This document discusses acute respiratory distress syndrome (ARDS). It defines ARDS as acute lung injury caused by severe pulmonary damage that results in fluid leakage into alveoli. ARDS can be directly caused by lung issues or result from systemic problems. Chest X-rays show diffuse bilateral opacities in ARDS. While CT scans reveal ground-glass opacification and consolidation. The appearance on imaging depends on the early or late stage. Severity is graded based on the Ichikado CT scoring system from 1 to 6. Understanding the underlying cause and appearance on tests helps manage ARDS.
ALL THE QUESTIONS ARE HAVING VERY STANDARD ANSWERS FROM THE STANDARD BOOKS)
REF : ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE.
COMPREHENSIVE IMAGE BASED REVIEW OF PATHOLOGY BY SONI .
GARG & GUPTA PATHOLOGY REVIEW & GENETICS.
ALL THE QUESTIONS ARE HAVING VERY STANDARD ANSWERS FROM THE STANDARD BOOKS)
REF : ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE.
COMPREHENSIVE IMAGE BASED REVIEW OF PATHOLOGY BY SONI .
GARG & GUPTA PATHOLOGY REVIEW & GENETICS.
A concise presentation on clubbing. Can be used for revising or presenting or for teaching purposes.
PS: You may use this presentation without any restriction.
In this presentation all images of Chapter 18 from Grainger and Allison have been discussed.
Our aim is to discuss authentic material .
This is only for educational purposes.
In this chapter air space infilteration have been discussed. Ground glass haze and consolidation are discussed in detail.
A concise presentation on clubbing. Can be used for revising or presenting or for teaching purposes.
PS: You may use this presentation without any restriction.
In this presentation all images of Chapter 18 from Grainger and Allison have been discussed.
Our aim is to discuss authentic material .
This is only for educational purposes.
In this chapter air space infilteration have been discussed. Ground glass haze and consolidation are discussed in detail.
Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid resulting in severe dyspnoea, hypoxemia and diffuse pulmonary infiltrates.
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
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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
2. ARDS
• Acute respiratory distress syndrome (ARDS) is
a form of acute lung injury and occurs as a
result of a severe pulmonary injury that
causes alveolar damage heterogeneously
throughout the lung.
• It can either result from a direct pulmonary
source or as a response to systemic injury.
3. Neonatal respiratory distress
syndrome
• This is a distinct entity from neonatal
respiratory distress syndrome, which is caused
by surfactant deficiency in premature babies.
4. ARDS mimics Acute intersitial
pneumonitis
• ARDS has a similar clinical presentation and
histological features of those seen in acute
interstitial pneumonitis (AIP), showing extensive
diffuse alveolar damage (DAD)
• Both conditions likely represent the same
pathology, with AIP probably accounting for
some of the idiopathic cases of ARDS.
5. Pathology ARDS
• Lung damage results in leakage of fluid into alveoli, so
decreased arterial oxygenation.
• lung injury of acute onset, within one week of an apparent
clinical insult and with the progression of respiratory
symptoms
• bilateral opacities on chest imaging not explained by other
pulmonary pathology (e.g. pleural effusion, pneumothorax, or
nodules)
• respiratory failure not explained by heart failure or volume
overload ( heart size is normal on xray)
• decreased arterial PaO2/FiO2 ratio
– mild ARDS: 201-300
– moderate ARDS: 101-200
– severe ARDS: ≤100
6. History
• History and etymology
• It was first described in 1967 by Dave G
Ashbough
• Hall mark of ARDS
• Increased alveolar–capillary permeability to
fluid, proteins, neutrophils and red blood
cells (resulting in their accumulation into the
alveolar space)
10. ARDS on plain Chest Xray
• Chest radiographic findings of acute respiratory
distress syndrome are non-specific and resemble
those of typical pulmonary edema or pulmonary
hemorrhage
• There are diffuse bilateral coalescent opacities
• The time course of ARDS may help in
differentiating it from typical pulmonary edema.
11. Chest xray– B/L diffuse pulmonary
opacity
• Chest x-ray features usually develop 12-24
hours after initial lung insult as a result of
proteinaceous interstitial edema
• Within one week, alveolar pulmonary edema
(hyaline membrane) occurs due to type 1
pneumocyte damage.
12. ARDS vs Cardiogenic lung oedma
• In contrast to cardiogenic pulmonary edema,
which clears in response to diuretic therapy,
ARDS persists for days to weeks
• Also, as the initial radiographic findings of
ARDS clear, the underlying lung appears to
have a reticular pattern secondary to type 2
pneumocyte proliferation and fibrosis
13. ARDS on CT
• bilateral symmetrical changes is more
common in extrapulmonary ARDS and
asymmetrical in pulmonary ARDS
• ground-glass opacification: a non-specific sign
In acute ARDS likely represent edema and
protein within the interstitial and alveolar
spaces
• bronchial dilatation within areas of ground-
glass opacification
14. ARDS on CT—early & late phase
• Early phase—pulmonary opacification with
dense consolidation in most dependent region
merging into background ground glass
attenuation
• Non dependent region is either normal or
hyperextended
15. Why inhomogeneous appearance
• increased weight of overlying lung
causing compressive atelectasis posteriorly,
which produces dense opacification
• supported by the fact that with the positional
change from supine to prone, the density
gradient can quickly redistribute accordingly
• In the non-dependent portions, the lung may
be of normal attenuation, or it may be lower if
mechanically ventilated.
16. Late phase-- variable
• Complete resolution: may occur in some cases
• coarse reticular pattern and ground-glass
opacification in the anterior (non-dependent)
part of the lungs: considered more typical
later-stage CT appearances
• areas of mixed reticular and ground-glass
opacification
• pulmonary cysts or bullae of varying
sizes (probably develop as a result of
prolonged ventilation)
17. Ichikado CT scoring of ARDS-1-6
• normal attenuation --grade 1
• ground-glass attenuation --grade 2
• airspace consolidation– grade 3
• ground-glass attenuation with traction
bronchiolectasis or bronchiectasis grade 4
• airspace consolidation with traction
bronchiolectasis or bronchiectasis grade 5
• Honeycombing grade6
22. CT score ARDS
• To calculate the overall "CT score", each lung zone
(upper, middle, lower) are interrogated, and the
extent of each CT finding is estimated to the nearest
10%. Then that percentage of CT finding (should be
100% in each zone) is multiplied by the CT findings
point scale and this results summed for each zone.
There should be one of the scores for each zone,
which are then summed to calculate a final "CT
score" Overall CT scores of survivors were
significantly lower than those of nonsurvivors (P =
0.0003). Also, the CT score was independently
associated with mortality.