1) Color vision deficiency is the reduced ability to see color differences due to an absence of color-sensitive pigments in the eye. It is usually genetic and most common in men.
2) There are two main types - red-green deficiency which makes distinguishing red and green difficult, and blue-yellow deficiency which affects blue and green/yellow.
3) The Ishihara test is commonly used to test for red-green deficiency using plates with colored dots that form numbers visible to those with normal color vision but not for those with deficiencies.
Colour vision , How to check color vision, About colour vision, Types of colour vision , Color vision tests , Theories of colour vision , Characteristics of colour vision , Causes of colour vision , Colour blindness , Defects of colour vision , Optometry , Causes of colour vision , All about color vision , Colour disability , monochromatism , Determine colour deficiency patients ,
Presented by our respected teacher
Mohammad Siddique (Optometrist)
thank u sir
Final Year Student Of Optometry at ISRA School Of Optometry
All Rights Reserved
This PowerPoint included all of the optical and non-optical aspects, uses, advantages, and disadvantages, as well as detailed notes on how to use each aspect.
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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!
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.
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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
- 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
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
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.
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
1. Colour Vision Deficiency
Presented by :
Optometrist (intern) Asma Al-Jroudi
Saudi Arabia, Riyadh, King Abdulaziz University Hospital
30 Dec 14
2. • What Is Color Vision Deficiency?
• Causes Of Color Vision Deficiency
• Types Of Color Vision Deficiency
• Tretments Of Color Vision Deficiency
• Ishihara’s Test
• Conclousion
3. What is Colour Blindness?
• Color blindness, or color vision deficiency, is the
inability or decreased ability to see color, or
perceive color differences, under normal lighting
conditions.
•This condition results from an absence of color-
sensitive pigment in the cone cells of the retina,
the nerve layer at the back of the eye.
4. What is Colour Blindness?
• Cones are the coulored light receptors in back of
the eye: Red light receptors, Blue light receptors
and Green light receptors.
• Colour blindness occurs when one or more of the
cone types are defected.
5. Causes of Color Blindness
• Genetic:
Many more men are affected than women.
• Acquired :
Chronic illness, Accidents, Medications and Age.
6. There are two main types of CVD:
• Red-Green deficiency
Where people are unable to distinguish certain
shades of red and green; it is the most commonly
inherited type..
• Blue-Yellow deficiency
This is a rare condition where it is difficult to
distinguish between blue and green, yellow may
appear as a pale grey or purple.
7. Protanopes: do not see RED
Deutranopes: do not see GREEN
Tritanopes: do not see either YELLOW or BLUE
8.
9. • There is currently no treatment .
• Colour filters or contact lenses can be used in
some situations to enhance the brightness
between some colours.
• For acquired colour vision deficiency, once the
cause has been established and treated, your
vision may return to normal.
Treatment
10. Treatment
• Genetherapy
September 2009, the journal Nature reported
that researchers at the University of Washington
and University of Florida were able to give
trichromatic vision to squirrel monkeys, which
normally have only dichromatic vision, using gene
therapy.
12. Ishihara’s test
• The most common is the Ishihara Plate test.
• Can test for red/green colour blindness but not
blue colour blindness.
• This is the test most likely to be used for routine
colour vision screening in schools or medicals.
• Contains 24 plates of circles created by irregular
coloured dots in two or more colours.
13. Four Different Types of Plates
1. Vanishing design:
Individuals with normal colour vision could
recognize the figure.
2. Transformation design:
Individuals with colour vision defect should see a
different figure from individuals with normal
color vision.
14. Four Different Types of Plates
3. Hidden digit design:
Only individuals with colour vision defect could
recognize the figure.
4. Classification design:Intended to determine the
type of color vision defect ( protanopia or
deuteranopia) and the severity of it.
15. Steps & Procedure
1. Obtain the chart in the back of the book
Note: before adminstering this test; you should be
tested first.
2. Explain the procedure to the pt.
3. Ask pt first to read the plates with both eyes
(with a corrective glasses if there is one)
4. Test pt’s monocularly, one eye at a time.
5. Record those frames the pt misses.
18. Plates 1-17
2nd =8 3rd=29
• Red-green deficiency would read it as:
2nd plates=3 , 3rd plate= 70
• Those with total colour blindness cannot read any
figures.
19. Plates 1-17
4th = 5 5th = 3 6th = 15 7th = 74
• Red-Green deficiency will read it as :
4th =2 , 5th = 5, 6th=17, 7th=21
• Those with total color blindness cannot read any
figures
20. Plates 1-17
• 8th =6 ,9th=45 ,10th =5 , 11th =7 ,12th =16 ,13th =73
• Majority of thoes with CVD can not read them or
read them incorrectly.
21. Plates 1-17
14th & 15th plates
• Normal and total colour blindness people can not read
any numeral.
• Only thoes with Red-Green deficiency can read them
as: 14th= 5 ,15th=45
22. Plates 1-17
16th=26 17th=42
• protanopic would read it as:
16th=6, 17th=2
• Deutaneropic would read it as:
16th=2 , 17th=4
23. Plate no. 18
• In tracing the lines between the two X’s, the
normal trace along purpule and red lines.
• In protanopia and strong protanomalia Purple
line is traced.
• In deutaneropia and strong deutanomalia Red
line is traced
24. Plate no.19
• Majority of normal and thoes with total colour
blindness are unable to follow the line.
• In tracing the line between the two X’s majority
of thoes with Red-Green deficiencies trace along
the line.
25. Plate no.20
• Normal will trace the bluish-green line.
• The majority of thoes with colour vision
deficiencies are unable to follow the line.
26. Plate no. 21
• Normals will trace the orange line.
• The majority of thoes with colour vision
deficiencies are unable to follow the orange line
or will follow a different line.
27. Plate no. 22
• Normals will trace the the line that connects the
bluish-green and yellowish-green lines.
• Red-Green deficiencies will trace line connecting
bluish-green and purple.
• Thoes with total colour blindness can not trace any
line.
28. Plate no.23
• Normals will trace the line connecting purple and
orange
• Red-Green deficiencies will trace line connecting
bluish-green and purple.
• Thoes with total colour blindness can not trace
any line.
30. Analysis The Results
• If 13 (out of 24) or more plates are read normally,
the color vision is regarded as normal.
• If only 9 or less than 9 plates are read normally,
the color vision is regarded as deficient.
31. Conclosion
• Colour blind people face many difficulties in
everyday life.
• Problems can arise in even the most simple of
activities including choosing and preparing food,
gardening, sport, driving a car and selecting
clothing.
• Colour blind people can also find themselves in
trouble because they haven’t been able to pick
up a change in someone’s mood by a change in
colour of their face.