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MRCP > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Asthma Exacerbation - Features

A

Breathlessness
Cough
Wheeze
Chest tightness

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2
Q

Asthma Exacerbation - Investigations

A

PEFR - % of the patients best or predicted score . Predicted is used if no accurate best in last 2 years. Calculated using age and height

Pulse Ox - if under 92% life threatening. Note if shock or anaemia present then inaccurate

ABG

CXR - not normally required but can r/o pnuemonia

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3
Q

Features in more severe asthma exacerbation

A

Tachypnoea
Tachycardia
Inability to complete sentences
Silent chest

Note 50% of those with severe exacerbation won’t have any of these!

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4
Q

ABG in asthma exacerbation

A

Most asthma exacerbation will show resp alkalosis unless hypercapnia has developed

Hypercapnia - means near fatal - normally occurs at PEFR of 20%

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5
Q

Epidemiology

A

Peak incidence - 20-30 yrs

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6
Q

Moderate attack - Asthma

A

PEFR 50-75% and no features of severe attack

All patients with asthma exacerbation should have 40-50mg Pred OD for 5 days or until symptoms resolve

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7
Q

Severe attack - Asthma

A

PEFR 33-50%
RR 25 or over
HR 110 or over
cant complete sentance

Admit if fail to respond to initial management

SABA can be given using inhaler

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8
Q

Life-threatening Asthma

A

PEFR under 33%
Spo2 under 92%
Pao2 under 8
Silent chest
Cyanosis
Decreased resp effort
Arrhythmia
Reduced GCS
Hypotension

Requires Admission ASAP

SABA has to be given via neb

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9
Q

Near Fatal Asthma

A

Hypercapnia or mechanical ventilation

Requires Admission ASAP

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10
Q

Generic Management of Asthma exacerbation

A

SAMA - Ipratropium - life threatening + near fatal or in those that have not responded to steroid and SABA. 0.5mg 4-6 hrly

Mg Sulfate / IV Aminophylline - can be used as a next step

Ventilation - can be considered if all else fails

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11
Q

Exacerbation of COPD - epidemiology

A

More in Men
Peaks at ages 60 - 70

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12
Q

Causes of COPD exacerbations

A

Infections:
- S.Pneumoniae, Haemophillus and Moraxella
- Viral - rhinovirus, influenza, etc

Non Infectious
- Air Pollution - smoke, emissions, dust etc
- Allergens
- PE
- Non compliance to meds

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13
Q

Pathophysiology of COPD Exacerbation

A

In COPD airways are obstructed due to inflammation and have higher compliance due to emphysema destruction

  1. Increased inflammation + oedema + bronchospasm - limits exp flow
  2. Worsening of gast trapping - inc ventillation perfusion mismatch
  3. Resp muscles fatigue (neuromechnical decoupling) - reduced resp drive
  4. Cardiac dysfunction worsens more due to inc pulm vascular resistance
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14
Q

Modified Anthonisen Criteria - COPD

A

2 major symptoms or 1+1 then can make Dx

Major:
- SoB
Inc sputum volume
Inc sputum purulence

Minor
- Cough
Wheeze
Nasal discharge
- Sore throat
- Fever

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15
Q

Assessment of COPD Exacerbations

A

Assessment should focus on if need to come into hospital or not

Rapid onset
Poor baseline functional status - ie LTOT
Comorbid
Signs of Hypoxia or Hypercapnia

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16
Q

Investigations in COPD Exacerbations

A

CXR
ABG
FBC
Sats

Sputum culture
Spirometry
CT

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17
Q

4 components of COPD Exacerbation management

A
  1. Respiratory Support
  2. Pharmacological management
  3. Optimisation for discharge
  4. Preventing exacerbations
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18
Q

o2 targets in COPD

A

88-92% if:

History fo T2RF requiring NIV
O2 below 94% when stable
Long standing hypercapnia

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19
Q

Resp support in COPD Exacerbations

A
  • supplemental o2
    - Serial ABGs - presentation and after 30-60min
    • NIV - persistent acidosis and hypercapnia or RR over 23 despite optimal treatment for one hour

Invasive mechanical ventilation:

the first 4 hours of NIV are key. If any of following decelop need invasive

  • Imminent resp arresst
  • Severe resp distressed
    Failure of NIV (acidotic under 7.25 or RR over 35
  • Persistnet or worsening acidsois ie under 7.15
  • GCS under 8
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20
Q

Pharmacological Management COPD

A

SABA and or SAMA
5 day course pred
IV Theophyline if inadequate response

Abx:
All 3 major symptoms or 2 major (one being inc sputum production or require NIV

21
Q

Prevention of COPD Exacerbations

A

Smoking cessation
Vaccines - Influenza and Pneumococcal
Pulm rehab
Azithromycin long term
carbocysteine / NAC

22
Q

ARDS - pathophysiology

A

Increased permeability of Alveolar capillaries leading to alveolar fluid accumulation

Causes:
1. Infection
2. Blood transfusion
3. Trauma
4. Smoke inhalation
5. Pancreatitis
6. Cardio-pulm bypass

23
Q

ARDS - Features

A

Acute onset hypoxia and bilateral pulmonary infiltrates in absence of cardiac failure

24
Q

Diagnostic Criteria - ARDS

A

Acute onset - within one week of risk factor

Pulm oedema (bilateral infiltrates on CXR)

Non cardiogenic

Hypoxic

25
Q

ARDS Management

A

Generally need ICU admission

Reverse Hypoxia
Organ support
Treat the cause

Possible evidence for prone positioning and muscle relaxation

26
Q

Allergic Bronchopulmonary Aspergillosis

A

Hypersensitivity reaction in response to colonisation of resp tract with Aspergillus fumigatus

27
Q

Aetiology of ABPA

A

Unlikely to occur in those without risk factors

Asthma - thick mucus in airways makes it harder to clear fungus

CF - impaired mucous clearance and airways inflammation

Atopy history - Aspergillus acts as antigen inducing TH2 cells to produce eosinophils

Other possible risk factors:
1. HLA associations - DR2 or DR5
2. IL-10 promoter polymorphisms
3. CFTR gene mutations
4. Surfactant protein polymorphisms

28
Q

Pathophysiology of ABPA

A

In those with risk factors inhalation of spores trigger a T1HS reaction.

Aspergillus acts as antigen stimulating TH2 cells to secrete cytokines. These promote IgE and IgG synthesis - these enhance eosinophil production and survival. These cause mediator release and vasoldiation with bronchoconstriction

Inflammation causes mucus production, airways hyperreactivity and bronchiecstasis.

29
Q

ABPA presentation and investigation

A

New or worsening cough with inc sputum (brown / black)
Wheeze
Blood (inflammation and bronchiecstasis)
Chest Pain
Weight loss
fever

Occasionally may get associated chronic rhinosinusitis (allergic aspergillus sinusitis)

To diagnose
1. Skin Test - positive hypersensitivity to fungus - not specific

  1. Bloods - IgG and IgE against fungus. Serum total IgE. Eosinophilia (steroids mask this)
  2. CXR (Upper / middle lobe infiltrates). CT
30
Q

Management of ABPA

A

Initially - Steroids and adjunctive antifungal (if very poor functional status)

Remission - Maintenance of inhaled steroids

If cannot be weaned off of steroids without remission - Faily oral steroids and omalizumab (anti IgE therapy)

31
Q

Complciations of ABPA

A

Bronchiectasis - mostly central
Fibrosis
Reps failure
Pulm HTN

Side effects related to steroids.

32
Q

Chronic Asthma - Aetiology

A

Genetics + Env + Immunological

Env - allergens, resp infections, tobacco, occupational exposure. Antenatal smoking and RSV infection in pregnancy.

Immune - Asthma is the imabalance of immune response. This leads to cytokine production (IL 4,5 and 13) which causes eosinophilic inflammation and IgE production.

33
Q

Pathophysiology of Chronic Asthma

A

“Chronic inflammatory disorder secondary to T1HS”

Airway inflammation - pro-inflammatory mediators cause airway oedema, mucuous and constriction.

Bronchoconstriction - contraction of smooth muscle secondary to mediatiors

Hyper-responsiveness - excessive narrowing of airways to stimuli.

Mucous production and airway remodelling - chronic inflammation leads to changes in the airway wall. These include subepithelial fibrosis, inc msucle muss, gland hypertrophy and angiogenesis.

34
Q

Classification of Chronic Asthma

A
  1. Intermittent - less than once a week. Normal Pulm function between episodes. Nocturnal symptoms less than 2x a month
  2. Mild Persistent - More than once a week but less than once a day. More than 2x a month nocturnally. Normal Pulm function tests.
  3. Moderate Persistent - Daily with the use of SABA. Nocturnal symptoms more than once a week FEV1 and PEFR netween 60-80% predicted
  4. Severe Perisistent - Continuous daily symptoms limiting activity. Under 60% predicted pulm function
35
Q

Diagnosis of Chronic Asthma

A

FeNo - fractional exhaled nitric oxide. This is produced by nitric oxide synthase and one of these rises when there is rise in eosinophils.

Over 17 - All need FeNO and BDR

5-16 = all should have BDR. FeNo if there is normal spirometry or obstructive but with normal BDR

Under 5 - clinical judgement

36
Q

Tets used in Diagnosis of Asthma

A

FeNO - over 40ppb or 35 in kids

FEV1/FVC under 70%

BDR - improvement of 12% FEV1 or 200ml in adults. 12% or more in kids only.

37
Q

Management of Chronic Asthma

A

Step up each time not controlled or if symptoms more than 3x a week / night time waking

  1. SABA
  2. SBA and low dose ICS
  3. SABA + low does ICS + LTRA
  4. SABA + low dose ICS +LABA continue LTRA if worked)
  5. Switch ICS and LABA for MART (includes the low dose ICS)
  6. increase MART to mod dose ICS
  7. Add either ICS to high dose (not as MART), LAMA / theophylline or specialist referral

Low dose ICS - under 400mcg budenoside
Mod - 400-800mmcg
High os over 800mcg

38
Q

Complications of Asthma

A

Status asthamticus - severe persistent Asthma attack

Pneumonia

COPD

Pneumothorax

Osteoporosis - steroids
Anxiety and depression

39
Q

Bronchiectasis

A

Irreversibly dilated Bronchi + chronic Bronchial Inflammation and infection

Can be localised (one lobe) or generalised

A deficit of mucociliary clearance +/- immune function = microorganisms acquisition, colonisation and infection = chronic inflammation = dilation and thickening or bronchi = bronchial wall oedema = more infection = cycle repeats

40
Q

Aetiology of Bronchiectasis

A

Idiopathic - 45%
Post infection
Immunodeficiency
COPD
Connective tissue disorders
ABPA
Ciliary issues
Asthma
IBD
Aspiration
A1AT
Pinks
yellow Nail syndrome
congenital malformation

41
Q

Presentation and investigation of Bronchiectasis

A

Chronic Producitve couch + recurrent chest infections

up to 50% may have haemoptysis

Other:
Chest Pain
GORD - 20-40%
Rhinosinusitis

On exam:
Crackles clubbing and wheeze

Investigation - CXR, Sputum culture. High res CT (best)

On CT:
1. Bronchoarterial ratio over 1 - this is signet ring sign (lumen is alrger than artery)
2. Lack of tapering - bronchi should get smaller as they get closer to periphery
3. Bronchus visible within 1cm of pleural surface

Once diagnosed:
1. Bloods - IgE, FBC and investigate for ABPA.
Serum IgG and IGA + IgM - screen for immunodeficiency

42
Q

Cryptogenic organising Pneumonia

A

Diffuse interstitual lung disease which affects distal brocnhioles, alveolar ducts + wall. Unknown cause

50-60 y/o with cough, SoB, fever and malaise with no response to abx.

Leukocytosis on bloods and elevated ESR and CRP. Bilateral patchy or diffuse consolidation / ground glass on imaging

Treat as watch and wait or high dose steroids if severe

43
Q

Eosinophilic Granulomatosis with Polyangitis

A

Small to medium vasculitis.

Pathogenesis:
1. Prodromal allergic phase - asthma
2. Eosinophilic phase - tissue infiltration with eosinophils - gastroenteritis / pneuomonia
3. Vasculitic phase - endothelial damage - purpura, neuropathy and organ damage

Unknown cause but thought to be related to genes, env, immune (pANCA + high IgE) with infection can trigger

44
Q

Extrinisc Allergic Alveolitis

A

Also called Hypersensitivity Pneumonitis. Induced by immune response to rpt inhalation of antigens

Farmers lung, bird fanciers lung, Malt workers lung or issues with air conditioning

Acutely present with - 4-8 hour after expsosure - cough fever, malaise and SoB. Reslves after 1-2 days

Chronic - cough, weight loss, clubbing and pulm fibrosis

45
Q

Pathophysiology of Extrinsic allergic alveolitis

A

Antigen Exposure - small particles that can reach alveoli

Sensitisation - particles are processed by APC (antigen presenting cells) and present to T lymphocytes. These become activate and release cytokines.

Acute Inflammatory reaction - On re-exposure an inflammatory response is mounted. Leads to neutrophilic infiltration in alveoli leading to alveolitis. There is increased vasc permeability causing fluid accumulation in alveoli (impaired gas exchange)

Chronic Inflammation and Fibrosis - Repeated exposure causes lymphocytic alvooelitis and granuloma formation. Causes pulm fibrosis

46
Q

Investigation and management of EAA

A

Bloods
FBC - normocytic anaemia and inc WCC
ABG

Imaging
CXR
HRCT - can be normal.

Lung function - acute phase it is restrictive. In chronic will turn into obstructive

Management
Avoid causative agent
Steroids - note IPF is not steroid responsive. In EAA these need to be tapered down.

47
Q

Pathogens in EAA

A

Farmers Lung - Saccharopolyspora rectivirgula
Malt - Aspergillus Clavatus
Mushroom - Thermophillic

48
Q
A

MRCP (2 decks)

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