PULMONOLOGY Flashcards
What are the causes of COPD?
Smoking
a-1 antitrypsin deficiency
Dust e.g. cadmium, coal, cotton, cement, grain
What are the symtoms of COPD?
Cough (productive)
Wheeze
Dyspnoea
What are the signs of COPD?
Tachypnoea Accessory Muscles Hyperinflation Hyperresonence Reduced expansion Reduced breath sounds e.g. over bullae Reduced corticosternal distance Cyanosis Cor pulmonale (raised JVP)
What are the complications of COPD?
Acute exacerbations (+/- infection) Respiratory failure Polycythaemia abnormal increase in Hb Pneumothorax due to ruptured bullae Lung carcinoma
What are the stages of COPD?
FEV1 1 Mild >80% 2 Moderate 50-79% 3 Severe 30-49% 4 Very severe 30% \+ post bronchodilator FEV1/FVC <0.7
BUT the patient must be experiencing symptoms to diagnose
What are the signs of COPD on CXR?
Hyperinflation
Bullae
Flat hemidiaphragm
Hyperlucent lung fields
What are the investigations for COPD?
- Spirometry
- FBC
- CXR
- BMI
How is COPD managed?
- Stop smokinh
- Flu vaccine (annual) and pneumococcal vaccine (one-off)
- SABA OR SAMA
- FEV1 > 50% LABA or LAMA
FEV1 <50% LABA + ICS or LAMA - Oral theophylline (reduce if giving macrolide or fluoroquinolone)
Persistant exacerbation/ breathlessness: LABA+ICS_LAMA
Mucolytics for productive cough
What can improve survivial in COPD?
- Stop smoking
- Lung volume reduction surgery
- Long term O2 therapy
When should long-term O2 therapy be considered?
FEV1 <30% Cyanosis Polycythaemia Peripheral oedema Raised JVP PO2 <92% on room air
When should long-term O2 therapy be offered?
2 blood gasses, 3 weeks apart
pO2 < 7.3kPA or 7.3-.8kPA + 1 of…
- Secondary polycythemia
- Nocturna; hypoxaemia
- Peripheral oedema
- Pulmonary HTN
What microorganisms cause acute exacerbations of COPD?
H. Influenzae
S. Pneumoniae
Maroxella Catarrhalis
30% are viral
How are exacerbations of COPD managed?
Nebbed bronchodilator
7-14 days of prednisolone
Abx ONLY if sputum is purulent OR clinical signs of pneumonia
NIV when pH 7.25-35
What are ‘pink puffers’?
Primarily emphysema
Destruction in small airways leads to destruction of capillary beds so reduced O2 of Hb causing hyperventilation ‘puffers’ but with normal ABGs-less hypoxic so ‘pink’
TYPE 1 resp failure
What are ‘blue bloaters’?
Primarily chronic bronchitis
Redueced alveolar ventialtion so reduced O2 and reduced CO2
Cyanosed but not breathless (blue)
Chromic alveolar hypoxia leads to pulmonary HTN and R heart failure so oedematous (bloated)
Hypoxic drive maintains respiratory effor
What is Asthma?
TYPE I hypersensitivity (IgE) reaction causing CHRONIC INFLAMMATION OF THE AIRWAYS
REVERSIBLE BRONCHOSPASM (causing airway obstruction) due to:
- Bronchial muscle contraction
- Mucosal inflammation by mast cells and basophil degranualtion releasing inflammatory mediators
- Increased mucous production
What are the risk factors for Asthma?
Atopy: eczema, hayfever Not breast fed Maternal smoking Very clean house Multiple siblings Hygiene Aspirin Occupational
How does asthma present?
Widespread Expiratory Polyphonic Wheeze
Hyperinflated chest-hyperresonnance
Obstruction
Nocturnal cough
What are the investigations for Asthma?
PEF
Spirometry
FEV1(reduced)/FVC(normal) <70%
Reversed when given SABA (improvement >12% and increase in volume >200ml
How is Asthma managed?
SABA (Salbutamol) \+ ICS (Beclamethasone dipropionate or Fluicasone Proprionate) 100mch 2x2 \+ LEUKOTRIENE RECEPTOR ANTAGONIST (Oral monteleukast) \+ LABA (Salmeterol) (review LTRA) \+ Convert ICS and LABA to MART regimen (combined inhaler) with low maintenance ICS dose \+ Convert ICS to moderate dose 200mcg 2x2 \+ Increase ICS to high dose or Trial LAMA or THEOPHYLLINE
How is acute asthma classified?
Moderate:
- Worsening symptoms
- PEF <75% best/predicted
- No features of acute severe
Severe: any of
- PEF 33-50%
- RR >25
- HR >110
- Can’t complete sentances
Life-threatening: any of
- PEF <33%
- O2 <92% <8kPa
- Cyanosis
- CO2 normal
- Silent chest
- Poor respiratory effort and exhaustion
- Arrhythmias
- Hypotension
- Altered consciousnes
Near-fatal:
- Raised CO2
- Any need for ventilation assistance (low pH)
How is acute asthma managed?
Nebulise 5mg salbutamol through oxygen
Teotropium Bromide
Oral prednsiolone (continue 40-50mg 5 days after) or IV hydrocortisone
Magnesium sulphate IV
What is Pneumonia?
Inflammation of the alveoli in a lobar pattern
How is Pneumonia classified?
CAP v HAP
Acute v Chronic
Causative organism: bacterial v viral v fungal
Lung pathology:
- Lobar- S. Pneumoniae
Alveoli fill with plasma exudate and neutrophils-consolidation on CXR
- Broncho-patchy consolidation of different lobes
- Interstitial- H. Influenze
Accumulates of infiltrates into the alveolar walls, walls thicken, increased diffusion distance and irritated walls cause dry cough
What are the causative organisms of Pneumonia?
Streptococcus Pneumoniae
Staphylococcus Aureus
Haemophilus Influenzae
Klebisiella Pneumoniae
Atypical:
Mycoplasma pneumonia
Legionella pneumophillia
Chlamydia Psittaci
Fungal:
Pneumocystis jiroveci
What are the non-infective causes of Pneumonia?
- Aspiration Pneumonia
- Idiopathic interstitial Pneumonia
What is Streptococcal Pneumoniae Pneumonia?
Majority of cases
High fever
Rapid onset
Rusty sputum
>60 y/o
Associated with herpes virus
Vaccine available
What is Staphylococcal Pneumoniae Pneumonia?
After recent flu
IVDU
What is Haemophilus Influenzae Pneumonia?
COPD
Dry cough
What is Klebisiella Pneumoniae Pneumonia?
Alcoholics
Diabetics
‘Red-current jelly’ sputum
Upper lobes
Aspiration
Causes lung abscesses and empyema
How are the typical pneumonias treated?
Amoxicillin for 5 days
(Macrolide if penicillin allergic: doxycycline, Erythromycin or Clarithromycin)
If severe then add a macrolide for 7 days
Co-amoxiclav + clarithromycin/doxycycline/ceftriaxone/piptaz
What is Mycoplasma Pneumonia?
Atypical-won’t respond to penicillins as no peptidoglycan wall
Younger patients
Dry cough
Flu-like symptoms
Deranged LFTs
Bilateral CXR consolidation
Treat with macrolides e.g. Clarithromycin or Erythromycin
or Tetracyclines e.g. Doxycycline
What are the complications of Mycoplasma Pneumonia?
Complications: Cold agglutinins (IgM) cause (+ve test): Autoimmune haemolytic anaemia Thrombocytopenia Erythema multiforme Meningoencephalitis Guilla-Barre Peri/myocarditis Bullous myringitis (painful vesicles on tympanic emembrane-inflamed) Hepatitis Pancreatitis Acute gomerulonephritis
What is Legionella pneumophillia
legionnaire’s
Water tanks so air-conditioning
Flu-like fever Dry cough Bradycardia Confusion Pleural Effusion
Lymphopaenia
Hyponatreamia
Deranged LFTS
Macrolides Erythromycin or Clarithromycin
What is Chlamydia Psittacosis Pneumonia?
Parrots, poultry and sheep
Human to Human
Tetracyclines
What is Pneumocystis jiroveci Pneumonia?
HIV (most common opportunistic infection in AIDS) CD4+ <200
Dry cough Dyspnoea Fever Exercise-induced desaturation Absence of chest signs Bronchoalveolar lavage-silver stain shows cysts (sputum often fails to show PCP) CXR: Bilateral interstitial pulmonary infiltrates Ground glass opacity Pneumothorax is a common complication
Extrapulmonary (rare)
Hepatosplenomegaly
Lymphadenopathy
Choroid lesions
Co-trimoxazole
IV pentamidine
Steroids if hypoxic
What is Aspiration Pneumonia?
Foreign materials (e.g. saliva or food) entering the bronchiole tree
Risk factors:
- Incompetent swallowing
- Neurological diseases e.g. stroke and MS
- Intoxication
- Poor dental hygiene
- Impaired consciousness
- Impaired mucociliary clearance
- Prolonged hospitalisation/surgical procedures e.g. intubation
Chemical: acidic pneumonitis
Bacterial pathogens S. Pneumoniae, S. Aureus. H. Influenzae, Pseudomonas aeruginosa
What is Idiopathic Interstitial Pneumonia?
Non-infective pneumonia e.g. Cryptogenic organising pneumonia (bronchiolitis due to RA or amiodarone) can cause ground-glass opacity
What is Viral Pneumonia?
Damage to cells lining the airways/alveoli, alveoli fill with fluid impairing gas exchange
Severe viral pneumonia results in necrosis/haemorrhage into the lung parenchyma and presents like ARDS
Ground glass opacity (diffuse or patchy) on CXR
What are the risk factors for Lung Cancer?
SMOKING (x10)
Asbestos (x5)
(Arsenic, Radon, Nickle, Chromate)
What are the types of Lung Cancers?
Small Cell 15%
Non-Small cell:
- Squamous 35%
- Adenocarcinoma 30%
- Large-cell 10%
- Bronchial adenoma
How are Lung Cancers investigated?
- Contrast CT
- CXR (10% are reported as normal)
- Peripheral nodule
- Hilar enlargement
- Consolidation
- Lung collapse
- Pleural effusion
- Boney secondaries - Bronchoscopy to biopsy
- PET scan for Non-Small Cell to establish eligibility for treatment
- Cytology
- Sputum
- Pleural fluid - Lung function tests
How do Lung Cancers Present?
Cough Haemoptysis Dyspnoea Chest pain Slow resolving/recurrent pneumonia Cachexia Anaemia Clubbing Supraclavicular or axillary lymph nodes Hypertrophic Pulmonary Osteoarthropathy (wrist pain)
What are the paraneoplastic syndromes and complications for Small-Cell Lung Cancer?
- ADH (SIADH) hyponatreamia
- ACTH cushing’s
- Lambert-Eaton syndrome is like myesthenia
How is Small-Cell Lung cancer managed?
Nearly always disseminated (only ~20% are suitable for surgery)
May respond to radio and chemo-mostly used for palliation (reduce bronchiole obstruction)
What are the features, paraneoplastic syndromes and complications of squamous cell lung cancers?
Central, cavitating tumours
Finger clubbing
PTH-rp -> hypercalcaemia
TSH -> hyperthyroid
What are the features of Adenocarcinomas?
Typically peripheral
Most common in non-smokers
What are the features and paraneoplastic syndromes of Large-cell lung cancers?
Typically peripheral
Anaplastic, poor differentiation and poor prognosis
Secrete B-HCG
Gynaecomastia
How are Non-Small Cell Lung Cancers managed?
Excision if:
- SVC occluded
- FEV <1.5
- Malignant pleural effusion
- Vocal cord paralysis
Radiotherapy can be curatice
Add platinum-based chemo if advanced disease
What are the paraneoplastic syndromes/complications of Lung masses?
- Recurrent laryngeal nerve palsy
- Horner’s syndrome
- Phrenic nerve palsy
- Pericarditis
- SVC obstruction
- P.E (all malignancies)
What is Horner’s syndrome?
Damage to the sympathetic trunk (arises in spinal cord and ascends to head and neck), due to the presence of a Pancoast tumour in the apex of the lung. symptoms appear on the same side
- Miosis (constricted pupil. Light reflex is still present as this is parasympathetic)
- Partial ptosis (drooped eyelid or lower eyelid raised due to inactivated superior tarsal muscle)
- Anhidrosis (reduced sweating)
Flusging - Psuedoenopthalmos (inset eyeball)
What is Pulmonary Fibrosis (ILD)?
Scarring of the lung interstitium?
What are the causes of Upper Zone Pulmonary Fibrosis?
Allergic Bronchopulmonary ASPERGILLOSIS
Alveolitis
TB
EXTRINSIC ALLERGIC ALVEOLITIS (fungal spores, avian proteins)
Ankylosing Spondylitis
Sarcoidosis
Histiocytosis
Occupational e.g. silicosis-egg shell calcification of hilar lymph nodes
Pneumoconiosis (dust)
What are the causes of Lower Zone Pulmonary Fibrosis?
Bronchiectasis RA (others) Asbestos Drugs - Amiodarone - Methotrexate - Sulfasalazine (anti-rheum drugs) - Nitrofurantoin - Some dopamine receptor agonists
Idiopathic Interstitial
What is Idiopathic Interstitial LD?
A.K.A CRYPTOGENIC FIBROSING ALVEOLITIS
50-60 y, M>f
ANA +ve in 30%
Rhuem factor 1%
Poor prognosis,, 50% 5 year
What are the symptoms of Pulmonary Fibrosis?
Systemic:
- Flu-like
- Weight loss
- Malaise
arthralgia
Cor Pulmonale - sacral oedema - pitting oedema Clubbing Cyanosis Chest pain
Dry Cough
Fine inspiratory crackles bibasal
Exerctional dyspnoea (high R.R)
What are the investigations for Pulmonary Fibrosis?
Spriometry: restrictive CT: Honeycombing CXR: Ground glass opacity with lower lobe nodule shadows (reduced lung volume) ABG Type 1 RF, Type 2 if severe Biopsy: interstitial pneumonia Reduced transfer factor Broncho-alveolar Lavage: alveolitis
How is Pulmonary Fibrosis managed?
Give O2
Pulmonary rehab
Palliation
Transplant
What is Asbestosis?
Pleural plaques:
- MC
- 20-40 year latency
- Benign, no malignant changes
Diffuse Pleural thickening
Asbestosis:
- Severity is proportional to length of exposure
- 15-30 year latency
Mesothelioma:
- Malignant disease of the pleura
- Progressive SOB, Chest pain, pleural effusion
- Give palliative chemotherapy
What is Extrinsic Allergic Alveolitis?
Inhalation of allergens e.g. fungal spores or avian proteins resulting in a HYPERSENSITIVITY REACTION
ACUTE: alveoli infiltrated with acute inflammatory cells
(Fevers, rigors, myalgia, cough, dyspnoea, crackles)
CHRONIC: granuloma formation and obliterative bronchiolitis
(Dyspnoea (exertional), weight loss, Type 1 resp failure, Cor Pulmonale)
FBC, Raised ESR, ABG
CXR: U. Zone motelling/consolidation
BAL: lymphocytes and mast cells
Remove allergens, give O2, Long-term prednisolone
What is Allergic Bronchopulmonary Aspergillosis?
Allergy to aspergillus spores (RAST test)
Proximal BRONCHIECTASIS EOSINOPHILIA- IgE - Wheeze - Cough - Dyspnoea
CXR:
- Tram track
- Mass
- Parahilar ring shadow
- Central cystic/varicose
STEROIDS and ITRACONAZOLE
What are the causes of Bilateral Hilar Lymphadenopathy?
SARCOIDOSIS
TB (mycoplasma)
Malignancy (lymphoma, carcinoma)
Pneumoconiosis
Extrinsic Allergic Alveolitis
Hystiocytosis
What is Sarcoidosis?
MULTISYSTEM GRANULOMATOUS DISEASE
What are the features of sarcoidosis?
Conjunctivitis and keratoconjunctivitis
Uveitis
Facial Nerve Palsy
Pituitary dysfunction
Upper Zone lung fibrosis with bilateral hilar lymphadenopathy
Hepatosplenomegaly
Raised Ca2+: renal stones
Erythema nodosum
Acute arthropathy
What can be detected on investigation in Sarcoidosis?
Low Na+-ADH is produced ectopically
Raised serum ACE
Cytopenia = eosinophillia
Raised ESR
HyperCa2+
Lymphocytosis and lymphopaenia
Treat with Steroids and NSAIDS
What is Pleural Effusion?
Build up of fluid in the pleural space
Can be Exudate >30g/L
or Transudate <30g/L of protein
What are the features of Pleural Effusion?
Dullness on percussion
Reduced breath sounds and vocal resounnance
Reduced chest expansion
Non-productive cough
Dyspnoea
Pleuritic chest pain
What are the causes of Transudate Pleural Effusion?
Increased venous pressure
HEART FAILURE Hypoalbuminaemia (Liver disease or nephrotic syndrome) Hypothyroidism Meig's syndomre: - Ovarian tumour - ascites - Pleural effusion
What are the causes of Exudate Pleural Effusion?
Increased capillary leakiness
INFECTION (pneumonia, TB, Subphrenic abscess) CT disease (RA, SLE) Neoplasm (Lung cancer, mesothelioma, metastases) Pancreatitis PE Dressler's syndrome Yellow nail syndrome
What is Light’s Criteria?
25-35g/L protein
Exudate likely if…
Pleural fluid protein/ serum >0.5
Pleural fluid LDH/ serum >0.6
Pleural fluid LDH >2/3 the upper limit of normal serum
What else makes Exudative Pleural effusion more likely?
Low Glucose:
- RA
- TB
Raised Amylase:
- Acute pancreatitis
- Oesophageal perforation
Blood staining:
- Mesothelioma
- TB
- PE
What does imaging show in Pleural Effusion?
PA CXR
- Small: Blunted costophrenic angles
- Large: Concave border (unless pneumothorax too in which case flat border)
USS guided aspiration and detect seprations
Contrast CT to detect cause
What is measured in Pleural Fluid analysis?
pH Protein LDH Glucose Cytology Microbiology
How is Recurrent Pleural Effusion managed?
- Aspirate
- Pleurodesis: artificially obliterate the pleural space by adhering them together
- Indwelling pleural catheter
- Relieve symptoms
What is Lambert-Eaton syndrome?
Small cell lung cancer
Reduced release of acetylcholine
Muscle weakness, depressed reflexes and autonomic dysfinction- postural BP drop
What are the risk factors for a Pulmonary Embolism?
Sex-female Pregnancy Age Surgery Malignancy Oestroge (OCP/HRT) DVT (Prev PE) Immobility Colosal size (high BMI) A Lupus
What is the pathophysiology of a Pulmonary Embolism?
Risk factors contribute to Virchow’s triad:
Venous throbosis in the:
Popliteal/Femoral/Iliac veins embolises and travels through the venous system -> RA -> RV -> occlude pulmonary a artery causing a:
Saddle embolism occluding central arteries or saddle embolus
- Clot reduces blood flow (V/Q mismatch)
- Reduced CO2 delivery to lungs, builds up in blood, detected by medullary chemoreceptors increase R.R
- Low O2 detecetd by aortic/carotid receptors increase R.R and H.R - Saddle embolus causes PULMONARY HYPERTENSION -> back up of blood to heart -> RH strain
- Circulation to lung peripheries cut off leading to ischaemia and infarct (although infarct is rare due to lots of collaterals so only really occurs in patients with pre-existing poor flow to lungs e.g. COPD)
- irritates somatic endings on parietal pleura causing adrenergic response increase H.R and pleuritic chest pain
- ischaemic tissue becomes inflamed and adheres to pleura causing plueral rub and ARDS
How does Pulmonary Embolism present?
Triad:
- Dyspnoea/SOB
- Haemoptysis
- Pleuritic chest pain (focal and localised, with each breath)
Tachypnoea Tachycardia Cyanosis Hypotension Dizziness and syncope Pyrexia Signs of DVT Pleural rub Increased inflammatory cells -> increased vessel permeability -> ARDS
What is Well’s score?
3 Signs and symptoms of DVT 3 Alternative diagnosis less likely 1.5 Tachycardia 1.5 Immobile >3days/ surgery <4 weeks ago 1.5 Previous DVT/PE 1 Haemoptysis 1 Malignancy
> 4 means P.E is likely
How are Pulmonary Embolisms investigated?
- Do a CXR to rule out other diagnoses
- If wellsscore >4 then immediately do CTPA (V/Q if renal failure/contrast allergy) Give LMWH if delayed
If <4 do a D-Dimer and do above if +ve - ECG
- Tachycardia
- RBBB+R axis deviation
- S1Q3T3
Large S in I Large Q and inverted T in III
(Pulmonary angiography is gold standard BUT high risk of complications)
How are normal Pulmonary Embolisms managed?
- LMWH or FONDAPURINUX until INR >2.0 (3.5 in recurrent P.Es) or for 5 days (6 mo in CA patients)
- Warfarin within 24 hours for at least 3 months (definitely >3 mo if PE unprovoked)
How are Massive Pulmonary Embolism with Circulatory Failure managed?
THROMBOLYSIS
What is Homan’s sign?
Tender calf muscle when leg dorsiflexed
How are Pulmonary Embolisms prevented?
Give heparin e.g. deltaparin/Enoxiparin to all immobile patients
Stop oestrogen 4 weeks prior to surgery
What are the causes of Bronchiectasis?
Post-infective
- HIV TB
- Measles
- Pertussis
- Pneumonia
Cystic fibrosis
Bronchiole obstruction
- Cancer
- Foreign body
Immune deficiency
- Selective IgA
Allergic Bronchopulmonary Aspergillosis
Cilliary Dyskinesia
- Kartagener’s
- Young’s
RA
UC
Idiopathic
Yellow nail syndrome
What is the pathophysiology of Bronchiectasis?
Inflammation
Neutrophils, Cytokines
NO and O. radicals accumulate
Bronchial and prebronchial destruction
Elastic tissue lost
BRONCHIOLES PERMANENTLY DILATED (would usually taper)
What are the features of Bronchiectasis?
OBSTRUCTIVE PATTERN
- Persistent cough
- Purulent sputum
- Intermittent haemoptysis
- Clubbing
- Wheeze
- Coarse insipiratory crepitus
What are the complications of Bronchiectasis?
Pneumonia
Plueral effusion
Pneumothorax
Cerebral abscess
Amyloidosis
What is seen on CT in Bronchiectasis?
Signet rings where the artery looks much denser next to the airy bronchi
Clusters of grapes: appear to crowded together
Bronchi seen within 1cm of pleura as dilation makes them more visible
What is seen on CXR in Bronchiectasis?
Tram tracking: outlining of dilated and thickened bronchi
Cystic shadows
How is Bronchiectasis managed?
- Physical training
- Postural drainage BD
- Abx when axacerbated
( - Sometimes bronchodilators
- Immunisations
- Surgery if localised
What is Kartagener’s syndrome?
Primary CILLIARY DYSKINESIA-immobility
Associated with DEXTROCARDIA and SINUS INVERSUS
Causes recurrent SINUSITIS and INFERTILITY
What are the causes of ARDS?
Infection:
- Sepsis
- Pneumonia
Trauma
Smoking
Pancreatitis:
- Liver failure
Massive blood transfusions
Cardio-pulmonary bypass
What is the pathophysiology of ARDS?
Lung damage releases inflammatory mediatorys which increases permeability of alveolar capillaries causing fluid to accumulate in the alveoli = NON-CARDIOGENIC PULMONARY OEDEMA
What are the features of ARDS?
Dyspnoea Tachypnoea Tachycardia Peripheral vasodilation Cyanosis Bilateral FINE INSPIRATORY LING CRACKLES (pulmonary oedema)
How is ARDS investigated?
- CXR shows bilateral lung infilitration
- ABG shows low O2
- Pulmonary artery catheter measures pulmonary capillary wedge pressure which gives an idea of L atrial pressure, if >20mmHg then pulmonary oedema caused by cardiogenic issues
What are the diagnostic criteria for ARDS?
Acute Onset (<1 week)
CXR shows pulmonary oedema (bilateral infiltration)
Non-cardiogenic pulmonary oedema PCWP <19mmHg or NO CONGESTIVE HF
Refractory hypoxaemia
How is ARDS managed?
ITU
Respiratory support: oxygenate/ventilate with CPAP
Circulatory support
Treat sepsis
What is Pulmonary Oedema?
FLUID accumulates in the TISSUE and AIRSPACE of the lung resulting in impaired gas exchange and RESPIRATORY FAILURE
CXR is same as in HF
What are the causes of Pulmonary Oedema?
CARDIOGENIC: L ventricle fails to remove blood from pulmonary circulation
e.g. HEART FAILURE
NON-CARDIOGENIC: initial and rapid increase in PUMONARY VASCULAR PRESSURE due to vasoconstriction or blood flow causing parenchyma and vacular injury = LEAKY CAPILLARIES
- ARDS
- Drowning
- Fluid overload
- Aspiration
- Neurogenic
- Allergic
- Acute glomerulonephritis
What is Idiopathic Pulmonary Arterial Hypertension?
No known underlying cause
Risk factors: - Female - 20-40 - FHx (10% A.D) Cocaine
What are the features of Idiopathic Pulmonary Arterial Hypertension?
Increased pulmonary artery pressure >25mmHg at rest and >30mmHg on exercise
Progressive SOB
Cyanosis
Tricuspid regurgitation on ECHO
Raised JVP with prominent A wave
Loud O2
R ventricular heave
RHF
How is What Idiopathic Pulmonary Arterial Hypertension managed?
- Diuretics in RHF
- Anticoagulation
- Heart-lung transplant
- Vasodilator therapy
What is the gene mutation in Cystic Fibrosis?
A.R mutation of DELTAF508 on CHROMOSOME 7
(CF Transmembrane Conductance Regulator (CFTR))
1/25 people are carriers
What is the pathophysiology of Cystic Fibrosis?
Dysfunction of the CFTR protein (which is the Cl- ion channel in exocrine glands) means that less Cl- diffuses into secretions from the duct epithelial cells.
This reduces the H2O content of the peri-cilliary mucous (reduced osmotic gradient) leading to THICK and STICKY mucous (increased viscosity)
Reduced clearance of mucous means it accumulates and obstructs the secretory passageways in the GI, Resp and Genito-urinary tracts
This also reduces Cl- ABSORPTION in sweat glands so there is more Cl- in sweat (salty babies)
What are the GI tract features of Cystic Fibrosis?
BILIARY TREE-delayed passage of BILE causing LIVER INFLAMMATION resulting in
- GALLSTONES
- CIRRHOSIS
- PORTAL HTN
GI TRACT- reduced movement of INTESTINAL contents
- CHILDREN/ADULTS this causes DISTAL ILEAL OBSTRUCTION SYNDROME (DIOS)
- Neonates causes MECONIUM ILEUS (meconium is retained) resulting in JAUNDICE and RECTAL PROLAPSE
PANCREAS-can’t secrete DIGESTIVE ENZYMES
- STEATORRHOEA
- reduced FAT and PROTEIN absorption resulting in FAILURE TO THRIVE and reduced ADEK vitamin absorption
- OSTEOPOROSIS due to reduce VIT D
the enzymes DEGRADE the pancreas causing scarring and inflammation eventually resulting in
- DMT2
What are the Respiratory tract features of Cystic Fibrosis?
URT:
- Nasal polyps
- Sinusitis due to retained secretions
LRT: Resp failure causing Hypoxia - Cyanosis - Clubbing Cor Pulmonale Pneumothorax Haemoptysis Obstructive Lung disease: hyperinflation and abnormal spirometry Retention of secretions: BRONCHIECTASIS Chronic Productive Cough Bilateral Coarse Crackles Recurrent Chest infections
What are the Genito-urinary tract features of Cystic Fibrosis?
Vas deferens issues in utero leading to male infertility
Female subfertility
What are the common organisms in Cystic Fibrosis related chest infections?
- Staph Aureus
- Psuedomonas Aeruginosa
- Aspergillus
- Burkholderia cepacia
What are the investigations for Cystic Fibrosis?
- genetic screening
- Cl- IN SWEAT > 60MMO/L (Cl>Na)
- Faecal elastase
- Annual Glucose Tolerance Test
How is Cystic Fibrosis managed?
- Ursodeoxycholic acid in liver inflammation
- Pancreatic enzyme supplements
- Supplements (high fat and calorie diet)
- Chest physio BD
- Antibiotics
- Vaccinations
What is a Pneumothorax?
Presence of gas in the pleural space
What are the types of Pneumothorax?
Primary: no underlying lung pathology
Secondary: underlying lung disease
Closed: Pleuritic cavity pressure < atmospheric pressure
Open: Air can enter the chest from the outside
Tension: Pleuritic cavity pressure > atmospheric pressure
- One way valve formed between damaged tissue so gas continues to enter
- this significantly impairs respiration and/or blood circulation by putting pressure on the mediastinal/thoracic structures
What are the features of Pneumothorax?
- Chest pain
- Shortness of breath
- Reduced breath sounds on that side
- Hyperresonance
- Reduced vocal resonance and tactile fremitus ‘99’
How are Pneumothoraces managed?
PRIMARY:
Small <2cm: Monitor
Large: Syringe and Chest drain into 2nd intercostal space mid clavicular line
SECONDARY:
Small: Syringe and Chest drain
Surgery: Pleurodesis- stick pleura together or Pleurectomy-remove the pleural membranse
Will fail to inflate if there is an injury to a right main bronchus
What is Atelectasis?
BLOCKAGE or INCREASED PRESSURE in or around BRONCHIOLES
BASAL ALVEOLAR COLLAPSE causing COLLAPSE OF 1 or MORE LOBES
RESPIRATORY DIFFICULTY (Tachypnoea and Pleural Effusion)
AIRWAYS OBSTRUCTED BY BRONCHIAL SECRETIONS with REDUCED OR ABSENT GAS EXCHANGE
AIR IS TRAPPED
Causes by:
- TB
- Post-op
- Lack of surfactant in infants
What are the features of Tension Pneumothorax?
- Respiratory distress
- Tachycardia
- Cyanosis
- Reduced consciousness
Displacement of Apex HB
Resonance on tapping the sternum
Trachea displaced away from the collapse
JVP
What are the features of an Obstructive respiratory disease pattern?
Reduced FEV1
FVC normal or a bit reduced
FEV1/FVC= REDUCED
e.g. Asthma, COPD, Bronchiectasis
What is Bronchiolitis Obliterans?
Popcorn lung
Obstruction of smallest airways due to inflammation
What are the feature of a Restrictive respiratory disease pattern?
Reduced FEV1
Reduced FVC
equally
FEV1/FVC= NORMAL OR RAISED
e.g. Fibrosis (aspestosis, sarcoidosis), ARDS
Neuromusclar and Kyphoscoliosis
What are the causative organisms for TB?
MYCOBACTERIUM
TUBERCULOSIS
Bovis
Africanum
Non-mobile, rod bacili, obligate aerobe
What is the pathophysiology of TB?
Mycobacterium ENGULFED by ALVEOLAR MACROPHAGES but can’t kill so continue to multiply
Primary complex of TUBERCLE LADEN MACROPHAGES
CASEATING GRANULOMA
Local drainage into HILAR LYMPH NODES
Lymphocytes and epitheloid + LANGHERHAN’S GIANT CELLS
GHON COMPLEX: INFECTION IS CONTAINED
What are the features of Primary and Milliary TB?
Immune destruction of the lung - Fever - Cough: haemoptysis - Night sweats - Weight loss - Malaise - Breathlessness - Crackles - Pleural Effusion - Cavitation and fibrosis Seen on CXR
What conditions can reactivate TB?
- Diabetes
- CKD
- Haem malignancy
- Organ transplant
- Tumour necrosis
- Silicosis
- Low body weight
- HIV
- Substance abuse and IVDU
- Immunosupression i.e. STEROIDS
What are the extra-pulmonary features of Secondary TB?
- Larynx
- Lymph nodes -> cervical SCROFULODERMA
- CNS -> TB meningitis
- Renal spread to LUT
- GI due to swallowing
- Bones and Joints -> Vertebral bodies -> Pott’s
What is Pott’s (TB)?
In the spine
How is TB managed?
Rifampicin
Isonazid
Pyroxidine
Ethambutol
3 or 4 for 2/12
18/12 if CNS
What are the diagnostic tests for TB?
- NAAT and chromotography
- ACID FAST
- ZIEHL NEILSEN stain
- Auramine stain
- Culture is gold standard
- Tuberculin Sensitivity Test on skin (delayed-type hypersensitivity reaction)
- Gastric aspirates in children
Define: stridor
narrow or obstructed upper airways, sounf od turbulent airflow through larynx or bronchial tree
What is Obstructive Sleep Apnoea?
Throat muscles intermittently relax in sleep blocking airways, breathing repeatedly stops and starts
What are the predisposing factors for Obstructive Sleep Apnoea?
- MARFAN’S
- large tonsils
- Obesity -> loswe weight
- Macroglossia e.g. in Acromegaly, Hypothyroidism, Amyloidosis -> Can manage with intraoral devices
What are the consequnces of Obstructive Sleep Apnoea?
Daytime sleeping: EPWORTH sleepiness scale, multi-sleep latency test
Reduced arousal response in REM
HTN
Compensated RESPIRATORY ACIDOSIS
What is Thoracoabdominal movement paradox?
Reverses inspiration/expiration chest contractions: abdomen moves weirdly
