Respiratory Flashcards

1
Q

What type of hypersensitivity reaction is asthma?

A

Type I (IgE)

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2
Q

What type of hypersensitivity reaction is Goodpasture’s disease?

A

Type II (IgG)

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3
Q

What type of hypersensitivity reaction is SLE?

A

Type III (immune complex formation)

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4
Q

What type of hypersensitivity reaction is TB?

A

Type 4 (cell mediated)

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5
Q

What is a type I hypersensitivity reaction?

A

Reaction mediated by IgE antibodies.
(Allergy) ie anaphylaxis

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6
Q

What is type II hypersensitivity?

A

Cytotoxic reaction mediated by IgG or IgM antibodies.
(antibody binds to host cell which is perceived to be foreign destruction)
Goodpastures, Graves, Myasthenia Gravis

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7
Q

What is type III hypersensitivity?

A

Reaction mediated by immune complexes – deposited in vessel walls.
RA, post-strep glomerulonephritis, reactive arthritis, SLE

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8
Q

What is type IV hypersensitivity?

A

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

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9
Q

What happens in type I hypersensitivity?

A

IgE mediated, mast cell degranulation, antibody binding to antigen eg asthma, allergy

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10
Q

What happens in type II hypersensitivity?

A

IgG reaction – cytotoxic – IgG binds to cell and kills its – Rhesus haemolytic disease, Goodpastures,

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11
Q

What happens in type III hypersensitivity

A

Immune complex forms (soluble but saturates) – SLE, EAA

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12
Q

What happens in type IV hypersensitivity?

A

Cell mediated delayed (CD-4 cells are sensitized to infection but cant clear it - granuloma) – TB, sarcoid, Wegeners,

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13
Q

What is total lung capacity?

A

(5900ml): max volume of air/gas the lungs can contain/accommodate

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14
Q

What is vital capacity?

A

(4700ml): amount of effort that can be exhaled with max effort after max inspiration

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15
Q

What is tidal volume?

A

(500ml): Volume of air inspired (inhaled) and expired (exhaled) in a normal breath

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16
Q

What is inspiratory capacity?

A

(3500ml): max volume of air that can be inhaled after normal tidal expiration

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17
Q

What is expiratory reserve volume?

A

(1200ml): Volume of air exceeding tidal expiration that can be exhaled with max effort

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18
Q

What is inspiratory reserve volume?

A

(3000ml): Volume of air exceeding tidal inspiration that can be inhaled with max effort

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19
Q

What is functional residual capacity?

A

(2400ml): Volume of air remaining in the lungs after a normal tidal expiration

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20
Q

What is residual volume?

A

(1200ml): Volume of air that remains in lungs after expiration (keeps alveoli inflated)

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21
Q

What is FEV?

A

How much air a person can exhale during a forced breath

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22
Q

What is FEV1?

A

FEV in 1 second

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23
Q

What is FVC?

A

Total volume of air forcefully exhaled during FEV test

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24
Q

What is peak expiratory flow rate (PEFR)?

A

The peak flow rate during expiration

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25
How do you calculate total ventilation per minute?
Tidal volume x resp rate
26
What is COPD?
Irreversible progressive disorder of airway obstruction
27
What does COPD include?
Chronic bronchitis and emphysema
28
What causes COPD?
Smoking, fumes and dust, air pollution, genetics
29
How does COPD present?
Dyspnoea, tachypnoea, barrel chest SOB, chronic cough, recurring chest infections, wheeze
30
What measurement classifies COPD?
FEV1/ FVC \<70%
31
How is COPD managed?
1. SABA/ SAMA 2. LABA +LAMA OR LABA and ICS (if asthmatic features/ steroid responsive) 3. triple therapy. + smoking cessation, regular physical activity Other tx options: oxygen, abx in exacerbation, mucolytics, theophylline.
32
What might you want to rule out if no smoking history in COPD?
Alpha-antitrypsin deficiency
33
What vaccinations are given to someone with newly diagnosed COPD?
Pneumococcal and influenza
34
How are COPD exacerbations treated?
Oral pred. 30mg for 7-14 days
35
What is spirometry?
Post-bronchodilator measurement.
36
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
37
What are the stages of COPD?
1: FEV1 \>80% 2: FEV1 50-79% 3: FEV1 30-49% 4: FEV1 \<30% of predicted value
38
What are chronic bronchitis patients nicknamed?
Blue bloaters
39
What are emphysema patients nicknamed?
Pink puffers
40
What is chronic bronchitis?
Airway inflammation and narrowing Increased mucous production
41
What is emphysema?
Destruction and dilation of air spaces Can’t recoil and expel air
42
What is required to be diagnosed with chronic bronchitis?
Inflammation of bronchi with a productive cough for 3/12 for at least 2 years
43
How does chronic bronchitis present?
Hypoxemia, hypercapnia, cyanosis, wheeze, rales/ crackles, infection
44
How do you investigate chronic bronchitis?
Spirometry, Reid index
45
How is chronic bronchitis diagnosed?
FEV1/ FVC \<0.7, Reid index \>40%
46
How is chronic bronchitis managed?
Supplemental O2, abx + as with COPD
47
What is the pathophysiology of emphysema?
Alveoli permanently enlarge and lose elasticity Inflammatory: proteases break down structural collagen/ elastin in the alveoli
48
How does emphysema present?
Pink puffer: exhaling slowly through pursed lips to increase pressure in bronchi, dyspnoea, weight loss, cough, “barrel chest”
49
How is emphysema diagnosed?
Spirometry, CXR: increase ant-post diameter, flattened diaphragm, increased lung-field lucency (more black)
50
How is emphysema treated?
As with chronic bronchitis/ COPD
51
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)
52
What is restrictive lung disease?
Tissue damage results in reduced lung volume Low FVC, low FEV1 FEV1/FVC \>0.8 - normal ratio
53
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.
54
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
55
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.
56
What is PaO2 in hypoxia?
↓ PaO2 (\<8kPa), ↓ / ↔ PaCO2
57
What is PaCO2 in hypercapnia?
↓ PaO2 (\<8kPa), ↑ PaCO2 (\>6kPa)
58
What is respiratory failure?
Failure to maintain adequate gas exchange and characterised by abnormalities of arterial blood gas tension” = failure to oxygenate blood adequately
59
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
60
What are the respiratory centres?
Respiratory stimulus Act via effects on the brainstem respiratory centres in medulla oblongata and pons
61
What is asthma?
Paroxysmal and reversible airway obstruction.
62
What is the pathophysiology of asthma?
Airflow limitation Hypersensitivity What type? Inflammation and Airway Remodelling Hypertrophy of smooth muscle Increased number of goblet cells
63
What causes asthma?
Allergic: Allergen (environmental stimuli), genetics, hygiene hypothesis Non-Allergic: exercise, cold air, b-blockers (WHY?), infection
64
What exacerbates asthma?
Infection, trauma, allergens, pollution, smoking, stress, some medications
65
How does asthma present?
Diurnal variation (worse in morning), triggers, worse after NSAIDs/ B-blockers, wheeze, chest tightness, SOBOE, Unproductive cough
66
How is asthma investigated?
PEFR- peak flow diary, reversibility testing, asthma control questionnaire, FEV1/FVC \<70%
67
How is asthma treated?
1. SABA PRN - salbutamol 2. Regular ICS - beclometasone 3. LTRA - montelukast 4. LABA - salmeterol +/- Theophylline. If severe IgE mediated ?Omalizumab.
68
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
69
What is hypersensitivity pneumonitis?
Inflammation of the alveoli within the lung caused by type 3/ 4 hypersensitivity to inhaled organic dusts
70
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
71
How is hypersensitivity pneumonitis diagnosed?
Hx of symptoms after exposure to allergen, spirometry, lung biopsy- expansion of interstitium
72
How is hypersensitivity pneumonitis treated?
Avoid antigen, corticosteroids- prednisolone
73
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.
74
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.
75
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)
76
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
77
What are the problematic bacteria associated with cystic fibrosis?
Problematic bacteria include staph. aureus and pseudomonas aeruginosa
78
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.
79
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 1. Primary: no underlying lung disease, but risk factors include MALE, SMOKING, FAMILY HISTORY, CONNECTIVE TISSUE DISEASE (Marfans, Ehlers Danlos) 2. Secondary: underlying lung pathology that has caused it. 3. Trauma: injury inside the body (fractured ribs), injury outside the body (stab wound, gunshot, etc), medical procedure (catheter, biopsy, etc).
80
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.
81
How is pneumothorax investigated?
CXR (standing) - Gold standard Gold standard: CXR Absent lung markings Collapsed lung Tracheal deviation towards the pneumothorax
82
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
83
How does tension pneumothorax present?
Sudden onset breathlessness, pleural pain, reduced chest expansion, hyperresonant to percussion, reduced breath sounds. MEDICAL EMERGENCY
84
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.
85
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 ) ## Footnote Emergency needle thoracotomy
86
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
87
How does lung cancer present?
Cough, weight-loss, haemoptysis, dyspnoea, chest pain, anaemia, clubbing,
88
What cancers can metastasise to the lungs?
Brain, bone, prostate, breast, thyroid, kidney
89
What can small cell lung cancer cause?
Paraneoplastic syndromes - ectopic Cushing’s syndrome, hypertrophic osteoarthroparthy (clubbing), SIADH
90
How is lung cancer investigated?
CXR: hilum enlargement, pulmonary opacity, rib bone lesions, pleural effusion, lung collapse. Chest CT. Bronchoscopy. Needle or surgical biopsy
91
How is lung cancer treated?
Stage 1/2: surgery, radical DXRT, stage 3/4: chemo/ RT, laser therapy and stenting palliative care
92
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) 2. Associations: Asbestos exposure, occupational link with delayed onset after exposure 3. Symptoms: SOB, swollen abdomen, chest wall pain, fatigue, weight loss, fever, persistent cough, clubbing 4. Dx: CXR and CT, confirmed by tissue biopsy 5. Tx: Surgery, RT, Chemo (cisplatin and pemetrexed), pleurodesis. Often palliative
93
Why might a lung cancer patient present with a hoarse voice?
Laryngeal nerve palsy caused by tumour compression usually in L lung.
94
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)
95
Where do lung cancers most commonly metastasise to outside of the lungs?
96
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
97
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.
98
How does Wegener's granulomatosis present?
Haemoptysis, cough, wheeze, SOB, glomerulonephritis, saddle nose deformity, nosebleeds, hearing loss, sinusitis
99
How is Wegener's granulomatosis investigated?
Test for cANCA, CXR, renal biopsy
100
How is Wegener's granulomatosis treated?
Immunosuppressant drugs: Cyclophosphamide Steroids ie prednisolone plasma exchange kidney transplant
101
What is pneumonia?
Inflammation of the lung parenchyma: lung tissue. Acute LRTI
102
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
103
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.
104
How is pneumonia managed?
Amoxicillin +/- clarithromycin (for atypical pneumonia cover) Co-amoxiclav + clarithromycin for severe
105
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.
106
What are the risk factors for pneumonia?
Stroke, Myasthenia gravis, reduced consciousness, oesophageal disease/ reflux
107
What are the complications of pneumonia?
Pleural effusion Empyema – pus Lung abscess Respiratory failure Septicaemia Pericarditis
108
What is given to groups at risk of pneumonia?
Pneumococcal vaccine given to at risk groups \>65yrs old, Chronic disease, Diabetes mellitus, Immunosuppressed
109
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
110
What is CURB-65?
Mortality risk assessment for pneumonia ## Footnote 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.
111
What is TB?
Mycobacterium tuberculosis with caseating granulomas that eventually calcify within the lungs. Type 4 hypersensitivty.
112
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
113
How is TB investigated?
Man-toux test, Interferon GammaReleaseAssay, 3 sputum samples with Ziehl- Neelsen stain
114
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
115
What is a granuloma?
an aggregation of epithelioid histiocytes
116
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
117
What does A1AT cause?
Causes 2% of emphysema – RARE inherited
118
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
119
What is PE?
Emboli in lungs, usually from DVT below knees
120
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
121
How does PE present?
sudden onset dyspnoea, pleuritic chest pain, ?red swollen leg, haemoptysis, tachycardia, tachypnoea
122
How is PE investigated?
CT pulmonary angiogram (GOLD STANDARD), V/Q scan: mis-match, D-dimer (sensitive not specific)
123
How is PE managed?
Large clots: Oral anticoagulation (DOAC/ Warfarin), Fondaparinux, Unfractionated Heparin, LMWH then oral anticoagulation.
124
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.
125
Goodpasture's syndrome
1. What: Autoantibodies attack the basement membrane in the lungs and kidneys 2. Symptoms: Lungs: haemoptysis, chest pain, cough, SOB. Kidneys: haematuria, proteinuria, oedema, high blood urea, HTN. Systemic: malaise, weight loss, fatigue, fever 3. Dx: Biopsy to look for anti-GBM (glomerular basement membrane antibody) 4. Tx: Plasmapheresis, Immunosuppressant drugs: cyclophosphamide, prednisone, rituximab 5. Other: Antibodies attack alpha-3 subunit of type IV collagen. Type 2 hypersensitivity.
126
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\*
127
Pulmonary fibrosis
What: Progressive replacement of interstitial lung parenchyma with collagen/ scar tissue 2. Causes: Over-proliferation of type 2 pneumocytes, stimulating myofibroblasts to produce collagen 3. Symptom/signs: Coughing, SOB, cyanosis, digital clubbing 4. Dx: CT chest- “honeycombing” and thickening of interstitial walls, spirometry: decreased TLC, FVC and FEV1 5. Tx: Supplemental O2, antifibrotics (pirfenidone), lung transplant
128
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.
129
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
130
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