Insulin therapy is eventually needed for most patients with type 2 diabetes as their natural insulin production declines over time, despite oral medication use. Starting insulin when HbA1c levels remain above 7.5% on maximum oral drugs can help control blood glucose and reduce complications, though weight gain and hypoglycemia are risks that require education to minimize. Achieving long-term glucose targets may require an intensified insulin regimen of basal and bolus insulin in addition to an insulin sensitizer medication.
Ponencia en VII Curso Avanzado en Diabetes organizado por Sociedad Española de Diabetes (SED) y Sociedad Española de Endocrinología y Nutrición (SEEN). Madrid 14 diciembre 2018
Ponencia en VII Curso Avanzado en Diabetes organizado por Sociedad Española de Diabetes (SED) y Sociedad Española de Endocrinología y Nutrición (SEEN). Madrid 14 diciembre 2018
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 simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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3. Before Starting Insulin, Patients Spend an Estimated 10 Years
Above Target
10 35 Months*
27 Months*
9.1 Metformin
9 8.8 monotherapy
Sulfonylurea
8.2 monotherapy
8 7.6 7.7
A1C %
7.1
7 ADA goal
6
05
First HbA1c on Best HbA1c on Last HbA1c before
treatment treatment switch or addition
Modified: Monotherapy switched to another agent or additional agent added.
*Mean number of months until a new or additional treatment was started
Adapted from Brown JB, et al. Diabetes Care 2004;27:1535–40
4. Progressively declining beta cell function in T2D
‘waiting for failure’
Insulin ±oral drugs
Dual for lowering
100 Lifestyle Monotherapy therapy blood glucose
10
ß-cell function (%)
9
8
HbA1c (%)
7
6
HbA1c
5
ß-cell function
0 0
0 Time >15
(years)
Adapted from: Heine RJ et al. BMJ. 2006;333:1200-1204.
5. The impact of glycemic control on complications
The majority of people with type 2 diabetes fail to reach
recommended goals for glycemic control1
Intensive glucose control is associated with long-term reductions in
long-term diabetes complications—the legacy effect
17% 15% 15% 13% 9%
p=0.01 p=0.01 p=0.01 p=0.007 p=0.04
Diabetes Myocardial Microvascular Death Any diabetes
death infarction disease (any cause) endpoint
1. Del Prato, et al. Int J Clin Pract Suppl 2007;157:47-57
2. Holman et al, NEJM 2008;359:1577-1589
6. No HbA1C Threshold in Type 2 Diabetes
80
Myocardial infarction Epidemiologic
Adjusted Microvascular endpoints Data from the
incidence per UKPDS
60
1000 person
years (%) ADA Goal
40
20
?
0
5 6 7 8 9 10 11
Updated mean HbA1C (%)
Stratton IM, et al. BMJ. 2000;321:405-412.
6
10. “Clinical Inertia”
Failure to advance therapy when required
Last HbA1C Value Before Abandoning Treatment
10
9.6%
9.1%
9
8.8%
8.6%
8
% Mean HbA1C at
ADA Goal
last visit1
7
Sulfonylurea
Diet/Exercise Combination
Metformin
2.5 years 2.9 Years 2.2 Years 2.8 Years
1Brown et al. The Burden of Treatment Failure in Type 2 Diabetes. Diabetes Care 27: 1535-1540, 2004 10
11. Clinical Inertia: “Failure to advance therapy when required”
Percentage of Subjects advancing when HbA1C > 8%
At Insulin Initiation, the average patient had:
100 • 5 years with HbA1C > 8%
• 10 years with HbA1C > 7%
80
%Age of Subjects
66.6%
60 44.6%
35.3%
40
18.6%
20
0
Diet Sulfonylurea Metformin Combination
Brown et al. The Burden of Treatment Failure in Type 2 Diabetes.
Diabetes Care 27: 1535-1540, 2004 11
12. Clinical Inertia: “Failure to advance therapy when required”
4207 Person-Years of Followup
At Insulin Initiation, patients who had failed
combination therapy
• Had a median HbA1C of 9.9%
“The high median HbA1C that preceded the initiation of insulin in our population
is particularly troubling and suggests that there are substantial barriers to its
Initiation”
Cook et al: Glycemic Control continues to deteriorate after Sulfonylureas Are Added
to Metformin Among Patients with Type 2 Diabetes. Diabetes Care 28: 995-1000, 2005
12
13. Treatment Algorithm for Type 2
Diabetes in Adults*
Education/Nutrition/Exercise
Goals met FPG/SMBG goals not met after 1 month
Follow-up Every 3 Start Initial Oral Monotherapy
to 6 Months or Early Dual Oral Therapy
Therapy adequate Goals not met after 3 months
Continue Therapy Initiate/Modify Dual
HbA1c Every 3 to 6 Months Therapy
Therapy adequate Goals not met after 3 to 6 months
Continue Dual Therapy Add Evening Insulin or Third Oral Agent;
HbA1c Every 3 to 6 Months Consider Referral to Endocrinologist
Goal: FPG/SMBG <6.5 mmol/L; HbA1C <6.5%†
*Modified Texas Diabetes Council Algorithm. Feld S. Endocr Pract. 2002;8(suppl 1):40-82.
†American College of Endocrinology. 13
14. What should I tell people with Type 2
diabetes about insulin?
‘Most people with Type 2 diabetes eventually
need insulin because their own production of
insulin falls off with time and they therefore
inevitably become insulin deficient’
• Diabetes is caused by a progressive failure of insulin production
in people who are usually insulin insensitive (overweight)
15. Progression of Type 2 diabetes relates to
declining islet -cell function while insulin
insensitivity is unchanged
Time to need glucose-lowering
medication
2–4 years
5–7 years
-Cell 60 Insulin 60 8–10 years
function sensitivity
(%)
40 40
20 20
0 0
0 2 4 6 0 2 4 6
Years from diagnosis
Levy J et al. Diabet Med. 1998;15:290-296
16. Progression to Type 2 diabetes usually involves a
failure of insulin secretion in people who are already
insulin insensitive
500
400
(insulin response mU/l)
Insulin secretion
300 Normal – compensated insulin resistance
Normal
Normal
200
IGT
100 Diabetes
0
0 1 2 3 4 5
Insulin sensitivity
(glucose requirement mg/kg/min)
Adapted from Weyer C et al. J Clin Invest. 1999;104:787-794
17. What should I tell people
with Type 2 diabetes about insulin?
‘If you need insulin, it doesn’t mean you failed.
Tablets cannot control blood glucose forever, because
they don’t stop the problem of your own declining
insulin production getting worse’
• Islet -cell dysfunction worsens over time, regardless
of therapy
18. UKPDS: Islet -cell function and the progressive
nature of diabetes
100 Time of diagnosis
80
(% of normal by HOMA)
Islet -cell function
60
40 Pancreatic function
= 50% of normal
20
0
10 9 8 7 6 5 4 3 2 1 0 1 2 3 4 5 6
Years
HOMA = homeostasis model assessment
Holman RR. Diab Res Clin Pract. 1998;40(suppl):S21-S25;
UKPDS. Diabetes. 1995;44:1249-1258
19. What should I tell the person with Type 2
diabetes who needs
insulin, but doesn’t want to take it?
‘Insulin will not make your diabetes worse. In fact,
it will help control your glucose, so you’ll have
fewer complications and you’ll feel better.’
• Strict glycaemic control reduces the risks of both microvascular
and macrovascular complications
• People who start insulin usually feel much better for it
20. How should I start insulin therapy for my
patients with Type 2 diabetes?
• According to the IDF Global Guideline for Type 2
Diabetes
– Insulin is the most effective way of reducing hyperglycaemia
– Insulin can be started as a basal insulin alone or with premix
insulin
– Start insulin when glucose control on maximum tablets >7.5
% (HbA1c)
– Begin at low dose but titrate up rapidly in first month
IDF. Global Guideline for Type 2 Diabetes. 2005
21. Treat-to-Target: addition of detemir or NPH
to oral therapy
475 People with Type 2 Diabetes on 1 or 2 Oral Agents
Glycaemic Control Hypoglycaemia (events pt-yr-1)
Baseline HbA1c 8.5% 8.6%
0.0 12
-0.5
HbA1c
8
-1.0
NPH
-1.5 4
detemir
-2.0 -1.8%
-1.9%
P=NS 0
Final HbA1c 6.6% 6.8% 5.0 6.0 7.0 8.0 9.0
NPH insulin HbA1c (%)
Insulin detemir
Hermansen K et al. Diabetes Care. 2006;29:1269-1274
22. What are the problems associated with
insulin therapy?
• Weight gain is usual as glycosuria is reduced
• Hypoglycaemia will occur in some people – education is
needed
• Failure of dose titration to get adequate glucose control
• Worsening of control as islet β-cell failure progresses
• These risks can be minimized by
– use of insulin analogues in those with problems
– using basal insulin only when starting at lower HbA1c
– appropriate education on eating and physical activity
– active and continuing support for dose titration
– intensification of insulin regimens over following years
23. Conclusions
• Due to declining -cell function, insulin therapy will be necessary
for most patients with Type 2 diabetes
• Insulin effectively lowers HbA1c, thereby reducing the risks of
both micro- and macrovascular complications
• IDF Global Guidelines recommend starting insulin when glucose
control on maximum tablets >7.5 % (HbA1c)
• To maintain target glucose levels in the long-term, many patients
will require intensive insulin therapy (basal + bolus insulin) in
combination with an insulin sensitizer