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CP3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

CYSTIC FIBROSIS: Describe the clinical presentation of a patient with cystic fibrosis with respect to disease of the lung and pancreas and describe its inheritance

A

Mode of inheritance: Autosomal recessive

Clinical presentation:

  • Lung: Productive cough, dyspnoea, recurrent respiratory infections, progressive lung damage, spontaneous pneumothorax
  • ENT: Nasal polyps
  • Pancreas: Loss of exocrine function (digestive enzymes), DM in later stages
  • GI: Meconium ileus at birth, steatorrhoea secondary to malabsorption
  • General: Faltering growth, rickets, osteomalacia
  • Reproductive: Reduced/absent fertility
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2
Q

CYSTIC FIBROSIS: Describe the pathological changes in the lungs and the natural history of disease in a typical patient

A

Pathological changes:

A collection of unusually thick mucus in seen within the bronchi. The mucus acts as an ideal environment for the accumulation of bacteria, leading to respiratory infection.

The airways are dilated, with purulent secretions and chronic inflammation in the wall with granulomatous tissue (can lead to haemoptysis).

Fibrous scarring can occur, leading to respiratory failure.

Natural history:

  • Normally detected via the heel prick test, in the neonatal period
  • Faltering growth and recurrent chest infections seen throughout childhood
  • Infertility in males and reduced fertility in females
  • Complications in adult life include diabetes, rickets, osteomalacia
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3
Q

CYSTIC FIBROSIS: Outline the non-respiratory manifestations of cystic fibrosis

A

ENT: Nasal polyps, sinusitis

GI: Meconium ileus, malabsorption, intestinal obstruction, steattorrhoea

Pancreatic: Pancreatic insufficiency

Reproductive

Arthropathy

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4
Q

CYSTIC FIBROSIS: List the usual organisms causing lung infection

A
  • Haemophilus
  • Pseudomonas
  • Klebsiella
  • Strept. pneumoniae
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5
Q

CYSTIC FIBROSIS: Describe the main principles of treatment

A

Physiotherapy:

  • Postural drainage
  • Handheld devices to aid mucus drainage
  • Positive expiratory pressure mask

Medications:

  • IHD bronchodilator *to be given prior to physiotherapy*
  • Pancreatic enzyme supplementation: Creon
    • Fat soluble vitamin supplementation
  • Bile acid supplement (ursodeoxycholic acid)
  • Mucolytics
  • Antibiotics
    • Inhaled tobramycin for chronic Pseudomonas aeruginosa
  • Inhaled anti-inflammatory agent (macrolide, ibuprofen, corticosteroid)
  • CFTR modulator (e.g. ivacaftor)

Bilateral lung transplantation:

  • Reserved for when all other therapies have been exhausted
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6
Q

PNEUMONIA: Describe the typical presentation of a patient with CAP and the features that identify severe pneumonia, including the role of the CURB-65 tool for risk prediction

A

Symptoms/signs:

  • Productive cough
  • Dyspnoea and tachypnoea
  • Fever/chills/rigors
  • Cyanosis: Central (lips)
  • Confusion
  • New focal chest signs on examination
  • Pleuritic chest pain

THINK - could this be sepsis?

CURB-651 mortality risk prediction tool:

Confusion: AMT < 8

Urea (blood urea nitrogen) > 7 mmol/L

Respiratory rate > 30 breaths/minute

Blood pressure < 60/90 mmHg

> 65

Arrange urgent transfer to hospital if there is a score of 3 or >

Hospital assessment should be considered for scores of 1 or 2

1: CRB-65 severity score is used in the community setting

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7
Q

PNEUMONIA: Describe the pathology of acute lobar pneumonia and bronchopneumonia

A

Lobar pneumonia: Homogenous and fibrinosuppurative consolidation of one or more lobes

Bronchopneumonia: Suppurative peribronchiolar inflammation and subsequent patchy consolidation or one or more secondary lobules of a lung

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8
Q

PNEUMONIA: Describe the investigation of a patient presenting with CAP and interpret investigations

A

Investigations:

  • Observations
  • ABG
  • Sputum: MC&S
  • Bloods: FBC, U&Es, CRP, LFTs
  • Blood cultures: For all pts with moderate to severe disease
    • Sepsis screen: Blood cultures, lactate, urine output
  • CXR: Consolidation
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9
Q

PNEUMONIA: Describe the complications of pneumonia

A
  • Sepsis*
  • Pleural effusion
  • Pleural abscess*
  • Empyema (a collection of pus within the pleural cavity)*
  • ARDS (non-cardiogenic pulmonary oedema and severe lung inflammation)
  • Antibiotic associated c. diff colitis
  • Heart failure

* complications listed in the ACE study guide

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10
Q

PNEUMONIA: Create a treatment plan, including specification of observations, general supportive measures, appropriate antibiotic regimens, analgesia and physiotherapy

A

Observations:

  • Temperature, oxygen saturation, pulse, RR, BP

General supportive measures:

  • Oxygen
  • Ensure adequate fluid and nutritional intake
  • VTE prophylaxis

Antibiotic regimen:

  • Empirical broad-spectrum antibiotics immediately after diagnosis:
    • IV amoxicillin with clarithromycin or erythrocyclin
    • 5/7 course
  • Consider switch to PO according to treatment response
  • Switch to pathogen-targeted antibiotic therapy once sensitivities have been confirmed

Analgesia:

  • Paracetamol: 500 mg - 1000 mg every 4 hours, maximum 4g/day

Physiotherapy:

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11
Q

PNEUMONIA: Outline clinical management during recovery

A

* Radiological follow-up is required until the consolidation has cleared. Follow-up x-ray at 6 weeks should be organised to assess for resolution of consolidation and for persistent abnormalities of the lung parenchyma

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12
Q

TUBERCULOSIS: Describe the process of infection by the tubercle bacillus together with the route of spread and discuss the presentation of post-primary TB from reactivation of infection

A

Process of infection:

  • Inhalation of respiratory droplets that are released when an infected individual coughs
  • There is mild inflammatory response at the site of infection followed by spread to regional lymph nodes
  • Characteristic caseating granulomas form. Most heal by fibrosis and calcify without treatment.
  • A Ghon-focus forms

Route of spread:

  • Respiratory

Presentation of post-primary TB:

  • The primary complex may reactivate or there may be infection from an exogenous source
  • The granulomatous response causes the formation of an Assmann focus, leading to cavitation
  • The focus will normally heal and calcify but can progressively enlarge in patients who are immunocompromised
  • Symptoms:
    • Malaise, night sweats, anorexia, weight loss
    • Productive mucoid cough
    • Repeated small haemoptysis
    • Pleural pain
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13
Q

TUBERCULOSIS: Outline the investigation of a patient with suspected TB

A
  • Chest X-ray
    • Suggestive findings: Cavitation, pleural effusion, mediastinal or hilar lymphadenopathy, parenchymal infiltrates mainly in the upper lobes
  • 3 sputum samples with one morning sample
    • Microscopy for acid-fast bacilli, mycobacterium culture and molecular testing/drug sensitivity
  • ​Bronchoscopy with biopsy or bronchoalveolar lavage may be used if sputum samples are negative

​​Tests for latent TB

  • Mantoux test
  • Interferon-gamma release assay to be used in immunocompromised individuals
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14
Q

TUBERCULOSIS: List the common site of non-pulmonary TB infection and outline the pathological features

A

Miliary TB: A generalised haematogenous TB. Symptoms include fever, chills, weakness, malaise and progressive dyspnoea.

Lymphatic TB: Painless lymphadenopathy, typically of the posterior cervical and supraclavicular chains

Joint/spinal TB (Pott disease): Monoarthritis

Renal TB: Sterile pyuria

Cutanous TB: Erythema nodosum, lupus vulgaris

TB meningitis

TB pericarditis: Chest pain

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15
Q

TUBERCULOSIS: Outline common predisposing factors and outline the principles of treatment of confirmed cases and the principles of contact tracing

A

Predisposing factors:

  • Living in endemic areas (India, China, Indonesia, Nigeria, South Africa, Bangladesh, Ethiopia, Pakistan, Philippines)
  • Immunocompromised individuals
  • Close contact with other who have had TB
  • Alcohol/drug abuse
  • Living in crowded environment

Testing

Looking for immune response to TB (previous, latent or active TB)

1st: Mantoux test - induration of 5mm or more is positive

Positive Mantoux with no signs of active disease → IGRAs

  • Positive confirms latent TB

If there are signs of active infection:

  • CXR
  • Cultures - x3 sputum, blood cultures, lymph node biopsy/aspiration
  • NAAT

Principles of treatment:

The main goal is to cure the pt and prevent further transmission.

Whilst infectious, patients should remain isolated (either at home or in a hospital room).

Consists of:

  • An intensive phase: Lasts 8/52. Involves isoniazid, rifampicin, pyrazinamide and ethambutol.
    • ​Rifampicin and isoniazid for 6 months
    • Pyrazinamide and ethambutol for 2 months
    • Isolation for 2 weeks until on established treatment
  • A continuation phase: If sensitive to isoniazid and rifampicin, they are continued for 18/52.
  • Steroids for extrapulmonary disease

Principles of contact tracing:

  • Close contacts (prolonged, frequent or intense contact with the patient. Such as household contacts, partner etc.) should be assessed for symptoms of active TB or given testing for latent TB if asymptomatic
  • Notify public health of suspected cases
  • Social contacts (most workplace contacts) do not routinely require assessment. However, if the index case is particularly infectious or are known to be at high risk of developing TB then assessment is required
  • People who have had significant exposure in the last 1-2 years should be evaluated for active TB disease and latent TB disease

Side effects of treatment

Rifampicin - Coloured urine, tears

Isoniazid - Peripheral neuropathy. B6 usually prescribing prophylactivally

Ethambutol - Colour blindness and reduced VA

RIP all associated with hepatotoxicity

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16
Q

PNEUMOTHORAX: Describe its typical clinical presentation and the recognised risk factors together with the underlying pathology and investigations.

A

Clinical presentation:

  • Dyspnoea
  • Chest pain

Risk factors:

  • Smoking
  • FHx of pneumothorax
  • Chronic lung condition e.g. asthma, COPD, TB, CF
  • Trauma
  • Young, tall, thin males
  • Structural abnormalities e.g. Marfan syndrome, Ehlers-Danlos syndrome

Investigations:

  • Physical examination: Hyperresonance, reduced air entry, unequal chest expansion
  • CXR
  • Bloods: FBC, clotting
  • ABG - if PaO<span>2</span> is < 92% on room air

Underlying pathology:

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17
Q

PNEUMOTHORAX: Distinguish between simple and tension pneumothorax including features that aid in recognition of critically ill patients presenting with a tension pneumothorax

A

Tension pneumothorax: A one way valve develops that allows the entry of air into the pleural space but not out.

Clinical presentation:

  • Cardiopulmonary deterioration
    • Hypotension !EMERGENCY - suggests imminent cardiac arrest
    • Respiratory distress
    • Tachycardia
    • Shock
    • Low oxygen saturations
  • Mediastinal shift
  • Hydrosis
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18
Q

PNEUMOTHORAX: Describe treatment options

A

Percutaneous aspiration (needle thoracocentesis)

  • Indicated for:
    • Pneumothorax > 2cm (between the lung margin and chest wall) +/- breathlessness
    • Symptomatic pneumothorax < 2 cm
    • Tension pneumothorax
  • Insert local anaesthetic
  • Insert a cannula into the 2nd ICS, midclavicular line. Attach a 3 way tap and then a syringe to the 3 way tap. Aspirate air via the 3 way tap.
  • Aspirate until resistance, usually < 2.5 L

Intercostal underwater chest drain:

*MUST perform FBC and clotting to check for coagulopathy first*

  • Insert local anaesthetic
  • Insertion site may be identified using USS or by using the ‘safe triangle’
  • 4th ICS, mid-axillary line
  • Insert the needle, use a series of dilators to allow for eventual insertion of the chest drain, attach the chest drain to draining apparatus, secure the chest drain
  • Re-examine the patient and order a supine CXR to check the position of the drain
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19
Q

PNEUMOTHORAX: Outline the indications for surgical pleurectomy and pleurodesis

A

Indications for surgical pleurectomy1:

  • Those with persistent air leak at 48 hours should be considered for surgery
  • Open thoractomy2 and pleurectomy should be considered

Indications for medical pleurodesis3:

  • May be considered for patients refusing or not fit enough for surgery
    1: Pleurectomy involves removal of a small portion of the pleura, allowing for the lungs to adhere to the chest wall in the hope that this will prevent further accumulation of air between the lungs and the pleura
    2: Thoracotomy describes surgery to open the chest wall
    3: Involves the introduction of irritant drugs between the pleura and the lung to encourgae them to adhere to each other, preventing further accumulation of air
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20
Q

PNEUMOTHORAX: Describe the emergency treatment of tension pneumothorax

A
  1. Put out an immediate cardiac arrest call
  2. Immediate decompression: thoracocentesis or open thoracostomy (if secondary to trauma)
  3. High flow oxygen
  4. Chest drain insertion and hospital
21
Q

LUNG CANCER: Outline the major pathological classification of lung cancers and their prognosis

A
22
Q

LUNG CANCER: Describe the common clinical presentation and risk factors

A

Common clinical presentation:

  • RED FLAG symptoms: Weight loss, night sweats, malaise
  • Cough
  • Haemoptysis
  • Dyspnoea
  • Chest pain

Risk factors:

  • Smoking
  • Increasing age
  • Occupational exposure
  • COPD
  • FHx
23
Q

LUNG CANCER: List relevant investigations for lung cancer and interpret results

A

Investigations:

  • CXR
  • CT CAP/MRI

Investigations to consider:

  • Sputum cytology
  • Bronchoscopy
  • Biopsy
  • Bloods: FBC, Ca2+, LFTs
24
Q

LUNG CANCER: Outline local metastatic manifestations of lung cancer and describe the systemic non-metastatic manifestations including paraneoplastic syndromes

A

Local metastatic manifestations:

  • Hoarseness secondary to recurrent laryngeal nerve palsy
  • Atelectasis
  • Pleural effusion
  • Bronchial obstruction

Systemic non-metastatic manifestations:

(liver, brain, bone, adrenal gland)

  • Bone mets → Fractures and bone pain
  • Brain mets → confusion, personality changes, seizures, focal neurological deficit, nausea and vomiting
  • Paraneoplastic syndrome in SCLC:
    • A group of symptoms that may develop when substances released by some cancer cells disrupt the normal function of surrounding cells and tissues
    • Common paraneoplastic effects include: Hypercalcaemia, SIADH, Cushing syndrome, hypercoaguability, finger clubbing, symptoms similar to Myasthenia Gravis
25
Q

LUNG CANCER: Outline the treatment options for a patient with confirmed lung cancer

A

! Dependent upon the stage of the malignancy

  • Chemotherapy
  • Radiotherapy
  • Surgery
26
Q

PLEURAL EFFUSION: Classify causes of a pleural effusion

A
27
Q

PLEURAL EFFUSION: Describe the typical examination features of a pleural effusion

A

Symptoms:

  • Dyspnoea
  • Cough
  • Pleuritic chest pain

Examination findings:

  • Observations: Reduced chest expansion
  • Percussion: Dullness
  • Auscultation: Reduced air entry, increased vocal resonance

Looking for possible aetiology:

  • Signs/symptoms of malignancy
  • Peripheral stigma of kidney, liver or heart failure
    • ​?Organomegaly
  • Autoimmune conditions e.g. RA, SLE
28
Q

PLEURAL EFFUSION: Describe the aetiology and clinical features of an empyema

A

DEFINITION: A collection of frank pus within the pleural space.

Aetiology:

*Spread (e.g. from pneumonia) or direct innoculation*

  • Secondary to pneumonia: Spread of infection into the pleural space sees a complicated parapneumonic effusion, with progression to empyema
    • Therefore RF for empyema are the same as for pneumonia e.g. aspiration, immunocompromised, alcohol abuse and drug addiction
  • Iatrogenic aetiologies e.g. thoracic surgery, chest drain insertion, thoracentesis, aspiration of pleural effusions
  • Trauma e.g. infected haemothoraces

Clinical features:

*Symptoms of pleural effusion plus fever*

  • Dyspnoea, cough, pleuritic pain
  • Systemic symptoms: Fever
29
Q

PLEURAL EFFUSION: Discuss the investigation of a unilateral pleural effusion

A

Bloods:

  • Blood cultures
  • CRP
  • WBC count

Imaging:

  • CXR
  • Thoracic US

Thoracentesis:

  • Pleural fluid appearance/odour1/pH/total protein concentration/LDH level/glucose concentration/white cell diffential/MC&S

​NOTE the aspiration of frank pus is diagnostic of empyema and no other investigations are required to establish the diagnosis.

1: Putrid odour is suggestive of anaerobic infection

30
Q

PLEURAL EFFUSION: Discuss the management of pleural effusion and empyema

A

Management of pleural effusion:

*Dictated by the precipitating cause*

  • Congestive heart failure
    • ​Diuretics e.g. loop
    • Therapeutic thoracentesis if large or for the relief of symptoms
  • Infective e.g. pneumonia
    • Antibiotics
    • Therapeutic thoracentesis
      • ​Indicated if the effusion progresses to a complicated effusion or empyema
  • Malignant
    • ​Therapeutic thoracocentesis for symptomatic relief
    • In patients with a longer life expectancy a thoracoscopy with talc poudrage pleurodesis

Management of empyema:

THINK - May be septic at presentation

  • IV antibiotic treatment
  • Urgent pleural fluid drainage, inserted until US guidance
  • For patients who do not respond to tube thoracostomy (chest drain) surgery is indicated.
31
Q

INTERSTITIAL LUNG DISEASE/PULMONARY FIBROSIS: Describe the clinical and pathological features of interstitial lung disease

A

Clinical features:

  • Dypsnoea of exertion
  • Dry, paroxysmal cough
  • Abnormal breath sounds
  • Abnormal CXR or high-resolution CT
  • Restrictive pulmonary spirometry

Pathological features:

  • Fibrosis and remodelling of the interstitium
  • Chronic inflammation
  • Hyperplasia of type II pneumocytes
32
Q

INTERSTITIAL LUNG DISEASE/PULMONARY FIBROSIS: Outline the common causes and list the differential diagnosis in patients who present with established pulmonary interstitial fibrosis

A

Common causes:

  • Known cause:
    • Occupational exposure: Asbestosis, solicosis
    • Medications: Nitrofurantoin, bleomycin, amiodarone, sulfasalazine, busulfan
    • Hypersensitivity reaction
    • Infections: TB, fungi, viral
    • Gastro-oesophageal reflux
  • Systemic disease:
    • ​Sarcoidosis
    • RA
    • Connective tissue disease
    • Ulcerative colitis, renal tubular acidosis, autoimmune thyroid disease
  • Idiopathic

Different diagnosis:

  • Asthma
  • Bronchiectasis
  • COPD
  • Sarcoidosis
  • CT disorders
33
Q

INTERSTITIAL LUNG DISEASE/PULMONARY FIBROSIS: Outline the investigations and treatment options for patients with suspected interstitial lung disease

A

Investigations:

  • Lung function testing
    • Spirometry: Restrictive
    • Gas transfer (transfer constant of CO): Reduced
  • Chest X-ray
  • High resolution CT
  • Biopsy required if a confident diagnosis cannot be made from the above investigations

Treatment options:

  • Pulmonary rehabilitation
  • Lung transplantation
  • Ventilation
34
Q

EXTRINSIC ALLERGIC ALVEOLITIS (a.k.a. hypersensitivity pneumonitis): Outline the nature of the allergic reaction underlying EAA and how this is used to establish the diagnosis

A

Nature of the allergic reaction:

  • Non-IgE mediated immunological inflammation
  • Caused by repeated inhalation of non-human protein (e.g. plant or animal) or can be the result of a chemical conjugated to a human airway protein, e.g. albumin
  • ?Type 3 hypersensitivity reaction

Establishing diagnosis:

  • No pathognomic test is available. Diagnosis is achieved through a combination of history and corroborative tests:
    • High titre antibody against the suspected antigen
    • Abnormal CXR/CT
    • Abnormal pulmonary function tests
35
Q

EXTRINSIC ALLERGIC ALVEOLITIS (a.k.a. hypersensitivity pneumonitis): Describe the typical clinical presentation and list common causes

A

Clinical presentation:

*Dependent upon the concentration and frequency of exposure*

  • Acute HP illness: Fever, rigors, myalgia, dry cough, dyspnoea, fine bibasal crackles
  • Chronic: Dyspnoea, non-productive cough, weight loss/anorexia, clubbing, diffuse rales

Common causes:

  • Bacteria
    • ​Farmers lung, mushroom picker’s lung (Thermophilic Actinomycetes)
  • Animal proteins
    • ​Bird fancier’s/pigeon breeders lung
    • Malt workers lung
  • ​Reactive chemicals
  • Agents used in metal working
36
Q

EXTRINSIC ALLERGIC ALVEOLITIS (a.k.a. hypersensitivity pneumonitis): Outline the pathological consequences of repeated allergen exposure

A

Acute phase: Alveoli are infiltrated with acute inflammatory cells. Early diagnosis and prompt allergen removal can halt disease progression.

Chronic exposure leads to granuloma formation and obliterative bronchiolitis. There is very little inflammation. The fibrosis results in dyspnoea, weight loss, malaise and decreased DLCO.

37
Q

EXTRINSIC ALLERGIC ALVEOLITIS (a.k.a. hypersensitivity pneumonitis): Outline the treatment options and monitoring of treatment response

A

Treatment:

*The most important element is avoidance of the causative antigen*

  • Acute and sub-acute symptoms: Corticosteroid taper (increasing dose over 6/52)
  • Chronic symptoms: Long term low dose corticosteroid therapy i.e. Prednisolone 10 mg OD on alternate days

Monitoring:

Following avoidance and 1-2 weeks therapy with prednisolone PFT1 should be tested, as they will be as optimal as possible.

Prednisolone tapering is best monitored using PFTs, with the goal being optimal PFTs.

1: Pulmonary function tests allow for FEV1/FVC, FEV1 and gas transfer to be calculated

38
Q

OCCUPATIONAL LUNG DISEASE: Describe the clinical features of the main conditions associated with asbestos inhalation

A

Asbestos bodies: Not pathological

Pleural plaques: Normally asymptomatic

Pleural thickening: Normal asymptomatic. May be some mild restrictive deficit on spirometry

Asbestosis: Progressive dyspnoea, cough

Mesothelioma: Pleuritic chest pain, increasing dyspnoea, unilateral pleural effusion on CXR

39
Q

OCCUPATIONAL LUNG DISEASE: Describe the natural history of pleural plaques, mesothelioma and asbestosis

A

Pleural plaques: Not pathological. Act as a marker of exposure

Mesothelioma:

  • May be an extensive time period between exposure and tumour development
  • Caused by light exposure

Asbestosis:

  • Follows heavy exposure
  • An interval of 5-10 years from exposure to disease
40
Q

OCCUPATIONAL LUNG DISEASE: Discuss the effect of inhalation of coal dust on lung function and its relation to pneumoconiosis

A

Inhaled coal dust ingested by resident macrophages → subsequent death of macrophages allows for release of their enzymatic contents → causes inflammation and fibrosis

  • The above leads to coal workers pneumoconiosis, which is asymptomatic but often coexists with chronic bronchitis
  • CXR sees multiple opacities, especially in the upper zones
41
Q

OCCUPATIONAL LUNG DISEASE: Describe the pathology of simple and complicated coal workers pneumoconiosis (a.k.a. progressive massive fibrosis)

A

Simple coal worker’s pneumoconiosis:

  • Presence of coal macules (1-5 mm), which are round nodular opacities
  • Not associated with any clinically significant impairment in respiratory function although dyspnoea on exertion and a dry non-productive cough may develop as the disease progresses
  • COPD may develop as a complication of the condition

Progressive massive fibrosis:

  • Large opacities (1-10 cm) in the upper-mid zone seen *key ddx is lung carcinoma
  • Can progress of respiratory failure and cor pulmonale
42
Q

OCCUPATIONAL LUNG DISEASE: Demonstrate an awareness that patients exposed to coal and asbestos can obtain industrial compensation

A
43
Q

OCCUPATIONAL LUNG DISEASE: Demonstrate an awareness that asthma can be due to occupational factors

A

Explore the relationship of being in the work environment with symptoms, e.g. any improvement noted at weekends?

44
Q

OBSTRUCTIVE SLEEP APNOEA: Outline the clinical presentation of a patient with OSA, describe the use of sleep studies in its investigation and outline the principles of treatment

A

Clinical presentation:

  • Excessive daytime sleepiness (Epworth Sleepiness Score)
  • Loud snoring
  • Episodes of gasping and apnoeas
  • Restless sleep
  • Insomnia
  • Complications: MI, dysrhythmias, stroke, HTN, metabolic syndrome

Use of sleep studies:

  • Polysomnography: > 5 episodes per hour is sufficient in a symptomatic pt. An apnoea-hypopnoea index (AHI) > 15 epidoes/hour is confirmatory.

Polysomnography includes EEG, electro-oculographic recording, air flow assessment, EMG, capnography, oesophageal manometry, ECG and pulse oximetry.

Principles of treatment:

  • Aims are normalisation of AHI, control of hypertension and hyperglycaemia
  • Mild-moderate OSA: Weight loss, positional therapy
  • Severe OSA: CPAP, oral applicances
45
Q

RESPIRATORY FAILURE: Distinguish type-2 and type-1 respiratory failure and describe the implications of having a high arterial pCO2

A

Type 1 respiratory failure: Hypoxia

Type 2 respiratory failure: Hypoxia and hypercapnia

Implications of having a high arterial pCO2:

  • Clinical features include fatigue, headache, tachycardia, bounding pulse, CO2 retention ‘flap’ and papilloedema
  • Features of acidaemia:
    • Kussmaul respiration - ‘air hunger’, deep and laboured breathing
    • Cardiovascular dysfunction as acidosis is negatively ionotropic (contractability)
    • Potassium abnormalities: Acidosis leads to movement of K+ out of cells, leading to hypokalaemia if renal function is ok or hyperkalaemia if renal function is reduced
    • Cerebral dysfunction, manifesting as confusion or coma
    • Peripheral vasodilation and increased permeability
46
Q

RESPIRATORY FAILURE: Distinguish between acute and chronic type II respiratory and metabolic causes of acidosis

A

Acute vs Chronic Type II Respiratory Failure

  • Chronic type II respiratory failure would see hypercapnia and metabolic compensation, in the form of increased HCO3

Metabolic causes of acidosis

  • Increased production of acid (increased anion gap):
    • ​DKA: Elevated glucose and ketones
    • Lactic acidosis: Such as lactate accumulation occuring in shock or conditions in which there is increased anaerobic respiration e.g CCF. Metformin may also induce lactic acidosis
    • Renal failure: Decreased acid excretion and bicarbonate reabsorption
    • Toxic ingestions: Paracetamol overdose, rhabdomyolysis
  • GI or renal loss of bicarbonate (normal anion gap):
    • ​Renal tubular acidosis
    • GI losses: Diarrhoea, tube drainage

​​https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/metabolic-acidosis

47
Q

RESPIRATORY FAILURE: Describe the causes of ventilatory failure and outline the effect of chest wall and spinal deformity on respiratory function

A
  • Neuromuscular conditions: Myasthenia gravis, GBS, botulism
  • Intake of drugs that suppress ventilatory drive: Alcohol, benzodiazepines, opioids
  • Severe exacerbations of respiratory conditions: COPD, asthma *the most common causes of ventilatory failure*
  • Muscular dystrophy
  • Obesity
  • Trauma causing inability to inflate/deflate the chest wall e.g. flail chest

​Effect of chest wall and spinal deformity on respiratory function:

Compromises the neuromuscular competence to sustain alveolar respiration, such that the ‘load’ cannot be matched.

48
Q

RESPIRATORY FAILURE: Outline the conditions that cause ventilatory failure due to neuromuscular disease

A
  • Myasthenia Gravis
  • Guillain-Barre syndrome2
  • Amyotrophic lateral sclerosis1
  • Spinal cord lesions
  • Phrenic nerve injury (cervical spine injury - C3, 4, 5)
  • Botulism
  • Neuromuscular blockers: Succinylcholine (depolarising), rocuronium (non-depolarising)
  • Aminoglycosides

​1: ALS is a type of motor neuron disease, in which there is destruction of both upper and lower motor neurons responsible for voluntary movement.

2: Inflammation of neurons seein demyelination, and in extreme cases damage to the neuron itself. Presents with tingling, neuropathy, weakness and loss of sensation.

49
Q

RESPIRATORY FAILURE: Outline the treatment of acute respiratory failure

A

Type 1 respiratory failure - Hypoxia

Management:

  • Oxygen supplementation
  • Medical treatment: Bronchodilators, steroids, antibiotics
  • Surgical intervention e.g. pleurodesis

Type 2 respiratory failure - Hypoxia and hypercapnia

Management

  • NIV: CPAP, BiPAP
  • Invasive ventilation
  • Oxygen supplementation
  • Rehabiliation - physiotherapy

CP3 (14 decks)

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