1. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a genetic disorder that results in low levels of the G6PD enzyme in red blood cells.
2. The G6PD enzyme protects red blood cells from oxidative damage. Without sufficient G6PD, red blood cells are vulnerable to destruction when exposed to certain drugs or foods.
3. Primaquine, a drug used to prevent relapses of P. vivax malaria, can cause hemolysis or acute hemolytic anemia in people with low or intermediate G6PD levels due to its oxidative effects on red blood cells. It is important to test patients for G6PD status before administering primaquine to avoid
Discussion regarding Glucose 6 phosphate dehydrogenase deficiency and the genetics involved in inheritance of disease. The possible treatment options and mutations identified so far has also been discussed.
G6PDD is an inherited genetic disorder in the red blood cell enzyme known as G6PD. The effects of this disease are preventable by avoiding the triggers.
Presentation includes an account on overview about oral anti diabetics, toxicity of sulfonylureas, biguanides, alpha-glucosidase inhibitors, DPP4 inhibitor, SGLT2 inhibitor and its managemnt.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
More Related Content
Similar to 2.P.vivax and G6PD_PAVE_25112022_PSI.pptx
Discussion regarding Glucose 6 phosphate dehydrogenase deficiency and the genetics involved in inheritance of disease. The possible treatment options and mutations identified so far has also been discussed.
G6PDD is an inherited genetic disorder in the red blood cell enzyme known as G6PD. The effects of this disease are preventable by avoiding the triggers.
Presentation includes an account on overview about oral anti diabetics, toxicity of sulfonylureas, biguanides, alpha-glucosidase inhibitors, DPP4 inhibitor, SGLT2 inhibitor and its managemnt.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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.
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.
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.
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
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.
Follow us on: Pinterest
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
- 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
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.
1. 1
General information on G6PD deficiency
Plasmodium vivax malaria & Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency
Partnership for Vivax Elimination
2. P.vivax Life cycle in Humans
No test for liver
stage of vivax
NB: Some infections may not lead to
hypnozoites; some hypnozoites may not
relapses
S1.1
3. P. vivax malaria can relapse without a bite from an infected
mosquitoes a bite from an infected mosquito ted mosquito
Many relapses
weeks / months
after first infection
Illness, anemia,
possible
complications
including death
First
infection
Acute malaria
Obstacle to
malaria
elimination
Onward transmission
S1.1
`
`
`
4. P. vivax has a dormant liver stage which causes relapses
No test for liver
stage of vivax
NB: Some infections may not lead to
hypnozoites; some hypnozoites may not
relapses
Primaquine
(14-days)
[Chloroquine]
(3-days)
S1.1
5. Any questions?
• P. vivax malaria causes relapse of the malaria disease
• Relapse can lead to anemia, other illnesses and even death
• P. vivax malaria causes most malaria cases in countries / areas close to malaria
elimination
• P. vivax malaria is treated with chloroquine or an ACT to treat the acute malaria
infection and primaquine to prevent relapses
Key points to remember:
S1.1
6. What is G6PD deficiency?
By the end of this session you should be able to:
- Explain G6PD deficiency and how it affects P. vivax malaria care
S1.2
7. 7
Why is G6PD deficiency important for vivax patients?
WHO guidelines state that “the G6PD status of patients should be used to guide administration of
primaquine for preventing relapse” of vivax malaria.
To prevent drug-induced hemolytic anemia it is important to identify a patient’s G6PD status
before prescribing primaquine or tafenoquine for vivax malaria.
In Myanmar, the treatment for patients infected by P. vivax malaria is Chloroquine (CQ) (3 days)
and Primaquine (PQ) (14 days)
The dosage for PQ is usually a total dose of 0.25 mg/kg day over 14 days in G6PD normal patients or
eight weeks treatment with a weekly dose in G6PD deficient patients.
Partnership for Vivax Elimination
8. 8
What is G6PD Enzyme and its deficiency
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency: An X-linked recessive disorder which
results in the decreased activity of the G6PD enzyme.
G6PD enzyme protects red blood cells from oxidative stress:
Leads to decreased synthesis of NADPH (reduced form of nicotinamide adenine dinucleotide
phosphate)& glutathione (antioxidants)
NADPH helps restore glutathione stores so that glutathione can then reduce reactive oxygen
species (H2O2) to less harmful compounds (H2O).
The G6PD enzyme plays a critical role in protecting red blood cells (RBCs) from damage
and premature destruction from by-products of normal cell processes as well as external
challenges.
Many mutations have been identified that cause G6PD deficiency. Some of these mutations disrupt
the normal structure and stability of the enzyme – leading to low levels of G6PD activity inside the
red blood cells – or G6PD deficiency.
Partnership for Vivax Elimination
9. 9
• G6PD Status can be categorized as deficient, intermediate, or normal.
• People can have a mix of red blood cells – some with low G6PD activity and some with high G6PD activity.
If someone has mostly red blood cells with low G6PD activity, they are considered G6PD deficient.
If someone who has mostly blood cells with high G6PD activity, they are considered G6PD normal.
If someone has mixed blood cells, with high and low activity, they are considered G6PD intermediate. Only
females can be considered G6PD intermediate.
G6PD status
10. 10
G6PD
Gender Male Female
Low (deficient) <= 3.9 U/g Hb <= 3.9 U/g Hb
Gender Male Female
Medium (Intermediate) - 4-6 U/g Hb
G6PD status category by gender
Gender Male Female
Normal >= 4 U/g Hb >6 U/g Hb
11. Any questions?
• The G6PD enzyme helps protect red blood cells from damage
• If people have low or medium G6PD enzyme activity, they are at risk of hemolysis with anti-relapse
treatment
• About 0.5-8.6% of the Myanmar population is estimated having G6PD deficiency – it is important
to identify them before treating with primaquine
Key points to remember:
S1.2
13. What does it mean to have medium or low levels of G6PD?
G6PD activity level is inherited and affects 400 million people globally
More than 180 G6PD deficiency genetic variants ranging from mild to severe
G6PD deficiency is more common in males
People with low levels of G6PD activity can lead a totally normal life; they only need to
avoid certain medicines and food
G6PD enzyme activity
Normal
Deficient /
low
Normal
Deficient / low
Intermediate /
medium
G6PD enzyme activity
S1.2
14. 14
PQ effect on RBC
Due to PQ’s oxidant nature, Primaquine metabolites oxidize hemoglobin and generate
reactive oxygen compounds
leading to depletion of protective Glutathione (Bloom et al., 1983, Summerfield and
Tudhope, 1978) --- lead to a dose related hemolytic anemia.
The severity of hemolysis is determined by
dose of primaquine
extent of G6PD-deficiency
patient's physiological condition (Clyde, 1981, Youngster et al., 2010).
Partnership for Vivax Elimination
16. 16
PQ treatment effect on RBC among G6PD vivax/mix malaria
cases
Partnership for Vivax Elimination
17. Risks to patients with medium or low levels of G6PD
Most people with G6PD deficiency never experience any symptoms unless
exposed to certain foods or medicines
One serious potential side effect of some drugs taken by patients with low
or medium levels of G6PD activity is Acute Haemolytic Anaemia.
Haemolysis or Acute Haemolytic Anemia is when red blood cells to rupture
/ burst (haemolysis)
Red blood cells can be destroyed faster than the body can replace them
(acute hemolytic anemia - AHA)
S1.2
Trainers notes:
Background - P. vivax is a species of Plasmodium parasite, and one of the dominant species in this region/country. Like all malaria species, P. vivax has a complex life cycle. It infects a mosquito host, where sexual reproduction occurs, and then through, the mosquito infects its human host, where asexual amplification occurs.
Slide instructions: Ensure that the graphic is working prior to the training session. Explain each step of the life-cycle clicking through each stage.
Plasmodium vivax malaria is a parasitic disease, transmitted by mosquitoes in the genus Anopheles.
[CLICK]
Once a patient has been infected, an incubation period of approximately 2 weeks occurs as active liver stages develop without symptoms.
In humans, the infection consists of both a liver and a blood stage.
[CLICK]
It is the subsequent infection of red blood cells that provoke the symptoms of an acute attack of malaria.
[CLICK]
Some of the liver stage parasites do not immediately develop like that.
Instead they become dormant hypnozoites. These parasites are wholly silent and cannot be detected by any diagnostic means.
[CLICK]
Days, months or even years later, hypnozoites in the liver can awaken and cause a renewed attack of acute malaria called a relapse.
If a patient does not receive specific therapy against hypnozoites, they often suffer six or more relapses within the first year. Each one comes with acute illness and opportunity for transmission to the people around them.
Trainers notes:
Explain how the life-cycle of p vivax changes the number of p vivax malaria cases participants see in the clinic:
Patients can get sick from P vivax by being bitten by an infected mosquito
Once they have been bitten, they may get sick and transmit malaria onwards via mosquitoes biting them
They might also ‘relapse’ with p vivax again a few weeks or months after their first infection. If a patient relapses it means that the hynozoites ‘sleeping’ in their liver woke up and re-infected the patient. This infection was not spread from a mosquito.
Take 5-10 minutes to discuss the potential consequences of vivax malaria for patients and communities.
Prompts:
What do you think the consequences of relapses are on the patient?
How do you think relapses affect malaria in our communities?
Trainers notes
Remind participants about the life-cycle of P. vivax that you previously presented.
Highlight to participants the stage of the life-cycle that is affected by blood- and liver-stage treatment.
Note to participants that the blood-stage treatment (chloroquine/ACT) kills the blood-stage ring that we normally see in the blood slide
Primaquine treats the liver-stage of p. vivax.
Tell participants that if a patient is cleared of blood-stage parasites but has hynozoites, that we will not be able to detect them as there is no test that can currently do that
Note that some infections may not lead to hynozoites being formed, and some hynozoites may not lead to relapse
Trainers note
Ensure you highlight the key points of the session.
Take time to encourage participants to ask any questions about the session.
Let participants know that they can always ask questions of you during breaks or lunch as well.
Trainers notes:
Time: 30 minutes
Materials: Slide deck
Preparation: Ensure that you have located and inserted maps of the distribution of vivax malaria and G6PDd prevalence in your country on the slide ‘Malaria and G6PDd Distribution’
Trainers notes:
Ensure you highlight the key points of the session.
Take time to encourage participants to ask any questions about the session.
Let participants know that they can always ask questions of you during breaks or lunch as well.
Trainers notes:
Note to participants that Hemolysis is the destruction of red blood cells.
Hemolysis can occur due to different causes and leads to the release of hemoglobin into the bloodstream.
Take 2 minutes to ask participants if they have ever dealt with patients with hemolysis and specifically dark urine caused by hemolysis.