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Phase 3b > Respiratory > Flashcards

Respiratory Flashcards

1
Q

relevant points in the PMH/FH in breathlessness

A

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

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2
Q

drugs that can cause breathlessness due to fibrotic lung changes

A

o Antibiotics: nitrofurantoin

o Anti-rheumatoid drugs

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3
Q

measurement tools for breathlessness

A

WHO Functional Class
MRC Breathlessness Scale
Borg Scale
NYHA Class

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4
Q

Investigations for breathless patient

A

 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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5
Q

What is procalcitonin

A

 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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6
Q

CURB-65 criteria

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

management of T1 respiratory failure

A

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

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8
Q

treatment for acute eosinophilic pneumonia

A

steroids

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9
Q

causes of acute eosinophilic pneumonia

A

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

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10
Q

what is the pathophysiology of asthma

A

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

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11
Q

types of asthma

A

eosinophilic

  • atopic (fungal, aeroallergens, occupation)
  • non atopic

non eosinophilic
-non smoking, smoking, obesity related

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12
Q

symptoms of asthma

A

EPISODIC wheeze
cough + breathlessness,
diurnal variation
triggers

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13
Q

list 5 triggers for asthma exacerbation

A 
allergens 
exercise 
URTI/infection
menstrual cycle 
cold 
laughter/emotion
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14
Q

how to assess severity of asthma

A
  • how many inhalers
  • A+E, hospital admissions, ventilation, ITU/HDU care
  • requiring antibiotics/steroids?
  • RCP3
  • Asthma control test
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15
Q

what is the RCP3

A

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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16
Q

what questions are in the asthma control test

A

(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
17
Q

how can breathing/respiratory function contribute to acid-base

A

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.

18
Q

how can metabolism contribute to acid-base

A

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.

19
Q

what is henderson’s equation

A

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

HCO3 metabolic component (kidneys)
20
Q

asthma control test meaning

A

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

21
Q

signs of asthma on physical examination

A

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

22
Q

what is samter’s triad

A

nasal polyps
asthma
aspirin sensitivity

23
Q

investigations for asthma

A

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

24
Q

characteristics of severe asthma

A

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
25
Q

which individuals are at risk of asthma death

A 
o	On 3 or more classes of treatment 
o	Recent admission/frequent attender 
o	Previous near fatal disease 
o	Brittle disease 
o	Psychosocial factors
26
Q

differential diagnoses for asthma

A 
	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
27
Q

management of asthma

A

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)
28
Q

features of a moderate asthma attack

A

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

29
Q

features of a severe asthma attack

A

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

30
Q

features of life threatening asthma

A

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

31
Q

features of near fatal asthma

A

Raised PaCO2 and/or requiring ventilation with raised airway pressures

32
Q

immediate management of acute asthma

A

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

33
Q

monitoring during acute asthma management

A 
ABG: 2hrs 
PEFR: 15 - 30 mins 
oximetry - maintain 92% sats 
ECG: hypokalaemia 
BM: hyperglycaemia
34
Q

discharge requirements for acute asthma

A

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

35
Q

post-hospital management of acute asthma

A 
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)
36
Q

what causes simple stannosis

A

tin inhalation

37
Q

what causes silicosis

A

crystalline sillica dust inhalation

38
Q

what jobs are at high risk of silicosis

A 
o	Stone masonry and stone cutting 
o	Construction and demolition 
o	Pottery, ceramics and glass manufacturing 
o	Mining and quarrying 
o	Sand blasting
39
Q

what are 5 common triggers for occupational asthma

A

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

Phase 3b (9 decks)

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