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IMED3001 > Lower RTI2 > Flashcards

Lower RTI2 Flashcards

1
Q

What pattern do chronic interstitial lung diseases show on flow-volume loop?

A

Restrictive lung pattern on flow volume loop.

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2
Q

What are chronic interstitial lung diseases?

A

Heterogeneous group of disorders characterized predominantly by inflammation and fibrosis of the pulmonary connective tissue.

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3
Q

What are the types of chronic interstitial lung diseases?

A

Fibrosing diseases (usual interstitial pneumonia, non-specific interstitial pneumonia, cryptogenic organising pneumonia, autoimmune related pneumonia)

Granulomatous (Sarcoid, hypersensitivity pneumonitis)

Eosinophilic

Smoking related (Desquamative interstitial pneumonia, respiratory bronchitis)

Other

[important to know the categories not individual conditions]

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4
Q

What is honeycomb lung?

A

Thickening of septa between alveoli resulting in rigid lung with larger airspaces.

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5
Q

What is sarcoidosis?

A

Systemic granulomatous disease with unknown aetiology affecting liver, lung, and brain.

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6
Q

What lung condition is lung sarcoidosis very similar to?

A

TB, in its granulomatous nature.

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7
Q

How common is hilar lymphadenopathy in sarcoidosis?

A

90% of cases

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8
Q

What kind of granulomas are found in sarcoidosis?

A

Collection of big histiocytes with no necrosis in the middle.

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9
Q

What happens to the lungs in sarcoidosis?

A

Granuloma (non-necrotising) formation

Hilar lymphadenopathy

Pulmonary fibrosis

Lymph node enlargement

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10
Q

How is sarcoidosis diagnosed?

A

Other causes of symptoms must first be excluded.

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11
Q

What is pneumoconiosis?

A

Pulmonary fibrosis caused by inhaled dust.

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12
Q

Who is pneumoconiosis commonly seen in?

A

People who work in coal mines

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13
Q

What 2 blood supplies does the lung receive?

A

Pulmonary circulation (alveoli supply)

Systemic (Bronchial) circulation (Supply lungs until bronchioles prior to alveoli)

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14
Q

How many bronchial arteries does the lung receive?

A

2 on the left coming off descending aorta and 1 on the right

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15
Q

Can adults deal with losing bronchial arterial circulation?

A

Blood flow to bronchioles isn’t compromised too much due to nature of the anastomoses.

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16
Q

What happens if pulmonary circulation is broken?

A

Infarction of terminal airways.

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17
Q

What is an infarct?

A

An area of ischaemic necrosis caused by occlusion of vascular supply to affected tissue

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18
Q

What is the most common cause of pulmonary infarct?

A

Small/ medium sized Embolus (other causes include trauma and vasculitis) [big emboli kill before infarct even happens]

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19
Q

Where do lung infarcts tend to be?

A

Peripheral due to bronchial tree receiving anastomoses from pulmonary circulation and bronchial circulation.

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20
Q

What shape and colour do pulmonary infarcts tend to have?

A

Wedge-shape and haemorrhagic (red)

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21
Q

What are the types of emboli?

A

Thromboemboli

Air/gas emboli

Fat emboli

Amniotic fluid emboli

Septic emboli

Foreign body emboli

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22
Q

What provoking factors result in acute thromboemboli formation?

A

Surgery, burns, trauma, period of immobilisation, commencement of estrogen therapy, and pregnancy/post partum

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23
Q

What chronic factors cause thromboemboli to form?

A

Primary:

Clotting abnormalities (eg factor V leiden)

Secondary:

Obesity

Cigarette smoking

Hypertension

Age >60

Malignancy

24
Q

What are the 3 components that predispose to thrombis in virchows triad?

A

Endothelial injury

Abnormal blood flow

Hypercoagulability

25
Q

What are the 2 main effects of a pumlonary embolism?

A

Mechanical (stops blood flow and leads to mismatch between ventilation and perfusion, and increases right ventricular pressure)

Inflammatory cascade and thrombogenic effects (cytokines and other inflammatory mediators, damage to and activation of endothelium)

26
Q

What are the mechanical effects of a PE?

A

Blockage of blood from reaching the lungs

Ventilation Perfusion mismatch

Increased right ventricular pressure

27
Q

What are the inflammatory effects of a PE?

A

Cytokine production

Damage to and activation of endothelium promoting indiscriminate clotting

Consumption of platelets and clotting factors with paradoxical bleeding in DIC

28
Q

What is the effect of large emboli in the lungs?

A

Acute right heart failure and sudden death

“saddle embolus at bifurcation of pulmonary arteries.

Sudden onset shortness of breath, chest pain, collapse, unconsciousness

29
Q

What is the effect of smaller emboli?

A

Pulmonary haemorrhage with or without infarct, ventilation perfusion mismatch, and hypoxia.

Sudden onset shortness of breath and chest pain.

Can be single or multiple and can be symptomatic or asymptomatic.

Can lead to pulmonary hypertension and chronic RHF

30
Q

What are possible sequelae of a PE?

A

Based on degree and size of embolus:

Lysis can occur

Superimposed thrombus/inflammation/extension of infarct

Organisation and recanalisation

31
Q

How does air/gas embolism occur?

A

Surgery or trauma causes normal air emboli

Nitrogen can cause embolism (nitrogen decompression sickness)

32
Q

What causes fat emboli to form?

A

Fracture of long bones

Severe soft tissue injury

Burns

33
Q

What kind of cells are seen in fat emboli?

A

Adipocytes with or without associated haemopoietic marrow elements.

34
Q

What are the symptoms fat embolism syndrome?

A

Pulmonary insufficiency

Neurological symptoms (irritability, retlessness, delirium)

Intravascular coagulation with anaemia

Fatal in 5 - 15% of cases

35
Q

What causes amniotic fluid emboli?

A

In rare cases, a tear in placental membrane or rupture of uterine veins allow amniotic fluid into maternal circulation.

36
Q

What complications arise from amniotic fluid emboli?

A

Permanent neurological damage in 85% of survivors

Pulmonary oedema

DIC

Acute lung injury

37
Q

What is pulmonary hypertension?

A

Mean pulmonary artery pressure >=25mmHg or >30mmHg during exercise

38
Q

How can pulmonary hypertension arise?

A

Increase in pulmonary blood flow

Increase in pulmonary vascular resistance

Increase in left heart resistance to blood flow (mitral stenosis)

Idiopathic

39
Q

What are the groups of pulmonary hypertension by WHO classification?

A

Group 1: Pulmonary arterial hypertension

Group 2: Pulmonary hypertension owing to Left Heart Disease

Group 3: Pulmonary hypertension caused by lung disease

Group 4: Chronic thromboembolic pulmonary hypertension

Group 5: Pulmonary hypertension with unclear multifactorial mechanisms (idiopathic)

40
Q

WHO groups good way to remember it.

A

Pulmonary hypertension can be caused by:

Inflow: Left to right shunt

Pulmonary bed: Group 1/3/4/5

Outflow: Group 2. Pulmonary hypertension owing to left heart disease

41
Q

How is pulmonary circulation remodeled in people with pulmonary hypertension?

A

Genetic changes (Bone morphogenetic protein receptor 2)

Serotonin/other mediators

Inflammation

Endothelial damage and thrombosis

Hypoxia - oxidative damage

42
Q

What does bone morphogenetic protein receptor 2 do?

A

Member of transforming growth factor beta superfamily and is widely expressed in pulmonary artery endothelium.

End effect of mutations in this gene is dysfunction and proliferation of endothelial cells and vascular smooth muscle.

43
Q

How do people present in the clinic with pulmonary hypertension?

A

Right heart failure

Failure to oxygenate

Arrhythmias

In idiopathic group death from right heart failure occurs within 2 to 5 years in 80% of patients

Patients usually come in late into the course of the disease due to its lack of symptoms in the early stage.

44
Q

What symptoms are seen in right heart failure?

A

Chest pain

Abdominal discomfort

Peripheral oedema

SOB

45
Q

What are pathological findings of pulmonary hypertension?

A

Medial hypertrophy of pulmonary muscular and elastic arteries with intimal fibrosis

Pulmonary artery atherosclerosis

Right ventricular hypertrophy

End stage can form plexiform arteriopathy

Changes can involve entire pulmonary arterial system

Narrowing of vessel lumina

Increase vascular resistance

46
Q

How is pulmonary hypertension treated?

A

Depends on underlying cause, the cause is treated.

Group 1 have been treated with vasodilators with some success

Lung transplant provides definitive treatment for some patients

47
Q

Where do most pulmonary haemorrhages occur?

A

They occur focally due to what caused them (Tumour, abscess, infection, etc)

48
Q

How does diffuse pulmonary haemorrhage occur?

A

Range of settings and is usually associated with immunologically mediated or inflammatory diseases.

Can occur in DAD/ALI/ARDS patterns of interstitial lung disease

Some cases are idiopathic

49
Q

How do people with pulmonary haemorrhage present?

A

Haemoptysis

50
Q

How can localised pulmonary haemorrhage be diagnosed?

A

Haemoptysis and a thromboembolism/tumour/abscess/etc on chest scans

51
Q

What are the types of diffuse pulmonary haemorrhage?

A

Vasculitis associated

Without vasculitis

52
Q

What is goodpasture syndrome?

A

Uncommon autoimmune disease in which kidneys and lungs are damaged by autoantibodies against the non-collagenous domain of the alpha3 chain of collagen IV.

53
Q

What is Granulomatosis with pulmonary angiitis (Wegner’s granulomatosis)?

A

A systemic inflammatory disorder affecting blood vessels.

54
Q

What are the characteristic lung symptoms of granulomatosis with pulmonary angiitis (Wegner’s granulomatosis)?

A

Nodular lung lesions

Necrosis, vasculitis and granulomatous inflammation

Diffuse pulmonary haemorrhage.

55
Q

What results would serological tests show in granulomatosis with polyangiitis?

A

c-ANCA > p-ANCA

IMED3001 (46 decks)

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