The pancreas secretes several important hormones including insulin, glucagon, somatostatin, and pancreatic polypeptide. The endocrine part of the pancreas contains clusters of cells called islets of Langerhans. The main cell types in the islets are alpha cells which secrete glucagon, beta cells which secrete insulin and amylin, delta cells which secrete somatostatin, and F cells which secrete pancreatic polypeptide. These hormones regulate important metabolic processes like blood glucose levels. Insulin lowers blood glucose while glucagon raises it. Somatostatin inhibits the secretion of insulin and glucagon.
introduction to oral hypoglycemic agents with description about sulphonylurea and glinides along with their MOA, indication, side effects and brand name
In this PPTs you will get in depth information about insulin and the first class of oral hypoglycemic agents , Sulfonylurea.
useful for GPAT and Third Year B.Pharm students.
Oral hypoglycemic drugs are used only in the treatment of type 2 diabetes which is a disorder involving resistance to secreted insulin. Type 1 diabetes involves a lack of insulin and requires insulin for treatment. There are now four classes of hypoglycemic drugs:
introduction to oral hypoglycemic agents with description about sulphonylurea and glinides along with their MOA, indication, side effects and brand name
In this PPTs you will get in depth information about insulin and the first class of oral hypoglycemic agents , Sulfonylurea.
useful for GPAT and Third Year B.Pharm students.
Oral hypoglycemic drugs are used only in the treatment of type 2 diabetes which is a disorder involving resistance to secreted insulin. Type 1 diabetes involves a lack of insulin and requires insulin for treatment. There are now four classes of hypoglycemic drugs:
Sulfonylureas are most commonly used Oral Hypoglycemic drugs helpful in treating Diabetes Mellitus .
They show their effects on beta cells of the pancreas to release insulin which maintains the blood sugar level.
They are also called as ATP sensitive Potassium[K] channel blockers.
Sulfonylureas are most commonly used Oral Hypoglycemic drugs helpful in treating Diabetes Mellitus .
They show their effects on beta cells of the pancreas to release insulin which maintains the blood sugar level.
They are also called as ATP sensitive Potassium[K] channel blockers.
Pancreas makes a hormone called insulin. It helps your cells turn glucose, a type of sugar, from the food you eat into energy. Diabetes happens when one or more of the following occurs:
Your pancreas does not make any insulin.
Your pancreas makes very little insulin.
Your body does not respond the way it should to insulin
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from whic
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from which
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!
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
2. PANCREAS
The pancreas is an organ of the digestive system and endocrine system. It is located in
the abdomen behind the stomach and functions as a gland.
The pancreas has both an endocrine and a digestive exocrine function.
The endocrine part of pancreas is made up of small bundles of cells called as Islet of
Langerhans.
3. PANCREAS
There are five main types of endocrine cells in Pancreas as follows.
Alpha cells = secretes Glucagon
Beta cells = secretes Insulin
Delta cells = secretes Somatostatin
Gamma cells = secretes Pancreatic Polypeptide (PP)
Epsilon cells = secretes Ghrelin
4. GLUCAGON
Glucagon is a hormone that raises blood glucose levels by stimulating the liver to
convert its glycogen into glucose.
It is secreted by alpha cells of Islet of Langerhans.
Alpha cells make up to 15-20% of total Islet cells.
5. PHARMACOLOGICAL ACTION
Glucagon’s main pharmacologic activities are to increase blood glucose and relax
smooth muscle of the GI tract. The mechanisms of action for its GI effects are poorly
understood.
Glucagon causes Lipolysis and Ketogenesis.
Glucagon enhances Gluconeogenesis and urea formation.
It primarily increases blood glucose by stimulating hepatic glycogenolysis.
Glucagon increases alanine uptake by liver and hepatic glucose output.
6. PHARMACOLOGICAL ACTION
Glucagon stimulates insulin secretion and hepatic ketone body formation in presence
of low insulin levels.
Glucagon secretion is stimulated by Low levels of blood glucose (hypoglycemia),
Norepinephrine, Arginine, Cholecystokinin (CCK), Gastrin, Glucocorticoids etc.
Glucagon secretion is inhibited by High blood glucose, Somatostatin, GABA, Fatty
acids.
7. PHARMACOKINETICS
Glucagon must be administered parenterally as it is destroyed in the gut after oral
dosing.
After intravenous injection, maximum glucose levels are attained within 30 minutes;
hyperglycemic effects persist up to 90 minutes after dosing.
Glucagon is degraded in the plasma, liver and kidneys; in humans, plasma half-life is
around 10 minutes.
8. USES/INDICATION
In small animals, glucagon is used to increase blood glucose in patients with excessive
insulin levels (Insulinomas).
In Dairy cows, glucagon is used in the treatment of fatty liver syndrome.
In human medicine, glucagon is used in treating the cardiac manifestations of beta-
blocker and calcium-channel blocker overdoses.
10. ADVERSE EFFECTS
Adverse Effects of Glucagon is very rare.
Nausea and vomiting can be observed after administration.
Hypokalemia and Hypersensitivity reactions.
11. DOSAGE
Dogs and Cats
For hypoglycemic treatment
1 mg of glucagon is reconstituted per manufacturer directions and then added to
mL of 0.9% Sodium Chloride.
Initially give a 50 ng/kg bolus IV and then administer at 5-15 ng/kg/min. (ng=
nanogram)
Cattle
For treatment of fatty liver in dairy cows
5 mg glucagon in 60 mL of normal saline SC, every 8 hours (15 mg/day) for 14 days
12. INSULIN
Insulin is a pancreatic hormone secreted by beta cells of islet of Langerhans that is
used to treat diabetic ketoacidosis, uncomplicated diabetes mellitus and as adjunctive
therapy in treating hyperkalemia.
Aside of Insulin, the other secretions of Beta cells are:
Proinsulin
C peptide
Islet amyloid polypeptide (IAPP or amylin): Slows gastric empyting and prevents spikes
in blood glucose level
Gamma- aminobutyric acid (GABA)
13. STRUCTURE OF INSULIN
Insulin is composed of two peptide chains referred to as the A chain and B chain.
A and B chains are linked together by two disulfide bonds, and an additional disulfide
is formed within the A chain.
The A chain consists of 21 amino acids and the B chain of 30 amino acids as shown in
figure below.
16. PHARMACOLOGICAL ACTION
Insulin facilitates uptake and entry of glucose in the muscles, adipose and several other
tissues.
Insulin stimulates the liver to store the glucose in form of glycogen.
Insulin promotes synthesis of fatty acid in liver.
Insulin Inhibits breakdown of fat in adipose tissue.
The hormone stimulates lipogenesis, increases protein synthesis, and inhibits lipolysis
and free fatty acid release from adipose tissues.
Insulin promotes an intracellular shift of potassium and magnesium.
18. USES/INDICATIONS
Insulin preparations have been used for the treatment of diabetic ketoacidosis,
uncomplicated diabetes mellitus, and as adjunctive therapy in treating hyperkalemia.
19. PHARMACOKINETICS
Insulin is metabolized mainly by the liver and kidneys and also muscle and fat to a
lesser degree.
It is metabolized by enzymatic reduction to form peptides and amino acids.
Insulin is filtered by the renal glomeruli and is reabsorbed by the tubules, which also
degrade it.
The half-life of insulin is less than ten minutes.
20. PRECAUTIONS AND ADVERSE EFFECTS
Precautions
Do not inject insulin at the same site day after day or lipodystrophic reactions can
occur.
There is not much contraindication for insulin.
Adverse Effects
Hypoglycemia
Insulin-induced hyperglycemia i.e. Somogyi effect
Local reactions to the foreign proteins.
21. DOSES
Dogs and Cats
For treatment of diabetic ketoacidosis use regular insulin Initial Dose: 0.2 U/kg IM into
muscles of the rear legs; repeat IM doses of 0.1 U/kg hourly.
For treatment of severe hyperkalemia give regular insulin 0.25–0.5 U/kg slow IV bolus
followed by 50% dextrose solution.
Cattle
For treatment of ketosis give PZI insulin 200 Units (total dose) SC once every 48
22. DIABETES MELLITUS
Diabetes mellitus is a chronic, metabolic disease characterized by elevated levels of
blood glucose, which leads over time to serious damage to the heart, blood vessels,
eyes, kidneys and nerves.
Most symptoms secondary to hyperglycemia are polyuria, polydipsia and polyphagia.
23. CLASSIFICATION OF DM
Insulin Dependent Diabetes Mellitus (IDDM) or Type 1 DM
Non-Insulin Dependent Diabetes mellitus (NIDDM) or Type 2 DM
Gestational Diabetes mellitus
Malnutrition related DM (MRDM)
Other types
24. IDDM OR TYPE 1 DM
It results from the failure of pancreas to produce enough insulin or it is insulin
dependent DM.
It is also known as Juvenile Diabetes since age of onset is juvenile.
Ketonuria is common but the body weight remains normal.
For treatment of IDDM, Insulin is necessary.
25. NIDDM OR TYPE 2 DM
It begins with insulin resistance, a condition in which cell fails to respond to insulin
properly.
It is also adult onset diabetes since adult are mostly affected.
Mostly body is obese and there is no ketonuria.
Treatment with Insulin is usually not required.
27. HYPOGLYCEMIC DRUGS / ANTI DIABETIC
DRUGS
A) Injectable Hypoglycemic Drugs i.e. Insulin
B) Oral hypoglycemic drugs
1) Sulfonylureas
(a) First generation: Tolbutamine, Chlorpropamide, Tolazamide, Acetohexamide
(b) Second generation : Glibenclamide, Glipizide
Acts indirectly
They stimulate β-cells and release insulin
30 % of β-cells most be active for their action.
Should not be used in pregnancy because they are teratogenic.
Mainly used in NIDDM.
28. HYPOGLYCEMIC DRUGS / ANTI DIABETIC
DRUGS
2) Biguanides: Metformin, Phenphormin, and Buformin
Acts directly by increasing insulin sensitivity.
Generally metformin is the first medication prescribed for Type 2 DM (NIDDM).
It has No effects on β-cells.
Effective in IDDM also.
Lactic acidosis is harmful side effect.
29. HYPOGLYCEMIC DRUGS / ANTI DIABETIC
DRUGS
Metformin
Oral anti-hyperglycemic agent that is useful in the treatment of non-insulin
diabetes mellitus (NIDDM) in cats.
It is contraindicated in patients hypersensitive to it, with renal dysfunction, metabolic
acidosis, or temporarily when iodinated contrast agents are to be used.
Adverse effects may include lethargy, anorexia, vomiting, & weight loss
30. HYPOGLYCEMIC DRUGS / ANTI DIABETIC
DRUGS
3) Meglitinides
Meglitinides modulate β-cell insulin release.
Meglitinides are oral medications used to treat type 2 diabetes.
They work by triggering production of insulin.
4) Thiazolidinediones: Decreases Insulin resistance
5) Alfa-glycosidase inhibitors: delay CHO absorption
31. SOMATOSTATIN
Somatostatin is a polypeptide made up of 41 amino acids.
Somatostatin also known as growth hormone-inhibiting hormone (GHIH) is produced
by delta cells of Islet of Langerhans and hypothalamus.
Somatostatin is a polypeptide made up of 41 amino acids.
It inhibits Insulin and Glucagon secretion and also functions as neurotransmitter in
Brain
Somatostatin is secreted in response to high level of other endocrine hormones.
Somatostatin secretion is inhibited by low levels of other endocrine hormones.
32. SOMATOSTATIN
Action
Somatostatin decreases gastrointestinal functions by decreasing motility, secretion and
absorption.
It Inhibits secretion of gastrin and secretin.
It decreases splanchnic blood flow.
It decrease the release of Insulin and Glucagon.
It also functions as neurotransmitter in Brain.
Pharmacokinetics
Half life is 2-4 min
Synthesized in two forms i.e. somatostatin-14 and somatostatin-28
33. SOMATOSTATIN
Pharmacokinetics
Half life is 2-4 min
Synthesized in two forms i.e. somatostatin-14 and somatostatin-28
Indication
Somatostatin analogs are used for treatment of tumors secreting vasoactive intestinal
peptide, carcinoid tumors, glucagonomas and various pituitary adenomas.
It is also used to treat acromegaly
34. SOMATOSTATIN
Adverse Effects
Steatorrhoea
Diarrhea and loose stools.
Malabsorption
Gastrointestinal cramps and occasional nausea.
Somatostatin inhibits gallbladder contractions, and some patients treated with
Sandostatin developed gallstones.
35. PANCREATIC POLYPEPTIDE (PP)
Pancreatic polypeptide (PP) is a polypeptide secreted by PP cells in the endocrine
pancreas predominatly in the head of pancreas.
It consists of 36 amino acids.
Action
The function of PP is to self-regulate pancreatic secretion activities.
It also has effects on hepatic glycogen levels and gastrointestinal secretions.
36. PANCREATIC POLYPEPTIDE (PP)
Plasma PP has been shown to be reduced in conditions associated with increased food
intake and elevated in anorexia nervosa.
Peripheral administration of PP has been shown to decrease food intake in rodents.. It
is the antagonist of CCK and inhibits the pancreatic secretion which is stimulated by
cholecystokinin.
37. GHRELIN
Ghrelin is a hormone that is produced and released mainly by the stomach with small
amounts also released by the epsilon cells of pancreas.
Ghrelin is termed the 'hunger hormone' because it stimulates appetite, increases food
intake and promotes fat storage.
Action
Ghrelin exerts wide physiological actions throughout the body, including growth
hormone secretion, appetite and food intake, gastric secretion and gastrointestinal
motility, glucose homeostasis, cardiovascular functions, anti-inflammatory functions,
reproductive functions, and bone formation.