These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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An approach to Interstitial Lung Disease / Diffuse Parenchymal Lung DiseaseThomas Kurian
YouTube link: https://youtu.be/gPr31qrivUc
An approach to Diffuse Parenchymal Lung disease / Interstitial Lung disease with emphasis on the idiopathic causes.
An approach to Interstitial Lung Disease / Diffuse Parenchymal Lung DiseaseThomas Kurian
YouTube link: https://youtu.be/gPr31qrivUc
An approach to Diffuse Parenchymal Lung disease / Interstitial Lung disease with emphasis on the idiopathic causes.
Idiopathic Interstitial Pneumonias
Group of diffuse parenchymal lung diseases
Unknown etiology
Varying degrees of inflammation and fibrosis
In cases where diagnosis cannot be made because of overlap of CT and histological findings; Chrug & Muller proposed a three seperations on HRCT for chronic interstitial diseases.
Interstitial Lung Diseases [ILD] Approach to ManagementArun Vasireddy
Diffuse (interstitial) lung disease includes a wide variety of relatively uncommon conditions presenting with characteristic clusters of clinical features and marked by an immune response. There are over 200 specific diffuse lung diseases, many of unknown etiology. The combined incidence is 50 per 100,000, or 1 in 2000 people. Because these conditions cause aberrant lung function, morbidity and mortality due to lung injury and fibrosis are not uncommon. Both environmental and genetic factors are believed to contribute to the development of diffuse lung disease. Antigen processing and presentation are important in the development of the immune response seen in the disease, and it is thought that the likely candidate genes predisposing patients to this category of disease are those of the major histocompatibility complex. Genes that affect the immune, inflammatory, and fibrotic processes may also influence who develops the disease. If we can identify the genes that cause diseases characterized by lung injury and fibrosis, we can eventually develop genetic interventional approaches to treatment.
2 types (a) cellular NSIP
(b) Fibrotic NSIP (more common)
Fibrosis may involve alveolar septa, peribronchivascular interstitium, interlobular septa and visceral pleura.
Prognosis of fibrotic NSIP is worse , cellular NSIP has good prognosis.
HRCT finding may show both, airspace and interstitial patterns
HRCT in Diffuse Lung Diseases - II (Honeycombing, UIP pattern, IPF)Bhavin Jankharia
This is the second part of this series on HRCT in diffuse lung diseases, focussing on the diagnosis of honeycombing, UIP pattern and IPF and the associated complications and differential diagnoses
Idiopathic Interstitial Pneumonias
Group of diffuse parenchymal lung diseases
Unknown etiology
Varying degrees of inflammation and fibrosis
In cases where diagnosis cannot be made because of overlap of CT and histological findings; Chrug & Muller proposed a three seperations on HRCT for chronic interstitial diseases.
Interstitial Lung Diseases [ILD] Approach to ManagementArun Vasireddy
Diffuse (interstitial) lung disease includes a wide variety of relatively uncommon conditions presenting with characteristic clusters of clinical features and marked by an immune response. There are over 200 specific diffuse lung diseases, many of unknown etiology. The combined incidence is 50 per 100,000, or 1 in 2000 people. Because these conditions cause aberrant lung function, morbidity and mortality due to lung injury and fibrosis are not uncommon. Both environmental and genetic factors are believed to contribute to the development of diffuse lung disease. Antigen processing and presentation are important in the development of the immune response seen in the disease, and it is thought that the likely candidate genes predisposing patients to this category of disease are those of the major histocompatibility complex. Genes that affect the immune, inflammatory, and fibrotic processes may also influence who develops the disease. If we can identify the genes that cause diseases characterized by lung injury and fibrosis, we can eventually develop genetic interventional approaches to treatment.
2 types (a) cellular NSIP
(b) Fibrotic NSIP (more common)
Fibrosis may involve alveolar septa, peribronchivascular interstitium, interlobular septa and visceral pleura.
Prognosis of fibrotic NSIP is worse , cellular NSIP has good prognosis.
HRCT finding may show both, airspace and interstitial patterns
HRCT in Diffuse Lung Diseases - II (Honeycombing, UIP pattern, IPF)Bhavin Jankharia
This is the second part of this series on HRCT in diffuse lung diseases, focussing on the diagnosis of honeycombing, UIP pattern and IPF and the associated complications and differential diagnoses
the scenario given at the start of ppt z nt interstitial lung diseases... its a similar diseases to it.... diagnose it urself to differniate it and hv better command over diffferntial diagnosis.
HRCT in Diffuse Lung Diseases - I (Techniques and Quality)Bhavin Jankharia
The first part of a series on HRCT in diffuse lung diseases. This covers how to obtain good quality scans, which are the basis of learning how to interpret HRCT studies in the setting of diffuse lung diseases.
Dr Kishore Kumar Ubrangala, MD
Professor, Dept. of Medicine,
Yenepoya Medical College,
Yenepoya (Deemed to be) University, Mangalore, India.
sankish@gmail.com
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
It contains :
- Notes on Embryology, Anatomy and Physiology of respiratory system
- Cardinal symptoms in respiratory diseases
- Diagnostic procedures
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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
It contains :
- The new GOLD classification of severity
- The new GOLD treatment guidelines for the treatment of
COPD
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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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Updates on Acute respiratory distress syndromeHamdi Turkey
These lecture notes were made by Dr. Hamdi Turkey (Pulmonologist at Taiz university)
** Contents:
- Historical view on ARDS
- New definition of ARDS
- Precipitating risk factors
- Pathophysiology of ARDS
- Clinical picture, Diagnosis, Management and Prognosis
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. The interstitium of the lung is not normally visible radiographically; it becomes visible only when
disease (e.g., edema, fibrosis, tumor) increases its volume and attenuation.
The interstitial space is defined as continuum of loose connective tissue throughout the lung
composed of three subdivisions:
(i)the bronchovascular (axial), surrounding the bronchi, arteries, and veins from the lung root to
the level of the respiratory bronchiole
(ii) the parenchymal (acinar), situated between the alveolar and capillary basement membranes
(iii) the subpleural, situated beneath the pleura, as well as in the interlobular septae.
3. DPLD
Known cause – drugs, CVD, asbestos Granulomatous - sarcoidosis Idiopathic interstitial pneumonias Other forms – LAM, LCH
IPF IIP other than IPF
NSIP COP
RB-ILD DIP
AIP LIP
IIPs comprise a
heterogeneous
group of diffuse
parenchymal lung
diseases (DPLD) of
unknown cause
Include seven entities
Idiopathic Interstitial Pneumonias
7. Do not represent 'diseases' per se
Idiopathic - unknown cause
Interstitial pneumonia - injury to lung
parenchyma by varying patterns of
inflammation and fibrosis
All truly idiopathic or cryptogenic?
Common findings in collagen vascular
diseases and drug-related lung diseases
Idiopathic Interstitial Pneumonias
8. Achieving the correct diagnosis is a dynamic process
–diagnosis may take time
–may have to be revised at several stages
Final diagnosis only after all the data have been
reviewed by
Pulmonologist
Radiologist
Pathologist
Clinico-radiologic-pathologic diagnosis
•C-R-P diagnosis
Idiopathic Interstitial Pneumonias
Diagnosis
9. History
Nature of the first symptoms
dyspnoea /OE, cough +/–, little sputum
Progression
Comorbid diseases
CTD – arthritis, rashes, raynaud’s, dysphagia
Immune deficiency diseases
Drugs
Environmental / occupational exposures - with dates & durations
Asbestos, silica
Smoking status
Previous malignancies and treatment
Family history of lung diseases
11. Interstitial lung disease may result in four patterns
of abnormal opacity on chest radiographs and CT
scans: linear, reticular, nodular, and
reticulonodular
These patterns are more accurately and specifically
defined on CT
Radiology
16. Waiting for clinical / radiological deterioration before
obtaining biopsy is not recommended
– Delays diagnosis
– Least helpful when obtained late in the course of the
illness or after commencement of treatment
– Pt receives unnecessary or inappropriate treatments
CTD-associated ILD – biopsy is not usually performed
Surgical lung biopsy
17. Establishes a firm clinicopathological diagnosis
Prevents unnecessary exposure to toxic treatments
Confirms or excludes alternative diagnoses
– sarcoidosis, LAM, LCH, PAP, lymphangitis
carcinomatosis, occupational diseases
Benefits of Surgical lung biopsy
18. TBLB
– Not useful for most IIPs
• except AIP and occasionally COP
• Tissue obtained is very small
• May not be representative
– 1ry role is to exclude sarcoidosis, neoplasms and certain
infections
FOB
BAL
– Not essential
– Done as part of the diagnostic workup of a DPLD
• to exclude infection, tumour
• Rarely diagnostic – PAP, LCH
19. IPF/ UIP
UIP is a histological diagnosis
Has distinctive HRCT findings and they are usually
shown at lung biopsy
If the UIP pattern is of unknown cause the disease
is called
– Idiopathic pulmonary fibrosis (IPF)
IPF accounts for more than 60% of the cases of UIP
20. Requires exclusion of other known causes of UIP
– Drug toxicities – a long list
•Commonly cytotoxic agents
– Environmental exposures (asbestos, silica)
– Collagen vascular diseases
IPF/ UIP
21. Key features
1. Dense fibrosis with frequent honeycombing
2. Fibroblastic foci at the edges of the scars
3. Patchy lung involvement
4. Subpleural and paraseptal distribution
Pertinent negative findings
1. Lack of active lesions of other DPLDs
2. Lack of marked interstitial chronic inflammation
Granulomas – inconspicuous or absent
1. Lack of substantial organic dust deposits - asbestos
2. Lack of marked eosinophilia
UIP histology criteria
22. Age of onset > 50 yrs
–usually present > 6/12 after the onset
M > F – slightly
Dyspnoea
–the most prominent and gradual
–Occasionally – periods of rapid decline
• accelerated phase
intercurrent viral infection
• development of organizing pneumonia
• Diffuse alveolar damage
• Cough – paroxysmal
• Constitutional symptoms – unusual
Clinical features
23. Finger clubbing – 25-50%
Fine end-inspiratory crackles
– bases → other areas
Rt. Ht failure & leg oedema
Medium length of survival 2.5-3.5 yrs
Clinical features
BAL
–Neutrophil α extent of reticular damage
–E - mild – moderate
–L - not a feature
24. Peripheral reticular opacities
–most marked at the bases
Honeycombing
Lower lobe volume loss
–in emphysematous pt volume loss may be absent
Whenever long standing reticulation with a lower lobe and peripheral preference is seen also think
of ‘UIP’
Occasionally CXR may be normal
25.
26. General
– Oxygen therapy
• For patients with documented hypoxia
– SpO2 < 89%
– PaO2 < 55 mmHg
• Improves exercise tolerance
– Adequate nutrition
– Immunizations (pneumococcal, influenza)
Pulmonary rehabilitation
– Treatment of PHT
– Single-lung transplantation is a viable
option
management
27. Pirfenidone (antifibrotic)
–Reduces acute exacerbations and reduction in FVC
N-acetyl cystein (antioxydant)
N Engl J Med 2005;353:2229-42
–NAC 600 mg PO tid added to prednisone and azathioprine,
preserves vital capacity and FVC and DLCO
28.
29. Clinical
diagnosis
/ Histo.
Clinically CXR
B
A
L
HRCT findings / HRCT
distribution Treatment
IPF/CFA
– UIP
65 yrs
M:F =3:2
Insidious
Reticular ops,
loss of volume
> Basal
N
Reticular honeycombing,
traction b’ectasis, focal GGO
(rare)
Peripheral, subpleural, basal
Steroids + Aza
+ N AC
V poor
prognosis
Median
Survival 3yrs
NSIP –
NSIP
50-55yrs
M:F =1:1
Insidious
GGO, reticular
op
N, L
GGO, consolidation, reticular
changes, honeycombing (rare)
Peripheral, subpleural, basal,
symmetrical
≈ to IPF
Intermediate
Prognosis
Median
Survival 6-7yrs
COP –
OP -
Buds of
fibroprolif
erative
tissue in
alv. spaces
55 yrs
M:F =1:1
Subacute
Consolidation
– B/L patchy
N
B/L multifocal consolidation,
GGO, nodules
Subpleural, peribronchial
Steroids
Good
response
30. AIP – DAD
50 yrs
M:F =1:1
Acute onset
(≈ARDS)
GGO /
consolidation –
diffuse, progressive
Diffuse consolidation,
GGO, with lobular sparing
Diffuse
BAL - L
No proven Rx
IV Methylpred:
Cyclophos
Very poor prognosis
Die < 6/12
DIP –
Extensive
accum of
m’ph in
intra-
alveolar
spaces
40-50 yrs
M:F =2:1
Insidious.
Exclusively
in Smokers
GGO GGO, reticular lines,
centrilobular nodules
Subpleural, basal
Better response to
smoking cessation
and systemic steroids
than IPF
Good prognosis
RB-ILD –
RB Accum.
of m’ph in
peribronc
alveoli
40-50 yrs
M:F =2:1
Insidious.
Smoking
related
Bronchial wall
thickening, GGO
Bronchial wall thickening,
centrilobular nodules,
patchy GGO
Diffuse
Resolve with
smoking cessation
alone in most cases
Good prognosis
LIP –
LIP
40-50 yrs
M:F =1:5
Insidious
Reticular ops,
nodules
Centrilobular nodules,
GGO, septal &
bronchovascular
thickening, thin walled
cysts, L’adenopathy
Diffuse
Intermediate prognosis