INTRODUCTION TYPES CAUSES EPIDEMIOLOGY RISK FACTORS SIGN AND SYMPTOMS COMPLICATIONS MANAGEMENT

1. CURRENT MEDICAL
MANAGEMENT OF
DIABETES MELLITUS
PRESENTED BY: Ghaza Khan
DEPARTMENT: Pharmacy
CLASS: Final Prof

2. Diabetes Mellitus
About 422 million people worldwide,
particularly in low-and middle-income
countries, are either deficient of Insulin, a
pancreatic hormone, or their bodies can't use it
effective. And, more importantly, it is one of the
leading causes of death in the world.

3. INTRODUCTION
Diabetes is a life long(chronic)disease and is a
group of metabolic disorder characterized by
high levels of sugar in blood(hyperglycemia)
with disturbances of carbohydrates , fat and
protein metabolism resulting from defects in
insulin secretion , insulin action or both.

4. STAGES
There are two stages:
1. Normoglycemia
2. Hyperglycemia

5. What causes Diabetes?
 Diabetes causes vary depending on genetic
makeup, family history, health and environmental
factors.
 There is no defined diabetes cause because the
causes of diabetes vary depending on the
individual and the type.

6. PANCREAS
 The endocrine component of the pancreas consists
of islet cells (islets of Langerhans) that create and
release important hormones directly into the
bloodstream. Two of the main pancreatic hormones
are insulin, which acts to lower blood sugar,
and glucagon, which acts to raise blood sugar.
Insulin is released by the 'beta cells' in the islets of
Langerhans in response to food.

7. INSULIN

8. PATHOPHYSIOLOGY

9. TYPES
There are three main types of diabetes mellitus:
 Type 1 DM
 Type 2 DM
 Gestational Diabetes

10. INCIDENCE OF DM
 TYPE 1 (7%)
 TYPE 2 (90%)
 GESTATIONAL (5% OF ALL
PREGNANCIES)

11. TYPE 1 DM
• Results from the pancreas failure to produce
enough insulin.
• This form is previously referred to as “insulin-
dependent DM”.
• Type 1 diabetes occurs when some or all of the
insulin-producing cells in the pancreas are
destroyed. This leaves the patient with little or no
insulin. Without insulin, sugar accumulates in the
bloodstream rather than entering the cells. As a
result, the body cannot use this glucose for energy.

12. TYPE 1 DM

13. TYPE 2 DM
 Begins with insulin resistance , a condition in which
cells fail to respond to insulin properly.
 This form was previously referred to as “non insulin-
dependent DM”.
 Type 2 diabetes is much more common than type 1
diabetes.
 In people with insulin resistance, the pancreas "sees"
the blood glucose level rising. The pancreas responds
by making extra insulin to maintain a normal blood
sugar. Over time, the body's insulin resistance gets
worse. In response the pancreas makes more and more
insulin. Finally, the pancreas gets "exhausted". It cannot
keep up with the demand for more and more insulin. It
poops out. As a result, blood glucose levels start to rise.

14. TYPE 2 DM

15. GESTATIONAL DIABETES
 It is the third main form and occurs in pregnant
women without previous history of diabetes.
 Gestational diabetes mellitus (GDM) is a condition
in which a hormone made by the placenta prevents
the body from using insulin effectively. Glucose
builds up in the blood instead of being absorbed by
the cells.
 Unlike type 1 diabetes, gestational diabetes is not
caused by a lack of insulin, but by other hormones
produced during pregnancy that can make insulin
less effective, a condition referred to as insulin
resistance.

16. GDM

17. COMPARISON OF TYPE 1 AND TYPE
2

18. SIGNS AND SYMPTOMS
The classic symptoms of untreated diabetes are :
 Weight loss
 Polyuria (increased urination)
 Polydipsia (increased thirst)
 polyphagia (increased hunger)
Symptoms may develop rapidly (weeks or months)
in type 1 DM , while usually develop much more
slowly and may be absent in type 2 DM.

19. SIGNS AND SYMPTOMS
In addition they also include:
 Blurry vision
 Headache
 Fatigue
 Slow healing of cuts
 Itchy skin
A number of skin rashes that can occur in diabetes
are collectively known as diabetic dermadromes.

21. RISK FACTORS

22. RISK FACTOR

23. Complications
Diabetes increases your risk for many serious health problems. The
good news? With the correct treatment and recommended lifestyle
changes, many people with diabetes are able to prevent or delay the
onset of complications.
 DKA (ketoacidosis) & ketones
 Neuropathy
 Skin complications
 Eye complications
 Foot complications
 Kidney disease (nephropathy)
 Cardiovascular disease (CVD)
 High blood pressure
 Stroke

24. EPIDEMIOLOGY
 The number of people with diabetes rose from
108 million in 1980 to 422 million in 2014.
 The global prevalence of diabetes among
adults over 18 years of age rose from 4.7% in
1980 to 8.5% in 2014 (1).
 Between 2000 and 2016, there was a 5%
increase in premature mortality from diabetes.
 Diabetes prevalence has been rising more
rapidly in low- and middle-income countries
than in high-income countries.

25.  In 2016, an estimated 1.6 million deaths were
directly caused by diabetes. Another 2.2 million
deaths were attributable to high blood glucose in
2012.
 Almost half of all deaths attributable to high blood
glucose occur before the age of 70 years. WHO
estimates that diabetes was the seventh leading
cause of death in 2016.

26. DIAGNOSIS
Can be diagnosed by demonstrating one of the
following:
• Fasting plasma glucose level ≥ 126mg/dl
• Plasma glucose ≥ 200mg/dl two hours after a 75g
oral load as in a glucose tolerance test.
• Symptoms of high blood sugar and casual plasma
glucose ≥ 200mg/dl.
• Glycated hemoglobin(A1C) , below 5.7% is
considered normal.

27. CRITERIA FOR DIAGNOSING
DIABETES

28. MANAGEMENT
• Lifestyle:
Good Nutrition
Regular exercise
Diet control to maintain blood pressure
• Medications (6 CLASSES OF DRUG)
Sulfonylureas, Biguanides, Meglitinide analogs,
Thaizolidinediones, Alpha glucosidase inhibitors, Dipeptidyl
peptidase-IV inhibitors
• Surgery
Pancreas transplant
kidney transplant
weight loss surgery

29. MANAGEMENT

30. Pharmacologic Treatment: Noninsulin
Therapies
 When considering appropriate pharmacologic
therapy, it is important to determine whether the
patient is insulin-deficient, insulin-resistant, or both.
Treatment options are divided into noninsulin
therapies—insulin sensitizers, secretagogues,
alpha- glucosidase inhibitors, incretins, pramlintide,
bromocriptine, and sodium-glucose cotransporter 2
(SGLT-2) inhibitors—and insulin therapies (insulin
and insulin analogues).

31. Noninsulin Therapies
Subgroup
Generic name
(Brand)
Route Comments
Insulin sensitizers
Biguanides Metformin Oral Weight loss
No
hypoglycemia
GI upset
Thiazolidinedi
ones
Rosiglitazone
Pioglitazone
Oral Weight gain
Peripheral
edema

32. Noninsulin Therapies
Insulin secretagogues
Sulfonylureas Chlorpropamide
Glimepiride
Glipizide
Glyburide
Tolazamide
Glyburide
Oral Hypoglycemia
Weight gain
Glinides Nateglinide
Repaglinide
Oral Weight gain

33. Noninsulin Therapies
Alpha-glucosidase inhibitors
Acarbose
Miglitol
Oral GI upset
No hypoglycemia
Incretins
GLP-1 receptor agonists
Short-acting (4-
6 hrs)
Exenatide
(Byetta)
SC Weight loss
GI upset
Intermediate-
acting (24 hrs)
Liraglutide
(Victoza)
SC Weight loss
Nausea
Long-acting (7
days)
Exenatide ER
(Bydureon)
Albiglutide
(Tanzeum)
Dulaglutide
(Trulicity)
SC Weight loss
Nausea

34. Noninsulin Therapies
Others
Pramlinitide Pramlinitide
(Symlin)
SC Weight loss
GI upset
Adjunctive
treatment with
insulin
Rapid-release
bromocriptine
Bromocriptine Oral Take within 2 hrs
of awakening
Nausea, stuffy
nose
SGLT-2 inhibitors Canagliflozin
(Invokana)
Dapagliflozin
(Farxiga)
Empagliflozin
(Jardiance)
Oral Polyuria UTIs

35. Regimens for Insulin Therapy.
Insulin
Regimen
HbA1c (%) Medication Pattern Diet Lifestyle Monitoring
Basal-only >7.5-10 Oral
medications
adequately
control
postprandial
glucose
excursions
High fasting
glucose with
minimal
glucose rise
during the
day
Small,
regular
meals; large
meals will
result in
postprandial
hyperglycemi
a
Reluctance
to do MDI;
requires oral
agents
Fasting
Basal-bolus
(MDI)
>7.5 Regimen can
be matched
to any
pattern to
achieve
glycemic
control
Regimen can
be matched
to any diet to
achieve
glycemic
control
Erratic
schedule,
motivated to
achieve tight
glycemic
control
Frequent
blood
glucose
monitoring
(minimum
before meals
and bedtime)

36. Regimens for Insulin Therapy.
Once- or Twice-Daily Premixed
Rapid-acting
analogue
and
intermediate
acting
>7.5 Oral agent
failure
(maximum
tolerated
dosages,
contraindicat
ions, cost
issues)
Any fasting
glucose;
glucose
rises during
the day
Large
suppers,
small
lunches
Consistent
daily routine,
reluctance to
do MDI
Fasting and
pre-supper
(if insulin is
administered
twice daily)
Regular and
NPH
>7.5 Oral agent
failure
(maximum
tolerated
dosages,
contraindicat
ions, cost
issues)
Any fasting
glucose;
glucose
rises during
the day
Isocaloric
meals or
larger
lunches
Consistent
daily routine,
reluctance to
do MDI
Fasting and
pre-supper
(if insulin is
administered
twice daily)

37. THANKYOU