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Diabetes mellitus, often simply
referred to as diabetes, is a group of
metabolic diseases in which a person
has high blood sugar, either because
the body does not produce enough
insulin, or because cells do not respond
to the insulin that is produced. This
high blood sugar produces the classical
symptoms of polyuria (frequent
urination), polydipsia (increased thirst)
and polyphagia(increased hunger).
Type 1 DM,(IDDM) OR Juvenile diabetes
Type 2 ( NIDDM ) OR Adult onset
diabetes
Gestational diabetes
Congenital diabetes
Cystic fibrosis
Monogenic diabetes
 Type 1 diabetes
Type 1 diabetes mellitus is
characterized by loss of the insulin-
producing beta cells of the islets of
Langerhans in the pancreas, leading to
insulin deficiency. This type can be
further classified as immune-mediated
or idiopathic.
The majority of type 1 diabetes is of the
immune-mediated nature, in which
beta cell loss is a T-cell-mediated
autoimmune attack There is no known
preventive measure against type 1
diabetes,
diabetes can affect children or adults,
but was traditionally termed "juvenile
diabetes" because a majority of these
diabetes cases were in children.
Type 2 diabetes
Type 2 diabetes mellitus is characterized by
insulin resistance, which may be combined
with relatively reduced insulin secretion.
The defective responsiveness of body tissues
to insulin is believed to involve the insulin
receptor. However, the specific defects are
not known.
Diabetes mellitus cases due to a known
defect are classified separately. Type 2
diabetes is the most common type.
Gestational diabetes mellitus (GDM)
It is resembles type 2 diabetes in several
respects, involving a combination of
relatively inadequate insulin secretion and
responsiveness.
It occurs in about 2%–5% of all pregnancies
and may improve or disappear after delivery.
Gestational diabetes is fully treatable,
but requires careful medical supervision
throughout the pregnancy. About 20%–50%
of affected women develop type 2 diabetes
later in life.
Etiologic Classification of Diabetes
Mellitus
I. Type 1 diabetes (cell destruction, usually
leading to absolute insulin deficiency)
A.Immune-mediated
B.Idiopathic
II. Type 2 diabetes (may range from
predominantly insulin resistance with relative
insulin deficiency to a predominantly insulin
secretary defect with insulin resistance)
Other specific causes of the types of
diabetes
•Genetic defects of cell function Genetic
defects in insulin action.
•Diseases of the exocrine pancreas—
pancreatitis, pancreatectomy, neoplasia,
cystic fibrosis, fibrocalculous pancreatopathy,
•Endocrinopathies-acromegaly, Cushing's
syndrome, glucagonoma, hyperthyroidism,
somatostatinoma, aldosteronoma
•Drug- or chemical-induced-Vacor,
pentamidine, nicotinic acid, glucocorticoids,
thyroid hormone, diazoxide, -adrenergic
agonists, thiazides, phenytoin, interferon,
protease inhibitors, clozapine
•Infections—congenital rubella,
cytomegalovirus.
Other genetic syndromes sometimes
associated with diabetes—Down's
syndrome,Turner's syndrome
Other etiologies for DM
Specific genetic defects in insulin
secretion or action,
Metabolic abnormalities that impair
insulin secretion,
Mitochondrial abnormalities
DM can result from pancreatic
exocrine disease when the majority
of pancreatic islets are destroyed.
•Hormones that antagonize insulin action
can also lead to DM. Thus, DM is often a
feature of Endocrinopathies
• such as acromegaly and Cushing's
disease.
•Viral infections have been implicated in
pancreatic islet destruction but are an
extremely rare cause of DM.
•Polyuria
•Polydipsia
•polyphegia
•Weight loss
•Lethargy
•weakness
•Fluctuation in blood glucose level lead to
Blurred Vision
•Boils/abscesses
•Skin itching problem
•Others tingling sensation in skin
Body pains do not away by the
pain killers
Delay wound healing
Increased glucose level lead to
agitation,irritability,
inattention,confusion ,coma
Diagnostic test:
Fasting plasma glucose = preferred test:
Positive test is glycemia of 126mg/dL or
higher after fasting at least 8 hours

Random plasma glucose of 200mg/dL or
higher along with symptoms of diabetes

Post prandial glucose of 80 to 130 mg /dl
higher along with symptoms of diabetes
 Oral glucose tolerance test (OGTT) plasma glucose of
200mg/dL or higher done 2 hours after ingestion of 75
grams of glucose in water
 Diabetic urine tests
Complication:
Acute Complications of Uncontrolled
Diabetes:
(all directly caused by hyperglycemia)
--Polydypsia due to plasma glucose
hyperosmolarity
--Polyuria due to excess fluid intake and
glucose-induced osmotic diuresis
Weight loss due to calories loss as
glycosuria,leaving a negative calorie
balance
•--
Polyphagia due to glucosuria and
negative calorie balance
Poor wound healing, gingivitis, blurred
vision
Chronic Complications of Uncontrolled
Diabetes:
MACRO VASCULAR
Athrosclerosis
IHD
Stroke
Peripheral vascular disease
Micro vascular Diseases of
Diabetes
Diabetic Retinopathy
Nephropathy
Neuropathy
Diabetic foot
End stage Complications of
Uncontrolled Diabetes
1. Diabetic Ketoacidosis
2. Non ketotic hyperosmolarity
ORAL HYPOGLYCAEMIC MEDICATIONS
There are currently five classes of
oral anti-diabetic agents:
 Biguanides
Insulin Secretagogues – Sulphonylureas
Insulin Secretagogues – Non-
sulphonylureas
α-glucosidase inhibitors
Thiazolidinediones (TZDs)
Biguanides reduce hepatic glucose
output and increase uptake of
glucose by the periphery, including
skeletal muscle.
Example: metformin
Sulfonylureas were the first widely
used oral anti-hyperglycaemic
medications. They are insulin
secretagogues, triggering insulin
release by inhibiting the KATP
channel of the pancreatic beta
cells
First-generation agents
tolbutamide (Orinase brand name
)
acetohexamide (Dymelor)
tolazamide (Tolinase)
chlorpropamide (Diabinese)
Second-generation agents
glipizide (Glucotrol)
glyburide or glibenclamide
(Diabeta, Micronase, Glynase)
glimepiride (Amaryl)
gliclazide (Diamicron)
glycopyramide
gliquidone
Nonsulfonylurea secretagogues
Meglitinides
TYPES OF DRUGS:
repaglinide (Prandin)
nateglinide (Starlix)
Alpha-glucosidase inhibitors
TYPES OF DRUGS
miglitol (Glyset)
acarbose (Precose/Glucobay)
voglibose
Thiazolidinedione
pioglitazone
troglitazone
Short-term use:
Acute illness, surgery, stress and
emergencies
Pregnancy
Breast-feeding
Insulin may be used as initial
therapy in type 2 diabetes
in marked hyperglycaemia
Severe metabolic decompensation
(diabetic ketoacidosis, hyperosmolar
nonketotic coma, lactic acidosis,
severe hypertriglyceridaemia)
Long-term use:
If targets have not been reached
after optimal dose of combination
therapy, consider change to multi-
dose insulin therapy.

SURGICAL MANAGEMENT :
ISLET CELLS TRANSPLANATATION
:Insulin producing B cells taken
from donors pancreas &
transferred into a person with
diabetes, once transplanted the
donor islets begin to make &
release insulin actively & regulating
level of sugar in the blood
Nursing management:
NURSING DIAGNOSIS:
1) Deficient Fluid VolumeMay be
related to Osmotic diuresis (from
hyperglycemia
2) Nutrition: less than body
requirements May be related to
Insulin deficiency: decreased
uptake/utilization of glucose by the
tissues
3) Risk for Infection, [sepsis] Risk
factors may include High glucose
levels, decreased leukocyte
function, alterations in circulation
Preexisting respiratory infection, or
UTI
4) Risk for disturbed Sensory
Perception, Risk factors may
include Endogenous chemical
alteration: glucose/insulin
diabetes mellitus management prevent. ion
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diabetes mellitus management prevent. ion

  • 1.
  • 2.
  • 3. Diabetes mellitus, often simply referred to as diabetes, is a group of metabolic diseases in which a person has high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia(increased hunger).
  • 4. Type 1 DM,(IDDM) OR Juvenile diabetes Type 2 ( NIDDM ) OR Adult onset diabetes Gestational diabetes Congenital diabetes Cystic fibrosis Monogenic diabetes
  • 5.  Type 1 diabetes Type 1 diabetes mellitus is characterized by loss of the insulin- producing beta cells of the islets of Langerhans in the pancreas, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic.
  • 6. The majority of type 1 diabetes is of the immune-mediated nature, in which beta cell loss is a T-cell-mediated autoimmune attack There is no known preventive measure against type 1 diabetes, diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were in children.
  • 7. Type 2 diabetes Type 2 diabetes mellitus is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type.
  • 8. Gestational diabetes mellitus (GDM) It is resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.
  • 9. Etiologic Classification of Diabetes Mellitus I. Type 1 diabetes (cell destruction, usually leading to absolute insulin deficiency) A.Immune-mediated B.Idiopathic II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretary defect with insulin resistance)
  • 10. Other specific causes of the types of diabetes •Genetic defects of cell function Genetic defects in insulin action.
  • 11. •Diseases of the exocrine pancreas— pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, fibrocalculous pancreatopathy, •Endocrinopathies-acromegaly, Cushing's syndrome, glucagonoma, hyperthyroidism, somatostatinoma, aldosteronoma
  • 12. •Drug- or chemical-induced-Vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid hormone, diazoxide, -adrenergic agonists, thiazides, phenytoin, interferon, protease inhibitors, clozapine •Infections—congenital rubella, cytomegalovirus.
  • 13. Other genetic syndromes sometimes associated with diabetes—Down's syndrome,Turner's syndrome
  • 14. Other etiologies for DM Specific genetic defects in insulin secretion or action, Metabolic abnormalities that impair insulin secretion, Mitochondrial abnormalities DM can result from pancreatic exocrine disease when the majority of pancreatic islets are destroyed.
  • 15. •Hormones that antagonize insulin action can also lead to DM. Thus, DM is often a feature of Endocrinopathies • such as acromegaly and Cushing's disease. •Viral infections have been implicated in pancreatic islet destruction but are an extremely rare cause of DM.
  • 16.
  • 17. •Polyuria •Polydipsia •polyphegia •Weight loss •Lethargy •weakness •Fluctuation in blood glucose level lead to Blurred Vision •Boils/abscesses •Skin itching problem •Others tingling sensation in skin
  • 18. Body pains do not away by the pain killers Delay wound healing Increased glucose level lead to agitation,irritability, inattention,confusion ,coma
  • 19.
  • 20. Diagnostic test: Fasting plasma glucose = preferred test: Positive test is glycemia of 126mg/dL or higher after fasting at least 8 hours  Random plasma glucose of 200mg/dL or higher along with symptoms of diabetes  Post prandial glucose of 80 to 130 mg /dl higher along with symptoms of diabetes
  • 21.  Oral glucose tolerance test (OGTT) plasma glucose of 200mg/dL or higher done 2 hours after ingestion of 75 grams of glucose in water  Diabetic urine tests
  • 22. Complication: Acute Complications of Uncontrolled Diabetes: (all directly caused by hyperglycemia) --Polydypsia due to plasma glucose hyperosmolarity --Polyuria due to excess fluid intake and glucose-induced osmotic diuresis Weight loss due to calories loss as glycosuria,leaving a negative calorie balance •--
  • 23. Polyphagia due to glucosuria and negative calorie balance Poor wound healing, gingivitis, blurred vision Chronic Complications of Uncontrolled Diabetes: MACRO VASCULAR Athrosclerosis IHD Stroke Peripheral vascular disease
  • 24. Micro vascular Diseases of Diabetes Diabetic Retinopathy Nephropathy Neuropathy Diabetic foot
  • 25. End stage Complications of Uncontrolled Diabetes 1. Diabetic Ketoacidosis 2. Non ketotic hyperosmolarity
  • 26.
  • 27. ORAL HYPOGLYCAEMIC MEDICATIONS There are currently five classes of oral anti-diabetic agents:  Biguanides Insulin Secretagogues – Sulphonylureas Insulin Secretagogues – Non- sulphonylureas α-glucosidase inhibitors Thiazolidinediones (TZDs)
  • 28. Biguanides reduce hepatic glucose output and increase uptake of glucose by the periphery, including skeletal muscle. Example: metformin
  • 29. Sulfonylureas were the first widely used oral anti-hyperglycaemic medications. They are insulin secretagogues, triggering insulin release by inhibiting the KATP channel of the pancreatic beta cells
  • 30. First-generation agents tolbutamide (Orinase brand name ) acetohexamide (Dymelor) tolazamide (Tolinase) chlorpropamide (Diabinese)
  • 31. Second-generation agents glipizide (Glucotrol) glyburide or glibenclamide (Diabeta, Micronase, Glynase) glimepiride (Amaryl) gliclazide (Diamicron) glycopyramide gliquidone
  • 32. Nonsulfonylurea secretagogues Meglitinides TYPES OF DRUGS: repaglinide (Prandin) nateglinide (Starlix)
  • 33. Alpha-glucosidase inhibitors TYPES OF DRUGS miglitol (Glyset) acarbose (Precose/Glucobay) voglibose
  • 35.
  • 36. Short-term use: Acute illness, surgery, stress and emergencies Pregnancy Breast-feeding Insulin may be used as initial therapy in type 2 diabetes
  • 37. in marked hyperglycaemia Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma, lactic acidosis, severe hypertriglyceridaemia)
  • 38. Long-term use: If targets have not been reached after optimal dose of combination therapy, consider change to multi- dose insulin therapy. 
  • 39.
  • 40. SURGICAL MANAGEMENT : ISLET CELLS TRANSPLANATATION :Insulin producing B cells taken from donors pancreas & transferred into a person with diabetes, once transplanted the donor islets begin to make & release insulin actively & regulating level of sugar in the blood
  • 41.
  • 42. Nursing management: NURSING DIAGNOSIS: 1) Deficient Fluid VolumeMay be related to Osmotic diuresis (from hyperglycemia 2) Nutrition: less than body requirements May be related to Insulin deficiency: decreased uptake/utilization of glucose by the tissues
  • 43. 3) Risk for Infection, [sepsis] Risk factors may include High glucose levels, decreased leukocyte function, alterations in circulation Preexisting respiratory infection, or UTI 4) Risk for disturbed Sensory Perception, Risk factors may include Endogenous chemical alteration: glucose/insulin