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Mosler > Respiratory station > Flashcards

Respiratory station Flashcards

1
Q

What are your differentials, and why?

A

Main differential = (Idiopathic) Pulmonary Fibrosis

Differentials-IPF,occupational lung disease,COPD,lung cancer,,sarcoidosis,heart failure,pleural effusion,pneumonia,COVID

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2
Q

What investigations would you do?

A

Bedside-Full set of obs

           ECG

           Urine dip-rule out extra pulmonary

manifestation of sarcoidosis such as interstial nephritis,nephroclacinosis

           ABG(respiratory failure)

   Peak flow

Blood-FBC(anemia,infection,polycythemia),U&E’s(exclude other causes,baseline),Bone profile(Hypercalcemia),Serum ACE(sarcoidosis),LFT(Baseline,exclude),BNP(HF),ESR and CRP high(inflammation),Autoantibodies(ANA 30%,Rheumatic factor 10%)

Imaging-HR-CT(gold standard)

          CXR  In IPF, decreased lung volumes and basal reticulation may be seen.

Special test-Spirometry,bronchial larvage

TC-DTPA-disease activity

lung biopsy

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3
Q

What is your management for this patient?

A

Approach to management in IPF:

Conservative

  • Best supportive care
  • Lifestyle changes-Smoking cessation
  • Oxygen
  • Pulmonary Rehab
  • Palliative care when appropriate
  • Physiotherapy ,OCT
  • Yearly Flu vaccination,pneumococcal vaccination
  • Avoid exposure,protective wear,compensation
  • Talking therapies
  • Social,finanical support
  • Carer support

Medical

  • Perfenidone - anti-fibrotic properties, can stabilize lung function
  • Nintedanib
  • Bronchodilaters
  • Medication review
  • Opiates

Surgical

  • Lung transplant
  • clinical trials
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4
Q

What would you see on spirometry? What would you see in COPD vs IPF?

A

COPD-productive cough,Strong smoking history,wheeze,pathphysio,Hyper inflation on CXR

IPF-Dry cough,clubbing,Bibasal crackles,Diffuse pulmonary infiltrates on CXR

Spirometry

COPD-Obstructive picture

IPF-Restrictive picture

  • Reduced FEV1 (<80% of the predicted normal)
  • Reduced FVC (<80% of the predicted normal)
  • FEV1/FVC ratio normal (>0.7)
  • DCLO would be low
    diffusing capacity of the lung for carbon monoxide (DLCO)
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5
Q

What is the prognosis of IPF?

A

Prognosis 3-4 years

5 Year survival is 50%

Death often results from progressive disease and respiratory failure. Others may die during an acute exacerbation - a sudden worsening of symptoms that may be secondary to a specific trigger (e.g. infection) or idiopathic in nature. IPF is also associated with pulmonary hypertension, lung cancer and blood clots.

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6
Q

What other signs can you see in IPF?

A

Idiopathic Pulmonary Fibrosis (IPF) is the most common of the idiopathic pneumonias. There is no evidence of an alternative cause eg. drugs, environmental exposure or a system condition.

It is chronic and progressive, and can be more common in males.

Clinical Features:

  • Insidious onset of shortness of breath and cough
  • Exertional dyspnoea
    Dry cough
  • Malaise(fatigue)
  • Weight loss
  • Arthralgia
  • Fever

Often patients will be diagnosed as recurrent chest infections before the diagnosis of IFP is considered.

Important things to look for in the examination are

Fine end-inspiratory crackles are oft described as velcro crackles(bibasal)
Clubbing
Acrocyanosis(Peripheral cyanosis)

A thorough examination of the cardiovascular system is also recommended

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7
Q

What are other causes of interstitial lung disease?

A

-

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8
Q

What are the risk factors for IPF?

A

Age,Male X2,family history, smoking

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9
Q

Typical ABG finding in IPF?

A

Type 1 respiratory failure (low PaCO2)

COPD-type 2 hypercapneic

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10
Q

CT findings of IPF?

A

Decreased lung volume,ground glass appearance,honey combing
High-resolution CT: an essential investigation in patients with suspected IPF. Characteristic changes include honeycombing (clusters of cystic air spaces), reticular opacities, traction bronchiectasis, emphysema and loss of lung volume - changes are predominantly seen in the bases and peripheries. The classic radiological appearence is called usual interstitial pneumonia (UIP), a term that may also be used, by some, interchangeably with IPF

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11
Q

What are the complication of IPF?

A

Cor pulmonale ,weight loss,infections,pulmonary hypertension

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12
Q

Bronchio-alveolar lavage findings?

A

increased neutrophils,esinophils,lymphocytes(better response to treatment)

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13
Q

What is difference between pink puffers and blue bloaters?

A

Oxford

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14
Q

What is the Management of COPD?

A

pulse notes

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15
Q

What is the management of an acute exacerbation COPD

A

pulse notes

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16
Q

What is the criteria for LTOT for COPD

A

Type II (hypercapnic) respiratory failure

Patients with COPD are at risk of developing type II respiratory failure (T2RF) i.e. PaO2 < 8 kPa and PaCO2 > 6.7 kPa. See notes titled ‘Ventilation’ for more details.

Oxygen therapy must be used carefully in patients with COPD, typically saturations of 88-92% are targeted. ABGs may be necessary to monitor for CO2 retention.

If patients have evidence of T2RF, oxygen therapy should be trialled using a venturi mask for 1 hour with repeat ABG. If there is persistent evidence of T2RF, or they decline during the trial period, then non-invasive ventilation should be considered (i.e. BiPAP). BiPAP refers to Bilevel Positive Airway Pressure, which helps to ‘blow off’ excess carbon dioxide and normalise pH.

Indications for BiPAP:

Acute or acute on chronic hypercapnic respiratory failure (not requiring tracheal intubation)
pH < 7.35
PCO2 > 6
Increased RR despite optimisation of oxygen therapy
Cardiogenic pulmonary oedema (refractory to CPAP - continuous positive airway pressure)
Type 1 respiratory failure and clinically tiring
Weaning from mechanical ventilation
Patients requiring BiPAP should be managed in a high-dependency unit (HDU) setting or a specialist ward with nurses who are able to look after patients receiving BiPAP. Moreover, before starting BiPAP it is crucial to discuss and set ceilings of care (often involves discussion with ITU), to exclude any contraindications (e.g. undrained pneumothorax, coma, facial trauma/burns, cardiovascular instability) and plan to continually monitor.

There are two settings on a BiPAP machine:

IPAP: inspiratory positive airway pressure (usually 10-15 cmH20)
EPAP: expiratory positive airway pressure (usually 4-5 cmH20)
The difference between the IPAP and EPAP is crucial to blow off carbon dioxide. Patients are typically started on 12/5 and a repeat ABG is completed after one hour, which guides response to therapy.

Further information on BiPAP and NIV is beyond the scope of these notes.

Long-term oxygen therapy
Patients with COPD may benefit from long-term oxygen therapy (LTOT).
Long-term oxygen therapy (LTOT) is reserved for patients who meet the following criteria:

Arterial Pa02 < 7.3 kPa, OR
Arterial Pa02 < 8 kPa with any of:
Pulmonary hypertension
Peripheral oedema
Secondary polycythaemia
LTOT is required for at least 15 hours a day for a benefit to be seen. Patients who smoke should be explained the dangers of mixing oxygen and cigarette
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17
Q

How can severity of COPD be assessed?

A

Oxford

18
Q

How can you assess the severitiy of SOB?

A

Assess excercise tolerance,adl-stairs,dressing
MRC dyspnea scale
MRC dyspnoea scale
The Medical Research Council (MRC) dyspnoea scale is used to grade the severity of breathlessness.
The MRC dyspnoea scale is divided from 1 to 5.

Breathlessness on strenuous exercise.
Breathlessness on hurrying or slight hill.
Walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace.
Stops to catch breath after 100 metres OR a few minutes of walking
Breathlessness on minimal activity (dressing) or unable to leave the house due to breathlessness

19
Q

What are the Indications and contraindications for lung transplant?

A

Indications

Failure of medical and surgical improvement of disease
less than 2 year survival from disease
Co2 retention
Progressive excercise tolerance
Increased o2 requirement
right heart failure

Contraindications

Incurable malignancy
age >69
Active incurable infection
Major organ system damage
morbid obesity
Alchol,smoking,drug use
steroids
20
Q

How does his caring responsibilties affect his state of health?

A

delay is coming to the health care setting

21
Q

What Support can be provided to Carers?

A 
Carer assessment
respite care 
Support networks 
education
Bereavement counselling
22
Q

What options are available for smoking cessation?

A

check notes

23
Q

Would you add any further medications for this patient?

A

Statin-80mg,assess his q risk

24
Q

What are the causes of erythema nodosum?

A 
NO cause found in 60% of cases
Drugs (antibiotics e.g., sulfonamides, amoxicillin)
Oral Contraceptives 
Sarcoidosis or Lofgren's syndrome 
Ulcerative Colitis, Crohns, Bechet's  
Micro: TB
   Viral: HSV, EBV, HIV, HepB, HepC
   Bacterial: Campylobacter, Rickettsiae, Salmonella, Psittacosis, Bartonella, Syphilis
   Parasitic: Amoebiasis, Giardiasis
25
Q

How can sarcoidosis cause hypercalcemia?

A

Hypercalcaemia is seen in around 15% of cases. This occurs due extra-renal synthesis of calcitriol causing 1-α hydroxylation of 25-hydroxyvitamin D and so increased levels activated vitamin D. This leads to increased levels of calcium.

26
Q

How can TB be investigated?

A

Pulmonary TB

Imaging forms a key part of the diagnostic process and all patients should have a chest X-ray and consideration given to CT chest.

Where possible three respiratory specimens - sputum samples (including one early morning sample) - should be sent for TB microscopy and culture. In those unable to produce spontaneous sputum either induced sputum or bronchoscopy and lavage may be used.

DNA polymerase chain reaction is a nucleic acid amplification technique that allows for rapid and accurate testing. It is an expensive test and is advised for use in certain settings. Rapid testing with nucleic acid amplification may used on specimens if there is suspicion for TB and:

Patient has HIV or
Rapid information on the species would change patient care or
A large contact-tracing initiative is being explored or
Aged 15 or younger
In children and young people slightly different testing may be used. For example gastric lavage can be used as an alternative to induced sputum or bronchoscopy and lavage in those unable to produce spontaneous sputum.

Extrapulmonary TB

The diagnosis of TB requires site specific testing. There are a huge range of possibilities so here we will discuss a few of the possibilities:

Pleural TB: Imaging with a chest X-ray +/- bronchoscopy. Three respiratory specimen, ideally spontaneously produced deep cough samples, one from the early morning. Pleural fluid may be taken for TB microscopy and culture and cytology.

Lymph node TB: Imaging may be with USS, CT or MRI. Samples may be taken by either aspiration or biopsy. In addition to the routine tests nucleic acid amplification may be performed on samples.

Genitourinary TB: Imaging may involve USS and IV urography. Direct visualisation of the fallopian tubes and ovaries can be acheived with laparoscopy. Three early morning urine samples can be sent for TB culture. Biopsy may be taken from affected site (e.g. endometrial curettings or renal biopsy).

Bacille Calmette-Guérin
The BCG is the worlds most utilised vaccine with an estimated 3 billion vaccinations administered.
Mantoux test

A Mantoux test (tuberculin skin test) is required prior to administration in those aged > 6 years, or younger if there is a history of exposure to TB.

A positive result contraindicates the vaccine due to the risk of a severe reaction. It does not indicate the patient is immune to TB.

BCG

BCG is a live attenuated vaccine. Its has variable efficacy but prevents severe disease in children. It is not particularly effective in adults.

It is also protective against leprosy (caused by a non-tuberculous mycobacterium) and is a treatment in bladder cance

27
Q

How can TB differentiated sarcoidosis and tb from x-ray

A

Upper zone cavitating. lesions-check note book

28
Q

How can sarcoidosis be investigated?

A

Investigations
Bilateral hilar lymphadenopathy is a characteristic finding in sarcoidosis.

Bedside

Observations
Spirometry
Mantoux test
Bloods

Full blood count
Renal function
ESR
Bone profile:
Hypercalcaemia is seen in around 15%.
Serum ACE:
Raised in around 70%, levels show a response to treatment. However, it is not accurate enough to be used diagnostically and has limited prognostic value.
Imaging

A CXR may reveal:

Bilateral hilar and mediastinal lymphadenopathy
Reticulonodular opacities
Airspace opacities
Pulmonary fibrosis
CXR findings may be used to stage disease - see the ‘Scadding staging’ chapter below. It should be noted no changes are seen in 20% of patients.

Depending on disease progression high-resolution CT may demonstrate:

Lymphadenopathy
Diffuse nodularity
Ground glass opacification
Fibrosis typically affecting
FDG PET may be used in select cases where there is ongoing diagnostic uncertainty, particularly where cardiac sarcoidosis is suspected.

Diagnosis
Tissue biopsy is needed to absolutely confirm a diagnosis of sarcoidosis, though it may not always be required.
Tissue biopsy is needed to confirm a diagnosis of sarcoidosis. This is of great importance as other conditions that can mimic radiographical appearances of sarcoidosis include other interstitial lung disease, malignancies and TB.

Clinical diagnosis may be made without the need for biopsy following other relevant investigation and discussion at specialist MDTs. The British Thoracic Society: Sarcoidosis Clinical Statement (2020) describe two scenarios where a clinical diagnosis can be made:

Lofgren’s syndrome: there should be no suspicion of other diagnoses. Patients should follow close monitoring and follow-up.
Long-standing pulmonary disease: with a classical initial presentation, with no suspicion of other diagnoses, and stable, typical, imaging findings following MDT discussion.
In those with suspected pulmonary sarcoidosis bronchoalveolar lavage ± transbronchial biopsy may be arranged. The classic histopathological finding in sarcoidosis is a noncaseating granuloma. These are collections of macrophages, epithelioid cells, t-lymphocytes (normally CD4 +ve) and giant cells that are noncaseating (or non-necrotising) - that is the centre has not undergone caseating necrosis. This is then surrounded by both T- and B- lymphocytes, mast cells and fibroblasts.

Brochoalveolar lavage can show features supportive of sarcoidosis including raised lymphocytes and a CD4/CD8 ratio > 4.

29
Q

How can sarcoidosis be managed?

A

As such the British Thoracic Society (BTS) state treatment should only be started if:

Potential danger of a fatal outcome or permanent disability or
Unacceptable loss of quality of life
As with all chronic diseases, patients should be offered support and counselling. The optimisation of lifestyle factors may involve smoking cessation, weight loss and dietary advice.

Indications for treatment with steroids:

  • Progressive or clearly symptomatic lung disease
  • Cardiac sarcoid
  • Neuro sarcoid
  • Uveitis
  • Hypercalcaemia

The aim of steroid therapy is to reduce inflammation and prevent further damage and fibrosis to tissues. Long term steroid use has multiple complications which should be balanced with therapeutic effects.

In patients who cannot tolerate steroids alternatives include methotrexate and Infliximab.

Steroids

Prednisolone has been the mainstay of management for many years. Typically initial treatment consist of:

High-dose induction: typically 20 - 40mg each day for 4 - 6 weeks
Dose tapering: the initial dose is gradually reduced (e.g. 5mg every two weeks)
Maintenance dose: typically 5 - 10mg each day
Patients should be monitored for steroid based complications and side-effects. Bone protection should be strongly considered in patients on prolonged courses.

Withdrawal of therapy may be trialled after the threat to organ/life has resolved. In those who relapse treatment is re-initiated and further attempts made at withdrawal at 6-12 month intervals.

Classical immunosuppressants

These are generally considered to be second line agents. Options include methotrexate, azathioprine, leflunomide and mycophenolate They may be used in patients:

With significant side-effects from steroids
Co-morbidities putting patient at greater risk of steroid-related side effects
Progressive pulmonary disease / unacceptable ongoing symptoms
Inability to taper steroids to an acceptable maintenance dose
Patient aversion to steroid therapy - may be used as initial therapy
All second line therapies have significant side effect profiles. Baseline full blood count, renal function, liver function and viral hepatitis screen should be arranged. Contraindications to treatment include an eGFR < 30, ALT greater than two times the upper limit of the normal range (unless only cause is sarcoidosis) or chronic hepatitis B/C.

Methotrexate, an antimetabolite, is generally the first choice of the second line agents. Doses are given weekly alongside folic acid supplementation to reduce the risk of myelosuppression. Side effects include the aforementioned myelosuppression, rashes, alopecia and pneumonitis.

Biologics

Biologic agents are considered third-line therapy. They are indicated after treatment failure and use is directed by specialist tertiary centres.

Anti-tumour necrosis factor (TNF) agents (e.g. infliximab) reduce inflammation by blocking the inflammatory cytokine TNF. They are known to trigger the reactivation of latent TB and as such patients must be screened and treated for latent TB.

Lung transplantation

Lung transplantation is a significant procedure that may be indicated in those with:

Advanced pulmonary fibrosis
Pulmonary hypertension
Bilateral transplant appears to have better outcomes than unilateral ones. Clinically significant recurrent disease is rare.

30
Q

What are some genetic predispositions for IPF?

A

Familial pulmonary fibrosis: this is thought to account for up to 5% of cases of IPF. Suspicion is raised in families with multiple cases of ILD. It appears to be autosomal dominant with variable penetrance.
Hermansky-Pudlak syndrome: it is characterised by partial cutaneous albinism, ocular albinism, immunodeficiency, nystagmus and pulmonary fibrosis. Depending on the variants and expression, features may vary.
Telomeropathies: telomeres are sections of non-coding DNA found at the end of chromosomes. There are a number of short telomere syndromes that give rise to a variety of pathologies including pulmonary fibrosis.

31
Q

What are the indication for Lung transplant in IPF?

A

In appropriately selected patients lung transplantation can offer a survival benefit and improve quality of life.

In the US 66% percent survive 3 years or more following transplant, with 53% surviving 5 years or more. It remains a major operation with significant post-operative risks including graft rejection and immunosuppressant (necessary post-transplant) related infections and malignancies.

32
Q

What are the causes of Clubbing?

A 
Cyanotic heart disease/Cystic fibrosis
Lung cancer,lung abscess
Ulcerative colitis
Bronchiectasis
Benign mesothelioma
IE,IPF
Neurogenic tumours
Gastrointestinal disease
33
Q

What causes sarcoidosis?

A

Sarcoidosis is a rare multisystem granulomatous disorder of unknown aetiology.
The aetiology, though poorly understood, is thought to involve immune dysfunction and T-cell overactivity. In the UK onset tends to be between the ages of 20 - 40.

It can have a wide-range of clinical manifestations and is able to affect most of the bodies systems though it most frequently affects the lungs causing a form of interstitial lung disease.

34
Q

What is criteria used to stage for Sarcoidosis?

A

Scadding staging
Scadding staging may be used to stage pulmonary sarcoidosis based upon chest radiograph findings.

0-normal
1-enlarged lymph nodes only
2-enlarged lymph nodes and parenchymal changes
3-parenchymal changes only
4-Lung fibrosis
35
Q

What’s the prognosis of sarcoidosis?

A

It is estimated there is a reduction in life expectancy in 6-8% of those with sarcoidosis.
Many patients with sarcoidosis will experience spontaneous regression and resolution of the disease. In those with pulmonary disease the chance of this can be predicted with the scadding staging (see above). The disease is known to be more severe in certain races, in black Americans mortality rates of 10% have been seen.

Pulmonary disease (including pulmonary fibrosis and pulmonary hypertension) is the predominant cause of sarcoidosis related death, implicated in around 70% of cases. Cardiac disease accounts for much of the remaining deaths.

36
Q

Ventilation

A

copal vs bipap

invasive vs non invasive

37
Q

Causes of upper and lower fibrosis

A

upper zone fibrosis is CHARTS, which is for Coal workers’ pneumoconiosis, Histiocytosis X, Ankylosing Spondylitis, Radiation, TB and Sarcoidosis/Silicosis.

Lower

BAD RASH
B: bronchiectasis
A: aspiration
D: DIP
R: rheumatoid arthritis associated-interstitial lung disease 1
A: asbestosis
S: scleroderma (progressive systemic sclerosis)
H: Hamman-Rich syndrome (Acute interstitial pneumonitis)

38
Q

What is the refferal criteria for patient with suspected lung ca?

A

Patients with suspected lung cancer require two-week wait referral for further review.
NICE guidelines NG 12: Suspected cancer: recognition and referral offer advice on referral for suspected malignancy. They advise two-week wait referral in patients with:

Suggestive CXR findings
Unexplained haemoptysis and aged over 40
Patients with evidence of SVCO or stridor require urgent referral and emergency admission to hospital for further review.

Consider urgent CXR (within 2 weeks) in those aged over 40 with:

Persistent or recurrent chest infection
Clubbing
Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
Chest signs indicative of lung cancer
Thrombocytosis
Consider urgent CXR (within 2 weeks) in those aged over 40 with two of the following or have ever smoked and have one of the following:

Cough
Fatigue
Shortness of breath
Chest pain
Weight loss
Appetite loss
39
Q

What are the causes of SVCO and how does it present?

A

-

40
Q

What is prognosis of SVCO

A

-

Mosler (9 decks)

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