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Y4 Respiratory Medicine > 3. Interstitial Lung Disease > Flashcards

3. Interstitial Lung Disease Flashcards

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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
How can sarcoidosis affect the heart, liver and spleen, nerves
Myopathy or arrhythmias Cirrhosis and splenomegaly Facial nerve palsy
26
What are general Sx of sarcoidosis and what are the resp Sx
Fatigue, malaise, fever, weight loss, hypercal (eg. polyuria, constipation, confusion, renal stones, polydipsia), lymphodenopathy, night sweats cough, dyspnea, and chest pain
27
Chest examination in Sarcoidosis
Infreq crackles, often normal chest exam
28
what Ix to stage sarcoidosis and how to divide stages
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]
29
PFT in sarcodiosis
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
What is a possible observation in sarcoidosis blood tests
Serum angiotensin converting enzyme raised
31
What skin test for sarcoidosis
Tuberculin skin test- usually negative in pts with sarcoidosis due to anergy ( originally positive due to TB infxn or BCG vaccine)
32
Similarity and diff between TB and Sarcoidosis
Both have infiltrates but only CXR has hilar lymphadenopathy?? Non-caseatinng granuloma in sarcoid vs caseating in TB
33
How to confirm sarcidosis dx
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
Tx for pulm sarcoidosis
Corticosteroids eg. predni if have sx of stage 2 and above
35
Complication of VTE
Chronic thromboembolic pulmonary hypertension
36
Where do bloot clouts usually arise
deep veins of legs, but thrombi may also originate in pelvis, arms, or right heart
37
Leg sx of DVT
Calf pain, tightening, swelling
38
What is Virchow;s triad, examples of what can affect it
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
How does a large settled central PE cause shock
- 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
High risk factors for PE
Fracture of lower limb, hospitalisation for HF or AF, hip or knee replacement, major trauma, MI, previous VTE, spinal cord injury, family history,
41
Moderate risk factors for VTE
Many, including CCF, HRT, RF, stroke, cancer, thrombophillia, porstpartum and many inflammatory causes eg. IBD
42
Weak risk factors for VTE
DM, HTN, bed rest, immobility due to sitting on car/plane, old, surgery (laparo), obesity, pregancy, varicose veins
43
Px complain of PE
Dyspnoea, pleuritic chest pain, cough, substernal chest pain, haemoptysis, fever, syncope, unilateral leg swelling
44
Ix for PE
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
Simplified wells score
2 or more means PE likely Previous PE/DVT, HR>100, surgery or immobilization within past 4 weeks, hemoptysis, active cancer, clinical signs of DVT ( leg swelling and pain with palpation of deep veins) , alternative Dx less likely than PE - 1 pt each
46
What to do if Well's score shows PE is unlikely
Arrange D-dimer, if positive then CTPA. Anticoagulate until scan is performed
47
What is D-dimer
Breakdown product of crosslinked fibrin
48
Specificity and sensitivity of D-dimer
High sensitivity but low specifity +ve doesn't mean PE, high false +ve, just use to rule out
49
Gold standard to dx PE
CTPA
50
Are pts with distal or central infarction in PE at higher risk of death
central
51
cardiac biomarker for PE
Troponin
52
Acut Tx for high risk PE pts
Alteplase Bolus + 2hr infusion Subsequent IV unfractionated heparin
53
Diff High risk and intermediate risk VTE pts
Shock in high risk
54
Diff Intermediate and low risk PE pts
Low risk have PESI Class II or below and sPESI =0
55
If pt cannot have thrombolysis, what should be done for high risk acute PE
Cathether directed lysis under ultrasound
56
What does fibrinolysis target
Plasminogen, which is converted into active plasmin that breaks down fibrin into FDPs
57
Tx of low risk PE
New approach - just give DOACs (apix, rivarox) immediately JUST OUTPT
58
Mech of heparin
Potentiates antithrombin III which inactivates thrombin (factor IIa), and many other factors
59
Difference between LMWH and UFH
LMWH preferentially inactivates factor Xa, little to no monitoring
60
Mech of action of warfarin
Vit K antagonist- inhibits epoxide reductase ( affects synthesis of factors II, VII, IX and X)
61
featurdd of intermediate risk PE
May have large clot load in pulm artery or saddle embolism
62
When should thrombolysis not be given in PE
If there is haemodynamic stability
63
When should chronic thromboembolic pulmonary hypertension be checked for
If pt describes onset of RH failure such as progressive breathlessness despite treatment, and peripheral oedema
64
When may indefinte doacs be considered
Young male with unprovoked event w/o any known cause
65
What should be used to determine stopping of anticaog in PE
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
Do crackles in IPF clear on coughing
NOOOOOO
67
Ix for hypersensitivity pneumonitis
CXR, CT, avian precipitins abs
68
What pattern is found in hypersensitivity pneumonitis on HRCT
Mosiac distr, with ground glass shadowing
69
Ix for dequative interstitial pneumonia
HRCT followed by transbronchial biopsy +BAL if HRCT atypical
70
Is clubbing common in hypersensitivity pneeumonitis
no
71
72
Does sacrcoidosis cause hypo or hypercalcaemia
Hyper
73
Bronchiectasis features
persistent productive cough. Large volumes of sputum may be expectorated dyspnoea haemoptysis abnormal chest auscultation coarse crackles wheeze clubbing may be present
74
Bronchiectasis Ix and finding
Signet ring sign, enlarged bronchi
75
Mx of bronchiectasis
physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis postural drainage antibiotics for exacerbations + long-term rotating antibiotics in severe cases bronchodilators in selected cases immunisations surgery in selected cases (e.g. Localised disease)
76
Cause of bronchiectasis
Chronic insult to bronchial tree - post infection, systemic diseases, CF etc.
77
Features of CF
Meconium ileurs, recurrent chest infections, malabsortion, may have liver disease short stature diabetes mellitus delayed puberty rectal prolapse (due to bulky stools) nasal polyps male infertility, female subfertility
78
What is cystic fibrosis resulting from
Autosomonal recessive genetic disorder resulting from mutations in CF transmembrane conductance regulator F508del mutation
79
Ix for CT
newborn screening programs, which typically involve measuring immunoreactive trypsinogen (IRT) in blood samples. Sweat chloride rest CFTR gene mutation
80
Mx of CF
Chest physiotherapy and postural drainage High-frequency chest wall oscillation Exercise Lumacaftor/Ivacaftor (Orkambi) for pts homozygous for delta F508 mutation
81
Well's Score
DVT sx and

Y4 Respiratory Medicine (6 decks)

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