Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels. The document outlines the types of diabetes (type 1, type 2, gestational), risk factors, pathophysiology, clinical manifestations, complications and diagnostic tests. It provides definitions of diabetes, discusses the anatomy and physiology of the pancreas, classifications of diabetes, causes and risk factors, pathophysiology, clinical manifestations, complications, and diagnostic evaluations. The summary focuses on key information about the different types of diabetes.

1. SEMINAR ON-
DIABETES MELLITUS
SUMITTED TO- SUBMITTED BY-
Prof. Dr. Mrs. SHREEMINI PILLAI SWATI YADAV
MEDICAL SURGICAL NURSING MS.c 1st year
P.G. College Of Nursing bhilai

2. CONTENTS
• INTRODUCTION
• DEFINITION
• INCIDENCE
• ANATOMY AND PHYSIOLIOGY OF PANCREAS
• CLASSIFICATION OF DIABETES
• CAUSES AND RISK FACTORS
• PATHOPHYSIOGY OF DIABETES
• CLINICAL MANIFESTATIOS OF DIABETES
• COMPLICATIONS
• DIAGNOSTIC EVALUATIONS
• MANAGEMENT OF DIABETES

3. INTRODUCTION
• Diabetes mellitus is a chronic metabolic disorder of impaired
carbohydrates, proteins and lipid metabolism.
• Diabetes mellitus is a group of metabolic disorder in which a person
has high blood glucose level either because the body does not
produce enough insulin or because cells do not respond to the insulin
that is produced.

4. DEFINITION
• As per WHO diabetes mallitus (DM) is defined as a heterogenous
matabolic disorder characterised by common feature of chronic
hypergycemia with disturbance of carbohydrate, fat and protein
matabolism.
• Diabetes is a chronic disease that occurs either when the pancreas
does not produce enough insulin or the body cannot effectively use
the insulin it produces. Uncontrolled diabetes may lead to serious
damage to many body systems especially the nervous and blood
vessels.

5. INCIDENCE OF DIABETES MELLITUS
• The development of diabetes is projected to reach pandemic
proportions over the next 10-20 years.
• International diabetes federation data indicate that by the year 2025
the number of people affected will reach 33 million -90% of these will
have Type 2 Diabetes.
• In most western societies the overall prevalence has reached 4-6%
and is as high as 10-12% among 60-70 years old people.

6. ANATOMY OF PANCREAS
• The pancreas is an elongated tapered organ located across the
back of the belly, behind the stomach. The right side of the
organ called The Head which is the widest part of the organ
and lies in the curve of the duodenum the first division of the
small intestine . The tapered left side extends slightly upward
called The Body and end near the spleen called The Tail.

8. • The pancreas is made up of two types of glands.
• EXOCRINE PART- The exocrine gland secrets digestive enzymes. These
enzymes are secreted into a network of ducts that join the main
pancreatic duct. This runs the length of the pancreas.
• ENDOCRINE PART- The endocrine gland which consists of the islets of
langerhans secrets harmone into the blood stream.

9. PHYSIOLOGY OF PANCREAS-
• The enzyme secreted by the exocrine gland in the pancreas help in
break down of carbohydrates, fats, proteins and acids in the
deuodenum. These enzymes travel down the pancreatic duct into the
bile duct in an inactive form. When they enter the duodenum, they
are activated. The exocrine tissue also secretes a bicarbonate to
neutralize stomach acid in the deuodenum.
• The main harmone secreted by the endocrine gland in the pancreas
are insulin and glucagon which regulate the level of glucose in the
blood and stomatostatin which prevents the release of insulin and
glucagon.

10. CLASSIFICATION OF DIABETES
• There are many types of diabetes mellitus. These may differ in cause,
clinical course and treatment. The main classification is:-
• 1. Type-1
• it is also known as insulin dependent diabetes mellitus(IDDM).
• 2. Type-2
• It is also known as non- insulin dependent diabetes mellitus (NIDDM).
• 3. Type-3
• Gestational diabetes mellitus (GDM).
• 4.Type-4
• This is associated with other conditions or syndrome.

11. 1)TYPE-1 DIABETES MELLITUS
• It is also known as IDDM or juvenile onset diabetes.
• Type-1 diabetes mellitus is the one in which the insulin producing pancreatic beta
cells are destroyed by autoimmune process which leads to absolute insulin
deficiency. As a result insulin injections are needed to control the blood glucose
levels. It usually occur before 30 years of age.
• Manifestations of type 1 diabetes occur when the persons pancreas can no longer
produce sufficient amount of insulin to maintain normal glucose.
• Once the insulin therapy has started and good control achieved the remaining beta
cells mass can temporarily provide sufficiant insulin to meet the body’s demand. In
this case the external insulin can be reduced or stopped on occation. Unfortunately
this ‘HONEYMOON PERIOD’ is short lived and as the beta cells mass reduces further,
the symptoms will reappear necessitating lifelong treatment with insulin.

12. • CAUSES AND RISK FACTORS OF TYPE-1 DIABETES
MELLITUS
• 1)GENETIC LINK :-
• It is inherited and is common in identical twins.
• The strongest link has been traced to the DR3 and DR4 genes in the
human leucocyte antigen(HLA) located on chromosome 6 (now known
as type 1 or diabetes 1 locus).
• 2)ENVIRONMENT FACTORS:-
• Environmental factors such as viruses are supposed to start
autoimmune processes that destroys beta cells.

13. PATHOPHYSIOLOGY OF TYPE1 DM-
• IN TYPE 1 Diabetes mellitus the autoantibodies responsible for beta
cells destruction are present for months to years before the onset of
symptoms.
• However individuals often present with initial symptoms when the
demand for insulin has been increased e.g. in response to a physical
or psychological stress such as illness, trauma, surgery, pregnancy or
bereavement. In such cases the additional metabolic demands posed
by the stressed state can no longer be met by the failing pancreas and
symptoms of diabetes become evident.

14. • The patients usually have the history of weight loss and the classical
symptoms of polydipsia, polyuria and polyphagia.
• The individuals with type 1 diabetes requires insulin from an outside source
(exogenous insulin) to sustain life.
• Without insulin the patient will develop diabetic ketoacidosis.

15. 2)TYPE-2 DIABETES MELLITUS
• Type 2 diabetes mellitus results from decreased sensitivity to insulin ( called as
insulin resistance) or from a decreased amount of insulin production.
• TYPE 2 diabetes mellitus is also known as adult onset diabetes (AODM) or non-
insulin dependent diabetes mellitus . it is most prevalent type of diabetes
accounting for 90-95%.
• However the insulin that is produced is either insufficient for the needs of the
body or is poorly used by the tissues or both. The presence of endogenous
insulin is the major distinction between type 1 and type 2 DM.
• It is treated mainly by diet and exercise. If elevated glucose level remains same,
oral hypoglycemic agents are given further insulin injections are required. It
occurs mainly in person older than 30 years of age.

16. RISK FACTORS-
• Includes being overweight or obese
• Being older, family history of having type 2 DM.
• Individuals with the metabolic syndrome are at an increased risk for the
development of DM type 2. Metabolic syndrome have 5 components-
• Elevated glucose level
• Abdominal obesity
• Elevated blood pressure
• High level of triglycerides
• Decreased level of HDLs.

17. ETIOLOGY
• 1) GENETIC FACTORS-
• THE genetics of type 2 DM is not yet fully understood it is likely multiple
genes are involved. Genetic mutations that leads to insulin resistance and
higher risk for obesity.
• Type 2 diabetes has a strong component, manifest in the high
concordance of diabetes in monozygotic twins.
• 2) AGE-
• The prevalence of type 2 diabetes rises significantly with increasing age
and can be as high as 1in 10 in the over 70s. glucose metabolism is known
to become less efficient from third or fourth decade of life.
• There are 4 major causes for the development of type2 DM-

18. 3) INSULIN RESISTANCE-
• A condition in which the body tissues do not respond to the action of
insulin because insulin receptors are unresponsive are insufficient in
number or both.
• Most of the insulin receptors are present on the skeletal muscles, fat
and liver cells. When insulin is not properly used the entry of glucose
into the cells is impeded resulting in hypergycemia.
• In early stages of insulin resistence the pancreas responds to high
blood glucose by producing greater amount of insulin, if beta cells
function is normal. This creates a temporary state of hyperinsulinemia.

20. • 1-The development of type 2 DM is a marked decrease in the
pancreas ability to produce insulin as the beta cells become fatigued
from the compensatory overproduction of insulin or when beta cell
mass is lost.
• 2-Inappropriate production of glucose by liver. Instead of properly
regulating the release of glucose in response to blood levels, the liver
does so in a haphazard way that does not correspond to the body’s
need at that time.
• 3-Altered production of harmones and cytokines by adipose tissues
(apokines). Apokines secreted by adipose tissues appear to play a role
in glucose and fat metabolism.

21. 4) ETHNIC AND ENVIRONMENTAL FACTORS-
• There are wide geographical variations in the incidence of type 2
diabetes. In western europe around 3% of the population develope
type 2 diabetes but in certain cercumscribed socities incidence upto
40% have reported e.g. among the Pima Indians Of North America and
the Nauru Islanders of the Pacific, where gross obesity is also very
common. These remarkably high prevalence are probably due to the
exposure of genetically isolated, diabetes-predisposed populations to
influences such as a westernised diet and reduced physical activity.

22. PATHOPHYSIOLOGY OF TYPE 2 DIABETES
• Type 2 diabetes mellitus results from decreased sensitivity to insulin ( called
as insulin resistance) or from a decreased amount of insulin produced.
• - TYPE 2 diabetes mellitus is also known as adult onset diabetes (AODM) or
non- insulin dependent diabetes mellitus . It is most prevalent type of
diabetes accounting for 90-95%.
• -In type 2 DM the pancreas usually continues to produce some endogenous
(self made) insulin.

23. • However the insulin that is produced is either insufficient for the
needs of the body or is poorly used by the tissues or both. The
presence of endogenous insulin is the major distinction between type
1 and type 2 DM.
• It is treated mainly by diet and exercise. If elevated glucose level
remains same, oral hypoglycemic agents are given further insulin
injections are required. It occurs mainly in person older than 30 years
of age.

25. 3)GESTATIONAL DIABETES
• IT is diagnosis of diabetes mellitus that applies only to women in whom
glucose intolerance develops or first discovered in pregnancy.
• Gestational diabetes mellitus developes during pregnancy and occurs in
about 2% to 10% of pregnancies.
• Women with GDM have higher risk for caesarean section and their
babies have high risk for perinatal death, birth injuries, and neonatal
complications.

26. RISK FACTORS-
• Obesity
• Advanced maternal age
• Family history

27. SCREENING TEST
• Women with an average risk for GDM are screened by using OGTT at
24 to 28 weeks of gestation.
• The glucose tolerance test is a medical test in which a standard dose
(70gm) of glucose is ingested by mouth and blood samples are taken
to rule out how quickly this glucose is cleared out from the body.

28. PATHOPHISIOLOGY OF GDM-
• GDM is usually the result of beta cell dysfunction on a background of
chronic insulin resistance during pregnancy and thus both beta cell
impairment and tissue insulin resistence represent critical
components of pathophysiology of GDM.

30. PREDIABETIC STATE –
• INDIVIDUALS diagnosed with prediabetes are at high risk for the
development of type 2 DM. Prediabetes is defined as impaired glucose
tolerance (IGT) impaired fasting glucose (IFG) or both.
• It is an intermediate stage between normal glucose homeostasis and
diabetes where the blood glucose levels are elevated but not too high
to meet the diagnostic criteria for diabetes. A diagnosis of IGT is made
if the 2 hour oral glucose tolerance test (ogtt) values are 140 to 199
mg/dl. IFG is diagnosed when fasting blood glucose levels are 100 to
125 mg/dl.

31. CLINICAL MANIFESTATIONS OF HYPERGYCEMIA
AND HYPOGLYCEMIA
• HYPERGYCEMIA HYPOGYCEMIA
• Fruity smell breaths excess sweating
• nausea and vomiting excessive hunger
• shortness of breath light headedness
• confusion fainting
• weakness shakiness and fatigue

32. 4) DIABETES MELLITUS ASSOCIATED WITH OTHER
DRUGS AND CONDITIONS-
• Drugs may induce hyperglycemia through a variety of mechanisms,
including alterations in insulin secretion and sensitivity, direct
cytotoxic effects on pancreatic cells and increase in glucose
production. List of drugs which can induce diabetes
• Coorticosteroids(prednisolone)
• Thiazide diuretics
• Beta-blokers
• Antipsychptics

33. • Statins
• Conditions in which blood glucose level are increased-
• Pancreatitis
• Cushing’s syndrome
• Unusual harmone secreting tumors
• Pancreatic cancer

34. CLINICAL MANIFESTATIONS
• TYPE1 DIABETES MELLITUS-
• The onset of type 1 DM is rapid the initial symptoms are usually
acute.
The classic symptoms are
• -Polyuria
• The osmotic effect of glucose produces the manifestation of
polydipsia and polyurea.
• -Polydipsia

35. • Polyphagia.
-When insulin deficiency prevents the utilization of glucose for energy
Polyphagia is the consequences of cellular malnourishment.
• Weight loss
- may occur because the body cannot get glucose and turns to other
energy sources such as fat and proteins.
• Weakness and fatigue
-may result because body cells lack needed energy from glucose.

36. COMPLICATOPN OF DIABETES MALLITUS 1 IS
KETOACIDOSIS
• Diabetic ketoacidosis is a life threatening and most common
complication of type1 diabetes that occurs when the body produces
high levels of ketones due to lack of insulin.
• Diabetic ketoacidosis occurs when the body cannot produce enough
insulin.

37. MECHANISM OF DIABETIC KITOACIDOSIS

39. The sign and symptoms of diabetic ketoacidosis
include-
• -Confusion
• -Frequent urination
• -Nausea and vomiting
• -Abdominal pain
• -Dehydration

40. Risk factors for diabetic ketoacdosis-
• Type1 diabetes and missing insulin doses frequently or being exposed
to a stressor requiring higher insulin doses, infections.
• Diabetic ketoacidosis is diagnosed by an elevated blood sugar level,
elevated blood ketones and acid of the blood (acidosis).

41. CLINICAL MANIFESTATIONS TYPE 2 DIABETES
MELLITUS
• The individuals with type 2 DM will experience some of the classic
symptoms associated with type 1diabetes including
• Polyuria and Polydipsia and Polyphagia.
• - Some symptoms which are mainly associated with type 2 diabetes
are-Fatigue
• - Recurrent infections
• -Recurrent vaginal yeast or candidal infections
• - Prolonged wound healing
• - Visual changes.

42. • The sign,symptoms and clinical features of type 2 diabetes, although
still marked are less severe than those of type 1 diabetes and are due
to the more gradual onset and the effects of hyperglycemia arising
from a relative deficiency of insulin.
• In type 2 diabetes, there is still some insulin being secreted as a result
ketogenesis is inhibited and as the hyperglycemia is less severe.
Dehydration is also less common.

43. COMPLICATIONS OF TYPE2 DIABETES MALLITUS-
• -Diabetic retinopethy
• -Kidney disease(nephropathy)
• -Diabetic neuropathy
• -Macrovascular problems

44. DIAGNOSTIC TESTS
• 1-FASTING BLOOD GLUCOSE-
-It is diagnosed by measuring blood glucose levels. It is normally less than
110mg/dl patient is said to be diabetic if the value is above 125mg/dl.
Critical value is 60 mg/dl to 500mg/dl. A fasting blood glucose sample is
taken.
• 2-RANDOM BLOOD GLUCOSE-
-The sample is taken at any time it requires no preparation. Elevated blood
glucose levels may occur after meals after stressfull event. Random blood
glucose 200 mg/dl or above on two separate samples indicate DM.

45. • 3- PRANDIAL BLOOD GLUCOSE-
-Sample is taken 2 hours after standard meals normally blood glucose
returns to fasting level within 2 hours. But smoking and drinking coffee
can give increased reading and heavy exercise gives decreased values at
2hrs.
• 4-GLYCOSYLATED Hb-
-It measures the amount of glycosylated hemoglobin as a percentage of
total hemoglobin.

46. -Glucose attaches itself to molecules and it cannot be separated
therefore as the level of blood glucose increases the level of glycosylated
Hb increases.
-This glucose remains attached to the red blood cells for the life of that
cell (approx. 120 days).
- Therefore the A1 c test provides a measurement of gycemic control
over previous 2 to 3 months with the increase in the A1c reflecting
elevated blood glucose levels.
• Eg:- HbA1c 6.5% means that 6.5% of the total hemoglobin has glucose
attached to it.

47. • 5- GLYCOSYLATED ALBUMIN-
-Glucose also attached to the albumin. The concentration of glycosylated
albumin represents the average blood glucose level.
• 6-ORAL GLUCOSE TOLERANCE TEST-
-The patient need a diet that offers 150grms of carbohydrates per day for
3 days. Then fasting blood glucose is taken. Client is given 75grms of
glucose to drink. And therefore the tolerance level of patient to glucose is
checked.
• 7-KETONURIA-
-The presence of ketone in urine indicates that the body is using fat as a
major source of energy.

48. • 8-PROTEINURIA-
-Presence of protein in urine indicates that protein is being used as a
major source of energy.
•MANAGEMENT-
• It includes combination of medication and dietary modification and
physical exercise.

49. 1-DIET MANAGEMENT-
• The main goal of dietary management is to help diabetic client to
improve metabolic control by making changes in nuitrition habits. It
includes-
• A)Improving blood glucose level and lipids levels
• B)Providing daily food intake plan.
• C)Help in weight management
• D)Providing adequate nuitrition

50. • Person’s dietary habit and lifestyle are very important to control this
state.
• A balanced nutritional plan is important for all patients it should
include community resources, follow patient’s appetite, likes and
dislikes, religion.
• Protein should be included in the diet. High protein intake increases
renal functioning and glomerulus filtration rate.
• Fat levels should be mentioned daily cholesterol intake should be
maintained in the diet. limit saturated fat and cholesterol.
• CARBOHYDRATES- It is important to take carbohydrates to meet the
energy requirements of the body. Complex carbohydrates should be
included in diet.
• Avoid food that are sweeten with sugar or honey such as cakes,
icecream, jams etc.

51. • 2-Physical exercise-
• Promote regular physical activity, exercise lowers the blood glucose
by increasing carbohydrate metabolism. Weight reduction increase in
insulin sensitivity maintaining the insulin levels, lowers B.P, reduces
stress and tension but hypoglycemia is a risk for those patient taking
insulin or oral hypoglycemic agents. Therefore meal planning and
medication are collectively planned.

52. • EXERCISE-
• Diabetes management is the responsibility of clients and their family .
patient requires consistent follow ups, updating knowledge and
reinforcement.
• Explain the patient and family the basic pathophysiology of diabetes
and how it is managed and observe the patient response.
• 1)Exercise programme should be started after taking history, physical
examination , foot evaluation , lab examination of blood glucose level.
• 2)Walking is the best tolerated exercise . stationary bicycle and
swimming could also be used. unplanned exercise can also be
dangerous for the clients using insulin or oral hypoglycemic agents.

53. • 3)To prevent complication from exercise the clients should be
adequately hydrated before starting exercise. They should have
carbohydrate before or after exercise. Patients having high glucose
level should wait to exercise as heavy exercises can raise the blood
glucose level by releasing stored glycogen.
• PHARMACHOLOGICAL MANAGEMNT-
• Insulin works to decrease the blood glucose level by promoting the
transport of glucose into the cells and inhibits the coversion of
glycogen and amino acids to glucose. Insulin injected into the
abdomen is absorbed fastest, whereas in leg and arm absorption
decreases.

54. • Many insulin preparation are available. It varies according to three main
characteristics-
• 1)TIME, COURSE-
• a)Rapid acting insulin-
• It has the onset of 10-15 mints. eg: Lispro (Humalog),Aspart
• b)Short acting insulin-
• It is called as crystalline zinc- insulin (CZI). It has an onset of 30 mints
before a meal.
• eg. Regular or Novolin
• c)Intermediate acting insulin-
• Called as regular insulin its onset of action is 3-4 hours. It is important for
the patients to have taken food around this time.

55. • eg. NPH
• d)Long acting insulin-
• Called ultra lente insulin or peakless insulin. They act within 6-8 hrs
for the duration of 20-30 hrs.
• eg. Glargine, Detemir.
• INSULIN DOSES-
• The starting dose of insulin is 0.5 unit/kg/day. 2/3rd dose is
commonly in morning and i/3rd dose is given in the evening. The
dose can be increased or decreased according to the food intake,
exercise stress or illness.

56. • INSULIN PUMP THERAPY-
• Small portable pump for the continuous administration of regular
insulin are used. Needle sites are changed daily 2-3 times a day,
glucose level is monitored. Its complication includes-
• 1)Infection at the injection site.
• 2)Hypoglycemia
• COMBINTION THERAPY
• It is defined as the use of two or more oral anti diabetic agents or an
oral agent combined with insulin.

57. • ORAL ANTI- DIABETIC AGENTS-
• 1)Sulfonylureas (hypoglycemic agents)-
• ACTION-
• -stimulate beta cells of the pancreas to secrete insulin.
• -improve binding between insulin and insulin recepters or increase the insulin receptors.
• Eg. Glimepriride, glyburide, glipizide.
• IMPLICATION-
• -Monitor patients for hypoglycemia.
• -Monitor blood glucose level and urine ketone level to assess the effectiveness of therapy.
• -Instruct patient to avoid alcohol.
• SIDE EFFECTS-
• -Hypogycemia
• -Mild G.I symptoms
• -Weight gain
• -Sulfa allergy

58. • 2)Meglitinides (hypoglycemic agents)
• ACTION
• -Stimulate pancreas to secrete insulin.
• -Used in type 2 diabetes to control blood glucose level.
• Eg. Repaglinide(trade name Prandin), mitiglinide, nateglinide
• SIDE EFFECTS-
• -hypogycemia
• -Weight gain
• -Drug-drug interactions with ketoconazole, rifampicin, isoniazid
• IMPLICATIONS-
• -Has rapid action and short half life.
• -Should be taken only if able to eat a meal immediately.
• -Monitor patients with impaired liver and renal function.

59. • 3)Thiazolidinediones (insuline stabalizers)-
• ACTION
• -Sensitize body tissues to insulin.
• -Stimulate the insulin receptors sites to lower blood glucose and improve action of insulin.
• Examples-
• -Pioglitazone
• -Rosiglitazone
• SIDE EFFECTS-
• Hypoglycemia,anemia, weight gain, decrease effectiveness of oral contraceptives
• Impaired platelet function.
• IMPLICATIONS-
• -Monitor blood glucose level for effectivness of therapy.
• -Monitor liver function test.
• -Arrange dietary teaching to establish weight control program.

60. • 4)Biguanides (insulin stabalizers)-
• ACTION
-Inhibit production of glucose by the liver.
- Increase body tissue’s sensitivity to insulin.
-Decrease hepatic synthesis of cholesterol.
- Used in type 2 diabetes to control blood glucose levels.
SIDE EFFECTS-
-Lactic acidosis
- Hypoglycemia if metformine is used in combination with insulin or other
antidiabetic agents.
-Contraindications with the patients with impaired renal or liver function or
alcohol abuse.

61. • IMPLICATIONS
• -Monitor for lactic acidosis and hypoglycemia
• -Monitor blood glucose and urine ketone levels to assess effectiveness of
therapy
• -Instruct patient to avoid use of alcohol.
• 5)Alpha glucosidase inhibitors-
• Examples- acrbose, miglitol
• -Delay absorption of complex carbohydrates in the intestine and slow
entry of glucose into systemic circulation.
• -Do not increase insulin secretion.
• -Used in type 2 diabetes to control blood glucose levels.

62. • SIDE EFFCETS-
• -Hypoglycemia (risk increased if used with insulin or other antidiabetic
agents.)
• -GI side effects- abdominal discomfort or distension.
• -These agents are effective in type 2 DM when the nuitrition and
exercise therapy fails.
• IMPLICATION-
• -Must be taken with first bite of food to be effective.
• -monitorfor G.I side effects (nausea, abdominal discomfort).
• -ALERT- Hypogycemia should be treated with glucose not with sucrose.

63. SURGICAL MANAGEMENT-
• 1)Pancreas transplantation
• 2)Pancreas and kidney transplantation.
• NURSING MANAGEMENT OF DIABETIC PATIENT-
• 1)ASSESSMENT
• History includes –
• 1)Symptoms of hyperglycemia and hypoglycemia
• Nephropathy
• Neuropathy
• Exercise schedule

64. • Dietary schedule
• Retinopathy
• 3)PHYSICAL EXAMINATION
• Blood pressure
• Weight
• Feet (because of the presence of numbness)
• Neurological examination.

65. • 4)LAB EXAMINATION-
• Albuminuria
• 24hr urine collection
• Lipid examination
• Blood glucose level

66. NURSING DIAGNOSIS-
• -Risk for fluid volume deficit related to polyuria and dehydration.
• -Fluid and electrolyte imbalance related to fluid loss or shifts.
• -Deficient knowledge about diabetes self-care skills or information.
• -Anxiety related to diabetes mellitus.

67. • NURSING INTERVENTIONS-
• 1)Maintaining fluid and electrolyte balance.
• 2)Monitoring and managing potential
• Complication.
• -Hypokalemia
• -Cerebral edema
3)Increasing knowledge about diabetes management.

68. EXPECTED OUTCOMES-
• 1)Achieves fluid and electrolute balance.
- Demonstrate intake and output balance
-Exhibits electrolye in normal limits.
-Exhibits vital signs that remain stable with resolution of Orthostatic
hypotension.
• 2)Demonstrate knowledge about DKA
-Identify factors leading to DKA
-Describe signs and symptoms of DKA.
-Describe short term and long term consequences
• 3)Absence of complication

69. • -Exhibits normal cardiac rate and rhythm and normal breath sounds.
• -Exhibits no jugular venous distensions.
• -Exhibits blood glucose and urine ketone levels within target range.