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

1. TREATMENT OF TYPE-II
DIABETES
PRESENTED BY:
HUSNA SAQLAIN,
PHARM D
GUIDED BY: Dr. S. P. SRINIVAS NAYAK,
ASSISTANT PROFESSOR,
SUCP,HYD

2. TYPE-II DIABETES:
 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.
 Symptoms include: dehydration, frequent urination, blurry vision, fatigue,tingling
sensation in your hands or feet.
 Diagnosis: Different diagnostic tests include A1c, fasting plasma glucose test and
oral glucose tolerance test(OGTT)

4. TREATMENT OF TYPE-II DIABETES:
 NON PHARMACOLOGICAL TREATMENT:
Medical nutrition therapy is recommended for all patients.
Weight loss: Losing weight can lower your blood sugar levels.Controlling portions and
eating healthy foods are simple ways to lose weight.
Healthy eating: It is important to center your diet around foods with fewer calories,
fewer refined carbohydrates especially sweets, more vegetables and fruits, more
foods with fiber.
Physical exercise: Aerobic exercise can improve insulin sensitivity and glycemic
control and may reduce cardiovascular risk and improve well being.

5.  Physical activity goals include atleast 150 min/week of moderate (50-70%
maximal heart rate) exercise.
 Ongoing diabetes education should emphasize self care behaviors including
healthy eating, being active, monitoring blood glucose levels, taking
medication, reducing risk of complications.
 Patients must be involved in decision making and have strong knowledge of the
disease and associated complications.
 Islet cell and whole pancreas transplantation is ocassionallyused in patients
who require immunosuppression for other reasons eg. (Kidney transplants).

7. PHARMACOLOGICAL THERAPY USING
ORAL HYPOGLYCEMIC DRUGS:
 Oral hypoglycemic drugs are used only in the treatment of type 2 diabetes which
is a disorder involving resistance to secreted insulin. The different classes of oral
hypoglycemic drugs include:
 BIGUANIDES: Metformin enhances insulin sensitivity of hepatic and peripheral
tissues, allowing for increased glucose uptake. It reduces A1c levels by 1.5%-
2%.Metformin reduces plasma triglycerides and low density lipoprotein and also
high density lipoprotein cholesterol.
 As it does not increase pancreatic insulin release hypoglycemia is uncommon
when used alone.
 DOSE: Start at 500mg orally twice daily with meals and
increase by 500mg weekly as tolerated until reaching glycemic goals or
2500mg/day.

8.  SIDE EFFECTS: The most common side effects are gastrointestinal, including
metallic taste in mouth, mild anorexia, abdominal discomfort and diarrhea. A
rare side effect includes lactic acidosis which usually occurs in the presence of
predisposing conditions that include renal insufficiency, heart failure, hypoxia,
serious acute illness.
 PHARMACOKINETICS: Metformin should be taken with meals and should be
started at low doses to avoid intestinal effects. These doses then can slowly be
increased as necessary to 2550mg/day.
 THIAZOLIDINEDIONES (GLITAZONES):
 TZD’s bind to the peroxisome proliferator activator receptor-gama located
primarily on fat and vascular cells,enhancing insulin sensitivity in muscle liver
and fat tissues indirectly. They increase glucose utilization and diminish glucose
production. Examples include Pioglitazone and Rosiglitazone.
DOSE: Pioglitazone: Initially 15 mg to 30mg
orally once daily.

9.  Rosiglitazone: Initiate with 2 to 4mg orally once daily with maximum
dose of 8mg/daily.
 SIDE EFFECTS:Fluid retention may occur perhaps because of peripheral
vasodilation and improved insulin sensitization in the kidney with increased
sodium and water retention. This may result in peripheral edema, heart
failure.and weight gain.
 PHARMACOKINETICS:These have peak plasma concentrations in humans within 2
hours of administration on an empty stomach. Food delays absorption by 1 or 2
hours. These are highly protein bound and are metabolized in the liver.the half
life of pioglitazone is 3 to 7 hourse.
 ALPHA-GLUCOSIDASE INHIBITORS:
 They inhibit the upper gastrointestinal enzymes that converts dietary starch and
other complex carbohydrates into simple sugars which can be absorbed. The result
is to slow the absorption of glucose after meals. The net effect is reduction in
post prandial glucose (40-50mg/dl).

10.  DOSE:ACARBOSE and MIGLITOL are the two common drugs. Initiate therapy with
very low dose (25 mg orally with one meal a day) and increase very gradually
(over several months) to maximum 50mg three times daily or 100mg three times
daily for patients above 60kg.
 SIDE EFFECTS: The most common side effects are flatulence, bloating,
abdominal discomfort, and diarrhea which can be minimized by slow dosage
titration.
 PHARMACOKINETICS: These drugs exert their effects topically by inhibition of
the carbohydrate digesting enzymes at the surface of the intestinal mucosa. The
drugs should be taken with the first bite of the meal so the drug is present to
inihibit enzyme activity.
 SHORT ACTING INSULIN SECRETAGOGUES (MEGLITINIDES OR
GLINIDES): Glinides stimulate insulin secretion from pancreatic beta cells by
binding a site adjacent to the sulphonylurea receptor. They require the presence
of glucose to stimulate insulin secretion. As glucose levels decrease to normal,
stimulated insulin secretion diminishes.

11.  DOSE: REPAGLINIDE: Start with0.5 to 2mg orally with maximum 4mg per meal.
NATEGLINIDE: Start with 120mg orally three times daily before each meal.
 SIDE EFFECTS: The main side effect is low blood sugar (hypoglycemia) and
weight gain.
 PHARMACOKINETICS: These drugs should be administered before each
meal(upto 30 minutes prior). If a meal is skipped, the medication should also be
skipped.It is useful in patients with renal insufficiency and those with erratic
meal schedules.
 SULPHONYLUREAS: Sulphonylureas enhance insulin secretion by binding to
the sulphonylurea receptor on pancreatic beta cells. All sulphonylureas are
equally effective in lowering blood glucose when administered in equipotent
doses. These are usually used as a second line option. These are often avoided
in favor of DPP-4 inhibitors or SLGT-2 inhibitors.
 DOSE: The starting dose of sulphonylureas is 1-2 mg once daily. It can be

12. Increased to a maximum of 8mg once daily.
 SIDE EFFECTS: The most common side effect is hypoglycemia. Other side effects
include weight gain, risk for cardiovascular events.
 PHARMACOKINETICS: They are absorbed rapidly and are highly protein bound and
are metabolized by the liver.
 SODIUM GLUCOSE CO TRANSPORTER-2 (SGLT-2) INHIBITORS: Inhibition
of SGLT-2 lowers the renal tubular threshold for glucose reabsorption and
glucosuria occurs at lower plasma glucose concentrations. In clinical care
practice, SGLT-2 inhibitors are considered to be second or third line therapy.
Older patients with stage 4 or 5 chronic kidney disease are not optimal treatment
candidates.
DOSE: CANAGLIFLOZIN: Initial dose is 100mg orally once daily, taken before the
first meal of the day.
DAPAGLIFLOZIN: Start at 5mg daily orally once daily in the morning with or
without food. The dose maybe increased to 10mg once daily in patients requiring

13. additional glycemic control.
 SIDE EFFECTS: Genitourinary tract infections, especially yeast infections
which occur more commonly in women.
 PHARMACOKINETICS: Rapid oral absorption, long elimination half life
allowing once daily administration an extensive hepatic metabolism
mainly via glucuronidation to inactive metabolites and a low renal
elimination as a parent drug.

14.  PHARMACOLOGICAL TREATMENT USING INSULIN:
Insulin: All available insulins are manufactured using recombinant DNA technology
and are highly purified. The most commonly used concentration is 100 units/ml.
Insulin is usually injected into the fatty tissue just under the skin. This is also called
as subcutaneous tissue.
TYPES OF INSULIN:
FAST ACTING INSULIN:
 Is absorbed quickly from your fat tissue(subcutaneous) into the bloodstream.
 Is used to control the blood sugar during meals and snacks and to correct high
blood sugars.
 Example: Rapid acting insulin analogs (Insulin Aspart, Insulin Lyspro)
Regular Human Insulin

15.  INTERMEDIATE ACTING INSULIN:
 Is absorbed more slowly and lasts longer.
 Is used to control the blood sugar overnight, while fasting and between meals.
Examples include NPH Human Insulin
Pre Mixed Insulin.
 LONG ACTING INSULIN:
 Is absorbed slowly has a minimal peak effect and a stable plateau effect that
lasts most of the day.
 Is used to control the blood sugar overnight, while fasting and between meals.
Examples include Insulin Glargine, Insulin Detemir.

17. COMPLICATIONS OF DIABETES:
 Diabetes increases your risk for many serious health problems.
 People with diabetes have an increased risk of developing a number of
serious health problems. Consistently high blood glucose levels can lead to
serious diseases affecting the heart and blood
vessels, eyes, kidneys, nerves and teeth. In addition, people with diabetes
also have a higher risk of developing infections. In almost all high-income
countries, diabetes is a leading cause of cardiovascular
disease, blindness, kidney failure, and lower limb amputation.
 Maintaining blood glucose levels, blood pressure, and cholesterol at or close
to normal can help delay or prevent diabetes complications. Therefore
people with diabetes need regular monitoring.

18.  Cardiovascular disease: affects the heart and blood vessels and may cause fatal
complications such as coronary artery disease (leading to heart attack) and
stroke. Cardiovascular disease is the most common cause of death in people with
diabetes. High blood pressure, high cholesterol, high blood glucose and other
risk factors contribute to increasing the risk of cardiovascular complications.
 Kidney disease (diabetic nephropathy): caused by damage to small blood
vessels in the kidneys leading to the kidneys becoming less efficient or to fail
altogether. Kidney disease is much more common in people with diabetes than in
those without diabetes. Maintaining near normal levels of blood glucose and
blood pressure can greatly reduce the risk of kidney disease.
 Eye disease (diabetic retinopathy): most people with diabetes will develop
some form of eye disease (retinopathy) causing reduced vision or blindness.
Consistently high levels of blood glucose, together with high blood pressure and
high cholesterol, are the main causes of retinopathy. It can be managed through
regular eye checks and keeping glucose and lipid levels at or close to normal.

20.  Nerve disease (diabetic neuropathy): diabetes can cause damage to the
nerves throughout the body when blood glucose and blood pressure are too
high. This can lead to problems with digestion, erectile dysfunction, and
many other functions. Among the most commonly affected areas are the
extremities, in particular the feet. Nerve damage in these areas is called
peripheral neuropathy, and can lead to pain, tingling, and loss of feeling.
Loss of feeling is particularly important because it can allow injuries to go
unnoticed, leading to serious infections and possible amputations.
 Pregnancy complications: Women with any type of diabetes during
pregnancy risk a number of complications if they do not carefully monitor
and manage their condition. To prevent possible organ damage to the
fetus, women with type 1 diabetes or type 2 diabetes should achieve
target glucose levels before conception. All women with diabetes during
pregnancy, type 1, type 2 or gestational should strive for target blood
glucose levels throughout to minimize complications.

21. NOVEL DRUGS FOR DIABETES:
Class Brand (Company) Year Launched
DPP-4 inhibitors
Onglyza (AstraZeneca) 2009
Nesina (Takeda) 2013
Tradjenta (Boehringer
Ingelheim)
2011
GLP-1R agonists
Adlyxin (Sanofi) 2016
Byetta (AstraZeneca) 2005
Bydureon (AstraZeneca) 2012
Januvia (Merck) 2006
Lyxumia (Sanofi) 2015
Tanzeum
(GlaxoSmithKline)
2014
Trulicity (Eli Lilly) 2014
Victoza (Novo Nordisk) 2010
Insulin analogues
Afrezza (MannKind) 2015
Apidra (Sanofi) 2006
Humalog (Eli Lilly) 1996
Humalog 200 (Eli Lilly) 2015

22. THANK YOU