This document summarizes the pharmacotherapy of diabetes mellitus. It describes the types of diabetes, diagnostic criteria, goals of treatment, and various classes of medications used to treat diabetes. The main drug classes discussed include insulin, sulfonylureas, meglitinides, incretin mimetics, DPP-4 inhibitors, metformin, thiazolidinediones, and SGLT-2 inhibitors. For each class, the mechanisms of action, pharmacokinetics, indications, and side effects are summarized. The document provides an overview of current best practices for treatment and medication management of both type 1 and type 2 diabetes.
Sulfonyl ureas pharmacology Presented by arjumandPARUL UNIVERSITY
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
The slides describe concept of distribution, Volume of distribution, factors affecting volume of distribution and the barriers to distribution. Blood brain barrier and placental barrier.
Sulfonyl ureas pharmacology Presented by arjumandPARUL UNIVERSITY
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
The slides describe concept of distribution, Volume of distribution, factors affecting volume of distribution and the barriers to distribution. Blood brain barrier and placental barrier.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
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
Approach to case of type 2 DM
lifestyle modificatios
indications to start drug therapy
classification of antidiabetic drugs , mechanism of action , adeverse drug effects , doses , drug interactions , how to add differents class of drugs to give combination therapy . over view insulin therapy
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
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.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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!
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.
NVBDCP.pptx Nation vector borne disease control program
Pharmacotherapy of diabetes mellitus (DM)
1. Pharmacotherapy of
diabetes mellitus (DM)
By Nehal M. Ramadan. M.B.B.CH, MSc, PhD
Lecturer of Clinical Pharmacology
Clinical Pharmacology department, Faculty of Medicine, Mansoura University,
Egypt
2. Diabetes mellitus
Def → a group of disorders that
develop due to
● Insulin deficiency → T1DM
● Insulin resistance → inadequate
actions of insulin in stimulating
the uptake of glucose by
peripheral tissues → T2DM
→ hyperglycemia + disturbances in
metabolism of CHO, fat, and protein.
3. Diagnostic criteria
Clinical symptoms +
● Fasting blood glucose > 126 mg/dL
● Random blood glucose > 200 mg/dL
● 2-hour post-prandial glucose level > 200 mg/dL
● Hemoglobin A1c (HbA1c ) level >= 6.5%
HbA1c → the percentage of hemoglobin in circulating erythrocytes that is
glycosylated → an index of the average blood glucose level over the preceding 2 to 3
months.
4. Treatment of
T1DM
→ Patients with T1DM have an
absolute requirement for exogenous
insulin.
→ Most generally accepted target
goal for HbA1c in T1DM is 7.0%
Improved glycemic control in
patients with T1DM ↓ long-term
microvascular & macrovascular
complications
5. Insulin -> MOA
● When blood glucose ↑ → more glucose
enters pancreatic β cell via GLUT2 →
glycolysis → ↑ the ATP/ADP ratio →
inhibition of the ATP-sensitive K+ channel
(KATP) → membrane depolarization →
activation of voltage-gated Ca++ channels
→ ↑ intracellular Ca++ → insulin
secretion.
● Released insulin rapidly reaches liver,
muscles, and adipose tissue → binds to
and activates insulin receptor (a tyrosine
kinase receptor) → promote translocation
of glucose transporters (GLUT4) from
intracellular vesicles to the plasma
membrane → ↑ glucose uptake into the
cell.
6. Pharmacokinetics
of insulin
Route of administration →
● SC → most common for maintenance,
● IV → emergency treatment of diabetic
ketoacidosis → (regular insulin only)
● Recently → insulin SC infusion pumps &
inhaled insulin formulations
● Proteolytic destruction in the GI tract
prevents oral administration
Insulin preparations →
with different pharmacokinetics to meet different
physiological functions of insulin →
● Maintenance of constant low plasma glucose
levels during fasting
● Lowering blood glucose peaks after meals.
7. Insulin
Preparations
Insulin Type Onset Preprandial Injection Timing Peak Duration
Rapid-acting
● Lispro
● Aspart
● Glulisine
10-15 min At start of meal 1-2 h 3-5 h
Short-acting
Regular
30 min 30 min before meal 2-4 h 6-8 h
Intermediate-acting
NPH
1 h 30 min before meal 6 h Up to 18 h
Long-acting
● Glargine
● Detemir
● Degludec
2 h Once daily Peakless Up to 24 h
Peak insulin level
For
control
of
postprandial
hyperglycemia
To
maintain
baseline
glucose
levels
8. Premixed insulin
preparations (biphasic)
→ A premixed preparations of intermediate-acting
insulin (NPH) + short- or rapid-acting insulin, are
available as vials for injection with syringes or as
insulin pens.
→ Faster onset & longer duration of action
→ Greater ease of use → but are less likely to
achieve good glycemic control.
→ NPH/regular 70/30, NPH/regular 50/50,
NP/lispro 75/25, NP/lispro 50/50, NP/aspart 70/30
9. Insulin regimens
● Basal-bolus insulin therapy → intensive insulin regimen
→ MULTIPLE daily SC injections → injection of a long-
acting insulin analogue (e.g, glargine) once daily to
establish a stable basal insulin level + injection of rapid-
acting insulin analogue three or more times daily
(before each meal) to provide appropriate post-meal
peaks in insulin levels.
● Continuous SC insulin infusion → insulin pump
● Conventional insulin therapy → split-mixed regimen →
TWO daily injections of a premixed preparation
NPH/regular (or NPH/lispro) → ⅔ of the total daily
dose is given before breakfast and ⅓ before dinner
10. Let’s calculate
→ Total daily insulin requirements =
Body weight x starting dose =
0.2 x 45 = 9 U/day
● For a basal bolus regimen →
Divide the total daily insulin
requirements into ⅓ and ⅔ →
➔ Long-acting insulin → ⅓ of total
daily dose → 3U at bed time
➔ Rapid-acting insulin → ⅔ → 6U,
divided on 3 injections just before
each meal → 2U each
● For split-mixed regimen →
Divide the total daily insulin
requirements into ⅓ and ⅔ →
➔ Premixed NPH/regular 70/30 → ⅔
of total daily dose before
breakfast→ 6U
➔ Premixed NPH/regular 70/30 → ⅓
before dinner→ 3U
An adolescent girl is recently diagnosed
with T1DM → her body weight is 45 kg.
1. Given the information that the
typical starting insulin dose is 0.2
U/kg/day → calculate the total daily
insulin requirements for this girl?
2. Explain how can you formulate
these daily insulin requirements
into →
a. Basal bolus regimen
b. Split-mixed regimen
(conventional)
11. Insulin SEs
2. Diabetic ketoacidosis →
● Develops over hours or days.
● Opposite causes → low insulin dose,
skipped dose
● Hyperglycemia, ketoacidosis, electrolyte
imbalance, and dehydration
Other SE →
3. General weight gain
4. Temporary visual disturbances → changes in
the refractile properties of the lens
5. Localized fat accumulation/atrophy → if insulin
is repeatedly administered at the same site
→ disturbance in local adipocyte lipogenesis
functions → prevented by rotating injection
sites.
6. Local allergic reactions
7. Systemic allergic reactions → rare
1. Hypoglycemia→
○ The most serious complication
○ Rapid onset
○ Usually occurs due to → insulin overdoses,
changes in timing of injections or in eating
patterns (skipped meal), or high levels of
exercise.
○ Severe hypoglycemia can cause
unconsciousness, convulsions, brain
damage, and death.
○ Management → rapid restoration of blood
glucose → by iv concentrated dextrose
solutions
12. Insulin indications
1. Absolutely indicated in all cases of T1DM
2. T2DM patients if →
● Not controlled on antidiabetic
drugs
● In pregnancy
● In complications like diabetic
ketoacidosis → regular insulin i.v. is
preferred
● Stressful conditions like infections
and surgery etc.
3. Acute hyperkalemia
13. Diabetic
ketoacidosis
1. IV fluids → to correct fluid depletion
2. Continuous iv infusion of regular insulin
→ to slowly ↓ plasma glucose levels at
a rate of 50 to 100 mg/dL/hr.
3. IV administration of KCl → to
counteract hypokalemia
4. Glucose should be added to the iv insulin
infusion when glucose levels fall <
250 mg/dL → why? → Insulin infusion
are usually sufficient to treat acidosis &
should be continued until plasma
bicarbonate level is above 15 mEq/L.
However, hyperglycemia is usually
corrected more rapidly than acidosis →
added glucose will guard against
development of hypoglycemia
1
2
3
4
5
6
14. Treatment of
T2DM
→ treated mainly with anti-diabetic drugs
→ starting with one or two antidiabetic
drugs (acc. to the degree of hyperglycemia)
→ there is a progressive loss of beta-cell
function in T2DM over years → need for
adding a 3rd antidiabetic drug and →
ultimately, use of insulin
→ for younger T2DM patients → a target
goal for HbA1c in T1DM is 7.0%
→ for older T2DM patients with
complicating medical conditions → HbA1c
8% may be an acceptable and safer target
Improved glycemic control in
patients with T2DM ↓ long-term
microvascular complications
17. s
Meglitinides
SUs & meglitinides → common MOA → bind to SU
receptors on the KATP channels → channel closure
→ membrane depolarization & Ca++ entry → ↑
insulin release.
➔ Sulphonylureas
◆ 1st generation → Tolbutamide and
chlorpropamide → less potent & higher
risk of SE
◆ 2nd generations → glyburide, glipizide,
and glimepiride → 100 times more
potent, longer duration of action &
;ower risk of SE
➔ Meglitinides
◆ Repaglinide and nateglinide → rapid
onset of action & short-duration
Sulphonylureas
Meglitinides
GLP-1 analogues
18. Pharmacokinetics
& SEs
● Hypoglycemia →
○ the most common
○ result from overdose, skipped meals,
inadequate ingestion of carbohydrate,
renal or hepatic disease.
● Weight gain →
○ Common
○ Released insulin → ↑ lipogenesis
● Skin rashes
● GIT disturbances → nausea, vomiting, and
cholestasis.
● Hematologic reactions → leukopenia,
thrombocytopenia, and hemolytic anemia.
SUs (2nd gen) Meglitinides
MOA Common ????
Route Oral
Onset Faster than SUs
Duration of action Long → 24 h Short → 2-3 h
Administration Once daily, shortly
before/with
breakfast
Multiple, shortly
before/with each
meal
Effect on FBG ↓ →
Effect on PBG ↓ ↓
HA1c % ↓ 2% 1%
Plasma protein
binding
> 90%
Elimination Hepatic metabolism → renal/biliary
excretion
Hypoglycemia &
weight gain
less than SUs
19. Incretins
➔ Incretins → hormones released
from endocrine cells in small
intestine in response to food →
act on specific Rs pancreatic β
cells → ↑ insulin secretion
(glucose-dependant insulin
secretion)
➔ Two incretin hormones in
humans → glucose-dependent
inosulintropic polypeptide (GIP)
and glucagon-like peptide-1
(GLP-1).
➔ Incretins are rapidly catabolized
by dipeptidyl peptidase-IV
(DPP-IV)
Other effects of incretins:
➔ ↑ proliferation of β cells.
➔ ↓ glucagon secretion
➔ GLP-1 →
◆ Delays gastric emptying
◆ ↓ appetite
◆ ↓ blood pressure
◆ ↑ lipolysis in adipose tissue
20. Incretin mimetics
(GLP-1 analogues)
MOA →
➔ Liraglutide & exenatide → synthetic analogues
of human GLP-1 + resistant to degradation by
DPP-IV → prolonged duration of action
➔ GLP-1 analogues → bind to GLP-1 receptors
on beta cell → ↑ intracellular cAMP →
● cAMP-mediated activation of calcium
channel → glucose-dependent insulin release
● ↓ glucagon secretion
➔ Delays gastric emptying
➔ ↓ appetite
➔ ↓ blood pressure
Sulphonylureas
Meglitinides
GLP-1 analogues
Administered SC , once or
twice daily
Newer GLP-1 analogues → Dulaglutide
→ has been linked to human Ig or
albumin → very slowly eliminated →
half-life of a week → administered
once weekly
21. Incretin mimetics
(DPP-4 inhibitors)
MOA →
➔ Gliptins → sitagliptin, saxagliptin,
linagliptin
➔ Competitive inhibitors of DPP-IV (enzyme
that inactivates endogenous incretins) →
2x to 3x ↑ in incretin levels → glucose-
dependant insulin release ↑
Administered orally, once daily
22. DPP-4 inhibitors
● GIT SEs → low risk
● Hypoglycemia → rare
● Weight → neutral
● Pancreatitis → no
● Thyroid C-cell tumors → no
● ↑ in upper resp. tract infections & UTIs
● Arthralgia and hypersensitivity
reactions
● GIT SEs → mild-moderate nausea,
vomiting, diarrhea → ↓ over time →
start with low dose
● Hypoglycemia → rare, unless
combined with insulin, sulfonylureas,
or meglitinides → ↓ dose of insulin, etc
● Weight → ↓
● Pancreatitis → slight ↑ → require further
investigations
● Thyroid C-cell tumors → only in rodents
● Antibody formation → GLP-1 analogues →
synthetic peptides → could be recognized as
antigens → incidence is high with exenatide
GLP-1 analogues
24. Metformin
MOA →
➔ 1st-line drug for ttt of T2DM → esp.
for obese ptns with insulin resistance
➔ 1ry & most imp. effects → in the liver
→ inhibition of gluconeogenesis → ↓
hepatic glucose output
◆ Maybe due to inhibition of the
mitochondrial electron complex 1 →
activation of 5′adenosine
monophosphate-activated kinase
(AMPK) → ↓ transcription of genes
for gluconeogenesis
➔ ↑ insulin sensitivity & ↑ glucose uptake
in skeletal muscle and adipose tissue
➔ ↓ glucose absorption from the
intestines
25. Metformin
● GIT SEs →
○ the most common SEs
○ Diarrhea (30% of ptns), nausea,
vomiting, and flatulence.
○ Usually subsides over time.
● Lactic acidosis →
○ Very rare (only 3 cases per
100,000 ptn)
○ Due to interference with hepatic
mitochondrial glucose oxidation
○ CI in ptns with renal or hepatic
disease, or alcoholics → higher risk
of lactic acidosis
26. Thiazolidinediones
MOA →
➔ Pioglitazone & rosiglitazone
➔ 1ry & most imp. effects → on skeletal
muscle and adipose tissue
◆ A lesser effect → on the liver.
➔ Agonists at the peroxisome proliferator–
activated receptor-γ (PPAR-γ) → ↑
transcription of insulin-responsive
genes → ↑ peripheral insulin sensitivity
(60%) in ptns with T2DM.
◆ ↑ number of GLUT4 glucose
transporters in cell membranes of
muscle and adipose tissue → ↑
peripheral uptake of glucose
27. Metformin
● Body weight → ↓
● CV SEs → ↑ plasma volume, edema,
and ↑ risk of developing heart failure →
not used as 1st-line therapy in T2DM
& CI in ptns with/at risk of heart failure.
● Body weight→ ↑
● Risk of bladder cancer → slight ↑ →
pioglitazone
● Osteoporosis & fractures → ↑ → as it ↓
bone mineral density
Pioglitazone
28. Drugs that ↓ glucose reabsorption
● SGLT-2 inhibitors
Low risk of hypoglycemia
29. SGLT-2 inhibitors
MOA →
➔ The newest oral drugs for T2DM →
canagliflozin, dapagliflozin, and
empagliflozin.
➔ SGLT-2 → responsible for reabsorption
of 90% of filtered glucose in PCT
➔ SGLT2 inhibitors → selectively inhibit
SGLT2 → ↓ renal glucose reabsorption →
↑ urinary glucose excretion → ↓ blood
glucose levels
➔ High glucose in renal tubules → osmotic
diuresis → ↑ urine volume → ↓ blood
pressure
➔ Loss of calories in urine → ↓ weight
Based on the fact that → efficacy of SGLT-2
inhibitors is dependent on renal glomerular
filtration of glucose → SGLT-2 inhibitors are CI
in ptns with glomerular filtration rates <
50 mL/min.
30. ● ↑ incidence of UTIs and genital
yeast infections → as they ↑
urinary glucose levels & facilitate
microbial growth.
● Volume depletion → as they cause
osmotic diuresis → cases of acute
renal injury; in susceptible ptns
(dehydrated, heart failure or low
blood pressure, or are taking other
drugs affecting the kidneys as
diuretics and angiotensin-
converting enzyme (ACE) inhibitors)
→ reversible.
SGLT-2 inhibitors ● Rarely diabetic ketoacidosis →
euglycemic
● ↑ risk of osteoporosis and bone
fractures,
31. Drugs that ↓ glucose absorption
● α-glucosidase inhibitors
Low risk of hypoglycemia
32. MOA →
● Acarbose → a competitive
inhibitor of α- glucosidase enzyme
→ an intestinal enzyme that
converts oligosaccharides and
disaccharides to glucose → ↓
digestion & absorption of dietary
starch and disaccharides → ↓
postprandial blood glucose.
Acarbose SEs →
● Flatulence and abdominal bloating →
most common → result from delivery of
greater amounts of carbohydrate to
colon → exert an osmotic attraction for
water and are metabolized by bacteria.
● ↓ iron absorption.
N/B.. If ptns is on concurrent ttt with insulin
and acarbose, then he develops
hypoglycemia → should be treated with oral
glucose (dextrose) NOT sucrose → as sucrose
requires α-glucosidase activity for digestion
33. For T2DM→
● Metformin →
generally preferred as
first-line therapy
● For patients with CV
disease or chronic
kidney disease (CKD)
→ SGLT-2 inhibitors or
GLP-1 agonists →
recommended as first
line → proved to ↓ in
diabetes-related CV
complications
● Ptns requiring dual
therapy →
METformin +
1. GLP-1 analogues
2. SGLT inhibitors
3. DPP-4 inhibitors
4. TZD
5. SU
34. A 44-year-old man with a body mass
index of 34 kg/m2 was found to have
type-2 diabetes mellitus on routine
testing 3 months ago. He was advised
a low-energy, weight-reducing diet
and exercise. He has been unable to
comply with this, and recent
investigations show postprandial
blood glucose concentration is 250
mg/dl.
What would be the best drug to initiate
as first-line therapy for type-2
diabetes in this patient?
A. Gliclazide
B. Insulin
C. Metformin
D. Pioglitazone
E. Sitagliptin
35. A 34-year-old male patient has a past
medical history of Type 2 diabetes
and hypertension he has been
experiencing profound swelling in his
feet and lower legs for the past two
weeks
Medications:
● Metformin 850 mg tablet 1 po three times
daily;
● Gliclazide tablet two po twice daily;
● Pioglitazone 45 mg tablet 1 po once daily;
● insulin glargine inject 20 units
subcutaneously every evening;
● lisinopril 10 mg tablet 1 po once daily
Which diabetes medication is most
likely responsible for his new edema?
A. Gliclazide
B. Insulin
C. Metformin
D. Pioglitazone
36. A 52-year-old man presents to his
PCP’s office for a routine follow-up
visit on diabetes. His diabetes was
diagnosed one year ago and he has
only been prescribed metformin for
treatment. His metformin dose was
maximized last month, but his blood
glucose levels are still not at goal.
You need to add an oral agent that is
safe, and effective enough to
potentially attain a goal A1c of <7
percent.
What drug class do you recommend?
37. Which of the following
statements is correct
regarding insulin glargine?
A. It is primarily used to control
postprandial hyperglycemia.
B. It is a “peakless” insulin.
C. The prolonged duration of
activity is due to slow
dissociation from albumin.
D. It should not be used in a
regimen with insulin lispro or
glulisine.
E. It may be administered
intravenously in emergency
cases
38. A 78-year-old nursing home resident is
admitted to the acute medical unit after being
found collapsed in his room. A carer from the
nursing home is present and reports that he has
had regular 'hypos' recently. On admission he
was drowsy and the blood glucose was 45 mg/dl.
Following intravenous dextrose the patient's
condition significantly improved.
His medication on admission is as follows:
Metformin 1g bd
Glipizide 160mg od
Pioglitazone 45mg od
Aspirin 75mg od
Simvastatin 40mg od
What is the most appropriate initial
action?
A. Stop metformin
B. Stop pioglitazone
C. Stop gliclazide
D. Make no changes to the
medication
E. Stop all oral antidiabetic
medications