Respiratory Flashcards
(123 cards)
1
Q
What is COPD?
A
- Chronic Obstructive Pulmonary Disease
- Irreversible airflow limitation, usually progressive. Caused by persistent inflammatory response.
2
Q
What are the two diseases that comprise COPD?
A
- Emphysema.
- Chronic bronchitis.
3
Q
What is the clinical presentation of COPD?
A
SYMPTOMS:
- Chronic productive cough.
- SOB
- Fatigue (often due to sleep disruption).
- Decreased exercise tolerance.
SIGNS:
- Barrel chest.
- Expiratory wheeze
- Tachypnoea and ankle oedema (pulmonary hypertension).
- Crackles in lungs (emphysema).
4
Q
What are the differentials for COPD?
A
- Asthma. Earlier onset, often with FH of type 1 hypersensitivity. Daily variability of symptoms too.
- Congestive heart failure. Will have raised BNP.
5
Q
What is the pathophysiology of COPD?
A
Chronic inflammatory response to inhaled irritants. This causes:
- Airway remodelling/narrowing.
- Increased number of goblet cells.
- Mucous hypersecretion.
- Alveolar damage/collapse (emphysema).
- Vascular bed changes (pulmonary hypertension).
6
Q
What are the 2 most common causes of COPD?
A
- Smoking
- Occupational irritants (such as car fumes).
7
Q
What are the risk factors for COPD?
A
- Smoking.
- Old age.
- FH.
- Occupational exposure to chemicals.
8
Q
What are the investigations for COPD?
A
- Spirometry. Will show FEV1/FVC < 0.7, suggesting obstructive disease.
- Physical examination: Tachypnoea, use of accessory muscles, expiratory wheeze, coarse crackles.
- Sometimes CXR to exclude other pathologies.
- Alpha-1 antitrypsin (AAT) should always be measured at least once to check for AAT deficiency COPD.
9
Q
What is the treatment for COPD?
A
1st line:
- STOP SMOKING.
If not sufficient, add:
- SABA. Short-acting B agonist. (salbutamol) as a rescue inhaler for all patients.
2nd line:
- LABA + LAMA (salmeterol + tiotropium).
OR
- LABA + ICS (salmeterol + ciclesonide).
If extremely severe, consider oxygen therapy.
If sleep apnoea develops, consider ventilation overnight.
10
Q
What are the potential complications of COPD?
A
- Cor pulmonale. Right sided heart failure. Occurs due to pulmonary hypertension.
- Recurrent pneumonia. Usually Strep. Pneumoniae or haemophillus Influenza. (amoxicillin).
11
Q
What is asthma?
A
- Chronic inflammatory airway disease characterised by INTERMITTANT airway obstruction and hyper-reactivity.
12
Q
What are the two different types of asthma?
A
- Extrinsic. This is triggered by external, allergic factors. (Type 1 hypersensitivity, IgE mediated).
- Intrinsic. Triggered by non-allergic factors (e.g. stress, cold). Therefore, no IgE mediation.
13
Q
What is the clinical presentation of asthma?
A
- Expiratory wheeze
- Dyspnoea
- Chest tightness
- Dry cough (exacerbated by exercise/cold conditions).
- Night-symptoms indicate more severe asthma.
- Patients often have family members with asthma.
- Patients often have other allergy-related conditions.
- KEY FEATURE OF ASTHMA: Will have regular but distinctive exacerbations/attacks of disease.
14
Q
What is the pathophysiology of asthma?
A
Chronic inflammatory disease of the airways in response to an allergen (if extrinsic) or a non-allergic trigger (if intrinsic). Key features include:
- Smooth muscles of the airways constrict, narrowing the airways.
- Excess mucous is produced.
15
Q
What type of hypersensitivy is extrinsic asthma?
A
- Type I (IgE mediated).
16
Q
What are the diagnostic tests for asthma?
A
- Evidence of obstruction (Can be gained using PEF (peak expiratory flow) or spirometry during episodes/attacks).
- SABA trial. If SABA shows ability to REVERSE BRONCHIAL AIRWAY OBSTRUCTION DURING ATTACK, asthma is strongly suspected.
17
Q
What are the treatment options for asthma?
A
1) SABA (salbutamol) as releiver therapy.
2) Add in ICS (ciclesonide) as a maintinence therapy.
3) Add LTRA (montelukast) to the maintinence therapy.
18
Q
What are the two types of rhinitis?
A
- Allergic
- Non-allergic.
19
Q
What is the most common form of rhinitis?
A
- Hay fever. This is a type of seasonal allergic rhinitis that occurs due to pollen exposure in spring/summer.
20
Q
What is the pathophysiology of allergic rhinitis?
A
- Exposure to allergen.
- Dendritic cells present the allergen’s antigens to the immune system, triggering IgE production.
- IgE binds to mast cells, sensitising them.
- When re-exposure to the allergen occurs, mast cells degranulate to begin the inflammatory cascade:
- Histamine release.
- IL secretion.
- Migration of inflammatory cells.
21
Q
What are the two phases of effects seen following mast cell degranulation?
A
Early phase:
- Due to histamine.
- Within minutes of allergen exposure.
- Symptoms include pruritus, sneezing, rhinorrhea,
Late phase:
- Due to inflammatory cell infiltration.
- A few hours after initial exposure.
- Symptoms include nasal congestion/ mucus production.
22
Q
What are the risk factors for rhinitis?
A
- FH of atopic disease (allergic asthma, eczema etc.)
- Allergen exposure.
- <20 years old.
23
Q
What are the diagnostic tests used for rhinitis?
A
- Trials of antihistamines or intranasal corticosteroids.
- If needed, an allergy skin prick test.
24
Q
What treatment is given for rhinitis?
A
1st line:
- Avoidance of allergens (if possible).
- Anti-histamines.
2nd line or if rhinitis more severe:
- Intranasal corticosteroid (beclometasone or budesonide)
25
What is the clinical presentation of rhinitis?
- Pruritus.
- Rhinorrhea (thin discharge from nose).
- Red/swollen/watery eyes.
- Nasal congestion.
- Sneezing.
26
What is bronchiectasis?
- Permanent dilatation and thickening of the bronchi.
- Usually occurs as a result of recurrent/severe infection of the respiratory tract.
27
What is the clinical presentation of bronciectasis?
- Intermittent episodes of expectoration (coughing or spitting material up from the lungs) and infection, but as disease progresses can become more frequent (e.g. daily).
- Persistent, productive cough.
- Dyspnoea
- Wheezing/ crackling lungs.
28
What is the pathophysiology of bronchiectasis?
- Recurrent colonisation of the airways with microorgansisms, causing chronic inflammation. This results in:
- Permanently dilated and thickened bronchi.
- Increased mucous production.
- Impaired mucocilliary clearance.
29
What is the most common primary cause of bronchiectasis?
- Cystic fibrosis.
30
What is the criteria used to classify the severity of bronchiectasis called?
BSI: Bronchiectasis severity index.
31
What diagnostic tests are available for bronchiectasis?
- Spirometry. Shows an obstructive pattern of disease (FEV1/FVC \< 0.7).
- HRCT (high-resolution computed tomography). Can be used to see bronchial wall dilation and thickening. GOLD STANDARD.
- CFTR to check for CF.
32
What are the treatment options for bronchiectasis?
- Physiotherapy/exercises to aid mucocilliary clearance.
- Nebulised saline + salbutamol (pharmacological induction of mucociliary clearance).
- Amoxicillin is the first line of antibiotics if acute infection occurs.
NOTE: If patient also has COPD or asthma, choice of bronchodilator should be dependant on guidance for that condition.
33
What is cystic fibrosis?
- Severely life-limiting disease caused by autosomal recessive mutation, leading to abnormal CFTR chloride channels.
34
What is the clinical presentation of CF? (respiratory and gastric)
Signs associated with respiratory disease:
- Clubbing
- Wheeze
- Nasal polyps.
Symptoms:
- Recurrent respiratory complaints.
Signs/symptoms associated with pancreatic/intestinal disease:
- Failure to thrive
- Low BMI
- Increased appetite
35
What is the pathophysiology of cystic fibrosis?
How does it affect the pancreas, intestine, and respiratory systems?
- Mutation in the gene responsible for producing the CFTR chloride channels.
- Results in Cl transport channels on epithelial surfaces being dysfunctional, leading to mucous secretions being more thick and sticky. This causes:
- Pancreas. Blockage of the pancreatic ducts, and activation of the pancreatic enzymes trapped inside the pancreas. This leads to auto-destruction of the pancreas and a lack of digestive enzymes.
- Intestine. Formation of bulky stools, with the potential to cause intestinal obstruction.
- Respiratory. Reduced mucociliary clearance due to thicker secretions. This increases likelihood of chronic infection/inflammation, which leads to destruction of lung tissue.
NOTE: It is usually the respiratory aspect of CF that kills the patient.
36
What are the risk factors for CF?
- FH of CF.
- Both parents are carriers. (1 in 4 chance as the disease is autosomal recessive).
- White ethnicity.
37
How is CF monitored?
- CF patients should be seen approximately every 3 months by a CF specialist.
- Assessment of their lung function, diet and drugs will be carried out.
38
What are the diagnostic tests for cystic fibrosis?
- Sweat test. High levels of Cl- in sweat indicative of CF (98% sensitive).
- Heel-prick test (newborns). If positive, this only raises suspicion and a subsequent sweat test needs to be done for a conclusive result.
- Genetic testing. See if a mutation of a CFTR-coding gene is present.
39
What are the potential treatments for cystic fibrosis?
FOR ONGOING RESPIRATORY DISEASE:
1st line:
- Salbutamol (SABA) + inhaled saline + dornase alfa (all for mucociliary clearance).
- Inhaled tobramycin (antibiotic) if the patient has been colonised by pseudomonas aeruginosa.
- CFTR modulators (ivacaftor - all of these drugs end in "-ftor").
FOR ONGOING GI DISEASE WITH PANCREATIC INSUFFICIENCY:
- Pancreatic enzyme replacement (pancreatin)
- H2 antagonist (famotidine) or PPI (omeprazole) to keep the pH of the GI tract up, increasing the effectiveness of the pancreatin enzymes.
40
What are the main classes of lung cancer?
What is the basic epidemiology of each?
Mesothelioma (cancer of the pleura). Strongly associated with asbestos exposure.
Small cell carcinoma (highly malignant and aggressive).
Non small cell carcinoma. Most common. 3 subtypes:
- Adenocarcinoma. Most common lung cancer overall, and the most common lung cancer in non-smokers.
- Squamous cell carcinoma. Most common lung cancer in smokers.
- Large cell carcinoma.
41
What are the symptoms of lung cancer?
- Persistent cough.
- Haemoptysis.
- Weight loss.
- Fatigue.
- Clubbing.
- Chest/shoulder pain.
- Potential for lymphadenopathy.
- Horner's syndrome (sympathetic chain disturbance) or loss of sensation/atrophy in hand (brachial plexus disturbance).
- Recurrent laryngeal compression can cause hoarse voice.
42
Which lung cancer is most commonly found peripherally?
Which lung cancer is most commonly found centrally?
Peripherally - adenocarcinoma.
Centrally - large cell carcinoma.
43
What are the risk factors associated with lung cancer?
- Smoking
- FH (especially 1st degree relative).
- Radon exposure (mining).
- COPD
- Older age (median age is 70).
- Asbestos exposure (especially mesothelioma!)
44
What is the histological presentation of a small cell carcinoma?
- Small, densely packed cells.
- Anuclear.
45
What are the investigations used for lung cancer?
- CXR. Low sensitivity, so only used if the risk is low as it is cheap and quick.
- Contrast CT. Used straight away for higher risk patients (e.g. 70 year old smoker with chronic haemoptysis) or if CXR is worrying.
- Biopsy. Usually obtained by transbronchial needle aspiration. Allows for the typing/sub-typing of the cancer and planning of treatment.
46
What are the treatment options for pleural mesothelioma?
- Surgical (lobectomy/pneumonectomy) is GS. Unlikely to be curative for small cell carcinoma or mesothelioma.
- Radiotherapy.
- Chemotherapy. Cisplatin often the drug of choice.
47
Where does lung carcinoma commonly metastasise to?
- Bone (most common)
- Liver
- Brain
- Adrenal glands
- Lymph nodes.
48
What is the pathophysiology of Horner's syndrome
Disruption of the sympathetic nervous supply to one side of the face. Causes:
- Drooping eyelid.
- Pupil constriction.
- Absence of sweating on one side of the face.
49
What is the most common lung cancer in non-smokers?
- Adenocarcinoma
50
What is the most common lung cancer overall in the population?
- Adenocarcinoma.
51
What is the most common lung cancer in smokers?
- Squamous cell carcinoma (over half of the lung cancers seen in smokers).
52
What are the two types of COPD?
- Emphysema (Alveolar damage).
- Chronic bronchitis (long term inflammation of the bronchi).
53
What is alpha-1 antitrypsin deficiency?
- An autosomal codominant disorder.
- Mutation of the SERPINA1 gene at the protease inhibitor (PI) locus.
- Results in the production of mutant AAT, causing inflammatory lung damage and liver damage.
54
What is the clinical presentation of alpha-1 antitrypsin deficiency?
- Panacinar emphysema.
- Obstructive lung disease.
- Bronchiectasis.
- Liver disease
- Typical COPD presentation.
55
What is the main risk factor for alpha-1 antitrypsin deficiency?
- FH of AAT deficiency (could be one or two parents as the SERPINA1 mutation is co-dominant).
56
What are the investigations used for alpha-1 antitrypsin deficiency?
- AAT measurement. Low AAT raises suspicion.
- Spirometry. FEV1/FVC \< 0.7 indicates obstructive disease such as AAT deficiency.
57
What is the pathophysiology of alpha-1 antitrypsin deficiency?
- Mutation of the SERPINA1 gene at the protease inhibitor locus (PI).
- Results in the production of mutant alpha-1 antitrypsin.
- This mutant AAT results in less clearance of neutrophilic elastase, leading to inflammatory lung damage.
- Mutant AAT may polymerise and build up in the liver, causing liver disease.
58
What is the treatment for alpha-1 antitrypsin deficiency?
- Standard COPD treatment (Salbutamol for rescue, tiotropium LAMA for maintenance).
- Treat liver disease as appropriate: diuretics, transplant etc.
- Stop smoking
- Hep A/B vaccine
59
What is hypersensitivity pneumonitis?
- Inflammation of the alveoli and distal bronchioles.
- Caused by type III, non-IgE mediated allergic response.
SAME THINGS AS EXTRINSIC ALLERGIC ALVELOITIS.
60
What is the clinical presentation of Hypersensitivity pneumonitis? (symptoms and history)
**Exposure history is key:**
- Birds/cage cleaning.
- Mould.
- Occupational exposure to other allergens.
**Symptoms:**
- Dyspnoea.
- Cough
**Symptoms last only a few days and recur with each re-exposure to the allergen (acute hypersensitivity pneumonitis).**
61
How is hypersensitivity pneumonitis investigated?
- CXR. Patchy, nodular infiltrates.
- Spirometry. Restrictive disease pattern.
62
What is the treatment for hypersensitivity pneumonitis?
- Remove allergen (potentially change occupation).
- Prednisolone (corticosteroid) for 6 weeks.
63
What is an acute exacerbation of asthma?
Bronchospasm in response to allergen exposure/triggers
Causes acute exacerbation of the asthma symptoms
Results in a decrease of the patients PEF below their baseline
64
How will PEF change in an acute asthma exacerbation?
- PEF decreases below pateint's baseline.
65
What are the signs of life-threatening asthma?
What are the investigation findings in life-threatening asthma?
- Silent chest.
- Cyanosis.
- Hypotension.
- Exhaustion.
Investigations find:
- PEF \< 33% of predicted.
- SpO2 \< 92%
- NORMAL CO2 reading (would normally be reduced in asthma due to hyperventialtion).
66
What is the key sign of near fatal asthma? What immediate action should be taken?
- If CO2 becomes raised, near fatal asthma.
- Contact ICU/senior colleague.
67
What is the key investigation used during a life-threatening asthma attack?
- ABG.
- \<92% SpO2
- Normal (life threatening) or high (near fatal) PaCO2
68
What is the management for a life-threatening asthma attack?
- ABC
- Give O2
- High dose salbutamol (SABA)
- High dose ipratropium (SAMA).
- Oral prednisolone (corticosteroid).
- Monitor ABG. If PaCO2 becomes raised, contact ICU/senior colleague (near-fatal asthma).
69
What is occupational asthma?
What are the two types?
- Asthma caused by the workplace.
- Sensitisor-induced occupational asthma (90% of occupational asthma). This is type I, IgE mediated allergic response.
- Irritant induced occupational asthma. This is non-allergic inflammatory airway response due to occupational exposure.
70
How is occupational asthma diagnosed?
- Establish a relationship between asthma and the workplace.
- Spirometry (obstructive FEV1/FVC).
- Potentially a skin prick test (find the allergen).
71
What is the management of occupational asthma?
- Avoidance of the allergen (often involves a change of profession).
72
What is Goodpastures syndrome?
What is goodpastures disaese?
- Autoimmune disease affecting the lungs and kidneys.
- Goodpastures disease is a common cause of goodpastures syndrome - It involves the presence of anti-GBM antibodies that affect the alpha-3 chain in type IV collagen.
73
What are the key symptoms of goodpasture's syndrome?
- Reduced urine output (glomerulonephritis).
- Haemoptysis (Due to alveolar damage/potentially a lung haemorrhage).
74
How is goodpastures syndrome investigated?
- Renal function tests (Low GFR, raised creatinine and urea).
- Anti-GBM antibody testing (+ve)
- Renal biopsy (gold standard). Will reveal linear IgG staining on immunofluorescence.
75
What is the management for Goodpasture's syndrome?
- High dose prednisolone (corticosteroids).
- Plasmapheresis (Removal of the anti-GBM antibodies from the blood).
- Cyclophosphamide (alkylating agent).
- Stop smoking (reduced risk of pulmonary haemorrhage).
76
What is Wegener's granulomatosis?
What is the alternative name?
Vasculitis involving a classic triad:
- Upper resp tract.
- Lower resp tract.
- Kidneys.
Alternative name: granulomatosis with polyangitis.
77
What is the key test used for suspected Wegener's syndrome?
- ANCA +ve
78
How is Wegener's syndrome differentiated from Goodpasture's syndrome?
- Wegener's has +ve ANCA test, whereas Goodpasture's has +ve Anti-GBM antibody test.
- Wegener's shows linear IgG deposits on lung biopsy, whereas Wegener's shows granulatomas.
79
How is Wegener's syndrome treated?
- Prednisolone.
- Cyclophosphamide (alkylating agent).
80
What is PE?
- DVT embolises, and then gets trapped in the respiratory tract.
81
What factors contribute to DVT formation?
Virchow's triad:
- Venous stasis.
- Trauma.
- Hypercoagulability.
82
What scores is used to determine DVT risk?
Well's score.
\>4 - high risk of DVT.
≤4 - Low risk of DVT.
83
What are the key symptoms of PE?
- Dyspnoea.
- Pleuritic chest pain.
- Symptoms of DVT (e.g. calf swelling).
84
What is the immediate management for a PE?
Well's score ≤4 :
- Carry out a D-dimer test. If +ve, move on to CTPA and administer apixiban.
Wells score \>4 :
- Straight to CTPA
- Administer apixiban (anticoagulant).
Haemodynamic instability:
- O2 + fluids.
- Consider vasopressin for hypotension.
85
What is the long term management post-PE?
- Continue apixiban (anticoagulant) for 3 months.
86
What is pulmonary fibrosis?
- Formation of scar tissue in the lungs associated with progressive dyspnoea.
87
What are the symptoms of pulmonary fibrosis?
What are the signs of pulmonary fibrosis?
Symptoms:
- Progressive dyspnoea.
- Cough.
Signs:
- End-expiratory crackles.
- Finger clubbing.
88
What are the investigations for pulmonary fibrosis?
- Spirometry - restrictive pattern (FEV1/FVC \>0.7).
- CXR - Will show fibrotic tissue.
89
What is the management for IDIOPATHIC pulmonary fibrosis?
- Pirfenidone (a pyridone).
90
What is the management for pulmonary fibrosis?
Management is limited:
- Stop smoking.
- Pulmonary rehabilitation.
- At-home oxygen therapy for hypoxia.
Consier a lung transplant if patient is suitable.
91
What is pneumonia?
Lung inflammation associated with consolidations or interstitial lung infiltrates.
92
What is CAP?
What is the most common infective organism?
What is the first line treatment?
Community Acquired Pneumonia.
Pneumonia presenting as an outpatient/less than 48 hours in hospital.
Most common cause is strep. pneumoniae (Gram +ve cocci)
Amoxicillin 1st line.
93
What is HAP?
What are the main causative organsims?
What is the treatment for HAP?
Hospital Acquired Pneumonia.
Acquired after 48 hours or more in hospital.
Causative organisms include: E.coli, MRSA, Pseudomonas aeruginosa, klebsiella aeruginosa etc.
Treatment is co-amoxiclav + gentamycin.
94
What are the typical symptoms of pneumonia?
- Mucopurulent (green/yellow), smelly sputum.
- Productive cough.
- Dyspnoea.
- Fever.
95
How is the severity of pneumonia graded?
What implications does this have for treatment?
CURB-65.
Confusion? +1
Urea high? +1
Respiratory rate \>30? +1
Blood pressure lower than 60/90? +1
65 of older? +1.
3-5 = severe. Manage in hospital.
2 = moderate. Manage with short stay in hospital.
1 = low severity. Manage as outpatient.
96
What are the investigations used for pneumonia?
When are they used?
Investigations only usually used in moderate (2) or severe (3-5) pneumonia (CURB-65 score).
CXR - Shows shadowing.
Sputum/ blood culture - allows for pathogen detection/ antibiotic sensitivity testing.
97
What is sarcoidosis?
- Chronic granuloamtous (non-caseating) disorder that affects the lungs, skin and eyes.
- No identifiable cause.
98
Which disease(s) are associated with non-caseating granulomas?
Which disease(s) are associated with caseating granulomas?
Non-caseating: Sarcoidosis and Crohn's disease.
Caseating: Mycobacterium tuberculosis (TB).
99
How does sarcoidosis typically present?
- Cough
- Dyspnoea
- Uveitis (Red, painful eye; vision loss; photophobia)
100
What are the investigations for sarcoidosis?
- CXR. Upper lobe bilateral infiltrates. Hilar adenopathy.
- Tuberculin test -ve. (Excludes TB).
- Bronchial needle biopsy. Will show non-caseating granulomas (DIAGNOSTIC/GOLD STANDARD).
101
What is the management for sarcoidosis?
- No proper treatment yet established.
- Late stages use corticosteroids (prednisolone).
- Consider DMARD (methotrexate).
102
What is pleural effusion?
- Fluid collection in the space between the visceral and parietal pleura in the abdomen.
103
What are the signs and symptoms of pleural effusion?
SIGNS:
- Absent breath sounds.
- Dullness to percussion.
SYMPTOMS:
- Dyspnoea.
- Cough.
**- Pleuritic chest pain** (key symptom)
104
What are the investigations for pleural effusion?
- CXR. Blunted costophrenic angle raises suspicion.
- USS thorax. Shows fluid in the pleural space.
- Thoracentesis + appropriate histological study. Can show underlying cause (cancer? pneumonia?).
THORACENTESIS NOT NEEDED IF CLEARLY DUE TO CHF.
105
What is the management of CHF pleural effusion?
- Loop diuretic (furesomide).
- Therapeutic thoracentesis if effusion is large.
106
What is the management of bacterial pleural effusion?
- Antibiotics depending on the microbiology (usually amoxicillin, as commonly strep. pneumoniae).
107
What is the management of malignant pleural effusion?
- Oncological management.
108
What is a pneumothorax?
- Air infiltrates and accumulates in the pleural space.
109
What are the different classifications of pneumothorax?
- Primary. No underlying pulmonary disease.
- Secondary. Occurs when there is an underlying pulmonary disease.
- Spontaneous. Occurs with no trauma.
- Traumatic. Occurs with trauma.
- Tension. Results in positive pressure in the pleural space, leading to displacement of mediasteinal structures and compromise of cardiovascular function.
110
What is the most common type of patient seen with a pneumothorax?
- Young, slender male who smokes.
111
What are the signs and symptoms of pneumothorax?
Which ones are indicative of a tension pneumothorax?
Symptoms:
- PLEURITIC chest pain.
- Dyspnoea.
- Cough.
Signs:
- Ipsilateral reduced breath sounds.
- Ipsilateral hyper-resonance on percussion.
TENSION PNEUMOTHORAX:
- Hypoxia.
- Tracheal deviation contralaterally to lesion.
- Hypotension/loss of consciousness/tachycardia.
112
What is the key investigation used to diagnose pneumothorax?
- Erect CXR. Will show radiolucency, and loss of the visceral pleural edge in the area of the pneumothorax.
113
What is the management of a pneumothorax?
Normal pneumothorax:
- Needle aspiration (or chest drain if larger).
Tension pneumothorax:
- High flow oxygen if sats low.
- IMMEDIATE CEHST DECOMPRESSION (Large bore cannula in the second intercostal space, then replaced with a chest drain).
**If tension pneumothorax suggested, do not wait for confirmatory erect CXR.**
114
What is pulmonary hypertension?
What does this result in pathologically?
- Increased resistance and pressure in the pulmonary arterioles.
- Causes increased strain on the right side of the heart, and back pressure of blood into the systemic venous circulation.
115
What are some examples of common pulmonary hypertension causes?
- Left heart dysfunction (e.g. Mitral/aortic valve diseases).
- COPD.
- Pulmonary embolism.
- Vasculitis.
116
What are the key signs and symptoms of pulmonary hypertension?
Signs:
- Raised JVP (KEY).
- Peripheral oedema.
- Hepatomegaly.
- Tachycardia.
Symptoms:
- SOB (KEY).
- Syncope.
117
What are the investigations for pulmonary hypertension?
- ECG. Shows RAD, RVH, RBBB.
- CXR. Dilated pulmonary arterioles, RVH.
- BNP. Raised in HF (associated with pulmonary hypertension).
118
What is the management of pulmonary hypertension?
- Treat the underlying disease.
- If CHF is occuring, use of loop diuretics (e.g. furesomide).
119
What is the microbiological presentation of TB?
Mycobacterium Tuberculosis.
Acid-fast, atypical bacilli.
Needs Ziehl-neeson stain for identification.
120
What are the public health considerations surrounding TB?
- Isolate patient for 5 days to 2 weeks at the start of treatment to reduce transmission.
- Inform the authorities (notifiable disease).
- Contact trace and offer TB screening to contacts where appropriate.
121
What are the signs and symptoms of TB?
- Cough for 2-3 weeks that started non-productive and has become productive. KEY SYMPTOM.
- Low grade fever. KEY SYMPTOM.
- Weight loss.
- Malaise.
- Haemoptysis.
122
What are the investigations used for TB?
- CXR. Shows upper lobe infiltrate.
- Sputum sample + culture. (Acid fast, atypical bacilli on Ziehl neeson stain).
123
What is the management for TB?
- Isolate the patient for 5 days - 2 weeks.
- Contact tracing + appropriate contact TB testing.
Drugs:
- Isoniazid. Can cause tingling/numbness.
- Rifampicin. Blood in urine.
- Ethambutol. Can cause visual disturbances.
- Pyrazinamide. Can cause arthralgia.
