Interstitial lung disease (ILD) is a term that includes over 150 chronic lung disorders where the lung tissue becomes damaged, inflamed, and scarred. This makes it difficult for oxygen to travel into the bloodstream, causing shortness of breath and cough. Idiopathic pulmonary fibrosis is a chronic, progressive ILD of unknown cause where lung tissue becomes thickened and stiff. Sarcoidosis is a systemic disease characterized by non-caseating granulomas that commonly involves the lungs, causing inflammation and fibrosis. It has various stages of involvement and generally improves spontaneously but can progress in 15% of patients.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
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.
A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
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.
A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
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.
Interstitial lung diseases (ILDs) are a group of more than 200 different disorders that cause scarring in the lungs. Scar tissue in the lungs can make it harder for you to breathe normally. In ILDs, scarring damages tissues in or around the lungs’ air sacs and airways.
My Goals::::
1-Relationship of thorax to neck .
2-relationship of thorax to upper limb.
3-relationship of thorax to breasts : pleural cavity - pleural and Lung .
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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 Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
2. Definition & Background
Interstitial lung disease (ILD) is a common term that includes more
than 150 chronic lung disorders. When a person has ILD, the
lung is affected in three ways. First, the lung tissue is damaged
in some known or unknown way. Second, the walls of the air
sacs in the lung become inflamed. Finally, scarring (or fibrosis)
begins in the interstitium (or tissue between the air sacs), and
the lung becomes stiff.
When the interstitium becomes scarred and thickened, it is much
more difficult for oxygen to travel from the air into the
bloodstream. Patients with interstitial lung disease, then, will
develop symptoms which are the result of lung malfunction,
like shortness of breath and cough.
3. The terms interstitial lung disease, pulmonary fibrosis, interstitial
pulmonary fibrosis, and diffuse parenchymal lung disease often
used to describe the same condition.
Classification:
“Known” vs. “Unknown”
-”without” or “with” granulomas
4. Examples of Known Etiology: without granulomas
ARDS
Occupational and environmental inhalants
(e.g. asbestos, gases, aerosols)
Drugs
Aspiration
Radiation
Lymphangitic spread of carcinoma
5. Examples of Known Etiology: with granulomas
Occupational and environmental inhalants
-Beryllium
-Hypersensitivity pneumonitis (an allergic disorder)
- Talc
Infectious agents
- AFB (Acid-fast bacillus)
- Fungi
9. Signs & Symptoms
The most common symptoms are shortness of breath
with exercise and a non-productive cough. Some patients
may also have fever, weight loss, fatigue, muscle and
joint pain, and abnormal chest sounds,
depending upon the cause.
Clubbing can also be seen.
10. -PFT usually shows a restrictive pattern
-The FEV1/FVC ratio is usually normal
-It shows reduced lung volumes (low vital capacity, low total lung
capacity)
Pulmonary Function Test
Arterial blood gases typically show mild hypoxemia.
Patients tend to hyperventilate and have a reduced PCO2 and
compensated respiratory alkalosis, mostly as a result of increased
respiratory rate.
11. Check Medications
Immunosuppressive or chemo agents
- Bleomycin, methotrexate, cyclophosphmide
Antibiotics
- Macrobid
Cardivascular drugs
- Amiodarone
Vasoactive and neuroactive
- Sansert and dilantin
12. Occupational ILD
There are 3 categories of occupational lung disease
1. Hypersensitiviy pneumonitis
2. Organic dusts (byssinosis)
3. Inorganic dusts (asbestosis, silicosis, coal workers’
pneumoconiosis, and berylliosis)
14. Idiopathic Pulmonary Fibrosis
Definition: (IPF) is an inflammatory lung disease of unknown origin
that causes lung fibrosis and restrictive lung disease. It
characteristically involves only the lung and has no extrapulmonary
manifestations except clubbing. Typically seen in decade 5 of life, it
affects men and women equally.
Etiology uncertain (autoimmune?) It is a diagnosis of
exclusion
Accounts for 50% of ILD’s
Male = female, average age = 55
Smoking worsen disease
10% may have low titers of ANA or RF
15.
16.
17. IPF presentation
Dyspnea and cough and diffuse infiltrative process on CXR
Clubbing is common
History of progressive exercise intolerance
Dry crackles at lung bases
Like many ILD’s, PFT’s show a “restrictive” pattern (low TLC,
normal FEV1/FVC, low DLCO)
Treatment: corticosteroids + or – cyclophosphamide or
azathioprine (20-30% of patients show improvement. This
disease progresses to death. Single-lung transplantation is an
option for some late-IPF patients. Pneumococcal and influenza
vaccines should be given.
18. Diagnosis :
Chest x-ray reveals reticular or reticulonodular disease.
High-resolution CT may show ground-glass
appearance. As IPF progresses, imaging will show
extensive fibrosis with honeycomb pattern.
confirmed in about 25% of patients by transbronchial
biopsy. If transbronchial biopsy is not sufficient, a
thorascopic-guided lung biopsy or open lung biopsy
should be done-especially when there is any
suggestion that there may be an infection involved or
in younger patients.
Note : lung biopsy to exclude vasculitis and infections
19. Treatment :
Pharmacologic treatment: includes pirfenidone, a new
small-molecule compound that has antifibrotic effects
(shown to significantly reduce a decline in lung
function and IPF disease progression) also
corticosteroids + or – cyclophosphamide or
azathioprine (20-30% of patients show improvement.
This disease progresses to death
Non-pharmacologic treatment for eligible patients
includes lung transplantation (shown to reduce the risk
of death by 75% as compared with those who remain
on the waiting list).
20. Sarcoidosis
A disease characterized by the presence of granulomatous tissue.
This is a systemic disease which involves eyes, brain, heart, lungs, bones and
kidneys, skin, liver and spleen.
On pathology a non-caseating granuloma composed of histiocytes, giant
cells and lymphocytes.
In advanced lung disease fibrotic changes are seen.
21. Clinical presentation :
Hypercalcemia or hypercalciuria due to increased
circulation of vitamin D produced by macrophages
• Elevated angiotensin-converting enzyme (ACE) (60% of
patients)
• Abnormalities in LFTs (30% of patients with liver
involvement, with 90% of patients being symptomatic)
• Skin anergy
• PFTs normal or showing a restrictive pattern
• Uveitis and conjunctivitis (>25% of patients) (give all
patients with suspected sarcoidosis an ophthalmologic
examination)
22. Etiology
Unknown, likely immunological basis.
Clinical Features
Four stages are identified:
Stage 0: No obvious intrathoracic involvement
Stage 1: Bilateral hilar lymphadenopathy, often
accompanied by arthritis, uveitis and erythema
nodosum.
Stage 2: Pulmonary parenchyma is also involved,
changes in mid and upper zones.
Stage 3: Pulmonary infiltrates and fibrosis without
adenopathy.
25. Risk factor :black people , 20-40 age
Sarcoidosis can involve almost any organ system, but pulmonary
involvement is most common. Ocular, cutaneous, myocardial,
rheumatologic, GI, and neurologic manifestations can also occur.
Dermatologic manifestations occur in 25% of patients with
sarcoidosis; they include lupus pernio, erythema nodosum, non-
scarring alopecia, and papules. Commonly, sarcoidosis is
discovered in a completely asymptomatic patient, usually in the
form of hilar adenopathy on chest x-ray.
There are 2 distinct sarcoid syndromes with acute presentation:
• Lofgren syndrome includes erythema nodosum, arthritis, and
hilar adenopathy.
• Heerfordt-Waldenstrom syndrome describes fever, parotid
enlargement, uveitis, and facial palsy.
28. Lung involvement in sarcoidosis occurs
in 90% of patients at some time in their
course. Hilar and left paratracheal
adenopathy is the most common
presentation. Interstitial lung disease
with or without hilar adenopathy can
also be a presentation of sarcoidosis.
29. Diagnosis :
The definitive diagnosis of sarcoidosis rests on biopsy of
suspected tissues, which show noncaseating granulomas.
Chest x-ray findings can show 4 stages of disease (the
stages are not progressive):
• Bilateral hilar adenopathy
• Hilar adenopathy with reticulonodular parenchyma
• Reticulonodular parenchyma alone
• Honeycombing of bilateral lung fields with fibrosis
Transbronchial biopsy
30. Pulmonary Function
No impairment occurs in stages 0 and 1.
In stages 2 and 3 restrictive changes are seen.
Treatment and Prognosis
85% of these patients improve spontaneously, but 15% may develop
progressive fibrosis and respiratory failure.
31. Treatment :
Generally in the setting of organ impairment, a trial of
steroids may be used, giving a high dose for 2 months
allowed by tapering the dose over 3 months. There are
certain scenarios in which steroids are mandatory: uveitis,
sarcoidosis involving the CNS and heart, and patients who
develop hypercalcemia. (Prednisone 0.5- 1 mg/kg initially,
then tapered and continued for 6 months to 1 year.)
Eighty percent of patients with lung involvement from
sarcoidosis remain stable, or the sarcoidosis
spontaneously resolves. Twenty percent of patients
develop progressive disease with evidence of end-
organ compromise.
