Case 1:Poorly controlled type 2 diabetes on triple oral therapies
Case 2:Morning hypoglycemia on premixed InsulinCase 3
Case 3:Newly diagnosed D.M Type1D.M or type 2 D.M ?
Mr. AH is a 70-year-old man who was diagnosed with T2DM 10 years ago. He was initially treated with lifestyle management and metformin.
3 years later, his doctors advised him to add long acting basal insulin analogue to metformin, reached to 40U/day .
Other current medical conditions include: hypertension, hypothyroidism, and mild osteoporosis without fracture history.
Current medications; Metformin 1000 mg bid, long acting basal insulin analogue 40U/day , Candesartan 16 mg qd, Alendronate 70 mg once weekly, Levothyroxine 100 mg qd.
Physical exam: BMI 26 kg/m2, BP 140/80 mmHg, otherwise unremarkable.
His current FPG 140 mg/dL and HbA1c 8.5%. Kidney and liver functions are normal.
SGLT2I The paradigm change in diabetes managementPraveen Nagula
Just like ARNI, SGLT2I have changed the face of diabetes management and they have a good profile in multimodality management because of pleiotropic effects
This is a case on Diastolic heart failure with Type 2 Diabetes mellitus. Here we have discussed the pharmaceutical care plan (SOAP) about the treatment and non pharmacological approaches to treat the specified conditions
Irritable Bowel Syndrome: An Update in Pathophysiology and Management Monkez M Yousif
Irritable bowel syndrome is the commonest health problem in hospital outpatient clinics and in private health care facilities and represents a big challenge for patients and physicians. This presentation discusses a different aspect of the disease from pathophysiology, clinical presentation and management
Intensification Options after basal Insulin RevisitedUsama Ragab
Intensification Options revisited
By Dr. Usama Ragab Youssif
Add an OAD
Add a short-acting insulin at mealtime
Switch to premixed insulins
Novel insulin combinations
Basal insulin/GLP-1 RA combinations
Type 2 dm gdm new updates & guidelinesSachin Verma
Type 2 diabetes is a multifactorial disorder characterised by progressive pancreatic beta-cell dysfunction and insulin- resistance, leading to relative insulin deficiency, chronic hyperglycaemia, and various complications.
The treatment options for this disorder, which aim at correcting one or other of the two major pathophysiological mechanisms, have been hamstrung by unacceptable side-effects, lack of patient acceptability, and loss of efficacy over time.
Mr. AH is a 70-year-old man who was diagnosed with T2DM 10 years ago. He was initially treated with lifestyle management and metformin.
3 years later, his doctors advised him to add long acting basal insulin analogue to metformin, reached to 40U/day .
Other current medical conditions include: hypertension, hypothyroidism, and mild osteoporosis without fracture history.
Current medications; Metformin 1000 mg bid, long acting basal insulin analogue 40U/day , Candesartan 16 mg qd, Alendronate 70 mg once weekly, Levothyroxine 100 mg qd.
Physical exam: BMI 26 kg/m2, BP 140/80 mmHg, otherwise unremarkable.
His current FPG 140 mg/dL and HbA1c 8.5%. Kidney and liver functions are normal.
SGLT2I The paradigm change in diabetes managementPraveen Nagula
Just like ARNI, SGLT2I have changed the face of diabetes management and they have a good profile in multimodality management because of pleiotropic effects
This is a case on Diastolic heart failure with Type 2 Diabetes mellitus. Here we have discussed the pharmaceutical care plan (SOAP) about the treatment and non pharmacological approaches to treat the specified conditions
Irritable Bowel Syndrome: An Update in Pathophysiology and Management Monkez M Yousif
Irritable bowel syndrome is the commonest health problem in hospital outpatient clinics and in private health care facilities and represents a big challenge for patients and physicians. This presentation discusses a different aspect of the disease from pathophysiology, clinical presentation and management
Intensification Options after basal Insulin RevisitedUsama Ragab
Intensification Options revisited
By Dr. Usama Ragab Youssif
Add an OAD
Add a short-acting insulin at mealtime
Switch to premixed insulins
Novel insulin combinations
Basal insulin/GLP-1 RA combinations
Type 2 dm gdm new updates & guidelinesSachin Verma
Type 2 diabetes is a multifactorial disorder characterised by progressive pancreatic beta-cell dysfunction and insulin- resistance, leading to relative insulin deficiency, chronic hyperglycaemia, and various complications.
The treatment options for this disorder, which aim at correcting one or other of the two major pathophysiological mechanisms, have been hamstrung by unacceptable side-effects, lack of patient acceptability, and loss of efficacy over time.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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
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
Evaluation of antidepressant activity of clitoris ternatea in animals
Case studies in the managment of type 2 diabetes
1. Case Studies In The
Management of Type 2
Diabetes
Nasser Al-Juhani, MD,FRCP (U.K),ArBIM.SBIM,PHMD
Consultant of Endocrinology & Metabolic diseases
2. Rreceived honoraria/consultation fees from AstraZeneca, Sanofi,
Eli Lilly, Novo Nordisk, Boehringer Ingelheim, Merck, AstraZeneca
and Pfizer.
DISCLOSURE
4. • A 55-year-old man with
type 2 diabetes for 10 years.
• Background retinopathy
• C/O poluria,polydepsia and 4 Kg
weight loss over past 3 months
• Wt=70,Ht=166 cm, BMI is 25.4.
• Metformin 1 g BID po
• Empagliflozin 10 mg OD po
• Sitagliptin 100 mg od
• Normal renal & liver function
• eGFR 58
• Urine:albuminuria + ,no ketones
• ECG: normal
• HbA1c is 9.0 %.
1.1 What is your next treatment (s)
recommendation?
A. Add Gliclazide MR
B. Add repaglinide
C. Add pioglitazone
D. Add basal insulin
E. Add GLP-1 RA
Case 1
5. When to consider insulin in T2DM?
• Uncontrolled on 3 agents start INSULIN
• When 2 OAD being used-maximally
& AIC is not at goal ≥ 7%
If AIC < 8.5
Add 3rd OHA or insulin
or GLP-1RA
If AIC >8.5
Add insulin (or
GLP-1RA)
3rd OHA :
AIC drop 1%
Greater cost
6. • A 55-year-old man with
type 2 diabetes for 10 years.
• Background retinopathy
• C/O poluria,polydepsia and 4 Kg
weight loss over past 3 months
• Wt=70,Ht=166 cm, BMI is 25.4.
• Metformin 1 g BID po
• Empagliflozin 10 mg OD po
• Sitagliptin 100 mg od
• Normal renal & liver function
• eGFR 58
• Urine:albuminuria + ,no ketones
• ECG: normal
• HbA1c is 9.0 %.
1.2 What will you select as the basal
insulin for this patient?
A. NPH
B. Glargine U100
C. Glargine U 300
D. Detemir
E. Premixed insulin 70/30
Case 1
7. The Next Generation of Basal Insulin
with a Smoother PK/PD Profile than Lantus®
TOUJEO
•Smoother PK/PD
profile than Lantus®
•Full 24h coverage
•Less hypos than
Lantus
•Improved patient
experience
LANTUS
• Once daily
• Less hypos
than NPH
• Treat to target
NPH
PK/PD Profile: Pharmacokinetic/Pharmacodynamic Profile
8. Starting Basal Insulin+ OHA(S)
• Glargine 300 (Toujeo®) : 14 u at bedtime ,10 pm (0.2 U X 70 kg)
• Continue oral agent (s) at same dosage
• Daily FBG
• REQUEST PATIENT to increase basal dose 2 units
every 3 days to keep FBG target 80-130 mg/dl
During 6 & 12 months of follow-up
• Glaring -U300 dose was titrated to 45-U daily
• FBG averages 106 -115 mg/dL
• A1C = 6.6 – 6.9 %
5-18
9. At 2-year follow-up
• His weight increased 2 kg, BMI is 26.
• Background retinopathy/nephropathy
• Normal renal & liver function
• Has irregular eating habits; occasionally
misses meals during the day
• HbAic 8.1%
Case ……Con”d
57 yr man,DM2,Failure of 3 OADs Plus Basal insulin
Fasting
2H Post
breakfast
Pre
Lunch
2H Post
Lunch
Pre
dinner
2H Post
dinner
HbA1c
110 175 120 220 140 170 8.1%
• Metformin 1 g BID
• Empagliflozin 10 mg OD
• Sitagliptin 100 mg OD
• Glargine-U300) 45-U od pm
Target1 <110 <180 <130 <180 <130 <180 <7
Suspect PPH, IF FBG<130 mg/dl & AIC> goal >7%
10. A. Increase the dose of basal insulin
B. Add bolus insulin with lunch meal
C. Add bolus insulin with 3 main meals
D. Switch to twice daily premixed insulin
E. Add GLP-1 Receptor agonist
Choose the most suitable option?
11. How much rapid-acting analog at meal will you initiate?
Glulisine (Apidra®)
4 Units
OR
0.1-U/kg
12. Start Glulisine (Apidra®) 4 -U at lunch
INSTRUCT PATIENT to adjust rapid-acting analog dose
at meal by 2 units every 3 days until BG in the target.
Keep 2HPBG target 140-180 mg/dl
FBG target 80-130 mg/dl
Target HbAIC <7%
How do you adjust a rapid-acting analog at meals??
13. CASE 1 ……Con”d
6-Month Follow-Up
• Glargine 300 (Toujeo®) 46-U 10 pm
• Glulisine (Apidra®) 16-U at lunch and, patient is doing well
• Continue metformin 1 gm bid po/ Empagliflozin 10 mg od
• may D/C or continue Sitagliptin (more cost)
• A1C = 6.8%
• Patient feels well, has infrequent “ minor hypoglycemia,”
• Over time, if postprandial glucose becomes elevated at meals
other than lunch, add pre-meal insulin at that meal
14. Holman RR et al. Addition of biphasic, prandial, or basal insulin to oral therapy in type 2 diabetes. N Engl J Med 2007; 357(17): 1716–1730
>6 out of 10 basal insulin patients
will need another insulin to reach
target
After 1 year of treatment with basal oral therapy,
How many patients out of 10 will need another insulin?
15. When to target post-prandial blood glucose?
ADJUST BASAL insulin Controls pre-meal glucose
1st Fix the Fasting & Pre-dinner (PRE-MEALS)
80-130 mg/dl (4.4-7 mmol/l)
ADJUST BOLUS insulin :
if HbAic<8.0 %, the contribution of post-meal glucose becomes more
Pre-meal may be at target, but postmeal glucose values are high
Monitor 2-HPP
2hr PPG< 140-180 mg/dl (<10 mmol/l)
** AVOID HYPOGLYCEMIA <4 mmol/l( < 70mg/dl)
Controls post-meal glucose
16. Patient Not at Target with Basal
Insulin
Move on to
Multiple Daily Injections
Or
twice daily PreMix
Or
GLP-1 RA
18. 55-year-old man
T2DM x 10 years
Painful sensory neuropathy & nephropathy
eGFR 55, Creatinine 0.9 mg/dl
Erratic work schedule
sweating at some nights
Metformin XR 1500 mg od
Dapagliflozin 10 mg od
Premixed insulin analogue:
- 70/30 50 U am and 40 U pm
Hbaic 7.5%
FBG 200-280 mg/dl
• Morning hyperglycemia :
– Check blood sugar at bedtime and
between 2-3 a.m.
– Or Continuous glucose monitoring
Case 2
20. Classification of severity:
Non-severe versus severe symptomatic:
• Non-severe: Patient has symptoms but can
self-treat and cognitive function is mildly
impaired
• Severe: Patient has impaired cognitive
function sufficient to require external help
to recover (Level 3)
Reclassification of hypoglycaemia1–3
1. Seaquist ER et al. Diabetes Care 2013;36:1384‒1395.
2. International Hypoglycaemia Study Group. Diabetes Care 2017;40:155‒157.
3. Frier BM. Nat Rev Endocrinol 2014;10:711‒722.
Alert value for
hypoglycemia
Plasma glucose
3.9 mmol/L (< 70
mg/dl) and no
symptoms
Serious clinically
important
biochemical
hypoglycemia
Plasma glucose
3.1 mmol/l
(55 mg/dl)
Level 1 Level 2
21. Cause Bedtime 2-3 a.m. Fasting
Insufficient dinner rapid
acting dose/carbohydrate
consumption at night
High High High
Somogyi effect Normal Low High
Dawn phenomenon Normal Normal High
Morning hyperglycemia
22. Case 2
Shifting from premixed to Basal-Bolus insulin
For recurrent nocturnal HYPOGLYCEMIA
TDD= 90 U/day
80% of 90 U is 72 U
50% as basal: Glargine 300 (Toujeo®) – 36 units od 10:00 pm
36 U divided for three meals, (largest dose may given at largest meal) :
12 U before breakfast
12 U before lunch
12 U before dinner
24. 20-year-old male with newly
diagnosed DM
6 kg weight loss & polyuria for 1
month
Brother had T2DM
BMI 34.4 , acanthosis nigricans
Lab results:
BG 340 mg/Dl (18.8
mmol/l); A1C, 13%
Creatinine, 0.8 mg/dL
Ketones -ve
Anion gap, normal
In addition to Lifestyle modification
What is your next treatment
recommendation?
A. Metformin
B. Metformin plus Gliclizide
C. Metformin plus empagliflozin
D. Metformin plus liraglutide
E. insulin
Case 3
25. When should insulin be started in T2DM?
Newly diagnosed T2DM:
• ADA/EASD 2020
Consider
initial injectable combination
GLP-1 RA+Basal insulin
or
prandial/basal insulin
IF HbAIC 10% or 2% above target
26. Case 3
20 Yr old male Newly diagnosed D.M,BMI 34.4,
AIC=13% (cont.)
Type 1 D.M or type 2 D.M ?
27. Physical exam
• Obese / acanthosis nigricans
suggest DM2
• Thin suggest DM1
Family history
• More with DM 2 but occurs
also with DM 1
Complication
• Suggests undiagnosed DM 2
Age at onset
• <30 year
• >30 year
Differentiating Type 1 Vs. Type 2 DM
28. • Fasting serum C-peptide levels
• Normal or High C-peptide :
• DM1 (with honey moon) or DM2
Follow up :SMBG
• If insulin dose is reduced and no
ketones, may consider a trial of
stopping insulin
• If glucose high or ketones+ , resume
insulin
Low C-peptide :
DM1 or late DM2- Insulin
Testing for antibodies
- GAD-65
- Islet-cell
- IA2
- Insulin
-ZS
• High…DM1
• Normal…Idiopathic DM1 or DM2
Differentiating Type 1 Vs. Type 2 DM
29. Conclusions
Insulin Treatment in Type 2 Diabetes
• Basal treatment NPH or (glargine100 or 300) , detemir, degludec
Start 10 U and titrate
• Bolus treatment premeal (Lispro/glulisine/aspart)
Start at 4 U premeal and titrate;
• Premixed therapy
• Start at 10 U BID and titrate
• Basal bolus therapy
• Start at 0.5 U/kg, 40-50% basal, 20% bolus each meal