Diabetes Mellitus, medical and nursing management with its Complecations

1. DIABETES
MELLITUS
Ms. Amandeep Kaur
MMCON

2. INTRODUCTION
Type 2 diabetes is sometimes called a “life style” disease as it
more common in people who don’t do enough exercise, have
an
unhealthy diet and obese.
Type 2 Diabetes was previously seen mainly in older adults,
however it is becoming more common in young children due to
obesity and overweight children.

3. HISTORY
The Indian physician
Sushruta in the 6th
century B.C. noticed
the sweet nature of
urine in such patients
and termed the
condition
MADHUMEHA.

4. Diabetes
Mellitus
Greek word
"diabainein"
meaning "to
siphon or pass
through"
Latin word
"mellitus"
meaning
"sweetened with
honey"
"To pass through sweetened with
Honey"

5. DIABETIC MELLITUS
DEFINITION:-
Diabetes is a group of metabolic diseases characterized by
hyperglycemia resulting from defects in insulin secretion,
insulin action, or both.

6. EPIDEMIOLOGY
Globally
382 million people had diabetes in 2013
By 2035, this number will rise to 592
million
In India
65.1 million people had diabetes in 2013
By 2035, this number will increase by
70.6%

7. Courtesy: 2015 International Diabetes Federation
Epidemiology

8. ANATOMY OF PANCREAS
 The adult pancreas is a transversely oriented retroperitoneal
organ extending from the "C " loop of the duodenum to the
hilum of the spleen
EXOCRINEsecretion
 pancreatic juice enzymes promote the digestion of
carbohydrates, proteins and fats
ENDOCRINE secretion
 Insulin and glucagon- enter portal vein – transported directly
to the liver – regulate metabolism of carbohydrates, proteins
and fats.

9. PANCREAS
 15- 20% α cells synthesize and secrete GLUCAGON
 70- 80% β cells synthesize and secrete INSULIN
 1-8% δ cells synthesize and secrete
STOMATOSTATIN
and GASTRIN
 1-2% F- cells secrete PANCREATIC POLYPEPTIDE
which decreases the absorption of food from the GIT

10. INSULIN
 Polypeptide hormone produced by β- cells of islets of
Langerhans of pancreas
 Insulin is a protein made of 2 chains- alpha and
beta
 Anabolic hormone
STRUCTURE OF INSULIN

11. REGULATION OF INSULIN
SECRETION
 Factors stimulating insulin secretion :
Glucose: The effect is more predominant when glucose
is administered orally. Arise in blood glucose level is a
signal for insulin secretion.
amino acids:
gastrointestinal hormones: Gastrointestinal hormones
(secretin, gastrin) enhance the secretion of insulin.

12. REGULATION OF INSULIN
SECRETION
 Factors inhibiting insulin secretion
• Epinephrine is the most potent inhibitor of insulin release.
• In emergency situations like stress, extreme exercise and
trauma, the nervous system stimulates adrenal medulla to
release epinephrine.
• Epinephrine suppresses insulin release and promotes energy
metabolism by Mobilizing energy-yielding compounds-
glucose from liver and fatty acids from adipose tissue

13. TERMINOLOGY
Gluconeogenesis : The synthesis of glucose from non-
carbohydrate precursors( e.g. amino acids, glycerol)
Glycogenesis: The formation of glycogen from glucose.
Glycogenolysis : The breakdown of glycogen to glucose

14. ACTIONS OF
INSULIN
Stimulation of the activity of glycolytic enzymes Reduces
the activity of the enzymes of gluconeogenesis Increased
synthesis of glycogen
Increased uptake of of glucose by resting skeletal
muscles Reduction of blood glucose level
Reduction of lipolysis and stimulation of lipid synthesis

15. INSULIN
 Pancreas secretes 40-50 units of insulin daily in two
steps:
• Secreted at low levels during fasting ( basal insulin
Secretion.
• Increased levels after eating (prandial).
• An early burst of insulin occurs within 10 minutes of
Eating.
• Then proceeds with increasing release as long as
hyperglycemia is present.

19. CLASSIFICATION
 Classification by American diabetic association 2009 :
• Type 1 diabetes
• Type 2 diabetes
• Gestational diabetes mellitus (GDM)
• Secondary DM:
Hormonal problems, pancreatic disorders, drugs

20. TYPE 1 DM
 Juvenile / IDDM(5 to 10%)
 Autoimmune destruction of pancreatic beta cells.
 Individual has an absolute insulin deficiency and no
longer produces insulin.
 Such patients are absolutely dependent on exogenously
administered insulin for survival.

22. TYPE 2
DIABETES
MELLITUS

23. TYPE 2 DM
 Most common type.
 Comprises 90 to 95% of DM cases.
 Most type 2 DM patients are overweight, and most are
diagnosed as adults.
 Approximately half of the patients are unaware of their
disease.

24. Peripheral
resistance to
insulin, especially
in muscle cells
Increased
production of
glucose by the
liver
Insulin secretary
defect of the beta
cells
• Obesity contributes greatly to insulin resistance.
• Insulin resistance generally decreases with weight loss.
TYPE 2 DM
The underlying pathophysiologic defect in type 2 DM is
characterized by the following three disorders:

25. COMPONENTS OF DM-II
Type 2
Diabetes
Insulin
Resistance
B-cell
Dysfunction

27. RISK FACTORS
 NON-MODIFIABLE:
 Age: 45 or more
 Race : African American, Asian American, Hispanic
or Latino.
 Familial history : a parent, or siblings with diabetes.

28. RISK FACTORS
 MODIFIABLE:
Pre diabetes
Heart and blood disease
Hypertension
Low HDL cholesterol and high triglycerides.
Obesity
Polycystic ovary syndrome
Physical inactivity

30. CLINICAL PRESENTATION
Patients can be asymptomatic
 Polyuria.
 Polydipsia.
 Polyphagia.
 Fatigue.
 Weight loss.
 Most patients are discovered while performing urine
glucose screening.

32. DIAGNOSIS
 Fasting Plasma Glucose
 Oral Glucose Tolerance Test
(OGTT)
 Glycoselated Hemoglobin (HbA1c)
 Urinalysis
• Glycosuria
• Ketone bodies

34. HBA1C
•Measures the amount of glycated haemoglobin in
blood.•HbA1c is not sensitive enough to detect DM but
is standard for the long term monitoring.
the gold

35. ADDITIONAL INVESTIGATIONS;
 Lipid profile
 Fundoscopic examination
 LFT ,
 Urine analysis
 ECG
 Test to assess other complications

36. Any one test should be
confirmed with a second
test, most often fasting
plasma glucose (FPG).
DIAGNOSTIC CRITERIA
• Classic signs of HYPERGLYSEMIA with CPG ≥200mg/
• OGTT ≥200mg/dL
• FPG ≥126mg/dL
• A1C ≥ 6.5%

37. CONDITION 2 HRS GLUCOSE
FASTING GLUCOS
E
HbA1C
UNIT Mg/dl Mg/dl %
Normal <140 <110 <6
Impaired fasting
glycemia
<140 110 – 126 6 -6.4
Impaired
glucose
tolerance
>140 <126 6 – 6.4
DM >200 >126 > 6.5

38. MANAGEMENT OF DIABETES
MELLITUS

39. The major components of the treatment of
diabetes are:
MANAGEMENT OF DM
• Medical Nutrition Therapy(Diet and Exercise)A
• Oral hypoglycaemic therapyB
• InsulinC

40.  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.
A. DIET

41. DIETARY MANAGEMENT
DIETARY MANAGEMENT
Follow individualized meal plan and snacks as
scheduled diet based on pts. wt., age, occupation and
activity.
Balanced diabetic diet – 50% CHO, 30% fats, 20%
CHON(Co2, H2o, O2, Nitrogen), vitamins and
minerals.
Meal should include more fiber and starch and fewer
simple or refined sugars.

42. DIETARY MANAGEMENT
 If taking insulin, eat extra food before periods of vigorous
exercise.
 Routine blood glucose testing before each meal and at
bedtime is necessary during initial control, during illness and
in unstable pts.
 Excessive salt intake is to be avoided. It should be
particularly restricted in people with hypertension and those
with nephropathy.

43.  Eat grains in the least processed state possible.
 Limit potatoes and refined grain products.
 Avoid concentrated sweets (jellies, jams, cakes, ice
cream).
 Choose foods with healthy fats.
 Have 3 meals and one or two snacks each day.
 Eat slowly and stop when full.
 Avoid periods of fasting and feasting, Do not skip
meals.
How to eat low Glycemic Index food

44.  Physical activity promotes weight reduction and
improves insulin sensitivity, thus lowering blood
glucose levels.
 Exercise same time and duration of day.
 People should, however, be educated about the
potential risk of hypoglycaemia and how to avoid it.
 Avoid during poor metabolic control.
 Avoid trauma to extremities.
EXERCISE

45. EXERCISE PRECAUTIONS
 Patients who have BS >200mg/dl and who have urine
ketones should not begin exercise until urine tests are
NEGATIVE.
 Use of proper footwear.
 Avoid exercise in extreme heat or cold.
 Have snacks after the exercise , to avoid post exercise
hypoglycemia.

46.  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)
vi.DPP4i
B. ORAL ANTI-DIABETIC
AGENTS

47. Oral Anti-diabetic Agents

48. BIGUANIDES
 Metformin : is the only drug of this class presently
available in market
 It does not cause hypoglycaemia
 MOA : They increase glucose uptake and utilisation in
skeletal muscle (thereby reducing insulin resistance)
and reduce hepatic glucose production
(gluconeogenesis).
 Pharmacokinetic : Metformin has a half-life of about
3 hours and is excreted unchanged in the urine.

49. METFORMIN
 Side effects :
-Dose-related gastrointestinal disturbances
-lactic acidosis is a rare but potentially fatal toxic effect
-Long-term use may interfere with absorption of vitamin B12
 Contra indications:
Renal failure
Hepatic disease
Heart failure or shock.

50. INSULIN SECRETAGOGUES
SULFONYLUREAS : Inhibit KATP Channel of ß-cells
First-generation agents
Tolbutamide
Acetohexamide
Tolazamide
Chlorpropamide
Second-generation
Glipizide
Glyburide
Glimepiride

51. SULFONYLUREAS
 Hypoglycemia is the most common and most serious
adverse event associated with SU therapy.
 Weight gain, regarded as a class effect of Su’s
 Contraindicaton: liver failure, renal failure patients.
 Most sulfonylureas cross the placenta and enter breast
milk; as a result, use of sulfonylureas is contraindicated
in pregnancy and in breast feeding.

52. NON-SULFONYLUREA
SECRETAGOGUES
 MEGLITINIDES
• MOA: Inhibit KATP Channel of ß-cells
• Very fast onset of action, rapidly metabolized by liver
enzymes, with a peak effect within 1 hour, the
duration of action is 5–8 hr.
• Short duration of action and a low risk of
hypoglycaemia
• Medications in this Class: Repaglinide, Nateglinide.

53. THIAZOLIDINEDIONES
 ↓ Insulin resistance by making muscle and
adipose cells more sensitive to insulin. They also
suppress hepatic glucose production.
 Side effects: weight gain, oedema, Hypoglycemia
(if taken with insulin)
 Contraindication: patients with abnormal LFT or
CHF
 Medications in this class: Pioglitazone,
Rosiglitazone,

54. Α-GLUCOSIDASE INHIBITORS
 Acarbose : An inhibitor of intestinal α-glucosidase.
 MOA : It delays carbohydrate absorption, reducing the
postprandial increase in blood glucose .
 Unwanted effects : flatulence, loose stools or diarrhoea,
and abdominal pain and bloating.
 Like metformin, it is helpful in obese type 2 patients, and
it can be co-administered with Metformin.

55. TREATMENT OF TYPE 2 DIABETES
Diagnosis
Therapeutic Lifestyle Change
Combination Therapy - Oral Drug with Insulin
Combination Therapy - Oral Drugs Only
Monotherapy

56.  If glycaemic control is not achieved (HbA1c >
6.5%) 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%, FPG > 11.1 mmol/L), oral anti-
diabetic agents can be considered at the outset
together with lifestyle modification.
MONOTHERAPY

57. Combination oral agents is indicated in:
Newly diagnosed symptomatic patients with
HbA1c >10
Patients who are not reaching targets after 3
months on monotherapy
COMBINATION ORAL
AGENTS

58. DIABETES MANAGEMENT ALGORITHM

59. Short-term use:
 Acute illness, surgery, stress and emergencies
 Pregnancy
 Breast-feeding
 Insulin may be used as initial therapy in type 2 diabetes
 Severe metabolic decompensation (diabetic
ketoacidosis, hyperosmolar nonketotic coma, lactic
acidosis, severe hypertriglyceridaemia).
INSULIN THERAPY

60. Long-term use:
 If targets have not been reached after optimal
dose of combination therapy, consider change to
multi-dose insulin therapy.
INSULIN THERAPY

62. INSULIN INJECTION SITES

63. ROUTES OF ADMINISTRATION
 Subcutaneous for long term regular use
 Intravenous infusion in acute conditions- diabetes
Ketoacidosis, Perioperative period, Hyperosmolar
Nonketotic state ONLY NEUTRAL/ CLEAR
INSULIN CAN BE USED
 Intraperitoneal – Peritoneal dialysis patients
 Inhaled insulin- experimental

65. COMPLICATIONS OF
INSULIN THERAPY
Hypoglycemia
Lipodystrophy
Systemic allergic reactions
Insulin resistence

66. METHODS OF INSULIN
THERAPY
1. Insulin syringe:
2. Insulin pens
3. Jet injectors
4. Insulin Pumps

67. PATIENT EDUCATION
 Taking care of diabetes will help to reduce blood glucose,
blood pressure, and cholesterol levels in target ranges.
 Caring for your diabetes can also help prevent other health
problems over the years.
Follow your healthy eating plan every day.
Be physically active every day.
Take medicines every day.
Check blood glucose levels every day.

68. COMPLICATIONS
OF
DIABETES

69. COMPLICATIONS OF DIABETES
MELLITUS
I. Acute complications:
diabetic ketoacidosis
hypoglycemia
diabetic nonketotic hyperosmolar coma
II. Chronic complications:
 A. Microvascular
Retinopathy
Nephropathy
Neuropathy
Diabetic Foot
Dermopathy
b. Macrovascular
Cerbro-vascular.
Cardio-vascular.
Peripheral Vascular
Disease.

70. HYPOGLYCEMIA
 Hypoglycemia is the most frequent acute complication in
diabetes.
 Signs and symptoms are most common when blood
glucose levels fall <60 mg/dL.
 CAUSE:
Missing meals or excessive exercise
Alterations or errors in insulin dosage.
Alcohol ingestion.

71. CLINICAL MANIFESTATIONS OF
HYPOGLYCEMIA:
 Autonomic dysfunctions:
1. Hunger
2. Tremor
3. Palpitation
4. Anxiety
5. Pallor
6. Sweating
Neurologic dysfunctions:
1.Impaired thinking
2.Change of mood
3.Irritability
4.Headache
5.Convulsion
6.Coma

73. MANAGEMENT
 MILD (Self treated)
Oral fast acting carbohydrate (10- 15gm) – taken as
glucose drink or candy
 Severe :(semi conscious or comatose patient)
IV hypertonic glucose 25% or 50% concentration
Glucagons injection- i.m Glucagon (1mg)

75. DIABETIC KETOACIDOSIS
- It is a true emergency
- CAUSES: Omitting insulin in type 1 DM or increase
insulin requirements,
Infection
Trauma
Myocardial Infarction
Stroke
Surgery
Emotional stress
 Mortality rate is around 5%.

76. CLINICAL PRESENTATION

77. MANAGEMENT
 Fluid replacement: 0.9% Na.
 Insulin therapy for hyperglycemia: To restore the
metabolic abnormalities. Titrate the dose according
to the blood glucose level.
• 50U insulin in 50 ml NS iv via infusion pump
6U/hr initially
3U/hr when blood glucose < 270mg/dl
2U/hr when blood glucose < 180mg/dl
 Electrolyte correction.
 Acidosis correction.
 Treatment of precipitating cause.

78. HYPERGLYCEMIA HYPEROSMOLAR
NONKETONIC SYNDROME (HHNK)
 Occurs when there is insufficient insulin to prevent
hyperglycemia, but there is enough insulin to prevent
Ketoacidosis.
 Occurs in all types of diabetes, Esp Diabetes Type 2.
 Life threatening medical emergency.
 Characterized by :
 Plasma osmolarity 340 mOsm/L or greater normal: 280 -300).
 Blood glucose severely elevated, 600 - 1000 or 2000 (normal
70- 110).
 Undetectable ketonuria and Absence of acidosis.

79. HHNKS
 Major difference from diabetic ketoacidosis is the lack of
ketonuria because there is some residual ability to
secrete insulin in NIDDM.
CLINICAL MANIFESTATION:
 Altered level of consciousness (lethargy to coma)
 Neurological deficits: hyperthermia, motor and sensory
impairment, seizures
 Dehydration: dry skin and mucous membranes, extreme
thirst.

80. MACRO-VASCULAR
COMPLICATIONS
 Ischemic heart diseases.
 Cerebrovascular diseases.
 Peripheral vascular diseases.
Diabetic patients have a 2 to 6 times higher risk for development of
these complications than the general population

81. HYPERTENSION IN DM
 Mostly present at diagnosis
 Affects about 60% of patients
 Secondary to insulin resistance
 Increases risk for retinopathy, nephropathy
 Dyslipidaemia in DM
 Most common abnormality is  HDL and 
Triglycerides
 A low HDL is the most constant predictor of
Cardiovascular
disease in DM.

82. PERIPHERAL VASCULAR
DISEASE
 Increased risk for Types 1 and 2 diabetics.
 Development of arterial occlusion and thrombosis resulting
in gangrene.
 Gangrene from diabetes is themost common cause of non-
traumatic lower limb amputation.

83. SCREENING FOR MACROVASCULAR
COMPLICATIONS
1. Examine pulses for cardiovascular
diseases.
2. Lipid profile.
3. ECG.
4. Blood pressure.

84.  Microvascular complications are specific to longstanding
hyperglycaemia.
 Both Type1 DM and Type2 DM are susceptible to
microvascular complications.
 The duration of diabetes and the quality of diabetic
control are important determinants of microvascular
abnormalities.
MICROVASCULAR COMPLICATIONS

85. DIABETIC RETINOPATHY
 Affects 60 % of Type 2 diabetics
 progressive, irreversible vision loss.
Cotton wool spots
 Damage to the tiny blood vessels that supply the eye
• Micro aneurysms
• Scattered exudates
• Cotton wool spots (<5)
• Venous dilatations
NORMAL RETINA

86. DIABETIC NEPHROPATHY (DN)
Diabetic nephropathy is defined by persistent albuminuria
(>300 mg/day), decrease glomerular filtration rate and
rising blood pressure.
About 20 – 30% of patients with diabetes develop diabetic
nephropathy
- Manifested as:
- Microalbuminuria
- Progressive diabetic nephropathy leading to end-
stage renal disease

87. TREATMENT TO PREVENT
PROGRESSION TO DN
 All diabetic patients should be screened annually for
microalbuminurea.
 Tight glycemic control and management of the blood
pressure
 ACE-inhibitors are recommended to decrease the
progression of nephropathy
 Smoking cessation.
 Proteins restriction.
 Lipid reduction.

88. DIABETIC NEUROPATHY
 Damage to the Nerves due to hyperglycemia
 Typses of Neuropathies…
Sensory-Motor Polyneuropathy
• Numbness, paresthesias.
• Feet are mostly affected, hands are seldom affected.
• Complicated by ulceration (painless), charcot arthropathy
• Decreased deep tendon reflexes

89. DIABETIC NEUROPATHY
Autonomic neuropathy
 Can affect almost any system
- Manifested by orthostatic hypotension, diabetic
diarrhea, erectile dysfunction, and difficulty in
urination.

90. NURSING
MANAGEMENT

91. NURSING ASSESSMENT
Obtain history : it includes,
Current problems and General health history
Family history
Has the patient experienced polyuria, polydipsia,
polyphagia, and any other symptoms?
Number of years since diagnosis of DM?
Symptoms of complications?

92. NURSING ASSESSMENT
PHYSICAL EXAMINATION:
 General: Recent wt. loss or gain, fatigue, anxiety
 Skin: lesion, infections, dehydration,
 Eyes: changes in vision, “floaters, halos, cataracts…
 Cardiovascular: orthostatic hypotension, claudication
 GI: diarrhea, increased hunger and thirst
 GU: polyurea, nocturia
 Neurologic: numbness, and tingling of extremities

93. 1.Imbalanced nutrition : more than body requirement
related to intake of excess of activity expenditures.
Assess the current timings and content of meals
Advise patient on the importance of an individualized
meal plan in meeting weight loss goals.
Explain the importance of exercise in maintain /
reducing body weight.
Assist the patient to establish goals for weekly weight
loss and incentives to assist in achieving them.

94. 2. Risk for injury ( hypoglycemia) related to effects of
insulin, inability to eat.
Closely monitor blood glucose levels to detect
hypoglycemia.
Instruct the patient in the importance of accuracy in insulin
preparation and meal timings to avoid hypoglycemia.
Treat hypoglycemia promptly with 15 to 20 gm of fast
acting carbohydrates.
Encourage patients to carry sugar candy all times.
Encourage patient to wear identification bracelet

95. 3. Deficit knowledge related to use of oral hypoglycemic
agents.
Assess level of knowledge of disease and ability to care
self.
Assess adherence to diet therapy, monitoring procedures,
medication, treatment, and exercise regimen.
Assess for signs for hyperglycemia or hypoglycemia.
Perform skin and extremity assessment for peripheral
neuropathy or any injury in feet and lower extremities.

96. 4. Risk for impaired skin integrity related to decreased
sensation and circulation to lower extremities.
Assess feet and legs for skin temperature sensation, soft tissue
injures, corn, dryness, hammer toe,
Maintain skin integrity by protecting feet from break down.
Use heel protectors, special mattresses, foot cradles for patient
on bed rest.
Avoid Appling drying agent to skin. (alcohol)
Apply moisturizers to maintain suppleness and prevent
cracking and fissures.
Instruct patient in foot care guidelines

97. FOOT CARE
Patient should
Check feet daily
Wash feet daily
Keep toe nails short
Protect feet
Always wear shoes
Look inside shoes before
putting them on
Always wear socks
Break in new shoes
gradually

98. 5. Ineffective coping related to chronic disease and
complex self care regimen.
Discuss with the patient the perceived effect of diabetes
on lifestyle, finances, family life, occupation.
Explore previous coping strategies and skills that have
had positive effects.
Encourage patient and family participation in DM self
care regimen.
Assist family in providing emotional support.

99. SPECIAL PATIENT POPULATION
1. Adolescent Type 2 DM
- Type 2 DM is increasing in adolescent.
- Lifestyle modification is essential in these patients.
- If lifestyle modification alone is not effective,
metformin the only labeled oral agent for use in children
(10-16 years).

100. CONCLUSION
Type 2 diabetes is a “life style” disease,
characterized by hyperglycemia resulting from
defects in insulin secretion, insulin action, or both.
Caring for diabetes can also help prevent other health
problems over the years.