Type 1 diabetes is caused by the immune system destroying insulin-producing cells. Type 2 diabetes is caused by insulin resistance and relative insulin deficiency. Gestational diabetes occurs during pregnancy due to increased insulin needs. Diabetes is managed through diet, exercise, medication including insulin, and monitoring of blood sugar levels. Complications of uncontrolled diabetes include foot ulcers and infections, ketoacidosis, and other conditions.

3. CONTENT:
INTRODUCTION
 CAUSES
PATHOPHYSIOLOGY
TESTS
MANAGEMENT
COMPLICATIONS
MADE BY STUDENTS OF BAQAI MEDICAL UNIVERSITY,PAKISTAN

4. INTRODUCTION:
DIABETES:
Diabetes mellitus (DM) refers to a group of disorders characterized by absent or deficient insulin
secretion or peripheral insulin resistance, resulting in hyperglycemia and impaired metabolism.
Classification:
Classified in to three groups :
TYPE 1 DIABETES
TYPE 2 DIABETES
GESTATIONAL DIABETES

5. TYPE 1 INSULIN DEPENDENT (DM):
 This form is most common in children’s and in adults up to
 Age 30 years but may occur at any age.
 Type 1 diabetes are predisposed to ketoacidosis accumulation of ketone bodies in body tissues
and fluids
 Disease on set is sudden
 All type 1 diabetes requires insulin replacement therapy.
TYPE 2 NON-INSULIN DEPENDENT (DM):
 Most type 2 diabetes are above 40 years and obese
 Disease onset typically is gradual.
 Insensitivity to insulin in the target tissues
 Deficiency response of pancreatic beta cells to glucose
 Because of insulin secretion ketoacidosis is prevented
 Only in minority insulin replacement therapy is required

6. GESTATIONAL DIABETES :
 Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance
with onset or first recognition during pregnancy.
 Approximately 7% of all pregnancies are complicated by GDM.

7.  INDICATIONS:
 TYPE 1:

8.  TYPE 2:

9.  ETIOLOGY :
 TYPE 1:

10.  TYPE 2:

11. •GESTATIONAL DIABETES:

12. CAUSES:

13. TYPE 1 DIABETES CAUSES:
 Type 1 diabetes is caused by the immune system destroying
the cells in the pancreas that make insulin. This causes
diabetes by leaving the body without enough insulin to function
normally. This is called an autoimmune reaction.
 There is no specific diabetes causes, but the following triggers
may be involved:
 Viral or bacterial infection
 Chemical toxins within food
 Unidentified component causing autoimmune reaction
 Underlying genetic disposition

14. TYPE 2 DIABETES CAUSES:
 Type 2 diabetes causes are usually multifactorial. Often, the
most overwhelming factor is a family history of type 2
diabetes. There are a variety of risk factors for type 2
diabetes. These include:
 Obesity
 Living a sedentary lifestyle
 Increasing age
 Bad diet
 Other type 2 diabetes causes such as pregnancy

15. GESTATIONAL DIABETES CAUSES:
 The causes of diabetes in pregnancy(gestational diabetes) remain unknown.
However, there are a number of risk factors that increase the chances of
developing this condition:
 Family history of gestational diabetes
 Overweight or obese
 Polycystic ovary syndrome
 Have had a large baby weighing over 9lb
 Ethnicity

16. Pathophysiology

17. DIFFERENCE BETWEEN DIABETES MELLITUS TYPE I AND II:

18. PATHOPHYSIOLOGY OF DIABETES MELLITUS TYPE I:

19. PATHOPHYSIOLOGY OF DIABETES MELLITUS TYPE II:

20. Tests And investigations

21. TESTS FOR TYPE 1 AND TYPE 2 DIABETES AND PREDIABETES:
• GLYCATED HEMOGLOBIN (A1C) TEST: This blood test, which doesn't require fasting, indicates
your average blood sugar level for the past two to three months. It measures the percentage of blood
sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells.
The higher your blood sugar levels, the more hemoglobin you'll have with sugar attached. An A1C level
of 6.5 percent or higher on two separate tests indicates that you have diabetes. An A1C between 5.7
and 6.4 percent indicates prediabetes. Below 5.7 is considered normal.
If the A1C test results aren't consistent, the test isn't available, or you have certain conditions that can
make the A1C test inaccurate — such as if you're pregnant or have an uncommon form of hemoglobin
(known as a hemoglobin variant) — your doctor may use the following tests to diagnose diabetes:

22.  RANDOM BLOOD SUGAR TEST: A blood sample will be taken at a
random time. Regardless of when you last ate, a random blood sugar
level of 200 milligrams per deciliter (mg/dL) — 11.1 millimoles per liter
(mmol/L) — or higher suggests diabetes.

23.  FASTING BLOOD SUGAR TEST. A blood sample will be taken after an overnight fast. A
fasting blood sugar level less than 100 mg/dL(5.6 mmol/L) is normal. A fasting blood sugar
level from 100 to 125 mg/dL(5.6 to 6.9 mmol/L) is considered prediabetes. If it's 126 mg/dL (7
mmol/L) or higher on two separate tests, you have diabetes.

24.  ORAL GLUCOSE TOLERANCE TEST: For this test, you fast
overnight, and the fasting blood sugar level is measured. Then you
drink a sugary liquid, and blood sugar levels are tested periodically for
the next two hours.
A blood sugar level less than 140 mg/dL(7.8 mmol/L) is normal. A reading of more than 200
mg/dL(11.1 mmol/L) after two hours indicates diabetes. A reading between 140 and 199
mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates prediabetes.
If type 1 diabetes is suspected, your urine will be tested to look for the presence of a
byproduct produced when muscle and fat tissue are used for energy because the body
doesn't have enough insulin to use the available glucose (ketones). Your doctor will also
likely run a test to see if you have the destructive immune system cells associated with type
1 diabetes called autoantibodies.

25.  TESTS FOR GESTATIONAL DIABETES:
 Your doctor will likely evaluate your risk factors for
gestational diabetes early in your pregnancy:
 IF YOU'RE AT HIGH RISK OF GESTATIONAL DIABETES: —
for example, if you were obese at the start of your pregnancy;
you had gestational diabetes during a previous pregnancy;
or you have a mother, father, sibling or child with diabetes —
your doctor may test for diabetes at your first prenatal visit.
 IF YOU'RE AT AVERAGE RISK OF GESTATIONAL DIABETES:
 You'll likely have a screening test for gestational diabetes
 sometime during your second trimester — typically between
 24 and 28 weeks of pregnancy.


26. TREATMENT AND MANAGEMENT OF
DIABETES

27. MANAGEMENT AND TREATMENT:
How is diabetes managed?
There is no cure for diabetes, but it can be treated and controlled. The goals of managing diabetes are
to:
 Keep your blood glucose levels as near to normal as possible by balancing food intake with
medication and activity.
 Maintain your blood cholesterol and triglyceride (lipid) levels as near the normal ranges as possible
by decreasing the total amount of fat to 30% or less of your total daily calories, and by reducing
saturated fat and cholesterol.
 Control your blood pressure. (Your blood pressure should not go over 130/80.)
 Decrease or possibly prevent the development of diabetes-related health problems.

28. YOU HOLD THE KEYS TO MANAGING YOUR DIABETES BY:
 Following a balanced meal plan.
 Exercise regularly.
 Taking medication, if prescribed.
 Monitoring your blood glucose and blood pressure levels at home.
 Keeping your appointments with your doctor and having laboratory tests as ordered by your
doctor.

29. DRUG THERAPY:
Insulin and sulfonylurea's are used in treatment of diabetes mellitus:
Patients with type 1 diabetes mellitus are treated with insulin as well as diet and
exercise.
Patients with type 2 diabetes mellitus are initially treated with diet and exercise. If
those measures are not sufficient for glycemic control, they may be prescribed,
Sulfonylureas
Injectable glucagon-like peptide-1 (GLP-1) receptor agonists
Insulin
or a combination of these drugs.

30. EXAMPLES OF POSSIBLE TREATMENTS FOR TYPE 2
DIABETES INCLUDE:
METFORMIN (GLUCOPHAGE, GLUMETZA, OTHERS).
GENERALLY, METFORMIN IS THE FIRST MEDICATION
PRESCRIBED FOR TYPE 2 DIABETES.
SULFONYLUREAS.
MEGLITINIDES.
THIAZOLIDINEDIONES.
DPP-4 INHIBITORS.
GLP-1 RECEPTOR AGONISTS.
SGLT2 INHIBITORS.
INSULIN THERAPY.

31. Insulin
Insulin is required for all patients with type 1 DM if they become ketoacidotic without it; it is also helpful
for management of many patients with type 2 DM.
Insulin replacement in type 1 DM should ideally mimic beta-cell function using 2 insulin types to
provide basal and prandial requirements (physiologic replacement); this approach requires close
attention to diet and exercise as well as to insulin timing and dose.
When insulin is needed for patients with type 2 DM, glycemic control can often be achieved with basal
insulin combined with non- insulin anti-hyperglycemic drugs, although prandial insulin may be needed
in some patients.
MOA: Insulin lowers the blood glucose level by increasing glucose transport across cell
membranes, enhancing glucose conversion into glycogen inhibiting the release of free fatty acids from
adipose tissue, and inhibiting lipolysis and glycogenolysis.

32. Insulin Types
Insulin types are commonly categorized by their time to onset and duration of action.
Fast acting insulin products: Regular and semilente insulin (insulin zinc suspension)
Intermediate acting insulin products: lenth and NPH (isophane insulin suspension)
Long acting insulin products: PZI (protamine zinc insulin) and ultralente
Insulin mixtures: Some diabetics need a mixture of insulin types (E.g. Rapid acting to control
morning hyperglycemic and an intermediate acting insulin to control later hyperglycemia.
Administration: for routine use, insulin is administered by a subcutaneous
injection.

33. Sulfonylurea's (oral hypoglycemia)
Are used to control hyperglycemia in selected type 2 diabetics.
Indications: the drugs helps to reduce blood glucose level in type 2 DM that does not respond
to diet alone. Because the action of sulfonylurea's seen to depend on functioning beta cells. These
drugs should never be used in type 1 diabetics.
MOA: As acute action, sulfonylurea's stimulate beta cell tissues to secrete insulin. In the long term,
these drugs appear to reduce cellular insulin resistance.
Choice of agent:
First generation sulfonylurea's include acetohexamide, chlorpropamide, tolbutamide, and tolazamide.
Second generation sulfonylurea's, considerably more potent, include glipizide and glyburide.
The most clinically significant difference among sulfonylurea is duration of action.

34. GLINIDE:
postprandial glucose regulator and insulin secretagogues.
combine therapy of glinides with metformin and glitazone have better effect than
monotherapy (nateglinide and repaglinide ).
Weight gain is less of a problem with them than with sulphonylurea.
MOA:
Glinides culminate the release of insulin by increasing the function of pancreatic B
cells(like sulphonylureas) .
They have rapid onset and hence have shorter action.
Contraindication:
Metformin hypoglycemia.
Gemfibrozil(lipid lowering drug) hypoglycemia.

35. BIGUANIDES:
Biguanides are insulin sensitizers hence not cause hyperinsulinemia or
hypoglycemia.
It increase glucose uptake by tissues and decrease insulin resistance.
MOA:
Mainly inhibit hepatic gluconeogenesis hence reduce hepatic glucose output.
Modestly reduce hyperlipidemia.
Increase peripheral glucose uptake and utilization.
Contraindication:
In DM I patient with ketoacidosis.
In diabetic patient with renal and hepatic impairment.
In older patients and patient with CVD.

36. ALPHA-GLUCOSIDASE INHIBITORS:
acarbose and miglitol recommended for type 2 DM.
Postprandial glucose regulator.
MOA:
Acarbose specifically inhibit pancreatic alpha amylase which is responsible for
breakdown of starch to oligosaccharides.
While in general they inhibit alpha-glucosidase inhibitors which mainly
hydrolyze oligosaccharides to glucose.
Contraindication:
colon ulcer.
Inflammatory bowel disorder

37. Thiazolidinedione

abbreviated as TZD, also known as glitazones , are a class of heterocyclic compounds consisting of a
five-membered C3NS ring. The term usually refers to a family of drugs used in the treatment of diabetes
mellitus type 2
Members: Pioglitazone,Rosiglitazone,lobeglitazone.
MOA:
Thiazolidinediones or TZDs act by activating PPARs (peroxisome proliferator-activated
receptors), They are thus the PPARG agonists subset of PPAR agonists.
When activated, the receptor binds to DNA in complex with the retinoid X receptor (RXR), another
nuclear receptor, increasing transcription of a number of specific genes and decreasing transcription of
others. The main effect of expression and repression of specific genes is an increase in the storage of
fatty acids in adipocytes,
Contraindication:
The withdrawal of troglitazone has led to concerns of the other thiazolidinediones also increasing the
incidence of hepatitis and potential liver failure.

38. Disease management in pregnancy:
Approx 2%—3% of pregnant women with no history of DM develop diabetes
or impaired glucose tolerance– presumably from increased insulin requirements
of pregnancy.
tight glycemic control is especially important during pregnancy to avoid neonatal complications.
Continuous insulin infusion (via an insulin pump) or multiple insulin injections maybe required.
sulfonylurea's are contraindicated in pregnant women.
weight reduction is not recommended because this could compromise fetal development.
glucose tolerance usually normalizes within a few weeks after delivery.

39. COMPLICATIONS OF DIABETES
MELLITUS:

40. 1) DIABETIC FOOT:
 Presence of several characteristic diabetic foot pathologies such as
infection, diabetic foot ulcer is called diabetic foot syndrome. Due to
the peripheral nerve dysfunction associated with diabetes patients have
a reduced ability to feel pain.

41. PATHOPHYSIOLOGY:
INVESTIGATION:
There are mainly two tests which will be conducted before starting the treatment to determine the severity
of complication:
RADIOGRAPHY :
When lesion fail to heal.
A deep penetration ulcers present.

42. 2) BACTERIAL CULTURE TEST:
When superficial ulcer is present.
ORAL ANTIBIOTICS:
 Most commonly prescribed antibiotics are:
 Amoxicillin
 Metronidazole
 Flucloxacillin.
AMPUTATION OF ULCERATED AREA:
 When the condition results in a severe loss of tissue or a life-threatening infection, an amputation
may be the only option.
 A surgeon will remove the damaged tissue and preserve as much healthy tissue as possible. It
may take four to six weeks for your wound to heal completely.
Preventions:
 You can help avoid foot problems:
 First, control your blood sugar levels.
 Good foot hygiene .

43. 2 . DIABETIC KETOACIDOSIS:
Usually affectiing only type 1 diabetics results from an absence of insulin often a presenting
disorder in children with previously undiagnosed DM 1, this disorder is typically arises after a short
period of deteriorating glycemic control which results in hyperglycemia.
PATHOPHYSIOLOGY
:
 .
 Results from an absence of insulin in type
1 diabetes only.
Tissues become starved from glucose
 Low level of insulin means glucose can not nourish
the cell.
 To prevent the cell death from starvation body began
to breakdown fats and muscles to provide energy.
 Results in formation of bi products called ketones
which causes acidosis.

44. INVESTIGATION:
PHYSICAL FINDING:
 Acetone breath odour.
 Dry skin.
 Poor skin turgor.
 Abdominal pain.
 conciousness ranging from confusion to coma even causes death.
LABORATORY FINDING:
 Increase blood glucose and ketone bodies (acetone and acetoacetate).
 Low arterial blood pH and carbondioxide partial pressure values.
 Abnormal serum electrolytes values.
MANAGEMENT:
It includes :
 Fluid replacement.
 Electrolytes replacement.
 Insulin.

45. 3.HYPOGLYCEMIA:
In diabetic patients hypoglycemia occurs when there is too much insulin or not enough
glucose in blood hypoglycemia occur in both type 1 and 2 DM but mostly occur in type 1
because these patients receive an intensive treatment via direct insulin.
FACTORS :
•Due to imperfect insulin replacement.
•Over dosing of other diabetic medication.
•Skipping meal.
•Excessive exercising.
INVESTIGATION :
PHYSICAL FINDING:
•Hunger.
•Sweating.
•Confusion
•Somnolence
•Behavioural changes.

46. LABORATORY FINDING:
By simply using a glucose meter that will measure and display your blood sugar level.
MANAGEMENT:
Hypoglycemia can be manage by the flowing ways:
•Administer oral , rapidly absorbable glucose.
•If the patient is unable to swallow or irresponsive , administer SC and IV Gucagon or IV glucose.
•In severe hypoglycemia if mental state is altered hospitalization is recommended.

47. CHRONIC COMPLICATIONS:
Chronic complications or Micro vascular complications of diabetes are those long-term
complications that affect small blood vessels.
These typically include retinopathy, nephropathy.

48. DIABETIC RETINOPATHY:
“Disease of the retina which results in impairment or loss of vision”
There are three basic components of this damaging process.
•the blood vessels can leak
•they can make a special growth substance that makes other vessels grow
(VEGF = vascular endothelial growth factor)
•the vessels may eventually close and block.

49. Retinopathy is divided into two main categories
 No proliferative retinopathy
 proliferative retinopathy.
No proliferative retinopathy is the development of micro aneurysms, venous loops, retinal hemorrhages, hard
exudates, and soft exudates.
Proliferative retinopathy is the presence of new blood vessels, with or without vitreous hemorrhage. It is a
progression of no proliferative retinopathy.

50. TEST AND DIAGNOSIS:
Intravenous fluorescein angiography
Optical coherence imaging
MANAGEMENT:
Laser prevents blood vessel growth and prevents the bleeding.
Avastin injections are used to treat diabetic retinopathy. Avastin is an anti-VEGF drug. By blocking the
effect of VEGF, Avastin stops the new vessels growing and reduces retinal leakage for a while.

51. DIABETIC NEPHROPATHY:
Diabetic nephropathy is characterized by proteinuria,microalbuminuria,glomerular lesions and renal arteriosclerosis.
Test
• Urine test
• Blood test
Purpose
• To measure amount of albumin
• Micro albumin indicate that patient are at risk of developing
or may have early stage diabetic nephropathy
• Proteinuria or macroalbuminuria indicates that patient have
more advanced diabetic nephropathy that may be affecting
the ability of your kidneys to filter wastes.
• To measure the level of creatinine

52. MANAGEMENT:
Lifestyle measures (i.e. diet and exercise) + oral diabetes medicines or insulin can be used to control blood
glucose levels.
ACE inhibitors or angiotensin receptor blockers (ARBs) are also used because they decrease the amount of
protein in the urine and can prevent or slow the progression of diabetic kidney disease.

53. DIABETIC NEUROPATHY:
Diabetic neuropathy is nerve damage that is caused by diabetes.
TYPES:
1.Peripheral neuropathy
2.Autonomic neuropathy
3.Focal neuropathies
4.Proximal neuropathy

54. Tests
• Filament test
• Quantitative sensory testing.
• Nerve conduction studies.
• Electromyography
• Autonomic testing
Purpose
• Brush a soft nylon fiber over areas of
the skin to test sensitivity to touch.
• To assess how nerve respond to
vibration and changes in temperature.
• To measure how quickly the nerves in
arms and legs conduct electrical
signals.
• To measures the electrical discharges
produced in muscles.
• Done in patient with symptoms of
autonomic neuropathy to evaluate
blood pressure in different positions
and ability to sweat.
TESTS AND
DIAGNOSIS:

55. MANAGEMENT:
ANTI-SEIZURE DRUGS: Pregablin, Gabapentin and Carbamazipine.
ANTI DEPRESSANT: Tricyclic and Imipramine
SEROTONIN REUPTAKE INHIBITORS: Duloxetin.