Resp 1 Flashcards
Acute respiratory distress syndrome
- What happens in the disease?
- What can cause it?
- What clinical features are seen?
- What is seen on investigation?
NOTE: management generally in ITU
- increased permeability of capillaries in the alveoli leading to fluid accumulation in the alveoli
- > non-cardiogenic pulmonary oedema - smoke inhalation
- trauma - direct or long bone fractures causing fat embolism
- transfusion reaction
- acute pancreatitis
- infection: sepsis / pneumonia
- cardio-pulmonary bypass
3. acute onset within 1 week of symptoms - crackles throughout both lung fields - reduced O2 sats - dyspnoea - increased RR
mnemonic: one technically leads to the other
- CXR: pulmonary oedema -> bilateral infiltrates
pO2 <40kPa
Allergic bronchopulmonary aspergillosis
- What is it?
- What clinical features are often seen?
- What is seen on investigation?
- How is it managed?
- allergy to the fungus aspergillus
2.
- bronchiectasis
- bronchoconstriction: cough, dyspnoea, wheeze +/- previous label of asthma
- eosinophilia
- positive radioallergosorbent test to aspergillus
- oral glucocorticoids
- itraconazole sometimes used second line
Alpha-1-antitrypsin deficiency
- What is it?
- Where is the mutation for the disease located?
- What clinical features are seen?
- What investigation is done?
- lack of protease inhibitor produced by the liver -> cells aren’t protected from neutrophil elastase -> emphysema
- chromosome 14
- emphysema (most marked in lower lobes)
- liver:
- adults: hepatocellular carcinoma + cirrhosis
- children: cholestasis
- A1AT conc.
Altitude
- State the 3 types of altitude related illnesses and their clinical features.
- How would you manage the following (other than descent):
a) AMS prophylaxis
b) HACE treatment
1.
Acute mountain sickness (AMS) - headache, N+V
high altitude pulmonary oedema - clinical features of pulmonary oedema
high altitude cerebral oedema - headache, ataxia (loss of coordination + speech), papilloedema
- a) acetazolamide (carbonic anhydrase inhibitors)
if curious: causes primary metabolic acidosis, therefore resp. compensation by increased RR improving oxygenation
b) dexamethasone
Asbestos exposure
State what this can cause and their clinical features.
pleural plaques - do NOT undergo malignant change, therefore no follow up required
asbestosis
- lower lobe lung fibrosis
- symptoms of lung fibrosis: dyspnoea, reduced exercise tolerance
- related to length of exposure
mesothelioma
- progressive dyspnoea
- chest pain
- pleural effusion
Aspiration pneumonia
- What are the risk factors?
- What lobes are most likely to be effected?
- What organism is often the cause in alcoholics?
1.
- impaired conciousness
- poor dental hygiene
- impaired swallowing
- impaired mucociliary clearance
- surgical procedures (incl. intubation)
- right middle + right lower lobes
(because of more vertical nature of bronchus to these regions) - klebsiella
Atelectasis
- What is it?
- What are the clinical features?
- How is managed?
- basal alveolar collapse due to bronchial secretions blocking airways
- 72 hrs post op
- dyspnoea
- reduced sats
- position patient upright
- chest physiotherapy: breathing exercises
What are the most common causes of bilateral hilar lymphadenopathy?
- sarcoidosis
- TB
Bronchiectasis
- What is it?
- What clinical features are seen?
- What is seen on investigation?
- How is it managed?
- permanent dilation of the airways secondary to chronic infection/inflammation
(e. g. pneumonia, CF, aspergillus…) - persistent cough bringing up phlegm
- dyspnoea
- XR + CT
- tram tracks
- signet ring
4.
- physical training
- postural drainage
- ABx (exacerbations + severe cases)
Chest drain
- When would you insert a chest drain?
- Where should it be inserted?
- What are the relative contraindications for chest drain?
- What complication can be seen if a pleural effusion is drained too quickly (>1L in <6hrs)?
substance between visceral and parietal pleura
(e.g. air, liquid)
- mid axillary line, 5th intercostal space
- INR > 1.3
- platelets <75
- pulmonary bullae
- pleural adhesions
- re-expansion pulmonary oedema
- cough
- dyspnoea
What can cause finger clubbing?
cardiac
cyanotic congenital cardiac disease
bacterial endocarditis
respiratory
- lung cancer
- pyogenic conditions: abscess, bronchiectasis, cystic fibrosis, empyema
- TB
- asbestos: asbestosis, mesothelioma
other
- crohns
- cirrhosis, PBC
- Graves
(CCG)
Pneumoconiosis
most commonly coal pneumoconiosis
- What happens in this disease?
- Describe the staging in simple pneumoconiosis (often asymptomatic).
- Progressive massive fibrosis
a) What clinical features can be seen?
b) What is seen on investigation?
- macrophages remove foreign particles from alveoli and interstitium and then cleared with sputum
- > However, excessive dust causes this system to be overwhelmed causing macrophages to accumulate in lung tissue causing damage - Stage 1: small number of opacities, normal lung markings visible
Stage 2: large number of opacities, normal lung markings visible
Stage 3: large number of opacities and normal lung markings no longer visible
(30% of these progress to progressive massive fibrosis) - a)
- cough +/- black sputum
- dyspnoea on exertion
b)
- CXR: UPPER lobe fibrosis
- spirometry: mixed obstructive/restrictive picture
Metabolic Acidosis
- How is anion gap calculated?
(NOTE: inclusion of chloride level in question often indication of wanting to calculate anion gap)
- what type of metabolic acidosis is seen with
a) normal anion gap
b) raised anion gap - State the causes of metabolic acidosis with a
a) normal anion gap
b) raised anion gap
- (Na+ + K+) - (Cl- + HCO3-)
think positive ions minus negative ions
normal range is between 10-18
- a) bicarbonate loss
b) increased acid accumulation
3.
a)
- GI: diarrhoea, fistula
- renal tubular acidosis
- addisons
- acetazolamide
- ammonium chloride
b)
- lactate: shock, hypoxia
- urate: renal failure
- ketones: diabetic, alcohol
- acid poising e.g. methanol, salicytes
mnemonic: LUKA
NOTE: salicytes initially cause resp. alkalosis because stimulate resp. centre
What can cause metabolic alkalosis?
- vomiting
- diuretics
- hypokalaemia
- high aldosterone:
- primary hyperaldosteronism
- cushing’s syndrome
- congenital adrenal hyperplasia
mechanisms
ECF depletion (vomiting, diuretics) causes Na and CL loss and therefore activation of RAA system
hypokalaemia causes K to shift from cells into ECF, H+ goes into cells to maintain their neutrality
What can cause resp. acidosis?
NOTE: metabolic compensation implies minimum acute-on-chronic picture because takes days to make bicarbonate in response
- COPD
- acute asthma
- neuromuscular disease
- obesity hypoventilation syndrome
- sedatives: benzodiazepines, opiate overdose
