The document provides a comprehensive overview of diabetes mellitus, including its classification, pathophysiology, and management strategies. It discusses the two main types of diabetes, Type 1 and Type 2, highlighting their causes, clinical manifestations, and the importance of lifestyle and pharmacological interventions in management. Additionally, it covers diagnostic tests and the role of healthcare professionals in providing educational support and individualized care plans for patients.

1. By
Ms Saira Manzoor
Lecturer-SCN-STMU

2. Outline
• Definition
• Pathophysiology
• Health assessment
• Pharmacological management
• Nursing care
• Complications

3. Objectives
• Classify types of diabetes
• Explain pathophysiology of diabetes
• Perform health assessment of diabetic patient.
• Interpret diagnostic tests of diabetes
• Rationalize pharmacological management of diabetes.
• Plan patient teaching for diabetic management at home
• Rationalize Nursing Management of diabetic patient

4. Case study
• Ali, a 32-year- old, always complains of his increasing need for water.
He also feels an increasing need to urinate and always feels hungry.
There is tingling on his extremities and numbness. His once clear
vision is now experiencing cloudiness. He already feels tired just a few
hours after waking up even though he does not have any job and only
stays at home. He has a wound on his right knee that has been there
for weeks, but there has been no improvement.

5. Pancreas
The pancreas is made up of two major tissue types: the acini
and the islets of Langerhans.
acini secrete digestive juices into the duodenum
 islets of Langerhans secrete hormones into the blood.
 Each islet is composed of:
 Beta cells:secrete insulin and amylin,
 Alpha cells:secrete glucagon,
 Delta cells: secrete somatostatin

7. CONT..
Insulin lowers the blood glucose concentration by facilitating
the movement of glucose into body tissues.
Glucagon maintains blood glucose by increasing the release
of glucose from the liver into the blood.
Somatostatin inhibits the release of insulin and glucagon.
Somatostatin also decreases gastrointestinal activity after
ingestion of food.

8. Diabetes mellitus (DM)
 is a chronic disease characterized by insufficient insulin production in
the pancreas or when the body cannot efficiently use the insulin it
produces.
 This leads to an increased concentration of glucose in the bloodstream
(hyperglycemia).
 It is characterized by disturbances in carbohydrate, protein, and fat
metabolism.
 Sustained hyperglycemia has been shown to affect almost all tissues in
the body. It is associated with significant complications of multiple
organ systems, including the eyes, nerves, kidneys, and blood vessels.

9. Laboratory Investigations
Fasting Blood Glucose test:
 Glucose levels are measured after food has been withheld for at least 8
hours. An FPG level below 100 mg/dL is considered normal
 A level between 100 mg/dL and 126 mg/dL is significant and is defined as
impaired fasting glucose.
 If the FPG level is 126 mg/dL or higher on two occasions, diabetes is
diagnosed

10. Random/Casual
 A random plasma glucose is one that is done without regard to the
time of the last meal.
 A random plasma glucose concentration that is elevated (≥200 mg/dL)
in the presence of classic symptoms of diabetes such as polydipsia,
polyphagia, polyuria, and blurred vision is diagnostic of diabetes
mellitus at any age.

11. Glucose Tolerance test
 The oral glucose tolerance test is an important screening test for
diabetes. The test measures the body’s ability to store glucose by
removing it from the blood.
 In men and women, the test measures the plasma glucose response to
75 g of concentrated glucose solution at selected intervals, usually 1
hour and 2 hours.
 In pregnant women, a glucose load of 100 g is given with an additional
3-hour plasma glucose determination.
 In people with normal glucose tolerance, blood glucose levels return to
normal within 2 to 3 hours after ingestion of a glucose load, in which
case, it can be assumed that sufficient insulin is present to allow

12. Testing for Glycated Hemoglobin
 Glycated hemoglobin or glycosylated hemoglobin, HgbA1C, or A1C
reflects the average blood glucose levels over a period of
approximately 2 to 3 months.
 The longer the amount of glucose in the blood remains above normal,
the more glucose binds to hemoglobin and the higher the glycated
hemoglobin becomes.
 Normal values typically range from 4% to 6% and indicate
consistently near-normal blood glucose concentrations.

14. classification system of diabetes
• Diabetes has major classifications that include
1. Type 1 diabetes,
2. Type 2 diabetes,
3. Gestational diabetes, and
4. Diabetes mellitus associated with other conditions.
• The two types of diabetes mellitus are differentiated based on their
causative factors, clinical course, and management.

15. Pathophysiology

16. Pathophysiology
• Insulin is secreted by beta cells in the pancreas and it is an anabolic
hormone.
• When we consume food, insulin moves glucose from blood to muscle, liver,
and fat cells as insulin level increases.
• The functions of insulin include the
1. Transport and metabolism of glucose for energy,
2. Stimulation of storage of glucose in the liver and muscle,
3. Serves as the signal of the liver to stop releasing glucose,
4. Enhancement of the storage of dietary fat in adipose tissue, and
acceleration of the transport of amino acid into cells.
• Insulin and glucagon maintain a constant level of glucose in the blood by
stimulating the release of glucose from the liver.

17. Type 1 Diabetes Mellitus
• is characterized by destruction of the pancreatic beta cells.
• A common underlying factor in the development of type 1 diabetes is a genetic
susceptibility.
• Destruction of beta cells leads to a decrease in insulin production, unchecked
glucose production by the liver and fasting hyperglycemia.
• Glucose taken from food cannot be stored in the liver anymore but remains in the
blood stream.
• The kidneys will not reabsorb the glucose once it has exceeded the renal
threshold, so it will appear in the urine and be called glycosuria.
• Excessive loss of fluids is accompanied by excessive excretion of glucose in the
urine leading to osmotic diuresis.
• There is fat breakdown which results in ketone production, the by-product of fat
breakdown.

18. Causes
• Genetics. Genetics may have played a role in the destruction of the
beta cells in type 1 DM.
• Environmental factors. Exposure to some environmental factors like
viruses can cause the destruction of the beta cells.

19. Type 2 Diabetes Mellitus

20. Type 2 diabetes mellitus
• It has major problems of insulin resistance and impaired insulin secretion.
• Insulin could not bind with the special receptors so insulin becomes less
effective at stimulating glucose uptake and at regulating the glucose
release.
• There must be increased amounts of insulin to maintain glucose level at a
normal or slightly elevated level.
• However, there is enough insulin to prevent the breakdown of fats and
production of ketones.
• Uncontrolled type 2 diabetes could lead to hyperglycemic, hyperosmolar
nonketotic syndrome.
• The usual symptoms that the patient may feel are polyuria, polydipsia,
polyphagia, fatigue, irritability, poorly healing skin wounds, vaginal
infections, or blurred vision.

21. Causes
• Weight. Excessive weight or obesity is one of the factors that
contribute to type 2 DM because it causes insulin resistance.
• Inactivity. Lack of exercise and a sedentary lifestyle can also cause
insulin resistance and impaired insulin secretion.

22. Gestational Diabetes Mellitus
• With gestational diabetes mellitus (GDM), the pregnant woman
experiences any degree of glucose intolerance with the onset of
pregnancy.
• The secretion of placental hormones causes insulin resistance,
leading to hyperglycemia.
• After delivery, blood glucose levels in women with GDM usually
return to normal or later on develop type 2 diabetes.

23. • Weight. If you are overweight before pregnancy and added extra
weight, it makes it hard for the body to use insulin.
• Genetics. If you have a parent or a sibling who has type 2 DM, you are
most likely predisposed to GDM.

25. Clinical Manifestations-countinue
• Clinical manifestations depend on the level of the patient’s hyperglycemia.
• Polyuria or increased urination. Polyuria occurs because the kidneys remove
excess sugar from the blood, resulting in a higher urine production.
• Polydipsia or increased thirst. Polydipsia is present because the body loses more
water as polyuria happens, triggering an increase in the patient’s thirst.
• Polyphagia or increased appetite. Although the patient may consume a lot of
food but glucose could not enter the cells because of insulin resistance or lack of
insulin production.
• Fatigue and weakness. The body does not receive enough energy from the food
that the patient is ingesting.
• Sudden vision changes.The body pulls away fluid from the eye in an attempt to
compensate the loss of fluid in the blood, resulting in trouble in focusing the
vision

26. Clinical Manifestations
• Tingling or numbness in hands or feet. Tingling and numbness occur
due to a decrease in glucose in the cells.
• Dry skin. Because of polyuria, the skin becomes dehydrated.
• Skin lesions or wounds that are slow to heal. Instead of entering the
cells, glucose crowds inside blood vessels, hindering the passage of
white blood cells which are needed for wound healing.
• Recurrent infections. Due to the high concentration of glucose,
bacteria thrives easily.

28. Prevention
• Appropriate management of lifestyle can effectively prevent the
development of diabetes mellitus.
• Standard lifestyle recommendations, metformin, and placebo are
given to people who are at high risk for type 2 diabetes.
• It also included behavior modification strategies that can help
patients achieve their weight reduction goals and participate in
exercise.

30. Medical Management
• Here are some medical interventions that are performed to manage diabetes
mellitus.
• Normalize insulin activity. This is the main goal of diabetes treatment —
normalization of blood glucose levels to reduce the development of vascular and
neuropathic complications.
• Intensive treatment. Intensive treatment is three to four insulin injections per
day or continuous subcutaneous insulin infusion, insulin pump therapy plus
frequent blood glucose monitoring and weekly contacts with diabetes educators.
• Exercise caution with intensive treatment. Intensive therapy must be done with
caution and must be accompanied by thorough education of the patient and
family and by responsible behavior of patient.
• Diabetes management has five components and involves constant assessment
and modification of the treatment plan by healthcare professionals and daily
adjustments in therapy by the patient.

31. Nutritional Management
• The foundations. Nutrition, meal planning, and weight control are the
foundations of diabetes management.
• Consult a professional. A registered dietitian who understands diabetes
management has the major responsibility for designing and teaching this aspect
of the therapeutic plan.
• Healthcare team should have the knowledge. Nurses and other health care
members of the team must be knowledgeable about nutritional therapy and
supportive of patients who need to implement nutritional and lifestyle changes.
• Weight loss. This is the key treatment for obese patients with type 2 diabetes.
• How much weight to lose? A weight loss of as small as 5% to 10% of the total
body weight may significantly improve blood glucose levels.
• Other options for diabetes management. Diet education, behavioral therapy,
group support, and ongoing nutritional counselling should be encouraged

32. Meal Planning
• Criteria in meal planning. The meal plan must consider the patient’s food
preferences, lifestyle, usual eating times, and ethnic and cultural background.
• Managing hypoglycemia through meals. To help prevent hypoglycemic reactions
and maintain overall blood glucose control, there should be consistency in the
approximate time intervals between meals with the addition of snacks as needed.
• Assessment is still necessary. The patient’s diet history should be thoroughly
reviewed to identify his or her eating habits and lifestyle.
• Educate the patient. Health education should include the importance of
consistent eating habits, the relationship of food and insulin, and the provision of
an individualized meal plan.
• The nurse‘s role. The nurse plays an important role in communicating pertinent
information to the dietitian and reinforcing the patients for better
understanding.

33. • Reducing hypoglycemia. The patient must be cautioned to consume food
along with alcohol, however, carbohydrate consumed with alcohol may
raise blood glucose.
• Artificial sweeteners. Use of artificial sweeteners is acceptable, and there
are two types of sweeteners: nutritive and nonnutritive.
• Types of sweeteners. Nutritive sweeteners include all of which provides
calories in amounts similar to sucrose while nonnutritive have minimal or
no calories.
• Exercise. Exercise lowers blood glucose levels by increasing the uptake of
glucose by body muscles and by improving insulin utilization.
• A person with diabetes should exercise at the same time and for the same
amount each day or regularly.

34. Pharmacological Management

36. 36
Treatment
Type 1: Insulin must be injected or inhaled
Type 2: Food control, exercise, medicines
(1) agents which increase insulin secretion;
(2) agents which increase the sensitivity of target organs to insulin;
(3) agents which decrease glucose absorption
(4) Insulin needed for patients with serious complications or an
emergency.

37. 37
●Physiological & pharmacological actions of insulin
1. Sugar metabolism: Stimulates glucose uptake & use by cells;
inhibits gluconeogenesis →blood sugar↓
2. Fatty metabolism: Improves fatty acid transportation & fat
anabolism; inhibits fat catabolism & fatty acid and acetone body
generation
3. Protein metabolism: Improves transportation & protein anabolism;
inhibits protein catabolism & utilization in liver
Potassium : Stimulates K+ entering cells→blood K+↓
5. Long-term action: Improves or inhibits the synthesis of some
enzymes

38. 38
Effect of insulin on glucose uptake and metabolism. Insulin binds to its
receptor (1) which in turn starts many protein activation cascades (2). These
include: translocation of Glut-4 transporter to the plasma membrane and influx
of glucose (3), glycogen synthesis (4), glycolysis (5) and fatty acid synthesis (6).

40. 40
● Adverse reactions
1. Insulin allergy: itching, redness, swelling, anaphylaxis shock
2. Insulin resistance
3. Hypoglycemia: nausea, hungry, tachycardia, sweating, and
tremulousness.
＊ First aids needed while convulsions & coma happens
4. Lipodystrophy at injection sites: atrophy

41. Insulin Adjunct
• Pramlintide (Symlin) is an antihyperglycemic drug
• The drug is a synthetic analog of amylin, a natural hormone released by the
beta cells of the pancreas at the same time as insulin.
• The therapeutic actions of pramlintide are to slow gastric emptying time and
increase satiety, thereby leading to reduced calorie intake.
• Pramlintide is administered subcutaneously immediately prior to each meal.
• When initiating treatment, rapid- or short-acting insulin doses are usually
reduced by 50%.
• Adverse effects include nausea, vomiting, abdominal pain, headache,
dizziness, fatigue, coughing, allergic reaction, or arthralgia.
• The drug carries a black box warning that severe hypoglycemia may occur
during therapy

42. Oral Ant diabetic Drugs
42
Classification
• Sulfonylureas
• Thiazolidinediones
• Biguanides
• α-glucosidase inhibitors
• Meglitinides

46. І. Sulfonylureas
• Representative Drugs
1st generation:
tolbutamide chlorpropamide tolazamide
2nd generation:
glybenclamide glyburide
glipizide glymepride
3rd generation:
glyclazipe
46

47. • Hypoglycemic mechanism
1. Rapid mechanism: stimulation of insulin secretion
47
Sulfonylurea receptor in β-cell membrane activated
ATP-sensitive K+-channel inhibited
Cellular membrane depolarized
Ca2+ entry via voltage-dependent Ca2+ channel
Insulin release
2. Long term profit involved mechanism
①Inhibition of glucagon secretion by pancreas α cells;
②Ameliorating insulin resistance
③ Increase insulin receptor number & the affinity to insulin

48. Ⅱ. Thiazolidinediones (Tzds)
• Representative Drugs
rosiglitazone troglitazone
pioglitazone ciglitazone
• Pharmacological effects
●Improving function of pancreas β cells
●Ameliorating insulin resistance
●Ameliorating fat metabolic disorder
●Preventing and treating type 2 diabetes mellitus and their
cardiovascular complications
48

49. glitazone
• Mechanism of Action:
• increases the body's sensitivity to insulin
• Their primary action is the nuclear regulation of genes involved in glucose &
lipid metabolism and adipocyte differentiation
• Glitazones are ligands of the peroxisome peroliferator-activated receptor
gamma (PPAR-γ) part of the steroid and thyroid super family of nuclear
receptors
• PPAR-γ receptors are found in muscle, liver and fat
• PPAR-γ regulates the expression of genes involved in lipid and glucose
metabolism, insulin signal transduction, and adipocyte differentiation
• In persons with diabetes, a major site of TZD action is adipose tissue

50. • Mechanism (possible)
50
Peroxisome proliferator-activated receptor-γ(PPAR-γ) activated
Nuclear genes involved in glucose & lipid metabolism and
adipocyte differentiation activated
 Clinical use
Insulin resistance & type 2 diabetes mellitus
 Adverse reactions
Troglitazone occasionally induces hepatic injury

51. Ⅲ. Biguanides
• Representative Drugs
phenformin metformin
●Use for obese diabetes and type 2 diabetes
●Alone or co-administered with insulin or Sulfonylureas
●Metformin also used to treat atherosclerosis for down-regulation
of LDL& VLDL
●Ketonemia & lactic acidosis are major adverse reactions
51

52. Ⅲ. Biguanides(insulin sensitizer)
• decreases the liver's production of glucose via activation of AMP-activated
protein kinase (AMPK)
• Other possible mechanisms include:
• inhibits the breakdown of fatty acids used to produce glucose
• at very high doses it may increase the removal of glucose from muscle, the liver, and other
body tissues where it is stored

53. Ⅳ. α-glucosidase inhibitors
• Representative Drugs
acarbose voglibose miglitol
• Key points
● To inhibit digestion of starch & disaccharides via competitively
inhibiting intestinal α-glucosidase (sucrase, maltase, glycoamylase,
dextranase)
● Used alone or together with sulfonylureas to treat type 2 diabetes
● Main adverse reaction: flatulence, diarrhea, bellyache.
● Patients with inflammatory bowel disease & kidney impaired
forbidden.
53

54. Ⅴ. Meglitinides
• Representative Drugs
Repaglinide
• Key point
● To increase insulin release by inhibiting ATP-sensitive
K+-channel
● Unlike sulfonylureas, they have no direct effect on
insulin release
● Used alone or together with biguanides to treat type 2
diabetes
● Carefully used for patients with kidney or liver
impaired.
54

55. Nursing Management
• Nursing Assessment
• The nurse should assess the following for patients with Diabetes Mellitus:
• Assess the patient’s history. To determine if there is presence of diabetes, assessment of
history of symptoms related to the diagnosis of diabetes, results of blood glucose
monitoring, adherence to prescribed dietary, pharmacologic, and exercise regimen, the
patient’s lifestyle, cultural, psychosocial, and economic factors, and effects of diabetes on
functional status should be performed.
• Assess physical condition. Assess the patient’s blood pressure while sitting and standing
to detect orthostatic changes.
• Assess the body mass index and visual acuity of the patient.
• Perform examination of foot, skin, nervous system and mouth.
• Laboratory examinations. HgbA1C, fasting blood glucose, lipid profile, microalbuminuria
test, serum creatinine level, urinalysis, and ECG must be requested and performe

56. Diagnoses
• The following are diagnoses observed from a patient with diabetes
mellitus.
• Risk for unstable blood glucose level related to insulin resistance, impaired
insulin secretion, and destruction of beta cells.
• Risk for infection related to delayed healing of open wounds.
• Deficient knowledge related to unfamiliarity with information, lack of
recall, or misinterpretation.
• Risk for disturbed sensory perception related to endogenous chemical
alterations.
• Impaired skin integrity related to delayed wound healing.
• Ineffective peripheral tissue perfusion related to too much glucose in the
bloodstream

57. Planning and Goals
• Achievement of goals is necessary to evaluate the effectiveness of the therapy.
• Acknowledge factors that lead to unstable blood glucose.
• Maintain glucose in satisfactory range.
• Verbalize plan for modifying factors to prevent or minimize shifts in glucose levels.
• Achieve timely wound healing.
• Identify interventions to prevent or reduce Risk for Infection.
• Regain or maintain the usual level of cognition.
• Homeostasis achieved.
• Causative/precipitating factors corrected/controlled.
• Complications prevented/minimized.
• Disease process/prognosis, self-care needs, and therapeutic regimen understood.
• Plan in place to meet needs after discharge.

58. Nursing Priorities
• Restore fluid/electrolyte and acid-base balance.
• Correct/reverse metabolic abnormalities.
• Identify/assist with management of underlying cause/disease
process.
• Prevent complications.
• Provide information about disease process/prognosis, self-care, and
treatment needs.

59. Nursing Interventions
• Educate about home glucose monitoring. Discuss glucose monitoring at home with the
patient according to individual parameters to identify and manage glucose variations.
• Review factors in glucose instability. Review client’s common situations that contribute
to glucose instability because there are multiple factors that can play a role at any time
like missing meals, infection, or other illnesses.
• Encourage client to read labels. The client must choose foods described as having a low
glycemic index, higher fiber, and low-fat content.
• Discuss how client’s antidiabetic medications work. Educate client on the functions of
his or her medications because there are combinations of drugs that work in different
ways with different blood glucose control and side effects.
• Check viability of insulin. Emphasize the importance of checking expiration dates of
medications, inspecting insulin for cloudiness if it is normally clear, and monitoring
proper storage and preparation because these affect insulin absorbability.

60. • Review type of insulin used. Note the type of insulin to be
administered together with the method of delivery and time of
administration. This affects timing of effects and provides clues to
potential timing of glucose instability.
• Check injection sites periodically. Insulin absorption can vary day to
day in healthy sites and is less absorbable in lipohypertrophic tissues.

61. Evaluation
• To check if the regimen or the interventions are effective, evaluation must
be done afterward.
• Evaluate client’s knowledge on factors that lead to an unstable blood
glucose level.
• Evaluate the client’s level of blood glucose.
• Verbalized achievement of modifying factors that can prevent or minimize
shifts in glucose level.
• Achieved timely wound healing.
• Identified interventions that can prevent or reduce risk for infection.
• Evaluate maintenance of the usual level of cognition.

62. Teaching Survival Skills.
• Simple pathophysiology
a. Basic definition of diabetes (having a high
blood glucose level)
b. Normal blood glucose ranges and target
blood glucose levels
c. Effect of insulin and exercise (decrease
glucose)
d. Effect of food and stress, including illness and
infections (increase glucose)
e. Basic treatment approaches
2. Treatment modalities
a. Administration of insulin and oral
antidiabetes medications
b. Meal planning (food groups, timing of meals)
c. Monitoring of blood glucose and urine
ketones
3. Recognition, treatment, and prevention of
acute complications
a. Hypoglycemia
b. Hyperglycemia
4. Pragmatic information
a. Where to buy and store insulin, syringes, and
glucose monitoring supplies
b. When and how to contact the physician

64. Complications
• If diabetes mellitus is left untreated, several complications may arise
from the disease.
• Hypoglycemia. Hypoglycemia occurs when the blood glucose falls
to less than 50 to 60 mg/dL because of too much insulin or oral
hypoglycemic agents, too little food, or excessive physical activity.
• Diabetic Ketoacidosis. DKA is caused by an absence or markedly
inadequate amounts of insulin and has three major features of
hyperglycemia, dehydration and electrolyte loss, and acidosis.
• Hyperglycemic Hyperosmolar Nonketotic Syndrome. HHNS is a
serious condition in which hyperosmolarity and hyperglycemia
predominate with alteration in the sense of awareness.

65. ACUTE COMPLICATIONS OF DIABETES
• Hypoglycemia occurs when the blood glucose falls to less than 50 to
60 mg/dL (2.7 to 3.3 mmol/L) because of
1. too much insulin or
2. oral hypoglycemic agents,
3. too little food, or
4. excessive physical activity.
• Hypoglycemia may occur at any time of the day or night.

66. Clinical manifestations of hypoglycemia
• May be grouped into two categories:
1. Adrenergic symptoms - sweating,
tremor, tachycardia, palpitation,
nervousness, and hunger.
2. Central nervous system (CNS)
symptoms- the drop in blood
glucose level deprives the brain
cells of needed fuel for functioning.
3. In severe hypoglycemia, CNS
function is so impaired -Symptoms
may include disoriented behavior,
seizures, difficulty arousing from
sleep, or loss of consciousness
Signs of impaired function of the CNS may include
1. inability to concentrate,
2. headache,
3. lightheadedness,
4. confusion,
5. memory lapses,
6. numbness of the lips and tongue,
7. slurred speech,
8. impaired coordination,
9. emotional changes,
10. irrational or combative behavior,
11. double vision, and
12. drowsiness.

67. Management Treating with Carbohydrates
• Immediate treatment must be given
when hypoglycemia occurs.
• The usual recommendation is for 15 g
of a concentrated source of
carbohydrate such as the following,
• given orally:
• Three or four commercially prepared
glucose tablets
• 4 to 6 oz. of fruit juice or regular soda
• 6 to 10 hard candies
• 2 to 3 teaspoons of sugar or honey
• The blood glucose level should be
retested in 15 minutes
• a snack containing protein and starch
(eg, milk or cheese and crackers) is
recommended unless the patient
plans to eat a regular meal or snack
within 30 to 60 minutes
• In emergency situations, for adults
who are unconscious and cannot
swallow, an injection of glucagon 1 mg
can be administered either
subcutaneously or intramuscularly
• 25 to 50 mL of 50% dextrose in water
(D50W) may be administered IV.

68. Providing Patient Education
• Patients and family members must be instructed to recognize the
symptoms of hypoglycemia

69. DKA(Diabetic ketoacidosis)
• DKA is caused by an absence or markedly inadequate amount of
insulin.
• This deficit in available insulin results in disorders in the metabolism
of carbohydrate, protein, and fat.
• The three main clinical features of DKA are
• Hyperglycemia
• Dehydration and electrolyte loss
• Acidosis

71. Management
• Rehydration
• Restoring Electrolytes
• Reversing Acidosis- reversed with insulin, which inhibits fat
breakdown,

72. Hyperglycemic hyperosmolar nonketotic
syndrome (HHNS)
• It is a serious condition in which hyperosmolarity and hyperglycemia
predominate, with alterations of the sensorium (sense of awareness).
• At the same time, ketosis is usually minimal or absent.
• The basic biochemical defect is lack of effective insulin (ie, insulin
resistance).
• Persistent hyperglycemia causes osmotic diuresis, which results in losses of
water and electrolytes.
• To maintain osmotic equilibrium, water shifts from the intracellular fluid
space to the extracellular fluid space.
• With glycosuria and dehydration, hypernatremia and increased osmolarity
occur.

73. • Management The overall approach to the treatment of HHNS is
similar to that of DKA:
• Fluid replacement
• Correction of electrolyte imbalances
• Insulin administration.

75. LONG-TERM COMPLICATIONS OF DIABETES
• Macrovascular disease- changes in the medium to large blood vessels.
• Blood vessel walls thicken, sclerose, and become occluded by plaque
that adheres to the vessel walls.
• Eventually, blood flow is block
• Microvascular disease- (or microangiopathy) is characterized by
capillary basement membrane thickening.
• Two areas affected by these changes are the retina and the kidneys.

76. Neuropathy
• a group of diseases that affect all types of nerves, including peripheral (sensorimotor),
autonomic, and spinal nerves.
Peripheral Neuropathy Autonomic Neuropathy
• Peripheral neuropathy most commonly affects the distal
portions of the nerves, especially the nerves of the lower
extremities; it affects both sides of the body
symmetrically and may spread in a proximal direction.
• initial symptoms may include paresthesia's (prickling,
tingling, or heightened sensation) and burning sensations
(especially at night).
• As the neuropathy progresses, the feet become numb.
• Decreased sensations of pain and temperature place
patients with neuropathy at increased risk for injury and
undetected foot infection
Three manifestations of autonomic neuropathy are related
to the cardiac, gastrointestinal, and renal systems
• Cardiovascular symptoms range from a fixed, slightly
tachycardia heart rate and orthostatic hypotension to
silent, or painless, myocardial ischemia and infarction
• Delayed gastric emptying may occur with the typical
gastrointestinal symptoms of early satiety, bloating,
nausea, and vomiting. “Diabetic” constipation or
diarrhea (especially nocturnal diarrhea) may occur as a
result
• Urinary retention, a decreased sensation of bladder
fullness, and other urinary symptoms of neurogenic
bladder result from autonomic neuropathyHypoglycemic
Unawareness

78. References
• Waugh, A., & Grant, A. (2014). Ross & Wilson Anatomy and physiology
in health and illness. Elsevier Health Sciences. Chapter-16. page 389-
436.
• Grossman.S, Porth.M.C. (2009). Porth Pathophysiology concept of
altered health states (9th.ed). Philadelphia: Lippincott. Unit -XIV,
Chapter-56,57,58,59. page –
1431-1440,1445-1463,1489-1492,1500-1504,1509-1512.
• Porth, M. C. (2009). Essential of Pathophysiology (3rd.ed).
Philadelphia: Lippincott. Unit –XII, Chapter 42,43,44. Page 1081-
1109,1138-1153.

79. • Abrams, A., Lammon, C. and Pennington, S. (2009). Clinical drug
therapy. Philadelphia: Lippincott Williams & Wilkins.
• Adams,M., Holland,N.L.,& Urban,Q.C.(2014). Pharmacology for
Nurses-A Pathophysiologic Approach ((4th e.d).
• http//nurseslabs.com//diabetes-mellitus
• Brunner, L. S., & Suddarth, D. S. (2010). Text book of Medical-Surgical
nursing (12th e.d). Philadephia: Lippincott