This document discusses diabetes mellitus and its various types and complications. It defines diabetes as a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion or insulin action. There are two main types - type 1 diabetes which results from an absolute deficiency of insulin due to autoimmune destruction of pancreatic beta cells, and type 2 diabetes which is due to insulin resistance and inadequate insulin secretion. The document outlines the pathogenesis, clinical presentation, diagnostic criteria and long term complications of both types of diabetes, which can include damage to blood vessels, nerves, eyes and kidneys if not properly managed.
SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
General introduction to diabetes mellitusSnigdha Maity
Its very important topic in periodontology as Diabetes Mellitus has high impact on periodontium. So before going into details how it act on periodontium, we have to know what it is and how it is detected in blood. Here is the vast knowledge on diabetes mellitus
Pathophysiology of Diabetes Mellitus (Harrison’s Principles of Internal Medic...Batoul Ghosn
This presentation talks about the Pathophysiology part of Diabetes Mellitus I & II as well as Diabetic Ketoacidosis & Hyperglycemic Hyperosmolar State and Finally with Medical Nutrition Therapy in DIabetes Mellitus. It is made entirely from the Harrsion's Book 19th edition.
SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
General introduction to diabetes mellitusSnigdha Maity
Its very important topic in periodontology as Diabetes Mellitus has high impact on periodontium. So before going into details how it act on periodontium, we have to know what it is and how it is detected in blood. Here is the vast knowledge on diabetes mellitus
Pathophysiology of Diabetes Mellitus (Harrison’s Principles of Internal Medic...Batoul Ghosn
This presentation talks about the Pathophysiology part of Diabetes Mellitus I & II as well as Diabetic Ketoacidosis & Hyperglycemic Hyperosmolar State and Finally with Medical Nutrition Therapy in DIabetes Mellitus. It is made entirely from the Harrsion's Book 19th edition.
The endocrine pancreas
Islets of Langerhans (endocrine pancreas) contain 4 major
and 2 minor cell types.
●Major cell types:
1.β cell produces insulin.
2.α cell secretes glucagon.
3.δ cells contain somatostatin, which suppresses
both insulin and glucagon release.
• DM is a heterogeneous group of syndromes characterized by
an elevation of fasting blood glucose caused by absolute or
relative deficiency of insulin
• Hyperglycemia in diabetes results from defects in insulin
secretion ( destruction of β cells of the pancreas ), insulin
action, or most commonly both.
• Diabetes is the leading cause of adult blindness and
amputation and a major cause of renal failure, nerve damage,
heart attacks, and strokes.
• Most cases of diabetes mellitus can be separated into two
groups
- Type 1 (insulin-dependent DM)
- Type 2 (noninsulin dependent DM)
Type 1 Diabetes Mellitus
• Onset: usually during childhood
• Caused by absolute (complete) deficiency of insulin:
- Maybe caused by both:
1. autoimmune attack of b-cells of the pancreas, i.e. a
genetic determinant that allows the β cells to be
recognized as “nonself”
2. environmental factors as viral infection or toxins
• Rapid symptoms appear when 80-90% of the b-cells
have been destroyed
• Commonly complicated by diabetic ketoacidosis (DKA)
• Treated only by insulin
• the islets of Langerhans become
infiltrated with activated T
lymphocytes, leading to a
condition called insulitis .
• Over a period of years, this
autoimmune attack on the β cells
leads to gradual depletion of the
β-cell population. However,
symptoms appear abruptly when
80%–90% of the β cells have been
destroyed.
• At this point, the pancreas fails to
respond adequately to ingestion
of glucose, and insulin therapy is
required to restore metabolic
control and prevent lifethreatening ketoacidosis.
Metabolic changes of type 1 DM
1-Hyperglycemia: increased glucose in blood, Due to:
Decreased glucose uptake by muscles & adipose tissues &/or
Increased hepatic gluconeogenesis
2-Ketoacidosis:
• increased ketone bodies in blood (in untreated or
uncontrolled cases) results from increased mobilization of
fatty acids (FAs ) from adipose tissue, combined with
accelerated hepatic FA β-oxidation and synthesis of 3-
hydroxybutyrate and acetoacetate.
• in 25 – 40% of newly diagnosed type 1 DM
• in stress states demanding more insulin (as during
infection, illness or during surgery)
• In patients who have no compliance with therapy
3- Hypertriglyceridemia: increased TAG in blood
• Released fatty acids from adipose tissues are
converted to triacylglycerol. Triacylglycerol is
secreted from the liver in VLDL to blood.
• Chylomicrons (from diet fat) accumulates (low
lipoprotein lipase in DM due to decreased
insulin)
• Increased VLDL & chylomicrons results in
hypertriacylglyceridemia
INTERTISSUE RELATIONSHIP IN T1DM
Diagnosis of type 1 DM
• Clinically:
Age: during childhood or puberty (< 20 years of age)
- Polyuria (frequent urina
The renal actions of the most potent mineralocorticoid hormone Aldosterone are conceptualized as the 4 arrows in action, in the context of the regulation of the blood volume and pressure and the plasma electrolytes, sodium and potassium.
Mr. EasyG, a cartoon character, shows you the easy way to remember the direction and polarity of the 6 limb leads - the dirty half-dozen- important to localize the part of heart affected by the disease process(e.g. inferior infarct) and to determine the electrical axis of the heart.
Should neckties steal the show during a University Convocation Ceremony? Post-convocation rumblings of an academician from a private university in Kuala Lumpur, Malaysia
The whole cardiovascular physiology caters to blood flow through the organs, and blood pressure is just one of the factors favouring tissue blood flow (perfusion).
The concept is built up on basic transport mechanisms across the biological membranes including transcapillary or paracapillary transport. Attempt has been made to distinguish between the blood brain barrier and blood-CSF barrier. Cartoons were profusely used.
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
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.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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.
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.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
4. Diabetes mellitus
is a group of metabolic diseases characterized
by
hyperglycemia
resulting from
• defects in insulin secretion,
• defects in insulin action
(“insulin resistance”),
• or both.
long-term damage, dysfunction, and
failure of various organs, especially the
eyes
kidney
nerves
heart
blood vessels.
“Complications”
5. Classification of diabetes
Type 1 ( was called “insulin- dependent DM”/ juvenile type of DM) ( 5-10%)
Type 2 (was called “non insulin- dependent DM” /adult onset DM ) (90-95%)
The “pre-diabetic stage” (impaired glucose tolerance)
Gestational DM -any degree of glucose intolerance with onset or first
recognition during pregnancy [in 2-5% of all pregnancies]
Other specific types (1% - 2%)
– genetic syndromes (affecting insulin secretion or action)
– endocrinopathies (Acromegaly, Cushing’s syndrome, glucagonoma,
pheochromocytoma, thyrotoxicosis)
– diseases of pancreas (chronic pancreatitis, cancer)
– drug- or chemical-induced (corticosteroids, beta-blockers, thiazide
diuretics)
– infections (viral)
The main focus of this plenary
6. Type 1 Diabetes
“insulin- dependent DM”
“ juvenile-onset DM”
Type 2 Diabetes
“Non insulin-
dependent DM”
“ adult-onset DM”
7. Type 1 Diabetes
“insulin- dependent DM”
“ juvenile-onset DM”
Type 2 Diabetes
“Non insulin-
dependent DM”
“ adult-onset DM”
Many require insulin
i.e. insulin- dependent
May develop when
much older
Developing at younger
age groups
(childhood obesity)
8. Type 1 Diabetes Type 2 Diabetes
diabetes due to
insulin resistance and
inadequate compensatory
insulin secretory response
diabetes due to
absolute deficiency of
insulin
10. Pathogenesis
Susceptibility genes identified
e.g. HLA haplotypes DR3 & DR4.
cell-mediated autoimmune
destruction of the beta-cells
of the pancreas by auto-
antibodies
genetic
predisposition environmental factors
viral infections
stress
toxins e.g. rat poison
Type 1 Diabetes
absolute insulin deficiency
16. Sympathetic
nerves
Glucagon
Insulin
receptor (-)
receptor (+)
receptor (+)
receptor (-)
Sympathetic
nerves
Net effect: incr. glucagon secretion
Net effect: decr. insulin secretion
Paracrinepathway
(-)
(+)
Islets of
Langerhans
DM: Hyperglucagonaemia is a feature of DM
Beta-blockers may further impair insulin secretion
Start here
cells
cells
17. Natural history of Type 2 Diabetes
cell secretory response to
progressive insulin
resistance
(Blood glucose normal)
cells no longer able
to compensate
Type 2 Diabetes
18. Too late?
At the time of diagnosis, 50% of cell function has already been lost
( A study on patients in the UK)
Type 2 Diabetes
19. Clinical presentation of DM
• Asymptomatic (particularly type 2 DM)
• Features resulting from the effects of insulin
deficiency/resistance (review insulin actions)
– The 3 Polys :
• Polyuria / nocturia
• Polydipsia
• Polyphagia (in the presence of unintentional weight loss)
• Complications
– Acute: coma (ketoacidosis) (particularly type 1 DM)
– Chronic: macrovascular and microvascular
20. Pancreas beta cells
Insulin actions
Glucose
entry and
utilization
(oxidation,
storage)
Glucose
entry and
oxidation
TG synthesis
insulin actions: a review
21. Pancreas beta cells
Insulin actions
Glucose
entry and
utilization
(oxidation,
storage)
Glucose
entry and
oxidation
TG synthesis
Metabolic consequences of insulin deficiency/resistance
22. Clinical Features of DM due to insulin lack
Polyphagia
(decr. leptin?)
Starvation in the
midst of plenty
Hyperosmolar
hyperglycemic
syndrome (HHS)
Lactic
acidosis
Lactic
acidosis
Muscle protein breakdown
Acetoacetate,0H-butyrate, acetone
23. • Ketoacidosis - Life threatening – medical emergency!
Stressful situation
Positive feedback cycleStart here
24. Stressful situation
Positive feedback cycleStart here
• Treatment: Fluids(normal saline), I.V. insulin. Monitor plasma
glucose (and K+ as insulin promotes uptake of glucose and K+ by
muscles and adipose tissue)
Insulin
pump
Rehydration -
fluids
25. • hyperglycaemia
• Excess glucose attaches nonenymatically
to amino acids of proteins *“glycosylation”+
• Glycosylation of haemoglobin HbA1C
refects glycaemic control for the past 2
months (half life for RBCs)
• Glycosylation of plasma proteins
fructosamine levels refects glycaemic
control for the past 6 weeks(shorter half life)
Complications: pathogenesis
26. Complications: pathogenesis
• Hyperglycaemia
• Excess entry of glucose into non-insulin dependent
tissues
– Nerves
– Lens
– Kidneys
– Blood vessels
• Increased intracellular glucose metabolized to
sorbitol fructose increased osmotic load
influx of water osmotic cell injury
• E.g. lens cataract
27. Vascular complications: pathogenesis
• “glyocosylation”of collagen and other long-lived
proteins in tissues
• Irreversible formation of advanced
glycosylation end products (AGEs)
accumulation of AGEs over the lifetime of blood
vessel walls
– Protein cross-linking and trapping of plasma
lipoproteins in blood vessel walls
– Reduction in protein breakdown
– AGE binding to cell receptors/ endothelial dysfunction
• vasculopathy
33. (1) Symptoms (thirst, increased urination,
unexplained weight loss) + a random plasma glucose
concentration >200 mg/dL (11.1 mmol/L).
(2) Fasting plasma glucose (FPG) >126 mg/dL (7.0
mmol/L) after an overnight (at least 8-hour) fast
(3) Two-hour plasma glucose greater than 200 mg/dL
(11.1 mmol/L) during a standard 75-g oral glucose
tolerance test (OGTT)
[ should be confirmed on a later day with one of the
three methods listed]
34. Oral Glucose Tolerance Test (OGTT)
(how much one can tolerate a glucose load without undue rise in
plasma glucose levels; reflects how efficiently insulin can handle
the glucose load))
Procedure
Overnight fast
75 g glucose in 300 ml water given orally over 5 minutes
Basal plasma glucose & every 30 minutes for 2 hours
Urine tested for sugar
Indications
Borderline fasting (FPG) or postprandial PG
Persistent glycosuria
Glycosuria of pregnancy
Pregnant women with family history of DM or had large babies
37. American diabetic association. Diagnosis and classification of diabetes
mellitus. Diabetic care, 2004, 27 (Suppl. 1); 55-60.
Robbins Pathologic basis of disease. Pocket companion. Saunders.
Holt RIG and Hanley N. Essential Endocrinology and Diabetes. 5th ed.
2007, Blackwell.
Merck Manual. iPhone app. Agile Parters. www.Merck Manuals.com.
Diabetes power point file. Prof. Hla-Yee-Yee, IMU.