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Phase 2 v2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is COPD?

A
  • Chronic Obstructive Pulmonary Disease
  • Irreversible airflow limitation, usually progressive. Caused by persistent inflammatory response.
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2
Q

What are the two diseases that comprise COPD?

A
  • Emphysema.
  • Chronic bronchitis.
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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).
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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.
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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).
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6
Q

What are the 2 most common causes of COPD?

A
  • Smoking
  • Occupational irritants (such as car fumes).
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7
Q

What are the risk factors for COPD?

A
  • Smoking.
  • Old age.
  • FH.
  • Occupational exposure to chemicals.
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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.
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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.

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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).
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11
Q

What is asthma?

A
  • Chronic inflammatory airway disease characterised by INTERMITTANT airway obstruction and hyper-reactivity.
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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.
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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.
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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.
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15
Q

What type of hypersensitivy is extrinsic asthma?

A
  • Type I (IgE mediated).
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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.
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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.

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18
Q

What are the two types of rhinitis?

A
  • Allergic
  • Non-allergic.
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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.
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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.
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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.
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22
Q

What are the risk factors for rhinitis?

A
  • FH of atopic disease (allergic asthma, eczema etc.)
  • Allergen exposure.
  • <20 years old.
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23
Q

What are the diagnostic tests used for rhinitis?

A
  • Trials of antihistamines or intranasal corticosteroids.
  • If needed, an allergy skin prick test.
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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)

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25
Q

What is the clinical presentation of rhinitis?

A
  • Pruritus.
  • Rhinorrhea (thin discharge from nose).
  • Red/swollen/watery eyes.
  • Nasal congestion.
  • Sneezing.
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26
Q

What is bronchiectasis?

A
  • Permanent dilatation and thickening of the bronchi.
  • Usually occurs as a result of recurrent/severe infection of the respiratory tract.
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27
Q

What is the clinical presentation of bronciectasis?

A
  • 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.
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28
Q

What is the pathophysiology of bronchiectasis?

A
  • Recurrent colonisation of the airways with microorgansisms, causing chronic inflammation. This results in:
  • Permanently dilated and thickened bronchi.
  • Increased mucous production.
  • Impaired mucocilliary clearance.
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29
Q

What is the most common primary cause of bronchiectasis?

A
  • Cystic fibrosis.
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30
Q

What is the criteria used to classify the severity of bronchiectasis called?

A

BSI: Bronchiectasis severity index.

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31
Q

What diagnostic tests are available for bronchiectasis?

A
  • 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.
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32
Q

What are the treatment options for bronchiectasis?

A
  • 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.

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33
Q

What is cystic fibrosis?

A
  • Severely life-limiting disease caused by autosomal recessive mutation, leading to abnormal CFTR chloride channels.
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34
Q

What is the clinical presentation of CF? (respiratory and gastric)

A

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
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35
Q

What is the pathophysiology of cystic fibrosis?

How does it affect the pancreas, intestine, and respiratory systems?

A
  • 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.

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36
Q

What are the risk factors for CF?

A
  • FH of CF.
  • Both parents are carriers. (1 in 4 chance as the disease is autosomal recessive).
  • White ethnicity.
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37
Q

How is CF monitored?

A
  • 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.
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38
Q

What are the diagnostic tests for cystic fibrosis?

A
  • 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.
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39
Q

What are the potential treatments for cystic fibrosis?

A

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.
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40
Q

What are the main classes of lung cancer?

What is the basic epidemiology of each?

A

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.
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41
Q

What are the symptoms of lung cancer?

A
  • 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.
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42
Q

Which lung cancer is most commonly found peripherally?

Which lung cancer is most commonly found centrally?

A

Peripherally - adenocarcinoma.

Centrally - large cell carcinoma.

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43
Q

What are the risk factors associated with lung cancer?

A
  • Smoking
  • FH (especially 1st degree relative).
  • Radon exposure (mining).
  • COPD
  • Older age (median age is 70).
  • Asbestos exposure (especially mesothelioma!)
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44
Q

What is the histological presentation of a small cell carcinoma?

A
  • Small, densely packed cells.
  • Anuclear.
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45
Q

What are the investigations used for lung cancer?

A
  • 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.
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46
Q

What are the treatment options for pleural mesothelioma?

A
  • Surgical (lobectomy/pneumonectomy) is GS. Unlikely to be curative for small cell carcinoma or mesothelioma.
  • Radiotherapy.
  • Chemotherapy. Cisplatin often the drug of choice.
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47
Q

Where does lung carcinoma commonly metastasise to?

A
  • Bone (most common)
  • Liver
  • Brain
  • Adrenal glands
  • Lymph nodes.
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48
Q

What is the pathophysiology of Horner’s syndrome

A

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.
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49
Q

What is the most common lung cancer in non-smokers?

A
  • Adenocarcinoma
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50
Q

What is the most common lung cancer overall in the population?

A
  • Adenocarcinoma.
51
Q

What is the most common lung cancer in smokers?

A
  • Squamous cell carcinoma (over half of the lung cancers seen in smokers).
52
Q

What are the two types of COPD?

A
  • Emphysema (Alveolar damage).
  • Chronic bronchitis (long term inflammation of the bronchi).
53
Q

What is alpha-1 antitrypsin deficiency?

A
  • 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
Q

What is the clinical presentation of alpha-1 antitrypsin deficiency?

A
  • Panacinar emphysema.
  • Obstructive lung disease.
  • Bronchiectasis.
  • Liver disease
  • Typical COPD presentation.
55
Q

What is the main risk factor for alpha-1 antitrypsin deficiency?

A
  • FH of AAT deficiency (could be one or two parents as the SERPINA1 mutation is co-dominant).
56
Q

What are the investigations used for alpha-1 antitrypsin deficiency?

A
  • AAT measurement. Low AAT raises suspicion.
  • Spirometry. FEV1/FVC < 0.7 indicates obstructive disease such as AAT deficiency.
57
Q

What is the pathophysiology of alpha-1 antitrypsin deficiency?

A
  • 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
Q

What is the treatment for alpha-1 antitrypsin deficiency?

A
  • 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
Q

What is hypersensitivity pneumonitis?

A
  • Inflammation of the alveoli and distal bronchioles.
  • Caused by type III, non-IgE mediated allergic response.

SAME THINGS AS EXTRINSIC ALLERGIC ALVELOITIS.

60
Q

What is the clinical presentation of Hypersensitivity pneumonitis? (symptoms and history)

A

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
Q

How is hypersensitivity pneumonitis investigated?

A
  • CXR. Patchy, nodular infiltrates.
  • Spirometry. Restrictive disease pattern.
62
Q

What is the treatment for hypersensitivity pneumonitis?

A
  • Remove allergen (potentially change occupation).
  • Prednisolone (corticosteroid) for 6 weeks.
63
Q

What is an acute exacerbation of asthma?

A

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
Q

How will PEF change in an acute asthma exacerbation?

A
  • PEF decreases below pateint’s baseline.
65
Q

What are the signs of life-threatening asthma?

What are the investigation findings in life-threatening asthma?

A
  • 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
Q

What is the key sign of near fatal asthma? What immediate action should be taken?

A
  • If CO2 becomes raised, near fatal asthma.
  • Contact ICU/senior colleague.
67
Q

What is the key investigation used during a life-threatening asthma attack?

A
  • ABG.
  • <92% SpO2
  • Normal (life threatening) or high (near fatal) PaCO2
68
Q

What is the management for a life-threatening asthma attack?

A
  • 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
Q

What is occupational asthma?

What are the two types?

A
  • 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
Q

How is occupational asthma diagnosed?

A
  • Establish a relationship between asthma and the workplace.
  • Spirometry (obstructive FEV1/FVC).
  • Potentially a skin prick test (find the allergen).
71
Q

What is the management of occupational asthma?

A
  • Avoidance of the allergen (often involves a change of profession).
72
Q

What is Goodpastures syndrome?

What is goodpastures disaese?

A
  • 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
Q

What are the key symptoms of goodpasture’s syndrome?

A
  • Reduced urine output (glomerulonephritis).
  • Haemoptysis (Due to alveolar damage/potentially a lung haemorrhage).
74
Q

How is goodpastures syndrome investigated?

A
  • 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
Q

What is the management for Goodpasture’s syndrome?

A
  • 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
Q

What is Wegener’s granulomatosis?

What is the alternative name?

A

Vasculitis involving a classic triad:

  • Upper resp tract.
  • Lower resp tract.
  • Kidneys.

Alternative name: granulomatosis with polyangitis.

77
Q

What is the key test used for suspected Wegener’s syndrome?

A
  • ANCA +ve
78
Q

How is Wegener’s syndrome differentiated from Goodpasture’s syndrome?

A
  • 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
Q

How is Wegener’s syndrome treated?

A
  • Prednisolone.
  • Cyclophosphamide (alkylating agent).
80
Q

What is PE?

A
  • DVT embolises, and then gets trapped in the respiratory tract.
81
Q

What factors contribute to DVT formation?

A

Virchow’s triad:

  • Venous stasis.
  • Trauma.
  • Hypercoagulability.
82
Q

What scores is used to determine DVT risk?

A

Well’s score.

>4 - high risk of DVT.

≤4 - Low risk of DVT.

83
Q

What are the key symptoms of PE?

A
  • Dyspnoea.
  • Pleuritic chest pain.
  • Symptoms of DVT (e.g. calf swelling).
84
Q

What is the immediate management for a PE?

A

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
Q

What is the long term management post-PE?

A
  • Continue apixiban (anticoagulant) for 3 months.
86
Q

What is pulmonary fibrosis?

A
  • Formation of scar tissue in the lungs associated with progressive dyspnoea.
87
Q

What are the symptoms of pulmonary fibrosis?

What are the signs of pulmonary fibrosis?

A

Symptoms:

  • Progressive dyspnoea.
  • Cough.

Signs:

  • End-expiratory crackles.
  • Finger clubbing.
88
Q

What are the investigations for pulmonary fibrosis?

A
  • Spirometry - restrictive pattern (FEV1/FVC >0.7).
  • CXR - Will show fibrotic tissue.
89
Q

What is the management for IDIOPATHIC pulmonary fibrosis?

A
  • Pirfenidone (a pyridone).
90
Q

What is the management for pulmonary fibrosis?

A

Management is limited:

  • Stop smoking.
  • Pulmonary rehabilitation.
  • At-home oxygen therapy for hypoxia.

Consier a lung transplant if patient is suitable.

91
Q

What is pneumonia?

A

Lung inflammation associated with consolidations or interstitial lung infiltrates.

92
Q

What is CAP?

What is the most common infective organism?

What is the first line treatment?

A

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
Q

What is HAP?

What are the main causative organsims?

What is the treatment for HAP?

A

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
Q

What are the typical symptoms of pneumonia?

A
  • Mucopurulent (green/yellow), smelly sputum.
  • Productive cough.
  • Dyspnoea.
  • Fever.
95
Q

How is the severity of pneumonia graded?

What implications does this have for treatment?

A

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
Q

What are the investigations used for pneumonia?

When are they used?

A

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
Q

What is sarcoidosis?

A
  • Chronic granuloamtous (non-caseating) disorder that affects the lungs, skin and eyes.
  • No identifiable cause.
98
Q

Which disease(s) are associated with non-caseating granulomas?

Which disease(s) are associated with caseating granulomas?

A

Non-caseating: Sarcoidosis and Crohn’s disease.

Caseating: Mycobacterium tuberculosis (TB).

99
Q

How does sarcoidosis typically present?

A
  • Cough
  • Dyspnoea
  • Uveitis (Red, painful eye; vision loss; photophobia)
100
Q

What are the investigations for sarcoidosis?

A
  • CXR. Upper lobe bilateral infiltrates. Hilar adenopathy.
  • Tuberculin test -ve. (Excludes TB).
  • Bronchial needle biopsy. Will show non-caseating granulomas (DIAGNOSTIC/GOLD STANDARD).
101
Q

What is the management for sarcoidosis?

A
  • No proper treatment yet established.
  • Late stages use corticosteroids (prednisolone).
  • Consider DMARD (methotrexate).
102
Q

What is pleural effusion?

A
  • Fluid collection in the space between the visceral and parietal pleura in the abdomen.
103
Q

What are the signs and symptoms of pleural effusion?

A

SIGNS:

  • Absent breath sounds.
  • Dullness to percussion.

SYMPTOMS:

  • Dyspnoea.
  • Cough.

- Pleuritic chest pain (key symptom)

104
Q

What are the investigations for pleural effusion?

A
  • 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
Q

What is the management of CHF pleural effusion?

A
  • Loop diuretic (furesomide).
  • Therapeutic thoracentesis if effusion is large.
106
Q

What is the management of bacterial pleural effusion?

A
  • Antibiotics depending on the microbiology (usually amoxicillin, as commonly strep. pneumoniae).
107
Q

What is the management of malignant pleural effusion?

A
  • Oncological management.
108
Q

What is a pneumothorax?

A
  • Air infiltrates and accumulates in the pleural space.
109
Q

What are the different classifications of pneumothorax?

A
  • 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
Q

What is the most common type of patient seen with a pneumothorax?

A
  • Young, slender male who smokes.
111
Q

What are the signs and symptoms of pneumothorax?

Which ones are indicative of a tension pneumothorax?

A

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
Q

What is the key investigation used to diagnose pneumothorax?

A
  • Erect CXR. Will show radiolucency, and loss of the visceral pleural edge in the area of the pneumothorax.
113
Q

What is the management of a pneumothorax?

A

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
Q

What is pulmonary hypertension?

What does this result in pathologically?

A
  • 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
Q

What are some examples of common pulmonary hypertension causes?

A
  • Left heart dysfunction (e.g. Mitral/aortic valve diseases).
  • COPD.
  • Pulmonary embolism.
  • Vasculitis.
116
Q

What are the key signs and symptoms of pulmonary hypertension?

A

Signs:

  • Raised JVP (KEY).
  • Peripheral oedema.
  • Hepatomegaly.
  • Tachycardia.

Symptoms:

  • SOB (KEY).
  • Syncope.
117
Q

What are the investigations for pulmonary hypertension?

A
  • ECG. Shows RAD, RVH, RBBB.
  • CXR. Dilated pulmonary arterioles, RVH.
  • BNP. Raised in HF (associated with pulmonary hypertension).
118
Q

What is the management of pulmonary hypertension?

A
  • Treat the underlying disease.
  • If CHF is occuring, use of loop diuretics (e.g. furesomide).
119
Q

What is the microbiological presentation of TB?

A

Mycobacterium Tuberculosis.

Acid-fast, atypical bacilli.

Needs Ziehl-neeson stain for identification.

120
Q

What are the public health considerations surrounding TB?

A
  • 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
Q

What are the signs and symptoms of TB?

A
  • 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
Q

What are the investigations used for TB?

A
  • CXR. Shows upper lobe infiltrate.
  • Sputum sample + culture. (Acid fast, atypical bacilli on Ziehl neeson stain).
123
Q

What is the management for TB?

A
  • 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.

Phase 2 v2 (14 decks)

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