- Hemoptysis is the expectoration of blood from the respiratory tract below the level of the vocal cords. It can range from blood-streaked sputum to gross blood. It is classified as minor (<20mL/day), moderate (20-100mL/day), or massive (100-600mL/day).
- The bronchial arteries, which arise from the aorta, are responsible for 95% of hemoptysis cases as they have higher systemic pressure. The pulmonary arteries have lower pressure and carry only a small portion of cardiac output.
- Common causes of hemoptysis include tuberculosis, bronchiectasis, mycetoma, lung abscess, mitral stenosis, and
Hemoptysis is defined as coughing out blood.Definition, etiology,pathogenesis,diagnostic evaluation and management has been discussed in this power point presentation
Hemoptysis is defined as coughing out blood.Definition, etiology,pathogenesis,diagnostic evaluation and management has been discussed in this power point presentation
PATHOGENESIS OF BRONCHIECTASIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MED...Prof Dr Bashir Ahmed Dar
Dr Bashir Ahmed Dar associate professor medicine chinkipora sopore kashmir presently working in malaysia speaks about bronchiectasis.Bronchiectasis which is defined as the irreversible dilatation of the cartilage-containing airways bronchi or bronchioles.
Pleural effusion may be defined figuratively as the juice, oozing from the leaky lingerie of the lung. However the text book definition is the abnormal accumulation of fluid in the pleural space due to disturbances in the forces that keep the pleural fluid economy in equilibrium...
Atelectasis/Lung Collapse Part-1 by Dr Bashir Ahmed Dar Associate Professor M...Prof Dr Bashir Ahmed Dar
The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion.The incomplete expansion of lung may involve part of lung or entire lung.Most symptoms and signs are determined by the rapidity with which the collapse of lung occurs,the size of the lung area affected, and the presence or absence of complicating infection.
Rapid bronchial occlusion with a large area of lung collapse causes pain on the affected side, sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur.
Slowly developing atelectasis may be asymptomatic or may cause only minor symptoms. Middle lobe syndrome often is asymptomatic, although irritation in the right middle and right lower lobe bronchi may cause a severe, hacking, nonproductive cough.
DYSPNOEA IS DEFINED AS THE UNDUE AWARENESS OF UNPLEASANT BREATHING.WHEN THERE IS AMIS MATCH BETWEEN THE AFFERENT VENTILATORY SIGNALS AND THE EFFERENT RESPIRATORY SIGNALS IN THE BRAIN WE MAY GET AN UNIGNORABLE FEELING FOR NEED OF MORE AND MORE OXYGEN.
PATHOGENESIS OF BRONCHIECTASIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MED...Prof Dr Bashir Ahmed Dar
Dr Bashir Ahmed Dar associate professor medicine chinkipora sopore kashmir presently working in malaysia speaks about bronchiectasis.Bronchiectasis which is defined as the irreversible dilatation of the cartilage-containing airways bronchi or bronchioles.
Pleural effusion may be defined figuratively as the juice, oozing from the leaky lingerie of the lung. However the text book definition is the abnormal accumulation of fluid in the pleural space due to disturbances in the forces that keep the pleural fluid economy in equilibrium...
Atelectasis/Lung Collapse Part-1 by Dr Bashir Ahmed Dar Associate Professor M...Prof Dr Bashir Ahmed Dar
The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion.The incomplete expansion of lung may involve part of lung or entire lung.Most symptoms and signs are determined by the rapidity with which the collapse of lung occurs,the size of the lung area affected, and the presence or absence of complicating infection.
Rapid bronchial occlusion with a large area of lung collapse causes pain on the affected side, sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur.
Slowly developing atelectasis may be asymptomatic or may cause only minor symptoms. Middle lobe syndrome often is asymptomatic, although irritation in the right middle and right lower lobe bronchi may cause a severe, hacking, nonproductive cough.
DYSPNOEA IS DEFINED AS THE UNDUE AWARENESS OF UNPLEASANT BREATHING.WHEN THERE IS AMIS MATCH BETWEEN THE AFFERENT VENTILATORY SIGNALS AND THE EFFERENT RESPIRATORY SIGNALS IN THE BRAIN WE MAY GET AN UNIGNORABLE FEELING FOR NEED OF MORE AND MORE OXYGEN.
This slides gives you the Facts & Salient features of Liver Cysts / Interesting Case Reports covering Main Departments of Clinical side with Recent Advances made in the treatment of Liver cyst & Key points.
Management of Tetralogy of Falot - case presentation of a School going child presenting with central and peripheral Cyanosis, finger nail clubbing Grade IV with a history easy fatiguability and occasional Tet spells since the age of 2.
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.
- 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
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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. HEMOPTYSIS – definition
HEMOPTYSIS
• Expectoration of blood from da resp tract below da level
of vocal cords.
• can range from blood-streaking of sputum to the presence
of gross blood.
• Depending on da amount of blood loss, it has been
categorized… as minor, moderate, n massive.
3. Classification of hemoptysis
MINOR HEMOPTYSIS - bloodloss is 20ml/day
MODERATE HEMOPTYSIS – 20-100 ml/day
MASSIVE HEMOPTYSIS - 100- 600 ml/day
MASSIVE HEMOPTYSIS : bleeding is potentiallly life
threatening & blood loss is significant to compromise
resp function.
4. Anatomy
PULMONARY ARTERY :
entire cardiac output Low-pressure pulmonary
arteries & arterioles oxygenated in the pulmonary
capillary bed…………… Pulm @ only 5% of hemoptysis
BRONCHIAL ARTERY: higher systemic pressure but carry a
small portion of the cardiac output. Arise from aorta.
Nutitional source to airways, n lungs.
95% of hemoptysis.
5. D/D of HEMOPTYSIS
diff, from hemoptysis from other causes …
R/o NON PULMONARY like upper resp tract bleeding,
Bleeding from GI tract.
Alkaline pH, frothy, or the presence of pus may sometimes
suggest the lungs as the primary source of bleeding
differenciate hemoptysis from hemetemisis
7. Past HISTORY
Is there a history of prior lung, cardiac, or renal disease?
Is there a history of cigarette smoking?
Has the patient had prior hemoptysis, other pulmonary
symptoms, or infectious symptoms?
Is there a family history of hemoptysis or brain aneurysms
(suggesting hereditary hemorrhagic telangiectasia)?
Is there a history of skin rash? (Vasulitis, SLE)
What is the patient's travel history?
8. Previous HISTORY
Is there a history of bleeding disorders or use of
aspirin, NSAIDS, or anticoagulants?
Is there a history of upper airway or upper G.Icomplaints
or diseases?
Is pt having any liver disease.
9. Physical Examination
Skin rash -- vasculitis, systemic lupus erythematosus, fat
embolism, or infective endocarditis.
Telangiectasias -- hereditary hemorrhagic telangiectasia
Splinter hemorrhages -- endocarditis or vasculitis.
Clubbing is nonspecific, since it can occur in many chronic
10. Physical Examination
Audible chest bruit or murmur that increases with
inspiration -- large pulmonary AV malformations .
Cardiac murmurs -- congenital heart disease,
endocarditis with septic emboli, or mitral stenosis.
Legs should be examined carefully for possible deep
venous thrombi.
13. Tuberculosis
Active tubercular pneumonitis-
bronchiolar erosion
Rupture of Rasmussen’s aneurysm
(pulm. art)
Healed calcified LNE-eroding through
bronchial arteries into airway
Scar carcinoma
Development of bronchiectasis
Mycetoma formation
14. Bronchiectasis
Pathologically it is destruction of the
cartilaginous support of bronchial wall
and bronchial dilatation owing to
parenchymal retraction from alveolar
fibrosis
ANATOMICAL CHANGES:
o Bronchial artery hypertrophy
o Expansion of peribronchial & sub
mucosal bronchiolar arteriolar plexus
o Augmentation of anastomoses with
the pulmonaryarterial bed
16. MYCETOMA
Mechanical trauma of the vascular
granulation tissue by the movement of
the fungal ball in the cavity
Vascular injury from aspergillus
associated endotoxin
Aspergillus related proteolytic activity
Vascular damage from a type 3
hypersensitivity reaction
19. Lung abscess
Due to necrotizing effect of primary
infection and the inflammation that
involves pulmonary vasculature
20. MITRAL STENOSIS
Before valvotomy and mitral valve
replacement hemoptysis occurred in
20-50% of patients
In M.S - Lt atrial pressure – pulm veins
-pulmonary capillary bed-if pressure
exceeded inthe rt. atrial pressure-
blood flows in the retrograde direction
in the bronchial veins through the
bronchopulmnary anastomosis
21. carcinoma
83% with hemoptysis – squamous ca.
centrally located ,48% cavitate
Mechanism:
necrosis and inflammation of vessels
within tumour bed
Direct tumor invasion of the pulmonary
vasculature is rare
23. LOCALIZATION
o Physical examination and chest x-ray
were equivocal and not helpful in 55%-
60% of patients
o This poor localization of bleeding
reflects the fact that blood may be
widely distributed in the lung by
coughing
24.
25. LOCALIZATION
Early bronchoscopy :(48 hrs)
o Diagnostic yield is higher
o Likely hood of localizing site is more
o Accurate localization may direct
therapeutic interventioin
CT chest during active bleeding may be
misleading because aspirated blood
may mask underlying pathology or
incorrectly appear as a parenchymal
mass
26. CT Scan
o Use of early chest CT to help localize
the bleeding site and diagnose the
cause of hemoptysis
o The advantage of CT –diagnosing
bronchiectasis, lung abscess, and mass
lesions, including cancer, mycetomas,
and AVM’S
o The disadvantage of chest CT
diff in shiftin pt from ICU
27. LOCALIZATION
RBC SCAN
o Tc 99m-sulfur colloid isotope-labeled
RBC
o Reserved for the patients in whom
bronchoscopy couldn’t be performed
BRONCHOGRAPHY: replaced by HRCT
28. bronchoscopy vs HRCT
o Fiberoptic bronchoscopy and HRCT , each with
specific advantages in certain clinical situations
o HRCT picks all tumors seen by bronchoscopy
as well as several which were beyond
bronchoscopic range. On the other hand, HRCT
could not detect bronchitis or subtle mucosal
abnormalities which could be seen by
bronchoscopy
o HRCT was useful in diagnosing bronchiectasis
and aspergillomas, while bronchoscopy was
diagnostic of bronchitis and mucosal lesions
such as Kaposi's sarcoma
29. MANAGEMENT
o Adequate airway protection, ventilation,
and cardiovascular function
o Intubate if pt. has poor gas exchange,
rapid ongoing hemoptysis, hemodynamic
instability, severe SOB.
o protection of the nonbleeding lung
o Spillage of blood into the non-bleeding
lung can either block the airway with clot
or fill the alveoli and prevent gas
exchange.
o Need to know site of bleeding
30. MANAGEMENT
o Place bleeding lung in the dependant
position
o Selectiely intubate the nonbleeding
lung.
o Placement of a double lumen ETT
specially designed for selective
intubation of the right or left mainstem
bronchi
33. Bronchoscopic measures
BRONCHIAL IRRIGATION:
o Cold saline lavage (4c)
o Colon et al studied 25 pts
Bleeding stopped in 23 patients,,
2 patients rebleed
VASOCONSTRICTIVE AGENTS:
o Topical epinephrine (1:2000)
o Intravenous vasopressin
34. Bronchoscopic measures
ELECTROCAUTERY
ARGON PLASMA COAGULATION
BRONCHOSCOPIC BRACHYTHERAPY
TOPICAL COAGULANTS:
o Tsukamoto et al- 19 pts-
o 60% hemostasis with topical thrombin
o 100% - fibrinogen-thrombin solution
(re bleeding in 1 pt)
35. LASER COAGULATION
o Nd –YAG laser therapy for endobronchial
tumors
o Thermal effects vaporizes the superficial
layers and coagulate the deeper layers
o Seal vessels upto 1.5mm in diameter but
larger vessels maynot be adequately
controlled
o Even highly vascular tumors have a
propensity to bleed when subjected to
laser therapy
36. BALLOON TAMPONADE
o 4 Fr 100 cm Fogarthy balloon catheter
placed by the fibreoptic bronchoscope
and is inflated in the segmental and
sub segmental bronchus
o Inflated for 24-48 hrs
Advantages:
o Allows gas exchange
o Supports patient before embolization
or surgery
37. BALLOON TAMPONADE
o Disadvantages:
Ischemic mucosal injury
Post obstructive pneumonia
o Saw et al- 6/10 patients effective .
No rebleeding for 6wks- 9 months
o Swersky et al- 4/4 pts- effective.
Rebleeding in 2 pts
39. EMBOLIZATION
Alternative to surgery in pts with
bilateral disease, multiple bleeding
sites and borderline pulmonary reserve
o Halted active bleeding and stabilized
patients in 84-100%
o Long-term control of bleeding after
embolization range from 70%-88% with
f/u period of 1- 60 m
40. EMBOLIZATION
COMPLICATIONS:
o Chest pain-(24-91%)
o Dysphagia-(0.7-18.2%)
o Subintimal dissection of aorta or
bronchial artery
o Bronchoesophageal fistula
o Reflux of embolic material into systemic
circulationnecrosisofsmallbowel,occlusion
ofanterior tibial artery,seizure
41. SURGERY
• Conservative management of massive
hemoptysis carries a mortality rate of
50-100%
o Mortality rate for surgery performed
for massive hemoptysis- 7.1-18.2%
o However mortality rate increases
significantly upto 40% when surgery is
undertaken as an emergency procedure
42. SURGERY
SURGERY IS PROCEDURE OF CHOICE
o BRONCHIAL ADENOMA
o ASPERGILLOMA RESISTANT OT OTHER
TREATMENT
o HYDATID CYST
o THORACIC VASCULAR INJURY
43. Sx - contraindications
o Unresectable carcinoma
o Inability to lateralize the bleeding site
o Diffuse disease
Multiple AVM
Cystic fibrosis
o Arterial hypoxia
o Co2 retention
o Dyspnea at rest
44. Sx - complications
o Morbidity-23-54%
o Post- op BPF-10-14%
o Empyema
o Hemorrhage requiring re-exploration
o Hemothorax
o Resp insufficiency req proloned vent
o Mortality-10-50%
o -Gourin & garzon’s study:37% of active
bleeding died in comparision with 8%