- Type 2 diabetes accounts for over 90% of diabetes cases worldwide and is associated with obesity, lack of exercise, and poor diet. It is managed through lifestyle modifications including diet, exercise, oral hypoglycemic medications, and sometimes insulin therapy.
- The main treatment approaches involve dietary changes to control blood sugar and weight, regular physical activity, oral medications like metformin and sulfonylureas, and potentially insulin therapy if blood sugar levels remain uncontrolled.
- Close monitoring of blood sugar levels through self-testing and HbA1c levels helps guide treatment adjustments and ensure proper management of the disease.
Defines diabetes mellitus as a chronic metabolic disorder caused by insulin deficiency leading to hyperglycemia.
Highlights global diabetes statistics: >380 million globally, 1.56 million in Uganda (2014), 4.4% prevalence, and a significant undiagnosed population.
Classifies diabetes into: Type 1, Type 2, Gestational diabetes, and diabetes due to other causes.
Discusses Type 1 diabetes: diagnosis in childhood, autoimmune factors, environmental influences, and LADA.
Describes Type 2 diabetes: common in adults, links to obesity and lifestyle, with childhood cases rising.
Describes gestational diabetes, its risk factors, prevalence in pregnancies, and potential progression to Type 2 diabetes.
Lists symptoms of diabetes: polyuria, weight loss, fatigue, dehydration, complications like retinopathy and neuropathy.
Outlines diagnostic criteria for diabetes including blood sugar levels and testing methods like OGTT.
Discusses the approach to managing diabetes through thorough history taking and physical examination.
Lists investigations needed for diabetes management: urinalysis, blood glucose testing, and lipid profile.
Details treatment components: Diet, Exercise, Oral hypoglycemics, and Insulin therapy.
Emphasizes correct diagnosis, self-care, teamwork, and controlling cardiovascular risk factors.
Details dietary management focusing on nutrient balance, caloric intake, and glycemic control.
Discusses exercise benefits for weight reduction and improved insulin sensitivity.
Describes oral agents for diabetes management, categorization, and their application in treatment phases.
Details the combination therapy of insulin with oral anti-diabetic agents for improved glycemic control.
Presents a visual representation of diabetes management strategies.
Offers guidelines for oral medication use in diabetes, especially in special cases like pregnancy.
Discusses when to initiate insulin therapy, types of regimens, and insulin use in treatment.
Emphasizes self-monitoring practices and how to assess glycemic control through HbA1C measurements.
Highlights the need for patient education in self-management practices to take control of diabetes.
Diabetes Mellitus
Definition
A chronicdisorder of metabolism resulting from lack or reduced
effectiveness of endogenous insulin, characterized by hyperglycemia.
4.
Epidemiology
• >380 millionpeople worldwide have DM
• >90% have type 2 DM
• In Uganda in 2014 (adults 20-79yr);
- Approx 1.56 million pple have DM (est. 98,000 in yr 2000)
- Prevalence of 4.4%
- 693,200 cases were registered, 17,570 deaths
- Cost per person with DM = $ 84.9 ( Ugshs=257,247)
- Estimated undiagnosed DM= 520,500
Type 1 DM
•Usually diagnosed in childhood but can occur at any age
• Insulin deficiency from autoimmune destruction of pancreatic B cells
• Concordance among identical twins approx 30%
• >90% carry HLA DR3 +/- DR4
• Environmental factors have a role in disease;
-infection: mumps, cox sackie, CMV, EBV, rubella(in utero)
-diet: bovine serum antigen (BSA)
• Atleast 70-90% of pancreatic B cells destroyed
• Latent Autoimmune Diabetes of Adults(LADA)
9.
Type 1 cont…
•LADA
• Latent Autoimmune Diabetes in Adults (LADA) is a form of type 1
DM which is diagnosed in individuals who are older than the usual
age of onset of type 1 diabetes.
• Aka "Slow Onset Type 1" diabetes, and sometimes also Type 1.5
• Often, patients with LADA are mistakenly thought to have type 2
dm, based on their age at the time of diagnosis.
10.
Type 2 DM
•Common in adults > 40yrs
• Teenagers are now also increasingly being diagnosed
• Associated with obesity, lack of exercise, calorie & alcohol excess
• Concordance in identical twins approx. 80%
• Have B cell dysfunction and insulin resistance
• Typically progresses from IGT or IFG
• Maturity onset Diabetes of the Young (MODY)- Form of DM type 2
11.
Gestational diabetes
• Diabetesoccurring during pregnancy without prior hx of diabetes
• Usually resolves after pregnancy
• Occurrs in 4% of pregnancies
• Risk : >25yrs, +ve family hx, obesity
• Approx. 5-10% are found to have DM type 2 after pregnancy
• Have 20-50% chance of developing type 2 DM in the next 5-10yrs
13.
Clinical Features
• Polyuria,polydipsia & polyphagia
• Weight loss
• Fatigue
• Dehydration
• DKA
• Eyes- Retinopathy/ cataract
- ask for visual blurring or blindness.
- check for visual acuity, do fundoscopy
14.
Clinical features cont….
•Head : CN palsy
• Cvs- hypertension,MI
- take appropriate history,
- take bp
• GUT- nephropathy, erectile dysfunction, uti
• MSS- peripheral neuropathy, slow wound healing, foot ulcers,
wasting, obesity
• Skin- pigmentation, acathosis nigricans
15.
Diagnosis of DiabetesMellitus
• Symptoms of diabetes or testing urine for glucose and
ketones.
• random blood sugar(RBS) ≥ 11.1 mmol/L (200
mg/dL)
• Fasting plasma sugar(FBS) ≥ 7.0 mmol/L (126 mg/dL)
NB: FBS is the most reliable & convenient test for
identifying D.M in asymptomatic individuals.
16.
• Random isdefined as without regard to time since the
last meal.
• Fasting is defined as no caloric intake for at least 8 h
preceded by unrestricted carbohydrate diet for 3 days
before the test.
Indications for Oral Glucose Tolerance test(OGTT)
RBS: 7.8-11.0mmol/l (140-199 mg/dl)
FBS: 6.1-7.0mmol/l (110-126 mg/dl)
• The OGTT should be performed using a glucose load
containing the equivalent of 75 g anhydrous glucose
dissolved in water.
Treatment
• The majorcomponents of the treatment of diabetes
are:
• Diet and ExerciseA
• Oral hypoglycaemic
therapyB
• Insulin TherapyC
22.
Basic Principles• Correctdiagnosis is essential.
• lowering the blood glucose level but also correction of any
associated CVD risk factors such as
smoking,hyperlipidemias, and obesity
• Management of non-insulin-dependent diabetes mellitus
(NIDDM) requires teamwork.
• Self-care is an essential strategy. People with diabetes
should be encouraged and enabled to participate actively
in managing and monitoring their condition.
• Good control is important
23.
A. Diet
Dietis a basic part of management in every case.
Treatment cannot be effective unless adequate
attention is given to ensuring appropriate nutrition.
Dietary treatment should aim at:
◦ ensuring weight control
◦ providing nutritional requirements
◦ allowing good glycaemic control with blood
glucose levels as close to normal as possible
◦ correcting any associated blood lipid
abnormalities
24.
A. Diet (cont.)
•Dietary fat should provide 25-35% of total intake of
calories. Cholesterol consumption should be
restricted and limited to 300 mg or less daily.
• Protein intake can range between 10-15% total
energy (0.8-1 g/kg of desirable body weight).
Requirements increase for children and during
pregnancy
• Carbohydrates provide 50-60% of total caloric
content of the diet. Carbohydrates should be low
glycemic index and high in fibre.
25.
Exercise
• Physical activitypromotes weight reduction and
improves insulin sensitivity, thus lowering blood
glucose levels.
• Together with dietary treatment, a programme of
regular physical activity and exercise should be
considered for each person. Such a programme must
be tailored to the individual’s health status and
fitness.
• People should, however, be educated about the
potential risk of hypoglycaemia and how to avoid it.
26.
B. Oral Anti-DiabeticAgents
• There are currently four classes of oral anti-diabetic
agents:
i. Biguanides
ii. Insulin Secretagogues – Sulphonylureas
iii. Insulin Secretagogues – Non-sulphonylureas
iv. α-glucosidase inhibitors
v. Thiazolidinediones (TZDs)
27.
B.1 Oral AgentMonotherapy
If glycaemic control is not achieved (HbA1c > 6.5%
and/or; FPS > 7.0 mmol/L or; RPS >11.0mmol/L) with
lifestyle modification within 1 –3 months, ORAL
ANTI-DIABETIC AGENT should be initiated.
In the presence of marked hyperglycaemia in newly
diagnosed symptomatic type 2 diabetes (HbA1c >
8%, FPS > 11.1 mmol/L, or RPS > 14 mmol/L), oral
anti-diabetic agents can be considered at the outset
together with lifestyle modification.
28.
B.1 Oral AgentMonotherapy (cont.)As first line therapy:
Obese type 2 patients, consider use of metformin,
acarbose or TZD.
Non-obese type 2 patients, consider the use of
metformin or insulin secretagogues
Metformin is the drug of choice in overweight/obese
patients. TZDs and acarbose are acceptable alternatives
in those who are intolerant to metformin.
If monotherapy fails, a combination of TZDs, acarbose
and metformin is recommended. If targets are still not
achieved, insulin secretagogues may be added
29.
B.3 Combination OralAgents and Insulin
If targets have not been reached after optimal dose of
combination therapy for 3 months, consider adding
intermediate-acting/long-acting insulin (BIDS).
Combining insulin and the following oral anti-diabetic
agents has been shown to be effective in people with
type 2 diabetes:
◦ Biguanide (metformin)
◦ Insulin secretagogues (sulphonylureas)
◦ Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is
not an approved indication)
◦ α-glucosidase inhibitor (acarbose)
Insulin dose can be increased until target FPS is achieved
General Guidelines forUse of Oral Anti-
Diabetic Agent inDiabetes• Oral anti-diabetic agent s are not recommended for
diabetes in pregnancy
• Oral anti-diabetic agents are usually not the first line
therapy in diabetes diagnosed during stress, such as
infections. Insulin therapy is recommended for both
the above
• When indicated, start with a minimal dose of oral
anti-diabetic agent, while reemphasizing diet and
physical activity.
33.
C. Insulin Therapy
Short-termuse:
Acute illness, surgery, stress and emergencies
Pregnancy
Breast-feeding
Type 1
in marked hyperglycaemia
Long-term use:
If targets have not been reached after optimal dose of
combination therapy or BIDS, consider change to multi-dose
insulin therapy. When initiating this,insulin secretagogues
should be stopped and insulin sensitisers e.g. Metformin or
TZDs, can be continued.
34.
Insulin regimens
Themajority of patients will require more than one daily
injection if good glycaemic control is to be achieved.
However, a once-daily injection of an intermediate acting
preparation may be effectively used in some patients.
Twice-daily mixtures of short- and intermediate-acting
insulin is a commonly used regimen.
In some cases, a mixture of short- and intermediate-
acting insulin may be given in the morning. Further
doses of short-acting insulin are given before lunch and
the evening meal and an evening dose of intermediate-
acting insulin is given at bedtime.
Other regimens based on the same principles may be
36.
Monitoring of glycemiccontrol
• Self-monitoring of blood sugar by the patient.
• Measurement of glycated hemoglobin(HB1AC)
Rep. glycemic hx in previous 2-3 months; preceding
month contributes 50%
1% rise in HB1AC translates in 2.0mmol/l (35mg/dl)
increase in mean glucose
Frequency;
Good glycemic control; atleast twice a year.
Poor glycemic control or when therapy is changed or
most pts with type 1 DM; every 3 months
37.
Self-Care
Patients shouldbe educated to practice self-care.
This allows the patient to assume responsibility and
control of his / her own diabetes management. Self-
care should include:
◦ Blood glucose monitoring
◦ Body weight monitoring
◦ Foot-care
◦ Personal hygiene
◦ Healthy lifestyle/diet or physical activity
◦ Identify targets for control
◦ Stopping smoking
#5 Journal of Diabetes Research, Ronald Nyanzi, Robert Wamala & leonard atuhaire, Diabetes and the quality of life
International Diabetes Federation
WHO estimate for popn of UG who are diabetic by 2010= 328,000
#11 There is loss of abt20% B cell mass
Assctd with metabolic syndrome aka insulin resistance syndrome
Insulin resistance comes first
Central adipose releases a lot of FFAs that compete with glucose as energy source in peripheral tissues
Adipose also releases hormones eg adipokines and cortisol which alter insulin resistance
Inactivity is associated with down regulation of onsulin sensitive kinases & also increases accumulation of FFAs
#13 Insulin: promotes glycogen synthesis and storage, promotes peripheral uptake of glucose by muscle, stored as (muscle glycogen) and protein synthesis, promotes lipogenesis.
The main substates for gluconeogenesis are glycerol and amino acid,