This document discusses various causes of stridor and laryngeal obstruction in infants and children. It covers congenital lesions like laryngomalacia, subglottic hemangioma, and subglottic stenosis. It also discusses acquired causes such as laryngotracheobronchitis (croup), epiglottitis, diphtheria, and tuberculosis. For each condition, it describes the etiology, clinical features, diagnosis, and treatment. Physical examination findings and appropriate investigations are emphasized for assessing patients with stridor.
these emergencies often present to family practitioner...
some are trivial to the medical professional but are serious for the patient, while most are acute emergencies that require prompt referral and management to prevent further complications
pictures taken from google images...
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.
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
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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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
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
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
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The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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2. Stridor
Abnormal high pitched noisy respiration due to flow of air
through a partially obstructed narrowed lower airway
mainly larynx and tracheobronchial tree
Types
Inspiratory – supraglottis, glottis, hypopharynx
Expiratory (wheeze) – thoracic trachea, bronchi,
bronchioles
Biphasic – cervical trachea, subglottis
Stertor – snoring low pitched noise due to obstruction in
nasopharynx and oropharynx
Rales and crepitations – distal portion of bronchial tree
and alveoli
13. Laryngomalacia
Congenital laryngeal stridor
Excessive flaccidity of supraglottic larynx which gets
sucked in during inspiration producing stridor and
sometimes cyanosis
Pathology
Excessive softening of laryngeal skeletal framework ->
indrawing of aryepiglottic folds -> narrowing -> stridor
14. Clinical features
M:F 2:1
Low socio economic group
Intermittent low pitched inspiratory stridor develops
during first two weeks of life (rare at birth)
Aggravates on crying, feeding, exertion
Relieved in prone position, rest and sleep
Seen maximum at 9-12 months of age
Completely disappears after 2 years of age (5 years)
Normal cry and voice
In severe cases – feeding difficulty, failure to thrive and
cyanosis
15. Signs
Awake flexible laryngoscopy
Anterior collapse of arytenoid
Posterior collapse of epiglottis
Inward collapse of aryepiglottic folds
Omega shaped/tubular epiglottis
Prominent arytenoids
Normal vocal cords
16. Complications – GERD, recurrent URTI, OSA
D/D – laryngeal webs, cysts
Treatment
Conservative (90%)
- Reassurance
- Observation
- Treat the URTI
Tracheostomy
Surgery (10%) – when failure to thrive or cyanosis
- Supraglottoplasty (Aryepiglottoplasty)
17. Congenital laryngeal haemangioma
Subglottic haemangioma
Benign vascular malformation involving subglottis
C/F
Females mc
Asymptomatic for 3 to 6 months of age
With increase size progressive disease
Inspiratory or mostly biphasic stridor which is progressive
Appears with URTI
Aggravated by crying or agitation
Dyspnoea and cyanosis
Associated with cutaneous haemangioma or mediatinal
haemangioma
Rapid growth till 1 year of age then regress
18. Diagnosis
X Ray Neck – soft tissue seen
CT Scan/MRI with contrast – mass in larynx
DL Scopy – Reddish blue mass in subglottis
Biopsy
Treatment
Observation
Antibiotics and anti inflammatory
Steroids –IV dexamethasone, intra lesional
Intubation/tracheostomy
Resection – Co2 and KTP lasers/laryngofissure
19. Congenital subglottic stenosis
Abnormal thickening of cricoid cartilage or fibrous tissue
below the vc
Here subglottic diameter in full term <3.5 – 4 mm (normal
4.5 – 5.5 mm) and in preterm 3 mm (normal 3.5mm)
C/F
Evident after 1st week of life with URTI
Biphasic stridor
Dyspnoea
Normal cry
Grading I - <50% obstruction, II – 51-70% obstruction, III
– 71-99% obstruction, IV – no detectable lumen..
20. Diagnosis
X Ray Neck, CT/MRI
Bronchoscopy/MLS/DL Scopy
Treatment
Observation – improves as larynx grows
II/III/IV – tracheostomy
Excision – laser (Co2/KTP), Laryngotracheoplasty
21. Laryngeal web
Web formation most commonly in anterior part of larynx
due to arrest of development of larynx most commonly
seen in glottis (between vc)
C/F
Since birth
Small webs – asymptomatic
Inspiratory stridor
Dyspnoea or apnoea
Weak cry
Hoarseness
IDL – seen b/w anterior end of vc with concave sharp
posterior margin
22. D/D
From acquired web due to trauma or infection
Treatment
Excision by Laser/knife or laryngofissure
23. Acute epiglottitis
Supraglottic laryngitis
PAEDIATRIC
Marked oedema of epiglottis obstructimg the airway
Etiology
H influenza type B
Age – 2 to 7 years
Not in newborn as maternal immunity
Pathology
Severe cellulitis
Thick secretions
24. C/F
Rapid progress to respiratory distress within ½ hour
Abrupt onset and rapid progression
High grade fever (>40 C)
Dysphagia and odynophagia
Drooling of saliva
Hoarseness
Muffled (hot potato) voice
Tripod position- leans forward supporting on upper limb
Inspiratory stridor which increases in supine position
Retraction, nasal flaring, cyanosis, septicaemia
Pharynx is congested
25. Diagnosis
No tongue depressor/IDL
Examine in OT
Red and swollen (cherry red) epiglottis – sun rise sign
Oedema and congestion of supraglottis
X Ray Neck – swollen epiglottis – thumb sign
Throat swab
Blood culture
Leucocytosis
26. Complications
5-10% mortality
Reflux laryngospasm
Cardio-respiratory arrest
Otitis media
Pneumonia
Pericarditis
Meningitis
Prevention
Hib vaccine in children
27. Treatment
Hospitalization in ICU
Complete bed rest and voice rest
Intubation/tracheostomy under GA
Antibiotics- ampicillin, cephalosporins
IV fluids
IV steroids
Oxygen
28. Adult supraglottitis
Less severe
Marked oedema of supraglottis
Etiology
H Influenza, streptococci, staphylococci
C/F
Sore throat
Dysphagia
Pale oedematous supraglottis
Stridor
Treatment
Antibiotics, steroids, anti reflux treatment
Tracheostomy if needed
29. Acute laryngotracheobronchitis
Subglottic croup
Most common cause of infectious resp obstruction in
children
Etiology
Viral – parainfluenza I,II
Influenza A,B
Other viruses – myxovirus, adenovirus
Secondary bacterial infection
Males>females
Age group 3 months to 5 years of age
Involves subglottis (mc), trachea and bronchi
h/o URTI always
31. Diagnosis
Leucocytosis
X Ray Neck – tapered narrowing of subglottis –
steeple’s sign, wine bottle appearance – bottle sign
Chest X Ray – pneumonic patches
Flexible laryngobronchoscopy – subglottic narrowing
32. Treatment
Hospitalization
Humidification- soften crusts and thick secretions
Steam inhalation
Antibiotics
Oxygen
IV fluids
Steroids
Mucolytics – bromhexine
Nebulization with racemic adrenaline
Intubation/tracheostomy – if needed
Bronchoscopy – to remove secretions
33. Acute simple/non specific laryngitis
Acute inflammation of laryngeal mucosa of mild form
Etiology
Infections – URTI, tonsillitis, rhinitis or rhinosinusitis
First viral later bacterial
GERD
Allergy
Voice abuse
Burns
Trauma (endotracheal intubation)
More severe in children as subglottic area is narrower
34. Pathology
Hyperaemia of larynx
Formation of pseudo membrane
C/F
Abrupt onset
Hoarseness
Dysphonia
Pain throat
Fever
Dry cough worst at night
Stridor in children
Erythema and oedema of epiglottis, arytenoids and ventricles with
normal vocal cords earlier with later hyperemia of vc and subglottis
Pharyngeal and nasal congerstion
35. Treatment
Bed rest
Voice rest
Soft bland diet
Avoid smoking and alcohol
Steam inhalation with inhalant capsules
Cough sedatives
Antibiotics – cephalosporin, amoxy clav
Steroids
Anti reflux treatment
Tracheostomy/intubation if needed in childrens
36. Laryngeal diptheria
Etiology
Corynebacterium diptheriae
Secondary to faucial diptheria
Age < 10 years
Both sexes
Pesudomembrane formation
Exotoxins liberated
38. Complications
Cardiac – myocarditis, circulatory failure
Neurogenic – paralysis of palate, larynx and pharynx
Asphyxia and death due to airway obstruction
Diagnosis
Clinical
Throat swab
Smear and culture
39. Treatment
Diptheria anti toxin – 20000 to 100000 units IV as a
single saline infusion after test dose
Antibiotics – benzyl pencillin, erythromycin
Complete bed rest for 2 to 4 weeks
Oxygen
Steroids
IV fluids
DL Scopy for removal of diptheritic membrane
Intubation/tracheostomy
40. Tubercular laryngitis
Etiology
Mycobacterium tuberculosis
95% cases secondary to pulmonary TB, 5% primary
Route – infected sputum to larynx (mc), lymphatic,
haematogenic
Males (mc)
Age gp 20 – 40 years
Involves posterior part of larynx (mc – interarytenoid
region)
41. C/F
Weak voice
Hoarseness
Odynophagia and dysphagia
Hemoptysis
Hyperaemia of vc
Impaired adduction of vc
Mouse nibbled appearance of vc/ moth eaten appearance
due to ulcers
Pseudo edema of epiglottis – turban epiglottis
Bowing of vc
46. C/F
Hoarseness – worst in morning due to dryness of mouth
Constant clearing of throat
Throat discomfort/ FB sensation
Dry and irritating cough
Hyperaemia of larynx, vc dull red
Viscid secretions at vc and interarytenoid region
D/D – chronic specific laryngitis
Diagnosis – X Ray PNS/Chest X Ray, throat swab, flexible
laryngoscopy/biopsy
47. Treatment
Treat infections
Life style modifications for LPR
Avoid smoking, alcohol
Voice therapy/voice rest
Steam inhalation
Expectorant
Treat allergy
Steroid topic inhalers
Surgical – MLS, stripping of vc (one vc at a time)
48. Pachyderma laryngitis
Chronic lartyngitis affecting posterior part of larynx
Interarytenoid region, post vc
Males
Etiology
Alcohol, smoking, GERD
C/F
Hoarseness, irritation in throat
Symmetrical red grey granulations or whitish mass on both
vc (post part) and interarytenoid region, ulcer
Diagnosis – biopsy
Treatment – removal of granulations, anti reflux, speech
therapy
49. Atrophic laryngitis
Laryngitis sicca
Atrophy of laryngeal mucosa with crust formation associated
with atrophic rhinitis and pharyngitis
Females
C/F
Hoarseness of voice which improves on coughing and removal of
secretions
Dry irritating cough, dyspnoea
Atrophic mucosa covered with crusts which bleed on removal
Treatment – humidification, loosening of secretions (laryngeal
sprays containing glucose in glycerine, expectorants)
50. Lupus of larynx
Indolent tubercular infection associated with lupus of nose
and pharynx due to increased host resistance or decreased
bacterial virulence involving anterior parts of larynx
Epiglottis
Females
C/F
Painless, asymptomatic, no pulmonary TB
Scattered yellowish pink nodules in epiglottis which can
ulcerate
Complications – perichondritis, cartilage destruction
Treatment - ATT