Goodpasture’s syndrome
- What: Autoantibodies attack the basement membrane in the lungs and kidneys
- Symptoms: Lungs: haemoptysis, chest pain, cough, SOB. Kidneys: haematuria, proteinuria, oedema, high blood urea, HTN. Systemic: malaise, weight loss, fatigue, fever
- Dx: Biopsy to look for anti-GBM (glomerular basement membrane antibody)
- Tx: Plasmapheresis, Immunosuppressant drugs: cyclophosphamide, prednisone, rituximab
- Other: Antibodies attack alpha-3 subunit of type IV collagen. Type 2 hypersensitivity.
Sarcoidosis
Non caseating granulomatous inflammatory condition
Chest symptoms + extra-pulmonary manifestations ie erythema nodosum and lymphadenopathy
Bimodal: youngs adulthood and around 60. Women more than men. > in black people.
4 D’s of interstitial lung disease
o Dry cough
o Digital clubbing
o Dynspnoea
o Diffuse inspiratory crackles
- Erythema nodosum
Investigation
CXR: Enlarged hilar lymph nodes (bilateral hilar lymphadenopathy)
Raised serum ACE
hypercalcaemia
Gold standard: histology from biopsy (non caseating granulomas)
Management
Oral steroids
Methotrexate or azathioprine
Lung transplant
Granulomas: nodules of inflammation full of macrophages
*NB typical MCQ- 20-40y/o black woman – dry cough and SOB, nodules on shins suggesting erythema nodosum*
Pulmonary fibrosis
What: Progressive replacement of interstitial lung parenchyma with collagen/ scar tissue
- Causes: Over-proliferation of type 2 pneumocytes, stimulating myofibroblasts to produce collagen
- Symptom/signs: Coughing, SOB, cyanosis, digital clubbing
- Dx: CT chest- “honeycombing” and thickening of interstitial walls, spirometry: decreased TLC, FVC and FEV1
- Tx: Supplemental O2, antifibrotics (pirfenidone), lung transplant
Pulmonary hypertension
Pulmonary artery pressure PAP elevated >25mmHg
Asymptomatic or Shortness of breath on exertion, dyspnoea, syncope
If your pulmonary artery pressure is increased→ R ventricular hypertrophy → R heart failure → ascites/hepatomegaly
Causes: Drugs / congenital /idiopathic Left sided heart defects- MI/ valvular disorders Pulmonary disease- COPD, ILD etc Recurrent pulmonary embolisms
Tx- treat the underlying condition causing pulmonary hypertension
If untreated can lead to cor pulmonale
Cor Pulmonale = R sided HF secondary to pulmonary HTN.
Pleural effusion
Fluid in pleural space- stony dull to percussion. Decreased tactile vocal fremitus.
Diagnostic aspiration
Transudate <25g/L protein conc.
Causes hypoproteinemia- cirrhosis, nephrotic disease, malabsorption
Increased venous pressure - Cardiac failure, Constrictive pericarditis, Fluid overload
Exudate >35g/L protein conc - Leaky vessels so protein and fluid gets out.
Infection- pneumonia, TB. Inflammation- RA, autoimmune stuff. Malignancy
Large effusion causes tracheal deviation away from the pleural effusion side
Bronchiectasis
Chronic infection of bronchi/ bronchioles. Causes permanent dilation of airways.
H.influenzae, Strep.pneumoniae Staph aureus Pseudomonas aeruginosa
Causes
Anything that causes chronic inflammation or infection of the airways
CYSTIC FIBROSIS
Primary ciliary dyskinesia
post infection
Bronchopulmonary aspergillosis
Autoimmuine conditions
Symptoms
PERSISTENT cough. COPIOUS PURULENT sputum. haemoptysis
Signs
FINGER CLUBBING, course inspiratory crepitation
Ix
Sputum culture
CXR- TRAMLINE + RING SHADOWS cystic shadows
Spirometry of obstructive
Bronchoscopy- rule out obstruction, sample culture,
CF sweat test, Aspergillosis skin prick test
Tx
Physiotherapy to aid mucous drainage.
Bronchodilators or steroids may be useful depending on other underlying disease
