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Alex's MRCP Cards > Resp > Flashcards

Resp Flashcards

1
Q

O2 dissociation curve

A 
Right = raised oxygen delivery to tissues, raised acidity/CO2/temp/DPG
Left = lower oxygen delivery to tissues, lower acidity/CO2/temp/DPG
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2
Q

Bohr effect

A

Increasing acidity (or pCO2) means O2 binds less well to Hb –> better tissue oxygenation

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3
Q

Haldane effect

A

Increased pO2 means CO2 binds less well to Hb –> better CO2 elimination

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4
Q

Causes of raised TLCO?

A 
Asthma
Pulmonary hemorrhage (wegener's, goodpasture's)
Left-to-right cardiac shunts
Polycythemia
Hyperkinetic states
Male gender, exercise
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5
Q

Assessment for LTOT?

A 
Very severe airflow obstruction (FEV1 <
30% predicted). Assessment should be
'considered' for patients with severe
airflow obstruction (FEV1 30-49%
predicted)
•
Cyanosis
•
Polycythaemia
•
Peripheral oedema
•
Raised jugular venous pressure
•
Oxygen saturations 
 92% on room air
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6
Q

Indications for LTOT?

A 
pO2 of < 7.3 kPa or pO2 of 7.3 - 8 kPa and one of the
following:
• Secondary polycythaemia
• Nocturnal hypoxaemia
• Peripheral oedema
• Pulmonary HTN
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7
Q

How to assess for LTOT?

A

measurine arterial blood gases on 2 occasions at least 3 weeks apart in
patients with stable COPD on optimal
management

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8
Q

Recommended settings in NIV?

A

EPAP - 4-5
IPAP - 12-15
FiO2 - not >40%

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9
Q

CAP organisms

A 
Streptococcus pneumoniae (accounts for around 80% of cases)
•
Hemophilus influenzae
•
Staphylococcal aureus
•
Atypical pneumonias (e.g. due to Mycoplasma pneumoniae)
•
Viruses
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10
Q

Step pneumonia?

A

commonly causes reactivation of the herpes simplex virus resulting in ‘cold
sores and associated with foreign travel

  • Rapid onset
  • High fever
  • Pleuritic chest pain
  • Herpes labialis
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11
Q

Klebsiella pneumonia?

A

classically in alcoholics. CXR features may

include abscess formation in the middle/upper lobes and empyema. The mortality approaches 30-50%

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12
Q

Staph Aureus pneumonia?

A

normally causes pneumonia only AFTER a preceding influenzal viral
infection. Characteristically causes multiple abscesses in up to 25% of patients and empyema in 10%,
septicemia develops with metastatic abscess in other organs such as brain and bones

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13
Q

Bacterial organisms causing IECOPD?

A

Hemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis

Viral is most common

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14
Q

Mycoplasma pneumonia?

A
  • Affects youngerpatients frequently amongst those living in boarding houses (housings, hostels)
  • associated with erythema multiforme (target lesion) and cold
    autoimmune hemolytic anemia (IgM)
  • Diagnosis with serology, PCR, ?positive coombs test after 10 days

Treat with macrolides/tetracyclines

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15
Q

Mycoplasma features?

A
  • Flu-like symptoms classically PRECEDE a dry cough
  • Bilateral consolidation on x-ray

COMPLICATIONS

  • Cold agglutins (IgM) may cause an hemolytic anemia, thrombocytopenia
  • Erythema multiforme, erythema nodosum
  • Meningoencephalitis, Guillain-Barre syndrome
  • Bullous myringitis: painful vesicles on the tympanic membrane
  • Pericarditis/myocarditis
  • Gastrointestinal: hepatitis, pancreatitis
  • Renal: acute glomerulonephritis –> HAEMATURIA
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16
Q

PCP pneumonia extrapulmonary features?

A

Hepatosplenomegaly
Lymphadenopathy
Choroid lesions

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17
Q

PCP pneumonia investigations?

A

CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings e.g. lobar consolidation. May be normal

Exercise-induced desaturation

Sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate
PCP (silver stain)

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18
Q

What kind of organism is legionella?

A

Gram -ve bacilli

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19
Q

Legionella pneumonia features?

A

Flu-like symptoms
50% of cases have GI symptoms such as nausea, vomiting, diahrrhea and abdominal pain.
Dry cough
Lymphopenia
Hyponatremia
Deranged LFTs
Hematuria occurs and occasionally renal failure

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20
Q

Examples of EAA?

A

Bird fanciers’ lung (avian proteins)
Farmers lung (spores of micropolyspora faeni)
Malt workers’ lung (aspergillus clavatus)
Mushroom workers’ lung (thermophilic actinomycetes)

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21
Q

What type of hypersesnsitivity is EAA?

A

largely caused by immunecomplex
mediated tissue damage (type III hypersensitivity = acute phase) although delayed
hypersensitivity (type IV = chronic phase) is also thought to play a role in EAA, especially in the
chronic phase

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22
Q

Features/Ix EAA?

A

Acute: occur 4-8 hrs after exposure, SOB, dry cough, fever
Chronic: similar

CXR: upper lobe fibrosis
BAL (bronchoalveolar lavage): lymphocytosis
Blood: NO eosinophilia
Circulating IgG precipitant - no IgE therefore not allergy

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23
Q

Pathologies causing upper lung fibrosis?

A 
Extrinsic allergic alveolitis
Coal worker's pneumoconiosis/progressive massive fibrosis
Silicosis
Sarcoidosis
Ankylosing spondylitis (rare)
Histiocytosis
Tuberculosis
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24
Q

Pathologies causing lower lung fibrosis?

A

Cryptogenic fibrosing alveolitis
Most connective tissue disorders (except ankylosing spondylitis)
Drug-induced: amiodarone, bleomycin, methotrexate
Asbestosis

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25
Q

Features of asbestosis?

A

Progressive SOB
Chest pain
Pleural effusion

Pleural thickening
Pleural plaques (not premalignant) - occur after latent period of 20-40 years
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26
Q

Types of lung cancer and %?

A 
Squamous: 35%
Adenocarcinoma: 30%
Small (oat) cell: 15%
Large cell: 10%
Other: 5%
27
Q

Paraneoplastic features of lung ca?

A

Squamous cell: PTHrp (hypercalcaemia), clubbing, HPOA

Small cell: ADH (hyponatraemia), ACTH (cushings, HTN, hyperglycaemia, low K, alkalosis) , Lambert-Eaton syndrome (myasthenia)

Adeno - gynaecomastia

28
Q

Contraindications to lung ca surgery?

A

SVC obstruction, FEV < 1.5, MALIGNANT

pleural effusion, and vocal cord paralysis

29
Q

Locations of lung ca?

A

Small cell - central
Squamous - central
Adeno - peripheral

30
Q

Causes of cavitations on CXR?

A

Tuberculosis
Lung cancer (especially squamous cell)
Abscess (staph aureus, klebsiella and Pseudomonas)
Wegener’s granulomatosis
Pulmonary embolism
Rheumatoid arthritis
Aspergillosis, histoplasmosis, coccidioidomycosis

31
Q

Sarcoid?

A

Multisystem disorder of unknown aetiology characterized by non-caseating
granulomas.

It is more common in young adults and in people of African descent.

Sarcoidosis remits without treatment in approximately two-thirds of people.

32
Q

Investigations in sarcoidosis?

A

Diagnosis - no reliable test, largely clinical. ACE levels = sensitivity 60% specificity 70% - may have a role in monitoring disease activity.

Bloods - hypercalcaemia (10%) and raised ESR

Spirometry: may show a restrictive defect

Tissue biopsy: non-caseating granulomas

Gallium-67 scan - not used routinely

33
Q

Features of sarcoid with POOR prognosis?

A

Insidious onset, symptoms > 6 months

Absence of erythema nodosum

Extrapulmonary manifestations: e.g. Lupus pernio, splenomegaly

CXR: stage III-IV features

Black people

34
Q

CXR features in sarcoidosis?

A

0 = normal

1 = BHL

2 = BHL + infiltrates

3 = infiltrates

4 = fibrosis

35
Q

Indications for steroids in sarcoidosis?

A

Hypercalcemia

Worsening lung function

Eye (bilateral posterior uveitis is common eye manifestation)

Heart or neuro involvement

36
Q

Mikulicz syndrome?

A

chronic condition characterized by the abnormal enlargement of parotids,
lacrimal and salivary glands. The tonsils and other glands in the soft tissue of the face and neck may
also be involved. It is associated with sarcoidosis

37
Q

Causes of BHL?

A

Sarcoidosis
Tuberculosis

Lymphoma/other malignancy
Pneumoconiosis e.g. Berylliosis
Fungi e.g. Histoplasmosis, coccidioidomycosis (VHL + Cavitation in CXR)

38
Q

What is Lofgren’s syndrome?

A

Acute form sarcoidosis characterized by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia.

typically occurs in young females

excellent prognosis

Blood eosinophilia

39
Q

Caues of pulmonary eosinophiilia?

A 
Churg-Strauss syndrome (eosinophilia + asthma + hemorrhage)
Allergic bronchopulmonary aspergillosis
(ABPA)
Loffler's syndrome
Eosinophilic pneumonia
Hypereosinophilic syndrome
Tropical pulmonary eosinophilia
Drugs: nitrofurantoin, sulphonamides

Less common:
Wegener’s granulomatosis
Tropical pulmonary eosinophilia
Associated with Wuchereria bancrofti infection

40
Q

Organisms in bronchiectasis?

A

Hemophilus influenzae (most common)

Pseudomonas aeruginosa

Klebsiella spp.

Streptococcus pneumoniae

41
Q

Causes of bronchiectasis?

A

Post-infective: tuberculosis, measles, pertussis, pneumonia

Cystic fibrosis

Bronchial obstruction e.g. Lung cancer/foreign body

Immune deficiency: selective IgA, hypogammaglobulinemia

Allergic bronchopulmonary aspergillosis (ABPA)

Ciliary dyskinetic syndromes: kartagener’s syndrome, young’s syndrome

Yellow nail syndrome (associated with pleural effusion - exudates)

42
Q

Management of bronchiectasis?

A

Physical training (e.g. Inspiratory muscle training) - has a good evidence base for patients withnon-cystic fibrosis bronchiectasis

Postural drainage

IV antibiotics for exacerbations + long-term rotating antibiotics (nebulized ABX) in severe
cases

Bronchodilators in selected cases

Immunisations

Surgery in selected cases (e.g. Localised disease)

43
Q

Criteria for ARDS?

A

Acute onset

Bilateral infiltrates on CXR

Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)

pO2/FiO2 < 200 mmHg

44
Q

What is ABPA? Common question stem for this?

A

Results from an allergy to Aspergillus spores

Often give a history of bronchiectasis and eosinophilia

45
Q

Features of ABPA?

A

Bronchoconstriction: wheeze, cough, dyspnea
Bronchiectasis (proximal)

Eosinophilia
Flitting CXR changes
Positive radioallergosorbent (RAST) test to aspergillus
Positive IgG precipitins (not as positive as in aspergilloma)
Raised IgE

46
Q

Management ABPA?

A

Steroids

Itraconazole

47
Q

What is an aspergilloma?

A

a fungus ball which often colonises an existing lung cavity (e.g. secondary to TB,
lung cancer or cystic fibrosis)

48
Q

Features of aspergilloma?

A

Asymptomatic normally (cough, haemoptysis)

CXR shows round opacity
High titres aspergillus precipitins

49
Q

Mutation in CF?

A

Deletion at delta F508 on the long arm of

chromosome 7.

50
Q

Organisms in CF?

A

Staph aureus

Pseudomonas aeruginosa (Rx: Inhaled Tobramycin)

Burkholderia cepacia (can cause rapid fever, pneumonia, sepsis, wt loss - poor outcomes)

Aspergillus

51
Q

Sweat test for CF?

A

2 reliable positive results on 2 separate days is diagnostic for CF. it is positive when chloride is > 60

52
Q

Bronchiolitis obliterans?

A

Fibrous scarring of the small airways

It is seen following: toxic-fume inhalation; mineral-dust exposure; viral infection; mycoplasma and legionella infection; bone marrow, heart–lung and lung transplantation; rheumatoid arthritis; SLE; and as a side-effect of penicillamine

53
Q

Causes of exudates?

A

Infection: pneumonia, TB, subphrenic abscess

Connective tissue disease: RA ( glucose < 1.6, LDH > 700, pH < 7.2, R.F > 1:320, cholesterol), SLE

Neoplasia: lung cancer, mesothelioma, metastases

Pancreatitis

Pulmonary embolism

Dressler’s syndrome

Yellow nail syndrome

54
Q

Causes of transudates?

A

Heart failure

Hypoalbuminemia (liver disease, nephrotic syndrome, malabsorption)

Hypothyroidism

Meigs’ syndrome: triad of ascites, pleural effusion (right side) and benign ovarian tumor
(fibroma).

55
Q

Features of different types of lung mets?

A

Cavitation - squamous cell carcinoma.

Calcification - osteosarcomas and chondrosarcomas as well as metastases from papillary thyroid carcinoma.

Adenocarcinoma metastases spread along the walls of alveoli, instead of destroying the lung parenchyma, resulting in consolidation like that seen with pneumonia.

Haemorrhagic pulmonary metastases - choriocarcinoma and angiosarcoma.

Miliary pattern- renal cell carcinoma and malignant melanoma

56
Q

Causes of occupational asthma?

A

Isocyanates - the most common cause. Example occupations include spray painting and foam moulding using adhesives

Platinum salts

Soldering flux resin

Glutaraldehyde

Flour

Epoxy resins

Proteolytic enzymes

57
Q

NICE COPD management?

A

SABA or SAMA

If breathless then need to consider whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’

No asthmatic/steroidy features –> LABA + LAMA (if on SAMA switch to SABA)

Asthmatic/steroidy features - LABA + ICS —> triple therapy if remains breathless (LAMA + LABA + ICS - discontinue SAMA start SABA)

58
Q

Asthmatic/steroid responsive features for COPD management?

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%)

59
Q

Genotypes in A1AT?

A

PiZZ = 10% of normal enzyme

PiMZ = no lung dysfunction

60
Q

What can LRTAs unmask/precipitate?

A

Churg Strauss (eosinophilic granulomatosis with polyangiitis)

61
Q

Cherry red lesion?

A

Lung carcinoid

62
Q

Kartegener’s syndrome?

A

dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

63
Q

pH of pleural fluid for chest drain insertion?

A

7.2

Alex's MRCP Cards (13 decks)

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