eosinophilic - atopic (fungal, aeroallergens, occupation) - non atopic non eosinophilic -non smoking, smoking, obesity related

3 questions to assess severity of asthma: - are you still experiencing your day symptoms - do you have nocturnal waking - is it interfering with ADL

Respiratory Flashcards by Imma Nyamali

relevant points in the PMH/FH in breathlessness

 PMH: connective tissue disease (interstitial lung disease); previous history of DVT
 FH: VTE, emphysema (alpha-1-antitrypsin deficiency)

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drugs that can cause breathlessness due to fibrotic lung changes

o Antibiotics: nitrofurantoin

o Anti-rheumatoid drugs

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measurement tools for breathlessness

WHO Functional Class
MRC Breathlessness Scale
Borg Scale
NYHA Class

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Investigations for breathless patient

 Immediately: ABG
 Also: Blood tests, ECG, Chest X-ray
 Microbiology: blood cultures, sputum culture (MCS), Acid-fast bacilli, pneumococcal antigen (most common bacterial cause of pneumonia) urinary legionella antigen (severe pneumonia), PCR, procalcitonin

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What is procalcitonin

 Pro-peptide for calcitonin; produced mainly in thyroid neuroendocrine cells and cleaved prior to release upregulated by pro-inflammatory cytokines (IL-1, IL-6, TNF)
 Also released by macrophages in un-cleaved form
 Possible suppressed by interferons –> Distinguishes between bacterial and viral chest infections
• Only 60 – 70% accuracy: not used as part of official guidelines but can be used locally
• If levels are low, avoid antibiotics

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CURB-65 criteria

confusion
urea >7
respiratory rate > 30
BP < S:90 or D:60
Age greater than or equal to 65

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management of T1 respiratory failure

Type 1 respiratory failure: O2 to keep SaO2 above 94%

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treatment for acute eosinophilic pneumonia

steroids

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causes of acute eosinophilic pneumonia

 Usually smoking (or increase/resumption)
 Inhaled recreational drugs
 Medication
 Following lung infections: mainly parasites, also fungi viruses etc.

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what is the pathophysiology of asthma

bronchial hyperresponsiveness –> inappropriate contraction of smooth muscle –> hypertrophy and proliferation of smooth muscle –> inflammation and secretions –> narrow lumen –> airway obstruction

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types of asthma

eosinophilic

atopic (fungal, aeroallergens, occupation)
non atopic

non eosinophilic
-non smoking, smoking, obesity related

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symptoms of asthma

EPISODIC wheeze
cough + breathlessness,
diurnal variation
triggers

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list 5 triggers for asthma exacerbation

allergens 
exercise 
URTI/infection
menstrual cycle 
cold 
laughter/emotion

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how to assess severity of asthma

how many inhalers
A+E, hospital admissions, ventilation, ITU/HDU care
requiring antibiotics/steroids?
RCP3
Asthma control test

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what is the RCP3

3 questions to assess severity of asthma:

are you still experiencing your day symptoms
do you have nocturnal waking
is it interfering with ADL

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what questions are in the asthma control test

(out of 25)
in the past 4 weeks how often did your asthma:

prevent you from getting as much done at work/school/home
shortness of breath
cause you to wake up at night
used your inhaler
how would you rate your asthma control

how can breathing/respiratory function contribute to acid-base

Respiratory: When breathing is inadequate carbon dioxide (respiratory acid) accumulates. The extra CO2 molecules combine with water to form carbonic acid which contributes to an acid pH. The treatment, if all else fails, is to lower the PCO2 by breathing for the patient using a ventilator.

how can metabolism contribute to acid-base

Metabolic When normal metabolism is impaired - acid forms, e.g., poor blood supply stops oxidative metabolism and lactic acid forms. This acid is not respiratory so, by definition, it is “metabolic acid.” If severe, the patient may be in shock and require treatment, possibly by neutralizing this excess acid with bicarbonate, possibly by allowing time for excretion/metabolism.

what is henderson’s equation

Henderson equation:
[H+] is proportional to CO2 / HCO3-
CO2 respiratory component, (lungs)

HCO3 metabolic component (kidneys)

asthma control test meaning

25: well controlled
20-24: on target
less than 20: off target

signs of asthma on physical examination

 May be normal
 Wheeze: polyphonic, expiratory, widespread
 Absence of crackles, sputum and other signs

what is samter’s triad

nasal polyps
asthma
aspirin sensitivity

investigations for asthma

clinical diagnosis if obvious

 Blood count: eosinophils
 Tests for atopy and allergy
 Chest XR often useful to rule out cancer etc.
 [Oxygen saturations]
 Skin prick tests
 Lung function testing (spirometry, PEFR, reversibility challenge)
o Increased responsiveness to challenge agents (mannitol, methacholine)
 Exhaled nitric oxide (FeNO): marker of eosinophilic inflammation

characteristics of severe asthma

one major + 2 minor

major:
 Treatment with continuous or near continuous oral steroids
 Requirement for high dose inhaled steroids

minor 
	Additional daily reliever medication 
	Symptoms needing reliever medication on a daily/near daily basis
	Persistent airway obstruction 
	One or more emergency visits/yr
	3 or more steroid courses/yr
	Prompt deterioration with small changes to steroid dose
	Near fatal event in past

which individuals are at risk of asthma death

``` o On 3 or more classes of treatment o Recent admission/frequent attender o Previous near fatal disease o Brittle disease o Psychosocial factors ```

differential diagnoses for asthma

```  Bronchiolitis  Bronchiectasis* o Chronic infection  airway damage  Cystic fibrosis  Pulmonary embolism  CEA  Idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis)  Hyperventilation*  Bronchial obstruction – foreign body, tumour etc.  Vocal cord dysfunction*  Aspiration  Congestive cardiac failure  COPD ```

management of asthma

non-pharmacological: avoid triggers, smoking pharmacological - bronchodilators (SABA LABA LTRA LAMA, anticholinergics) - treat symptoms - steroids: reduce airway inflammation - biologics: omalizumab (anti-IgE) mepolizumab (anti-IL-5)

features of a moderate asthma attack

PEFR > 50% RR: <25 HR: <110 Normal speech, no other severe markers

features of a severe asthma attack

PEFR 33 - 50% RR: >25% HR > 110% Inability to complete full sentences

features of life threatening asthma

PEFR <33% SaO2 <92% PaO2 <8kPa normal PaCO2 altered consciousness, exhaustion, arrythmia, hypotension, silent chest, poor effort, cyanosis

features of near fatal asthma

Raised PaCO2 and/or requiring ventilation with raised airway pressures

immediate management of acute asthma

oxygen (40 - 60%) nebulised salbutamol 5mg + nebulised ipratropium 0.5mg prednisolone: 30 - 60mg (+/- hydrocortisone 200mg IV)

monitoring during acute asthma management

``` ABG: 2hrs PEFR: 15 - 30 mins oximetry - maintain 92% sats ECG: hypokalaemia BM: hyperglycaemia ```

discharge requirements for acute asthma

o Need to be off nebulisers for 24hrs before discharge o Educate: opportunity to prevent readmission o Achieve PEFR > 75% and <25% variability

post-hospital management of acute asthma

``` o Prednisolone for minimum 7 – 14 days o Step up treatment o Personalised Asthma action plan o Nurse led follow up o Early clinical review (48 hours at GP surgery) ```

what causes simple stannosis

tin inhalation

what causes silicosis

crystalline sillica dust inhalation

what jobs are at high risk of silicosis

``` o Stone masonry and stone cutting o Construction and demolition o Pottery, ceramics and glass manufacturing o Mining and quarrying o Sand blasting ```

what are 5 common triggers for occupational asthma

flour, isocyanates (industrial paints), wood, cleaning materials, resins