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Y4 Respiratory Medicine > 3. Interstitial Lung Disease > Flashcards

3. Interstitial Lung Disease Flashcards

1
Q

What is the function of the interstitium

A

For gas exchange

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2
Q

What ILD is cause by exposure to birds

A

Hypersensitivity penumonitis

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3
Q

What is the most common CTD assoc ILD

A

Rheumatoid ILD

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4
Q

What are the two main idiopathic ILDs

A

UIP/IPF and Sarcoidosis

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5
Q

Most common two Sx of ILD

A

Breathlessness and cough

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6
Q

Drugs associated with ILD

A

Amiodarone, methothrexate, Rituximab, nitrogurantoin, sulfsalazine, Bleomicyi and Leflunamide

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7
Q

What are common examinations in most ILDs

A

Clubbing (esp common in IPF and asbestosis)
and mid and late inspiratory bibabsal fine crackles
NOT common in Sarcoidosis

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8
Q

What are the infiltrates in ILD like

A

Bilateral diffuse nodular or reticular infiltrates

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9
Q

Are pleural effusions common in ILD

A

No

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10
Q

What is the pathological pattern of disease in IPF

A

Subpleural dominant disease
Honeycomb fibrosis
Grossly distorted lung architecture
Temporal and spatial heterogeneity
Fibroblastic foci

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11
Q

risk factors for IPF

A

Male, smoker

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12
Q

Is sputum produced in IPF

A

Usually no, only dry cough
BUT smokers may have chronic bronchitis also (respiratory bronchiolitis ILD)

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13
Q

Pathogenesis of IPF- what cells are involved

A

Fibroblasts transdiff into myofibroblats, secrete excess collagen and also accumulate and form fibroblastic focus
TII AEC hypertorphy and can’t transdiff to TI AEC

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14
Q

FEV1/FVC ratio in IPF

A

Normal (early disease) or increased due to disprop decrease in FVC

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15
Q

What does it mean if FVC less than 80

A

Likely to be RESTRICTIVE

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16
Q

FGold standard biomarker for IPF disease progression

A

> 10% decline in FVC over 6 -12 mo

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17
Q

What is one common observation on exercise tests for IPF pts

A

Destauration

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18
Q

CXR changes in IPF

A

Usually occur earliest in CPA - reticular and nodular opacification- left heart border more shaggy and diffuse, same for hemidiaphragm

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19
Q

Critical Inv in suspected IPF

A

HRCT
- Reticular patter made of intra-lobular lines (all) - due to intralob septal thickening
- Traction Bronchiectasis/ bronchiolectasis (almost all)
- Honeycomb cyst formation ( Most)
- ALL changes supleural and bnasally dominant

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20
Q

What is a possible UIP pattern

A

Sub pleural basal predominance and reticular abnormality , and no features inconsistent with UIP but no honeycombing

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21
Q

What to do if possible UIP pattern

A

Consider doing Surgical lung biopsy, if SLB shows UIP then confirmed, otherwise dx possible UIP

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22
Q

Tx fot UIP

A

Pirfenidone and Nintedanib

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23
Q

Non pharmalogical Tx of IPF

A

Smoking cessation, ambularotu and domicillary oxugen if prone to hypoxaemia, pulm rehabiliatation, maybe lung transplant

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24
Q

What characterises Sarcoidosis

A

Non-caseating granuloma

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25
Q

How can sarcoidosis affect the heart, liver and spleen, nerves

A

Myopathy or arrhythmias
Cirrhosis and splenomegaly
Facial nerve palsy

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26
Q

What are general Sx of sarcoidosis

A

Fatigue, hypercal (eg. polyuria, constipation, confusion, renal stones, polydipsia), lymphodenopathy, night sweats

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27
Q

Chest examination in Sarcoidosis

A

Infreq crackles, often normal chest exam

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28
Q

what Ix to stage sarcoidosis
and how to divide stages

A

CXR
Stage 1 - Bilat hilar lymphadenopathy with normal parenchyma. May also present with erythema nodosum ( typically on shins)
Stage 2 - BHL with lung infiltrates ( spare LZ)
Stage 3- Lung infiltrates without BHL]

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29
Q

PFT in sarcodiosis

A

Normal in stage 1 disease or mild 2 or 3 disease, but will have restrictive defect with more extensive disease
If endobronchial disease, may have obstructive defect

30
Q

What is a possible observation in sarcoidosis blood tests

A

Serum angiotensin converting enzyme raised

31
Q

What skin test for sarcoidosis

A

Tuberculin skin test- usually negative in pts with sarcoidosis due to anergy ( originally positive due to TB infxn or BCG vaccine)

32
Q

Similarity and diff between TB and Sarcoidosis

A

Both have infiltrates but only CXR has hilar lymphadenopathy?? Non-caseatinng granuloma in sarcoid vs caseating in TB

33
Q

How to confirm sarcidosis dx

A

Stage 1- usually don’t need histology if have erythema nodosum
Stage 2 and 3- biopsy. Skin lesion or lymph nodes if have. In lungs, transbronchial if possible, SLB sometimes

34
Q

Tx for pulm sarcoidosis

A

Corticosteroids eg. predni

35
Q

Complication of VTE

A

Chronic thromboembolic pulmonary hypertension

36
Q

Where do bloot clouts usually arise

A

deep veins of legs, but thrombi may also originate in pelvis, arms, or right heart

37
Q

Leg sx of DVT

A

Calf pain, tightening, swelling

38
Q

What is Virchow;s triad, examples of what can affect it

A

Blood flow, vessel wall, coagulability

  • Surgery can induce trauma to blood vessels
  • Venous stasis and dehydration can affect blood flow
  • Inflammatory healing process makes blood hypercoagulable
39
Q

How does a large settled central PE cause shock

A
  • Right ventricle pushes blood through circulation, will dilate due to increased afterload
    • This generates hormonal activation and myocardial inflammation
    • In due cause can drive RV ischaemia due to increased O2 demand
    • RV contractiluty will drop and will not load LV
    • Reduced LV stretch reduces stroke value and CO, resulting in hypo T and shock
    • Shock is main cause of death rather than hypoxaemia
40
Q

High risk factors for PE

A

Fracture of lower limb, hospitalisation for HF or AF, hip or knee replacement, major trauma, MI, previous VTE, spinal cord injury, family history,

41
Q

Moderate risk factors for VTE

A

Many, including CCF, HRT, RF, stroke, cancer, thrombophillia, porstpartum and many inflammatory causes eg. IBD

42
Q

Weak risk factors for VTE

A

DM, HTN, bed rest, immobility due to sitting on car/plane, old, surgery (laparo), obesity, pregancy, varicose veins

43
Q

Px complain of PE

A

Dyspnoea, pleuritic chest pain, cough, substernal chest pain, haemoptysis, fever, syncope, unilateral leg swelling

44
Q

Ix for PE

A

CXR may show distal wedge infarction
ECG changes - S1Q3T3 possible, or may just be sinus tachy
Echo- right ventricle larger than left, septum may go into LV, suggesting acute RV stress

45
Q

Simplified wells score

A

2 or more means PE likely
Previous PE/DVT, HR>100, surgery or immobilzation within past 4 weeks, haemoptysis, active cacner, clinincal signs of DVT, alternative Dx less likely than PE - 1 pt each

46
Q

What is D-dimer

A

Breakdown product of crosslinked fibrin

47
Q

Specificity and sensitivity of D-dimer

A

High sensitivity but low specifity
+ve doesn’t mean PE, high false +ve, just use to rule out

48
Q

Gold standard to dx PE

A

CTPA

49
Q

Are pts with distal or central infarction in PE at higher risk of death

A

central

50
Q

cardiac biomarker for PE

A

Troponin

51
Q

Acut Tx for high risk PE pts

A

Alteplase Bolus + 2hr infusion
Subsequent IV unfractionated heparin

52
Q

Diff High risk and intermediate risk VTE pts

A

Shock in high risk

53
Q

Diff Intermediate and low risk PE pts

A

Low risk have PESI Class II or below and sPESI =0

54
Q

If pt cannot have thrombolysis, what should be done for high risk acute PE

A

Cathether directed lysis under ultrasound

55
Q

What does fibrinolysis target

A

Plasminogen, which is converted into active plasmin that breaks down fibrin into FDPs

56
Q

Tx of low risk PE

A

New approach - just give DOACs (apix, rivarox) immediately

Give LMWH like dalteparin subcut for at least 5 days until INR therapeutic for 2 days, then give warfarin (overlap until INR stable)

57
Q

Mech of heparin

A

Potentiates antithrombin III which inactivates thrombin (factor IIa), and many other factors

58
Q

Difference between LMWH and UFH

A

LMWH preferentially inactivates factor Xa, little to no monitoring

59
Q

Mech of action of warfarin

A

Vit K antagonist- inhibits epoxide reductase ( affects synthesis of factors II, VII, IX and X)

60
Q

featurdd of intermediate risk PE

A

May have large clot load in pulm artery or saddle embolism

61
Q

Tx of intermediate risk PE

A

Indv case basis
But consider IV unfractionated heparin instead of LMWH as can stop if need thrombolysis

62
Q

When should thrombolysis not be given in PE

A

If there is haemodynamic stability

63
Q

When should chronic thromboembolic pulmonary hypertension be checked for

A

If pt describes onset of RH failure such as progressive breathlessness despite treatment, and peripheral oedema

64
Q

When may indefinte doacs be considered

A

Young male with unprovoked event w/o any known cause

65
Q

What should be used to determine stopping of anticaog in PE

A

DASH score - Dodimer elevated, Age (<50), Sex male, H- not hormone assoc ( female)
If 1 or lower can consider stopping

If on oestrogen containing hormones and now off it, -2 points

66
Q

Do crackles in IPF clear on coughing

A

NOOOOOO

67
Q

Ix for hypersensitivity pneumonitis

A

CXR, CT, avian precipitins abs

68
Q

What pattern is found in hypersensitivity pneumonitis on HRCT

A

Mosiac distr, with ground glass shadowing

69
Q

Ix for dequative interstitial pneumonia

A

HRCT followed by transbronchial biopsy +BAL if HRCT atypical

70
Q

Is clubbing common in hypersensitivity pneeumonitis

A

no

71
Q
A

Y4 Respiratory Medicine (6 decks)

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