Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Core clinical problems > 48. Cough/sputum/wheeze/sneezing > Flashcards

48. Cough/sputum/wheeze/sneezing Flashcards

1
Q

what are the atopic conditions

A

asthma, eczema, hay fever and food allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

presentation asthma

A

Episodic
Diurnal variability

Typical symptoms are:
Shortness of breath
Chest tightness
Dry cough
Wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

o/e asthma

A

normal when well

widespread “polyphonic” expiratory wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is key about the wheeze suggetsing asthma

A

WIDESPREAD

and polyphonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

differentials for localised monophonic wheeze

A

inhaled foreign body, tumour or a thick sticky mucus plug obstructing an airway

A chest x-ray is the next step.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

triggers asthma

A

Infection
Nighttime or early morning
Exercise
Animals
Cold, damp or dusty air
Strong emotions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

common drugs that can exacerbate/trigger asthma

A

beta blockers

nsaids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

tests for making an asthma diagnosis

A
  • Spirometry with bronchodilator reversibility
  • Fractional exhaled nitric oxide (FeNO)

Where there is diagnostic uncertainty after initial investigations, the next step is testing the peak flow variability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

results of spirometry with reversibility testing that suggest asthma

A

reversibility = greater than 12% increase in FEV1 on reversibility testing supports a diagnosis of asthma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does FeNO test involve

A

The test involves a steady exhale for around 10 seconds into a device that measures FeNO.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what may impact the result of FeNO

A

Smoking can lower the FeNO, making the results unreliable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

FeNO positive result?

A

a level above 40 ppb is a positive test result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is peak flow varibaility? what is a positive result

A

Peak flow variability is measured by keeping a peak flow diary with readings at least twice daily over 2 to 4 weeks.

NICE says a peak flow variability of more than 20% is a positive test result, supporting a diagnosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

aim of treatment asthma

A

complete control of symptoms and normal lung function

No daytime symptoms.
No night-time waking due to asthma.
No need for rescue medication.
No asthma attacks.
No limitations on activity including exercise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

principles of asthma management

A

Start at the most appropriate step for the severity of the symptoms
Review at regular intervals based on severity (e.g., 4-8 weeks after adjusting treatment)
Add additional treatments as required to control symptoms completely
Aim to achieve no symptoms or exacerbations on the lowest dose and number of treatments
Always check inhaler technique and adherence when reviewing medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the steps of asthma management in adults

A
  1. SABA
    • ICS
    • LTRA (e.g., montelukast)
    • LABA +/- LTRA
  5. MART inc low dose ICS
  6. MART inc moderate dose ICS
  7. Consider high-dose inhaled corticosteroid or additional drugs (e.g., LAMA or theophylline)
  8. Specialist management (e.g., oral corticosteroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when should you prescribe ICS for adults asthma

A
  • using SABA 3/7
  • symptoms 3/7
  • woken at night 1/7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

if on SABA and ICS asthma, what should you do?

A

add Leukotriene receptor antagonist (e.g., montelukast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is COPD

A

Long-term, progressive condition involving airway obstruction, chronic bronchitis and emphysema. It is almost always the result of smoking and is largely preventable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is chronic bronchitis

A

Chronic bronchitis refers to long-term symptoms of a cough and sputum production due to inflammation in the bronchi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is emphysema

A

damage and dilatation of the alveolar sacs and alveoli, decreasing the surface area for gas exchange.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

presentation copd

A

A typical presentation of COPD is a long-term smoker with persistent symptoms of:
Shortness of breath
Cough
Sputum production
Wheeze
Recurrent respiratory infections, particularly in winter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does copd not cause

A

clubbing
haemoptysis
chest pain

These symptoms should be investigated for a different cause, such as lung cancer, pulmonary fibrosis or heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the grades of the mrc dyspnoea scale

A

Grade 1: Breathless on strenuous exercise
Grade 2: Breathless on walking uphill
Grade 3: Breathlessness that slows walking on the flat
Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
Grade 5: Unable to leave the house due to breathlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what invetsigations should you do copd

A

spirometry with bronchodialtor reversibility testing
CXR
FBC
BMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what tests do you need for a diagnosis of copd

A

clinical presentation and spirometry results

Spirometry will show an obstructive picture with a FEV1:FVC ratio of less than 70%. There is little or no response to reversibility testing with beta-2 agonists (e.g., salbutamol). Reversible obstruction is more suggestive of asthma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

why get a cxr ?copd

A

will show hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

why get fbc copd

A

exclude secondary polycythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why get bmi copd

A

(weight loss occurs in severe disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

further tests copd

A

ECG and echocardiogram to assess for heart failure and cor pulmonale

CT thorax for alternative diagnoses such as fibrosis, cancer or bronchiectasis

Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

non-pharmacological management points copd

A

smoking cessation
pneumococcal and annual flu vaccine
Pulmonary rehabilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

1st step pharmacological copd management

A

SABA or SAMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

copd pt is on saba or sama but still uncontrolled, next step?

A

Do they have asthmatic features/features suggesting steroid responsiveness?

Yes: Long-acting beta agonist (LABA) and Inhaled corticosteroid (ICS) (+SABA/SAMA as required)

No: LABA and LAMA. if taking SAMA, switch to SABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

management copd

A
  1. SABA (e.g. salbutamol) or SAMA (e.g. ipratropium bromide)
  2. Do they have asthmatic features/features suggesting steroid responsiveness?
    Yes: Long-acting beta agonist (LABA) and Inhaled corticosteroid (ICS) (+SABA/SAMA as required)
    No: LABA and LAMA. if taking SAMA, switch to SABA
  3. Triple therapy: LABA + LAMA + ICS (+ SABA as required)
  4. Specialist guided
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3rd line treatment copd

A

Triple therapy LABA + LAMA + ICS (+ SABA as required)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

if tried triple therapy, next step copd management

A

Specialist guided
eg theophylline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what criteria determines whether a pt has asthmatic/steroid resposnsive features?

A

any previous, secure diagnosis of asthma or of atopy
a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

LABA and LAMA combination inhalers - examples

A

Anoro Ellipta, Ultibro Breezhaler and DuaKlir Genuair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

LABA and ICS combination inhalers - examples?

A

Fostair, Symbicort and Seretide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

LABA, LAMA and ICS combination inhalers - examples

A

Trimbow, Trelegy Ellipta and Trixeo Aerosphere

triple therpay - some begin with T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

indication LTOT COPD

A

chronic hypoxia (sats < 92%),

cyanosis, polycythaemia,

cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

factors which may improve survival copd

A

smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is cor pulmonale

A

right-sided heart failure caused by respiratory disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

causes cor pulmoanle

A

COPD (the most common cause)
Pulmonary embolism
Interstitial lung disease
Cystic fibrosis
Primary pulmonary hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

symptoms cor pulmonale

A

Often patients with early cor pulmonale are asymptomatic. Symptoms of cor pulmonale include:
Shortness of breath
Peripheral oedema
Breathlessness of exertion
Syncope (dizziness and fainting)
Chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

signs of cor pulmonale o/e

A

Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Parasternal heave
Loud second heart sound
Murmurs (e.g., pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

management cor pulmonale

A

loop diuretic
LTOT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

high yield things to remember bronchiectasis

A

finger clubbing

Pseudomonas colonisation

diagnosis by HRCT

Extended courses of 7-14 days of antibiotics for exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is bronchiectasis

A

permanent dilation of the bronchi, the large airways that transport air to the lungs. Sputum collects and organisms grow in the wide tubes, resulting in a chronic cough, continuous sputum production and recurrent infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

causes of bronchiectasis

A

Idiopathic (no apparent cause)

Postinfectious:
Pneumonia
Whooping cough (pertussis)
Tuberculosis

Alpha-1-antitrypsin deficiency
Connective tissue disorders (e.g., rheumatoid arthritis)
Cystic fibrosis
Yellow nail syndrome

51
Q

what is triad of yellow nail syndrome

A

Yellow fingernails, bronchiectasis and lymphoedema

52
Q

presenting symptoms bronchiectasis

A

Shortness of breath
Chronic productive cough
Recurrent chest infections
Weight loss

52
Q

signs of bronchiectasis o/e

A

Sputum pot by the bedside
Oxygen therapy (if needed)
Weight loss (cachexia)
Finger clubbing
Signs of cor pulmonale (e.g., raised JVP and peripheral oedema)
Scattered crackles throughout the chest that change or clear with coughing
Scattered wheezes and squeaks

53
Q

most common infective organisms bronchiectasis

A

Haemophilus influenza is most common !!!!
Pseudomonas aeruginosa

54
Q

xr findinfs bronchiectasis

A

Tram-track opacities (parallel markings of a side-view of the dilated airway)
Ring shadows (dilated airways seen end-on)

55
Q

what investigation is test of choice for diagnosing bronchiectasis

A

High-resolution CT (HRCT)

56
Q

management infective exacerbation bronchiectasis

A

Sputum culture (before antibiotics)
Extended courses of antibiotics, usually 7–14 days
Ciprofloxacin is the usual choice for exacerbations caused by Pseudomonas aeruginosa

57
Q

general management for bronchiectasis

A

general:
Vaccines (e.g., pneumococcal and influenza)
Respiratory physiotherapy to help clear sputum
Pulmonary rehabilitation

pharma:
long term abx for freq infections
Inhaled colistin for Pseudomonas aeruginosa colonisation
Long-acting bronchodilators may be considered for breathlessness
Long-term oxygen therapy in patients with reduced oxygen saturation

Surgical:
Surgical lung resection may be considered for specific areas of disease
Lung transplant is an option for end-stage disease

58
Q

when may a pt be on long term abx for bronchiectasis? what is the abx of choice

A

azithromycin) for frequent exacerbations (e.g., 3 or more per year)

59
Q

management of pseudomonas colonisation bronchiectasis

A

Inhaled colistin

60
Q

what is interstitial lung disease? what is fibrosis?

A

Interstitial lung disease includes many conditions that cause inflammation and fibrosis of the lung parenchyma (lung tissue). Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue.

61
Q

causes interstitial lung disease

A

Idiopathic pulmonary fibrosis (the most important to remember)
Secondary pulmonary fibrosis: drugs/other conditions
Hypersensitivity pneumonitis
Cryptogenic organising pneumonia
Asbestosis

62
Q

key symptoms interstitial lung disease (ILD)

A

Shortness of breath on exertion
Dry cough
Fatigue

63
Q

examiantion findings idiopathic pulmoanry fibrosis

A

Bibasal fine end-inspiratory crackles
Finger clubbing

64
Q

what does HRCT show ILD

A

ground glass apperance
honeycombing

65
Q

investigation of choice ILD

A

high-resolution CT scan (HRCT)

66
Q

spirometry ILD

A

restrictive pattern

67
Q

when there is diagnostic uncertainty interstitial lung disease, what invetsigations might you do

A

Lung biopsy
Bronchoalveolar lavage

68
Q

general management interstitial lung disease

A

Remove or treat the underlying cause
Home oxygen where there is hypoxia
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine
Advanced care planning and palliative care where appropriate
Lung transplant is an option, but the risks and benefits need careful consideration

69
Q

what is idiopathic pulmoanry fibrosis

A

Idiopathic pulmonary fibrosis features progressive pulmonary fibrosis with no apparent cause.

70
Q

presentation idiopathic pulmonary firbosis

A

It presents with an insidious onset of shortness of breath and dry cough over more than 3 months. It usually affects adults over 50 years old.

71
Q

prognosis idiopathic pulmonary fibrosis

A

The prognosis is poor, with a 2-5 years life expectancy from diagnosis.

72
Q

drugs for idiopathic pulmoanry fibrosis

A

Pirfenidone reduces fibrosis and inflammation through various mechanisms

Nintedanib reduces fibrosis and inflammation by inhibiting tyrosine kinase

73
Q

causes of drug induced pulmaonry fibrosis

A

Amiodarone (also causes grey/blue skin)
Cyclophosphamide
Methotrexate
Nitrofurantoin

74
Q

causes of secondary pulmoanry fibrosis (Secondary to other conditions)

A

Alpha-1 antitrypsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis
Sarcoidosis

75
Q

what is Hypersensitivity pneumonitis/Extrinsic allergic alveolitis

A

involves type III and type IV hypersensitivity reaction to an environmental allergens

Inhalation of allergens in patients sensitised to that allergen causes an immune response, leading to inflammation and damage to the lung tissue.

76
Q

main invetsigation and results which suggest hypersensitivity penumonotis

A

bronchoalveolar lavage
- Raised lymphocytes (lymphocytosis)

77
Q

what is bronchoalveolar lavage

A

Bronchoalveolar lavage is performed during a bronchoscopy procedure. The airways are washed with sterile saline to gather cells, after which the fluid is collected and analysed.
Raised lymphocytes (lymphocytosis) are suggestive of hypersensitivity pneumonitis.

78
Q

specific types of hypersensitivity pneumonitis

A

Bird-fancier’s lung is a reaction to bird droppings
Farmer’s lung is a reaction to mouldy spores in hay
Mushroom worker’s lung is a reaction to specific mushroom antigens
Malt worker’s lung is a reaction to mould on barley

79
Q

presentation hypersensitivity pneumonitis

A

acute (occurs 4-8 hrs after exposure)
dyspnoea
dry cough
fever

chronic (occurs weeks-months after exposure)
lethargy
dyspnoea
productive cough
anorexia and weight loss

80
Q

management hypersensitivity pneumonitis

A

avoid precipitating factors
oral glucocorticoids
Oxygen if req

81
Q

investigation findings hypersensitivity pneumonitis

A

imaging: upper/mid-zone fibrosis
bronchoalveolar lavage: lymphocytosis
serologic assays for specific IgG antibodies
blood: NO eosinophilia

82
Q

what is cryptogenic organising pneumonia? - presentation, invetsigation, management

A

focal area of inflammation lung tissue - can be idiopathic or triggered by infection, drugs and inflamamtory disorders

presentation: same as pneumonia, cxr same as pneumonia

invetsigation: lung biopsy

management: systemic corticosteroids

83
Q

what is asbestosis

A

Asbestosis refers to lung fibrosis related to asbestos exposure.

84
Q

what lung problems can asbestos cause

A

Lung fibrosis (asbestosis)
Adenocarcinoma
Mesothelioma (Pleural thickening)
Pleural plaques and pleural thickening w/o the more serious diseases ^

85
Q

what is allergic rhinitis

A

inflammatory disorder of the nose where the nose become sensitized to allergens such as house dust mites and grass, tree and weed pollens.

86
Q

classifications of allergic rhinitis

A

seasonal
perennial
occupation

87
Q

features allergic rhinitis

A

sneezing
bilateral nasal obstruction
clear nasal discharge
post-nasal drip
nasal pruritus

88
Q

Management allergic rhinitis

A

allergen avoidance

mild/mod:
- oral or intranasal antihistamines

mod/sev:
intranasal corticosteroids

a short course of oral corticosteroids are occasionally needed to cover important life events

89
Q

why should you not used decongestents for extended periods of time

A

there may be a role for short courses of topical nasal decongestants (e.g. oxymetazoline).

They should not be used for prolonged periods as increasing doses are required to achieve the same effect (tachyphylaxis) and rebound hypertrophy of the nasal mucosa (rhinitis medicamentosa) may occur upon withdrawal

90
Q

what is alpha-1 antitrypsin deficiency

A

genetic condition caused by low levels of alpha-1 antitrypsin.
Two main organs are affected by alpha-1 antitrypsin deficiency:

  • lungs: COPD/bronchiectasis (typically after 30 years old)
  • liver Dysfunction, fibrosis and cirrhosis of the liver (depending on the specific genotype)
91
Q

inheritance alpha-1 antitrypsin deficiency

A

autosomal co-dominant pattern

Co-dominant refers to when both gene copies are expressed and contribute to the outcome (neither is dominant or recessive over the other). The disease severity results from the combination of both copies of the gene.

92
Q

what is alpha-1 antitrypsin

A

Alpha-1 antitrypsin is a protease inhibitor.

Proteases therefore have free attack of tissues such as the lungs

93
Q

how does alpha-1 antitrypsin deficiency cause liver damage

A

Alpha-1 antitrypsin is produced in the liver.

in specific genotypes, alpha-1 antitrypsin gets trapped in the liver and is toxic to hepatocytes –> inflamamtion - fibrosis, cirrhosis and potentially hepatocellular carcinoma.

94
Q

diagnosis of alpha-1 antitrypsin

A

Low serum alpha-1 antitrypsin (the screening test)
Genetic testing

95
Q

how is lung damage assessed aloha 1 antitrypsin

A

Chest x-ray
High-resolution CT thorax
Pulmonary function tests

96
Q

management of alpha 1 antitrypsin

A

Non-pharmacological:
Stop smoking
Monitoring for complications (e.g., hepatocellular carcinoma)
Screening of family members

Pharmacological:
Symptomatic management (e.g., standard treatment of COPD)

Surgical:
Organ transplant for end-stage liver or lung disease

97
Q

liver biopsy alpha-1 antitrypsin deficiency

A

Liver biopsy shows periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment. These represent a buildup of the mutant proteins.

98
Q

epidemiology klebsiella

A

more common in diabetics and patients with a history of alcohol excess. It is also frequently caused by aspiration.

99
Q

where in lungs does klebsiella affect

A

upper lobes of the lungs.

100
Q

pneumonia in alcohol excess, aspiration or diabetes

A

klebsiella

101
Q

risk factors for lung abscess

A

most commonly forms secondary to aspiration pneumonia
poor dental hygiene, previous stroke and reduced consciousness are some of the risk factors for this

102
Q

features lung abscess

A

symptoms may develop over weeks
systemic features such as night sweats and weight loss may be seen
fever
productive cough
often foul-smelling sputum
haemoptysis in a minority of patients
chest pain
dyspnoea
signs
dull percussion and bronchial breathing
clubbing may be seen

103
Q

CXR lung abscess

A

fluid-filled space within an area of consolidation
an air-fluid level is typically seen

104
Q

management lung abscess

A

intravenous antibiotics
if not resolving percutaneous drainage may be required and in very rare cases surgical resection

105
Q

pulmonary fucntuon test sarcoidosis

A

restrictive

106
Q

what is sarcoidosis

A

Sarcoidosis is a chronic granulomatous disorder.

Granulomas are inflammatory nodules full of macrophages. The cause of these granulomas is unknown.

It is usually associated with respiratory symptoms but has many extra-pulmonary manifestations, such as erythema nodosum and lymphadenopathy.

107
Q

acute vs insidious sarcoidosis

A

acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia, purple lesions (lupus pernio)

insidious: dyspnoea, non-productive cough, malaise, weight loss

108
Q

what skin changes do you get sarcoidosis

A

lupus pernio
- Lupus pernio is specific to sarcoidosis and presents with raised purple skin lesions, often on the cheeks and nose.

Erythema nodosum
- Erythema nodosum is characterised by nodules of inflamed subcutaneous fat on the shins.

109
Q

risk factors sarcoidosis

A

Aged 20-39 or around 60
Women
Black ethnic origin

110
Q

what lung changes do you get sarcoidosis

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules

111
Q

what is lofgrens syndrome?

A

Lofgren’s syndrome refers to a specific presentation of sarcoidosis with a classic triad of symptoms:

Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)

112
Q

investigations sarcoidosis

A

Bloods:
Raised angiotensin-converting enzyme (ACE) (often used as a screening test)
Raised calcium (hypercalcaemia)

Imaging:
Chest x-ray may show hilar lymphadenopathy
High-resolution CT scanning may show hilar lymphadenopathy and pulmonary nodules
MRI can show central nervous system involvement
PET scan can show active inflammation in affected areas

Histology:
helps establish the diagnosis, often by bronchoscopy with an ultrasound-guided biopsy of mediastinal lymph nodes. Histology characteristically shows non-caseating granulomas with epithelioid cells.

ACE levels have a sensitivity of 60% and specificity of 70% and are therefore not reliable in the diagnosis of sarcoidosis although they may have a role in monitoring disease activity.

113
Q

why do you get kidney stones in sarcoidosis

A

hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

hypercalcaemia

114
Q

main CXR finding sarcoidosis

A

bilateral hilar lymphadenopathy

115
Q

management sarcoidosis

A

Conservative management is considered in patients with no or mild symptoms.

Oral steroids (for 6-24 months) are usually first-line where treatment is required.

Bisphosphonates protect against osteoporosis whilst on long-term steroids.
Methotrexate is a second-line option.
Lung transplant is rarely required in severe pulmonary disease.

116
Q

indications steroids sarcoidosis

A

stage 2 or 3 disease + symptomatic.

hypercalcaemia

eye, heart or neuro involvement

117
Q

stages x-ray sarcoidosis

A

A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis

118
Q

prognosis sarcoidosis

A

Sarcoidosis spontaneously resolves in around half of patients, usually within two years.

In some patients, it progresses to pulmonary fibrosis and pulmonary hypertension. Overall mortality is less than 10%.

119
Q

histology sarcoidosis

A

non-caseating granulomas with epithelioid cells.

120
Q

how to obtain sample for histology sarcoidosis

A

bronchoscopy with an ultrasound-guided biopsy of mediastinal lymph nodes.

121
Q

cause bibasal altelectasis

A

common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.

122
Q

management post-op bialteral altelectasis

A

positioning the patient upright
chest physiotherapy: breathing exercises

Core clinical problems (94 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions