This document discusses hyphema, which is blood in the anterior chamber of the eye. It defines hyphema and lists its potential causes such as trauma, medical conditions, and surgeries/medications. The document outlines methods for grading hyphema based on the amount of blood in the anterior chamber. It also discusses the clinical features, workup, potential complications like increased eye pressure, and treatment approaches like medical management with anti-inflammatory drugs and surgery if needed to prevent complications. The prognosis depends on factors like the severity of hyphema and any associated eye damage.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Glaucoma types, Pathogenesis, Diagnosis and TreatmentPranatiChavan
Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field.
There are two major types of glaucoma: open-angle glaucoma, which accounts for most cases and closed-angle glaucoma.
this tells about the overview of glaucoma and the primary open angle glaucoma
valve surgery and cyclodestruction surgery are not listed, however they are important
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
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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
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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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
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.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
5. PATHOGENESIS
Mechanism
Direct contusive force that causes antero-
posterior compression and equatorial expansion
leads to mechanical tearing of blood vasculature of
iris, ciliary body and TM.
Concussive force creating rapidly rising IOP with
in the vessels resulting in rupture of vessels
Penetrating injury leads to hyphema by
damaging the blood vessels and due to hypotony
6. GRADING
Grade 1: < 1/3th of AC
Grade 2: 1/3th
-1/2 of AC
Grade 3: > ½ of AC
Grade 4: Total
7. CLINICAL FEATURES
Blurring of vision
Photophobia
Pain
Headache
Blood or clot or both in the AC
Mean duration of elevated IOP is 6 days
Duration in uncomplicated hyphema is 5-6 days
8. WORK-UP
History
Mechanism of injury
Time of injury
H/o medication (Aspirin, Warfarin)
H/o Sickle cell disease
H/o Coagulopathy – bleeding gums, epistaxis
Examination
Rule out any rupture globe or penetrating injuries
Visual acuity
IOP
Slit lamp
B scan (gently)
CT scan - suspected orbital floor # or IOFB
9. COMPLICATIONS
Increased IOP:
Occlusion by clot, inflammatory cells, erythrocytic debris
Pupillary block due collar button shaped clot
Peripharal anterior synechiae: if hyphema > 01 week
Optic atrophy:
IOP > 50 mmHg for 5 days or >35 mmHg for 7 days.
Contusion to the optic nerve
Secondary to damage to short posterior ciliary arteries.
Sickle cell disease even at normal IOP
Secondary haemorrhage (rebleed): usually occurs after
day 4
Increase in size of hyphema
Layer of fresh RBCs over previous clot
Change of colour from dark red to bright red.
10. COMPLICATIONS
Corneal blood staining:
Factors which influence corneal blood staining:
Rebleeding
Prolonged clot duration
Sustained increase in IOP
Corneal endothelial dysfunction
Two main risk factors of corneal blood staining:
IOP >25 mm of Hg
> 6 days duration
Earliest signs:
straw coloured discoloration of deep stroma
presence of tiny yellow granules in posterior
1/3rd
of the cornea
11. MANAGEMENT
Quick absorption of blood
Prevention of complications
Avoidance of recurrence
Discontinuation of anti coagulation therapy
Limiting activities
Rest in semi upright position and head end elevation
Patching
12. OUTPATIENT MANAGEMENT
Walton et al:
no associated injury
hyphema < ½ of AC volume
satisfactory IOP
no blood dyscrasia
safe home environment
good patient compliance
good follow up
no time delay at presentation
13. MEDICAL MANAGEMENT
Anti inflammatory drugs - NSAIDs
Cycloplegics
Topical, oral and systemic anti glaucoma drugs
Steroids
Anti fibrinolytic drugs - tranexamic acid, TPA,
aminocaproic acid
Laser photocoagulation of bleeding points by
goino prism
14. Anti fibrinolytic agents: epsilon amino caproic acid
(EACA) and Tranexamic acid are used to prevent
rebleed
EACA (amicar) binds to lysine molecules in the
clot via lysine binding site and inhibits fibrin clot
digestion. Its dose is 100mg/kg every 4 hours to a
maximum dose of 30g/day by mouth for 5 days.
Tranexamic acid also has similar mechanism.
The results of various studies indicate that both
amicar and tranexamic acid have beneficial effect
on rate of secondary haemorrhage but none of
them had improved the final visual outcome.
15. Corticosteroids:
Stabilizes the blood-ocular barrier
Directly inhibits fibrinolysis
Decrease incidence of secondary haemorrhage.
Prednisolone (0.6 mg/kg) is effective in reducing
the incidence of rebleed
Statistical analysis indicates that coticosteroids
decreases the incidence of rebleeding without
having any effect on the long term visual outcome.
Cycloplegics:
Studies advocate use of Cycloplegics as they
relieve ciliary spasm and prevents formation of
PAS
16. SURGICAL MANAGEMENT
Indications (Walton et al):
Microscopic corneal blood staining
IOP > 60 mm of Hg for 2 days
IOP > 50 mm of Hg for >4 days
IOP > 35 mm of Hg for 7 days
Pre-existing glaucomatous optic atrophy
Risk of corneal blood staining (e.g 4 days after the
onset of glaucoma, > ½ - total hyphema with IOP >
25mmHg > 6 days
Risk of synechiae formation (e.g > 50% hyphema for
> 8 days
Visual obstruction in children at risk of amblyopia
Sickle cell disease if IOP >25 mm of Hg for >24 hours
or spikes repeatedly >30 mm of Hg
17. SURGICAL MANAGEMENT
Simple paracentesis - allow the clot to retract
Irrigation and aspiration
Through a large limbal incision: manual expression,
cryoextraction, ultrasonic emulsification
Clot expression and limbal delivery is usually
advocated 4 to 7 days after the initial injury, when clot
consolidation and retraction is at its peak.
Clot irrigation with trabeculectomy is reserved for
total hyphema
18. FOLLOW-UP
Hospitalised patient - Daily V/A, IOP, Slit lamp exam
After discharge - next follow up after 2-3 days
1 - 2 weeks as per severity
After 4 weeks - gonioscopy and fundus exam
19. PROGNOSIS
Determinants:
Amount of associated damage to other ocular
structures like choroidal rupture, macular scarring
Secondary hemorrahge (rebleed)
Complications of Glaucoma, corneal blood
staining or optic atrophy
Recovery of V/A is good in approx 75% of patients:
Hyphema <1/3 of AC -- V/A 6/12 or better in
80% cases
Hyphema >1/2 - 2/3 of AC -- V/A 6/12 or better
in 60% cases
Hyphema Grade IV -- V/A 6/12 or better in 35%
cases