This document summarizes computed tomography findings for various chest diseases. It describes imaging appearances of different types of pneumonia including streptococcus, staphylococcus, haemophilus influenzae, klebsiella and pseudomonas. It also discusses tuberculosis and various lung cancers such as adenocarcinoma, squamous cell carcinoma, small cell carcinoma and lymphoma. Key imaging features for differentiating benign from malignant lung nodules are provided. Imaging patterns for various infectious, inflammatory and neoplastic lung diseases are concisely described.
Imaging plays an important role in diagnosis and formulating differential diagnosis in case of Solitary pulmonary nodule. It helps in differentiating and predicting benign and malignant nodules.
Imaging plays an important role in diagnosis and formulating differential diagnosis in case of Solitary pulmonary nodule. It helps in differentiating and predicting benign and malignant nodules.
High resolution Computerised Tomagraphy is a radiological procedure done to diagnose lung diseases.In this powerpoint presentation indications for HRCT,common patterns observed in HRCT to diagnose common lung diseases have been described.
High resolution Computerised Tomagraphy is a radiological procedure done to diagnose lung diseases.In this powerpoint presentation indications for HRCT,common patterns observed in HRCT to diagnose common lung diseases have been described.
Empyema is a collection of pus in the cavity between the lung and the membrane that surrounds it (pleural space). Caused by an infection that spreads from the lung and leads to an accumulation of pus in the pleural space, the infected fluid can build up to a quantity of a pint or more, which puts pressure on the lungs, causing shortness of breath and pain. Risk factors include recent lung conditions like bacterial pneumonia, lung abscess, thoracic surgery, trauma or injury to the chest.
SHORT TALK ABOUT DIFFERENTIAL DIAGNOSIS BILATERAL HYPERLUCENT LUNGS , COMMON AND LESS COMMON CAUSES WITH CLUES TO DIAGNOSIS AND SOME EXAMPLES
HOPPING YOU LIKE IT
DR HISHAM ALKHATIB
CONSULTANT RADIOLOGIST
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.
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- 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
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
5. Pneumococcal Pneumonia
It is the most common cause of Pneumonia.
• It is more common in male, elderly, during winter or at the end of dry
season, usually following viral infection.
• Capsular polysaccharide types 14, 4, 1, 6A/6B, 3, 8, 7F, 23F, and 18C
are the most frequent causes of pneumococcal disease.
• Classically, pneumococcal pneumonia produces diffuse involvement
of most of a lobe and more than one lobe may be involved in 10–25%
of cases but spread of consolidation throughout an entire lung is
unusual.
6. Imaging
• Homogenous non segmental , parrenchymal consolidation involving
one lobe, multi lobar involvement is less common.
• More commonly involves lower lobe or posterior segment of upper
lobe.
• Minimal volume loss
• Air bronchogram is common
• Cavitation is rare.
• May present as round pneumonia in children
• Associated with pleural effusion in 60% cases.
9. Staphylococcus aureus
X ray
• Lobular pattern of bilateral , multifocal, patchy heterogeneous ,
segmental air space consolidation.
• Usually lower lobes are involved
• Absent air bronchogram.
• May progress to homogeneous air space consolidation.
• May develop abscess with cavitation.
• Cavity has irregular shaggy internal walls and air fluid level.
• Pleural effusion in 30 -50 %cases , progress to empyema in 50% cases.
10. • CT scan
• Focal or multifocal masses or nodules, may undergo cavitation
• Centrilobular nodules and tree in bud opacities may be present.
• Peripheral wedge shaped opacities with associated feeding vessel is
seen in hematogenous dissemination.
• Pneumatocele common in children . Responsible for spontaneous
pneumothorax.
• Empyema in 20% adult and 75% children
11.
12.
13. Haemophillus influenza
• X ray
• Patchy air space opacities – Bronchopneumonia
• Lobar consolidation in immunosuppressed.
• Reticulonodular opacities associated with consolidation.
• Cavitation is rare.
• Pleural effusion in 40% cases.
• Empyema rare.
• Slow resolution of disease.
16. Klebsiella
• X ray
• Usually involves upper lobe
• Homogenous , non segmental lobar consolidation.
• Lobar expansion causing bulging fissure sign is seen.
• Abscess formation in 50% cases.
• Pleural effusion or empyema in 70% cases.
17. • CT
• Necrotizing pneumonia is charecteristic
• Consolidation with or without cavitation.
• Scattered enhancing linear branching structure representing pulmonary
vessel in atelactic or consolidated lung – CT angiogram sign is seen.
• Centripetal resolution (periphery to central) with residual fibrosis is seen.
• Cavitation with narrowed or obliterated feeding bronchus impeding
drainage of necrotic lung.
• Large vessel thrombosis can be seen .
18.
19.
20. Pseudomonas
• X ray and CT finding varies in bacteremic and Non bacteremic
patients.
• Bacteremic patients – patients with systemic toxicity , shock, altered
mental status, non productive sputum.
• Non bacteremic pateints – hemodynamically stable with purulent
sputum.
21. 1) Bacteremic pt
X ray - pulmonary vascular congestion ->pulmonary edema ->
necrotizing bronchopneumonia.
• Within 2-3 days mixed alveolar opacities and cavitation may occur.
• Mutifocal nodules.
• Nodules coalesces to form opacities.
22. CT scan
• Multilobar air space consolidation , upper lobe predilection (82%)
• Nodular opacities in 50% cases
• May be Centrilobular with tree in bud appearance in 64% cases
• Or large randomly distributed nodules in 36% cases.
• Ground glass opacity may be seen .
• Bronchial wall thickening may be present.
• Pleural effusion unilateral in 18% and bilateral in 46% cases
23.
24. 2) Non Bacteremic patients-
X ray
• Bronchopneumonia pattern
• Multifocal , bilateral , nonsegmental consolidation lower lobe more
common.
• Abscess , empyema ,pleural effusion - rare
CT scan
• Reticular or nodular opacities are seen
25. Legionella
• X ray
• Patchy , peripheral non segmental consolidation.
• Progressing rapidly to other lobes and other lung.
• Nodular and mass like consolidation
• Cavitation and lymphadenopathy – Unusual.
• Pleural effusion 50 -66%
• CT
• Sharply demarcated peribronchovascular foci of consolidation with
Ground Glass Opacity
28. Tuberculosis
• Primary tuberculosis-
• Consolidation –usually unilateral, dense , homogenous; segmental,
lobar or multifocal . Rapidly progressive cavitary consolidation.
• Lymphadenopathy – typically unilateral usually right hilar, or right
paratracheal more common in children.
• Atelactasis – usually right sided and usually in children.
• Pleural effusion – unilateral and typically self limiting.
29. • Post Primary Tuberculosis
• Consolidation – patchy , heterogenous,involving apical and posterior
segment of upper lobes and superior segment of lower lobes, ill
defined borders, satelite nodules.
• Cavitation –thin or thick walled, focal or multi focal , air fluid level
may be seen.
• Nodular and linear opacities.
• Tuberculoma –solitary or multiple pulmonary nodule variable size
well defined or ill defined margins.may exhibit calcification.
• Pleural effusion unilateral or bilateral.
30. • CT
• Central low attenuation and peripheral enhancement of affected node
• Cavitations are seen
• Linear branching opacities and cetrilobular nodules (2-4mm) tree in bud
appearance is seen due to endobronchial spread of disease associated with
cavitary disease.
• Ill defined nodules (4-8mm)lobular consolidation, thick inerlobular septa.
• Milliary nodules (1-3mm) with random distribution , thick nodular
interlobular septa
31. • Tuberculoma – rim enhancement, calcification, satellite lesion in 80%.
• Bronchial narrowing withmural thickening.
• Upper lobe predominant bronchiectasis.
• Empyema, pleural calcification, bronchopleural fistula – rarely seen
32. PA chest radiograph of a 9-year-old boy with tuberculosis
demonstrates a coalescent right perihilar consolidation
with ipsilateral hilar and mediastinal lymphadenopathy
37. Solitary Pulmonary Nodule
• A solitary pulmonary nodule is defined as a single discrete pulmonary
opacity that is surrounded by normal lung tissue that is not
associated with adenopathy or atelectasis.
• Diameter of SPN should be less than or equal to 3cm
• Incidence 1-2 / 1000 chest X rays
39. Character Benign Malignant
Age Young Old
Smoking history Absent Present
Size of Nodule Small Large
Radiograph density High (Solid) Low (partly solid ,GGO )
Calcification Present – Diffuse , stippled, laminar
/concentric or popcorn
Absent or Eccentric
Border Well circumscribed , round
Appearance
Lobulated border , Irregular
Appearance
Margins Smooth Spiculated
CT volume doubling Time , change
in density
Less than 20 days OR more than
400 days
60 – 80 days sq cell carcinoma
120 days Adenocarcinoma
30 days Small cell carcinoma
40. • Other features indicating malignancy are
• Pleural Retractoins
• Feeding vessel (vessel sign)
• Vascular convergence
• Dilated bronchus leading into nodule
• Pseudocavitation & True Cavitation
48. Adenocarcinoma
• 4 entity of Adenocarcinoma is identified on CT
• 1. Atypical Adenomatous hyperplasia of Lung (<0.5cm)
• 2. Adenocarcinoma In Situ (0.5 – 3cm)
• 3. Minimally Invasive Adenocarcinoma (<3cm, with invasion <0.5cm)
• 4. invasive Adenocarcinoma
49.
50.
51.
52.
53. Squamous Cell Carcinoma
• Squamous cell carcinoma is defined as a malignant epithelial tumor
showing keratinization and/or intercellular bridges.
• It has rapid local growth and relatively late distant metastases.
54. Imaging
• Frequent secondary atelectasis (absent air bronchograms),
obstructive pneumonia, or mucoid impaction; may be dominant
radiologic abnormalities
• Central mass
• Bronchial wall thickening; thickened (>3 mm) intermediate stem line
(i.e., posterior wall of the bronchus intermedius) (lateral radiography)
• Peripheral lung nodule or mass
• Cavitation
• Lymphadenopathy
55.
56.
57. CT chest
• Irregular central mass with abrupt obstruction of bronchial lumen
• Post-obstructive consolidation , atelectasis ; contrast administration
may help differentiate tumor from adjacent consolidation and
atelectasis , as tumor typically enhances less than atelectatic lung
• Bronchial wall thickening
• Peripheral mass or nodule
• Cavitation
• Lymphadenopathy
60. Small Cell Carcinoma
• Small-cell carcinoma is a malignant epithelial tumor consisting of
small cells with scant cytoplasm, ill-defined cell borders, finely
granular nuclear chromatin, and absent or inconspicuous nucleoli.
Chest X ray
• Central mass
• Lymphadenopathy
• Peripheral nodule rarely.
61.
62. Large cell carcinoma
• Large-cell neuroendocrine carcinoma is defined as “a large-cell
carcinoma showing histologic features such as organoid nesting,
trabecular, rosette-like and palisading patterns that suggest
neuroendocrine differentiation and in which the latter can be
confirmed by immunohistochemistry or electron microscopy.
• It is an aggressive cell type of lung cancer that accounts for
approximately 9% of all lung carcinomas.
• These neoplasms are characterized by rapid growth and frequent
metastases at presentation.
63.
64. Lymphoma
• Focal or multi-focal nodules, masses, or consolidations
• Ground glass opacities, CT halo sign
• Air bronchograms (90%) ; bronchial stretching, narrowing or
dilatation; bubble-like lucencies; cavitation
• Reticular opacities
• Pleural effusion in up to 10% of cases
• Lymphadenopathy in 5–30% of cases
65.
66. Metastasis
• Bilateral multifocal well-defined nodules/masses; spherical morphology
• Variable size
• Multi-focal opacities with ill-defined borders; may mimic air space disease
• Most numerous in the lower lobes
• May exhibit associated hilar/mediastinal lymphadenopathy
• May exhibit associated pleural effusion
• Rarely ◦ Cavitation, ◦ Calcification ◦ Solitary nodule/mass ◦ Endobronchial
lesion; may exhibit atelectasis/consolidation ◦ Lymphangitic carcinomatosis