Fasting during Ramadan poses risks for people with diabetes, especially those with type 1 diabetes who should be advised not to fast. For those who insist, risks include hypoglycemia, hyperglycemia, dehydration, and diabetic ketoacidosis. Management requires individualizing plans based on risk factors, educating patients, adjusting medications like insulin and timing/doses, frequent glucose monitoring, proper nutrition and hydration, and medical supervision. The goal is reducing risks while allowing observance of religious practices.
Vanita R. Aroda, MD, prepared type 2 diabetes mellitus infographics for this CME activity titled, "Putting Basal Insulin Therapy to Work for Patients With Type 2 Diabetes Mellitus." For the full presentation, downloadable infographics, monograph, complete CME information, and to apply for credit, please visit us at http://bit.ly/2kdVkuJ. CME credit will be available until September 12, 2020.
SGLT2I The paradigm change in diabetes managementPraveen Nagula
Just like ARNI, SGLT2I have changed the face of diabetes management and they have a good profile in multimodality management because of pleiotropic effects
Anti-Obesity Pharmacotherapy: Where are we now? Where are we going?InsideScientific
Obesity is a treatable chronic disease. With nearly 2 billion individuals worldwide classified as being overweight and 650 million as having obesity, it is critical to optimize implementation of existing treatment interventions and develop novel therapies to mitigate the obesity pandemic. Anti-obesity medications are one of the essential tools in our medical toolbox to help patients achieve their health and weight goals.
In this webinar, Dr. Jastreboff discusses current use of anti-obesity pharmacotherapy, mechanisms involved, and agents in various stages of development with considerations for next steps. The presentation aims to inspire development of innovative therapeutics while optimizing use of existing agents to address the urgent need to effectively and sustainably treat millions of individuals with obesity around the world.
Key Topics Include:
- Understand the role of anti-obesity pharmacotherapy in the treatment of obesity
- Describe current anti-obesity pharmacotherapy
- Discuss anti-obesity medications under development
Diabetic Dyslipidemia
By Dr. Usama Ragab Youssif
ISMA CME Activity 2021
In Tolip EL Galala Hotel
-----------
Introduction
Physiology of lipid metabolism
Pathophysiology of diabetic dyslipidemia
Statin therapy (+/- ezetimibe) evidence and translation of evidence
Residual CV risk: excess TG
EPA therapy evidence and translation of evidence
Fasting Ramadan carry many hazards to diabetic need to fast. Uncontrolled patients have a liability to some dangerous complications like DKA,HYPOGLYCEMIA,HHS AND thromboembolism
Vanita R. Aroda, MD, prepared type 2 diabetes mellitus infographics for this CME activity titled, "Putting Basal Insulin Therapy to Work for Patients With Type 2 Diabetes Mellitus." For the full presentation, downloadable infographics, monograph, complete CME information, and to apply for credit, please visit us at http://bit.ly/2kdVkuJ. CME credit will be available until September 12, 2020.
SGLT2I The paradigm change in diabetes managementPraveen Nagula
Just like ARNI, SGLT2I have changed the face of diabetes management and they have a good profile in multimodality management because of pleiotropic effects
Anti-Obesity Pharmacotherapy: Where are we now? Where are we going?InsideScientific
Obesity is a treatable chronic disease. With nearly 2 billion individuals worldwide classified as being overweight and 650 million as having obesity, it is critical to optimize implementation of existing treatment interventions and develop novel therapies to mitigate the obesity pandemic. Anti-obesity medications are one of the essential tools in our medical toolbox to help patients achieve their health and weight goals.
In this webinar, Dr. Jastreboff discusses current use of anti-obesity pharmacotherapy, mechanisms involved, and agents in various stages of development with considerations for next steps. The presentation aims to inspire development of innovative therapeutics while optimizing use of existing agents to address the urgent need to effectively and sustainably treat millions of individuals with obesity around the world.
Key Topics Include:
- Understand the role of anti-obesity pharmacotherapy in the treatment of obesity
- Describe current anti-obesity pharmacotherapy
- Discuss anti-obesity medications under development
Diabetic Dyslipidemia
By Dr. Usama Ragab Youssif
ISMA CME Activity 2021
In Tolip EL Galala Hotel
-----------
Introduction
Physiology of lipid metabolism
Pathophysiology of diabetic dyslipidemia
Statin therapy (+/- ezetimibe) evidence and translation of evidence
Residual CV risk: excess TG
EPA therapy evidence and translation of evidence
Fasting Ramadan carry many hazards to diabetic need to fast. Uncontrolled patients have a liability to some dangerous complications like DKA,HYPOGLYCEMIA,HHS AND thromboembolism
In this slide set we present recommendations on the management of Diabetes during the period of Ramadan. Preparations prior to fasting, management during the period and adjustments to be made.
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Sehit Sener Gundem Secondary School Comenius Multilateral Project. Presentation About Ramadan. Name of our project is 'Biodiversity Conservation The Only Path To Our Survival'
This Presentation Prepared from IDF-DAR,BMJ,ADA & Other guidelines.It will cover to solve problems faced by the physicians during management of DM in the Holy Month of Ramadan specially monitoring of blood glucose,Drug doses,dietary and exercise advice etc.
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
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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
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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
- 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
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2. “ O you who believe! Fasting has been
prescribed to you as it was prescribed to
those before you so that you attainTaqwa
(self restraint , God Awareness)”
3. 1. Physically sick ( Quran 2: 184-185)
2.Traveler on a journey ( Quran 2: 184-185)
3.Women during menstruation
4. ? Pregnant and lactating women
5. Pre pubertal children
4. Diabetes MellitusType 1
Chronic Renal Failure including Renal
Transplant and Nephrolithiasis
Severe cardiac and pulmonary conditions
G.I. Bleed and acute ulcers
Severe Epilepsy
Severe Migraine
5. Estimated 1.1-1.5 billion Muslims worldwide.
Fasting during Ramadan is obligatory on
every adult Muslim.
Muslims fast for 29-30 days of lunar based
month.
Fasting starts before sunrise and end at
sunset and the duration of the day varies as
the season.
6. What are evidences we have to support
today’s talk
Epidemiology of Diabetes and Ramadan 2001
(EPIDIAR)
Approximately
▪ 43% patients with type 1 diabetes
▪ 79% of patients with type 2 diabetes fast during
Ramadan
7. Insulin secretion in healthy individuals is
stimulated with feeding, which promotes the
storage of glucose in liver and muscle as
glycogen.
In contrast, during fasting, circulating glucose
levels tend to fall, leading to decreased
secretion of insulin, levels of glucagon and
catecholamines rise, stimulating the
breakdown of glycogen, while
gluconeogenesis is augmented
8. As fasting becomes protracted for more than
several hours, glycogen stores become
depleted, and the low levels of circulating
insulin allow increased fatty acid release from
adipocytes.
Oxidation of fatty acids generates ketones
that can be used as fuel by skeletal and
cardiac muscle, liver, kidney, and adipose
tissue, thus sparing glucose for continued
utilization by brain and erythrocytes.
10. Threefold increase in the risk of severe
hypoglycemia in patients who were in the
intensively treated group and had an average
HbA1c (A1C) value of 7.0%.
2–4% of mortality in patients with type 1
diabetes.
Severe hypoglycemia was more frequent in
patients in whom the dosage of oral
hypoglycemic agents or insulin were changed
and in those who reported a significant change
in their lifestyle.
11. There is no information linking repeated
yearly episodes of short-term hyperglycemia
(e.g., 4-week duration) and diabetes related
complications.
Control of glycemia in patients with diabetes
who fasted during Ramadan has been
reported to deteriorate, improve, or show no
change.
12. Fivefold increase in the incidence of severe
hyperglycemia (requiring hospitalization)
during Ramadan in patients with type 2
diabetes (from 1 to 5 events 100 people1
month1) and
An approximate threefold increase in the
incidence of severe hyperglycemia with or
without ketoacidosis in patients with type 1
diabetes
13. Patients with diabetes, especially those with
type 1 diabetes, who fast during Ramadan are
at increased risk for development of diabetic
ketoacidosis, particularly if they are grossly
hyperglycemic before Ramadan.
14. Limitation of fluid intake during the
fast, especially if prolonged, is a cause of
dehydration.
Hyperglycemia can result in osmotic diuresis and
contribute to volume and electrolyte depletion.
Orthostatic hypotension, syncope, falls, injuries
and bone fractures may result.
Patients with diabetes exhibit a hypercoagulable
state due to an increase in clotting factors, a
decrease in endogenous anticoagulants, and
impaired fibrinolysis.
15.
16. Most often recommendation will be not to
undertake fasting.
However, patients who insist on fasting need
to be aware of the associated risks and be
ready to adhere to the recommendations of
their doctors for safe Ramadan.
Risk stratification
17. 1.Very high risk
Severe hypoglycaemia within the last 3 months prior to
Ramadan.
A history of recurrent hypoglycaemia.
Hypoglycaemia unawareness.
Sustained poor glycemic control.
Ketoacidosis within the last 3 months prior to Ramadan.
Type 1 Diabetes
Acute illness
Pregnancy
Patients on chronic dialysis
Patients who perform intense labour
Recommendations for Diabetic Individuals during Ramadan, Diabetes Care , vol 33, num. 8, August2010
18. 2. High risk
Patients with moderate hyperglycemia (average
blood glucose between 150 and 300 mg/dl,A1C 7.5–
9.0%)
Patients with renal insufficiency
Patients with advanced macrovascular complications
People living alone that are treated with insulin or
sulfonylureas
Patients living alone
Patients with comorbid conditions that present
additional risk factors
Old age with ill health
Drugs that may affect mentation
19. 3. Moderate risk
Well-controlled patients treated with short-
acting insulin secretagogues such as
repaglinide or nateglinide
4. Low risk
Well-controlled patients treated with diet
alone, metformin, or a thiazolidinedione who
are otherwise healthy
21. Individualization
Frequent monitoring of glycemia
Nutrition
The diet during Ramadan should not differ
significantly from a healthy and balanced diet.
The common practice of ingesting large amounts
of foods rich in carbohydrate and fat, especially at
the sunset meal, should be avoided.
22. Because of the delay in digestion and
absorption, ingestion of foods containing
“complex” carbohydrates may be advisable at
the predawn meal.
While foods with more simple carbohydrates
may be more appropriate at the sunset meal.
It is also recommended that fluid intake be
increased during nonfasting hours and that the
predawn meal be taken as late as possible
before the start of the daily fast.
23. Slow energy release foods (such as
wheat, semolina, beans, rice) should be taken
before and after fasting, whereas foods high in
saturated fat (such as ghee, samosas, and
pakoras) should be minimised.
Advise patients to use only a small amount of
monounsaturated oils (such as rapeseed or olive
oil) in cooking
Before and after fasting include high fibre foods
such as wholegrain cereals, granary
bread, brown rice; beans and pulses;
fruit, vegetables, and salads
24.
25. Individualization
Frequent monitoring of glycemia
Nutrition
Exercise
Normal levels of physical activity may be maintained.
Breaking the fast
All patients should understand that they must always
and immediately end their fast if hypoglycemia (blood
glucose of 60 mg/dl [3.3 mmol/l])
Fast should be broken if blood glucose exceeds 300
mg/dl (16.7 mmol/l).
Patients should avoid fasting on “sick days.”
26. Medical assessment
This assessment should take place within 1–2
months before (Rajab, Shaban)Ramadan.
Overall well-being of the patient and to the
control of their glycemia, blood pressure, and
lipids.
During this assessment, necessary changes in
their diet or medication regimen should be made
27. EducationalCounselling
It is essential that the patients and family receive
the necessary education concerning self-
care, including signs and symptoms of hyper and
hypoglycemia, blood glucose monitoring, meal
planning, physical activity, medication
administration, and management of acute
complications.
29. In general, patients with type 1
diabetes, especially if “brittle” or poorly
controlled, are at very high risk of developing
severe complications and should be strongly
advised to not fast during Ramadan.
Glycemic control at near-normal levels
requires use of multiple daily insulin
injections (three or more)
30. Diet-Controlled patients
Potential risk for occurrence of postprandial
hyperglycemia after the predawn and sunset
meals if patients overindulge in eating.
Distributing calories over two to three smaller
meals during the nonfasting interval may help
prevent excessive postprandial hyperglycemia.
The exercise program should be modified in its
intensity and timing to avoid hypoglycemic
episodes
31. In general, agents that act by increasing
insulin sensitivity are associated with a
significantly lower risk of hypoglycemia than
compounds that act by increasing insulin
secretion.
32. Metformin.
Patients treated with metformin alone may safely
fast because the possibility of hypoglycemia is
minimal.
However, it is suggested that the timing of the
doses be modified.
Recommendation is that two thirds of the total
daily dose be administered immediately before
the sunset meal, while the other third be given
before the predawn meal.
33. Glitazones.
Patients on insulin sensitizers (rosiglitazone and
pioglitazone) have a low risk of hypoglycemia.
Usually no change in dose is required.
34. Sulfonylureas.T
his group of drugs was believed to be unsuitable for
use during fasting because of the inherent risk of
hypoglycemia. Hence, their use should be
individualized and they should be utilized with
caution.
Use of chlorpropamide is absolutely contraindicated
during Ramadan because of the high possibility of
prolonged and unpredictable hypoglycemia.
Newer members of the sulfonylurea family (gliclazide
MR or glimepiride) have been shown to be
effective, resulting in a lower risk of hypoglycemia
35. Short-acting insulin secretagogues.
Members of this group (repaglinide and
nateglinide) are useful because of their short
duration of action.
They could be taken twice daily before the sunset
and predawn meals.
36. Patients treated with insulin
A major objective is to suppress hepatic glucose
output to near-physiologic levels during the fasting
period.
Judicious use of intermediateor long-acting insulin
preparations plus a short-acting insulin administered
before meals would be an effective strategy.
Using one injection of a long-acting insulin
analog, such as insulin glargine, or two injections of
NPH, lente, or detemir insulin before the sunset and
predawn meals may provide adequate coverage.
37. Patients treated with insulin
However, most patients will still require short-
acting insulin administered in combination with
the intermediate- or long- acting insulin at the
sunset meal to cover the large caloric load of Iftar.
Moreover, many will need an additional dose of
short-acting insulin at predawn.
38.
39.
40. Dehydration, volume depletion, and a tendency
toward hypotension may occur with fasting
during Ramadan.
Hence, the dosage of antihypertensive
medications may need to be adjusted to
prevent hypotension.
It is common practice that the intake of foods
rich in carbohydrates and saturated fats is
increased during Ramadan. Appropriate
counselling should be given to avoid this
practice.
41. Fasting during Ramadan for patients with
diabetes carries a risk of an assortment of
complications.
Patients with type 1 diabetes should be
strongly advised to not fast.
Hypo- and hyperglycemia may also occur in
patients with type 2 diabetes but generally
less frequently and with less severe
consequences compared with patients with
type 1 diabetes.
42. Patients who insist on fasting should undergo
pre-Ramadan assessment and receive
appropriate education and instructions related
to physical activity, meal planning, glucose
monitoring, and dosage and timing of
medications.
The management plan must be highly
individualized.
Close follow-up is essential to reduce the risk for
development of complications.