the most you like the most you will read

1. ENDOCRINE DISORDERS
By Addisu S.
March, 2021
1

2. Endocrine system
• The endocrine system consists of group of organs
to maintain a state of metabolic equilibrium, or
homeostasis, among the various organs of the
body.
• Endocrine glands secrete chemical messengers, or
hormones->regulate the activity of target organs.
• Hormones transported to their target organs via
the bloodstream are referred to as "endocrine"
hormones.
2

3. Endocrine system
• The hormones secreted by the endocrine system are
affected in large part by structures in the central nervous
system, such as the hypothalamus.
• Structures located in the brain, such as the pituitary
gland, are endocrine glands that influence the function
of a large number of other endocrine glands.
3

4. Endocrine glands
Endocrine glands secrete their products directly in to the
blood stream:
– Pituitary gland
– Pancreatic islets
– Thyroid gland
– Adrenal gland
• Exocrine gland: secrete their product via duct.
– E.G. Sweat glands, salivary glands etc.
4

5. 5

6. Endocrine glands …
• Endocrine diseases can be broadly classified as
– underproduction ,
– overproduction of hormones or
– mass lesions
• Hormones are classified as:
– Steroid hormones (e.g., Hydrocortisone),
– Peptide or protein hormones (e.g., Insulin),
– Amine hormones (e.g., Epinephrine), and
– Fatty acid derivatives (e.g., Retinoids).
6

7. Endocrine glands…
• These hormones act on the target tissues via altering the
function of the target tissue by interacting with chemical
receptors located either on the cell membrane or in the
interior of the cell.
7

8. Disorders of pancreas
8

9. Pancreatic islets
• There are four types of cells in the Langerhans.
– α cells secrete glucagon (increase glucose in blood),
– β cells secrete insulin (decrease glucose in blood),
– Delta cells secrete somatostatin (regulates/stops α
and β cells) and
– PP cells, or gamma cells secrete pancreatic
polypeptide
9

10. Pancreatic islet cells
• Insulin: Lowers blood glucose by facilitating glucose
transport across cell membranes of muscle, liver, in the
form of glycogen and adipose tissue is stored as
triglycerides.
• Glucagon: Increases blood glucose concentration by
stimulation of glycogenolysis.
• Somatostatin: Delays intestinal absorption of glucose
and release of Glucagon.
10

11. Insulin
• Insulin is a peptide hormone, produced by beta cells of
the pancreas, and is central to regulating carbohydrate
and fat metabolism in the body
• Insulin is an anabolic, or storage, hormone.
• When a person eats a meal, insulin secretion increases
and moves glucose from the blood into muscle, liver,
and fat cells.
11

12. Function of insulin
• Transports and metabolizes glucose for energy.
• Stimulates storage of glucose in the liver and muscle in
the form of glycogen)
• Signals the liver to stop the release of glucose.
• Enhances storage of dietary fat in adipose tissue.
• Accelerates transport of amino acids (derived from
dietary protein) into cells.
• Insulin also inhibits the breakdown of stored glucose,
protein, and fat. 12

13. Function of insulin
• Basal insulin is small amount of insulin that is normally
supplied by the pancreas and is present 24 hours a day,
whether or not the person eats.
• Bolus insulin refers to the extra amounts of insulin the
pancreas would naturally make in response to glucose taken
in the food.
• The amount of bolus insulin produced depends on the size of
the meal.
13

14. Function of Glucagon
• Glucagon is secreted by the alpha cells and is released
when blood glucose levels decrease and stimulate the
liver to release stored glucose.
• insulin and glucagon together maintain a constant level of
glucose in the blood by stimulating the release of glucose
from the liver.
• Initially, the liver produces glucose through the breakdown
of glycogen (glycogenolysis).
• After 8 to 12 hours without food, the liver forms glucose
from the breakdown of non carbohydrate substances,
including amino acids(gluconeogenesis).
14

15. Diabetes mellitus
• Diabetes mellitus is a group of metabolic diseases
characterized by elevated levels of glucose in the blood
(hyperglycemia) resulting from defects in insulin
secretion, insulin action, or both.
• The major sources of this glucose is from absorption of
ingested food in the GIT and formation of glucose by the
liver from food substances.
15

16. Diabetes mellitus
• Insulin, a hormone produced by the pancreas, controls
the level of glucose in the blood by regulating the
production and storage of glucose.
• In the diabetic state, the cells may stop responding to
insulin or the pancreas may stop producing insulin
entirely.
• This leads to hyperglycemia.
16

17. Diabetes mellitus…
• A major action of insulin is to lower blood glucose by
permitting entry of the glucose into the cells of the:
– liver,
– muscle, and
– other tissues, where it is either stored as glycogen or
used for energy.
17

18. Classification of Diabetes
The major classifications of diabetes are:
– Type 1 diabetes/IDDM
– Type 2 diabetes/NIDDM
– Gestational diabetes
• D.M. associated with other condition or syndrome
18

19. Type I DM
• Insulin-producing pancreatic beta cells are destroyed by
an autoimmune process.
• As a result, patients produce little or no insulin and
require insulin injections to control their blood glucose
levels.
• Type 1 diabetes is characterized by:
– an acute onset, usually before 30 years of age.
– affects approximately 5% to 10% of people with the
disease
– caused by the body attacking its own pancreas with
antibodies.
19

20. Type 2 DM
• The bodies of people with type 2 diabetes make insulin.
• But either their pancreas does not make enough insulin
or the body cannot use the insulin well enough. This is
called insulin resistance.
– Onset at any age, usually over 30 years,
– Usually obese at diagnosis,
– Causes include obesity, heredity, or environmental
factors.
– It is affecting 90% to 95%
20

21. Type 2 DM
• Decrease in endogenous insulin, or increased with
insulin resistance (decreased tissue sensitivity to insulin).
• Most patients can control blood glucose through weight
loss if obese.
• Oral ant-diabetic agents may improve blood glucose
levels if dietary modification and exercise are
unsuccessful.
21

22. Gestational diabetes
• Onset during pregnancy, usually in the second or third
trimester due to hormones secreted by the placenta,
which inhibit the action of insulin .
• Has risk for perinatal complications, especially
macrosomia (abnormally large babies).
• Treated with diet and, if needed, insulin to strictly
maintain normal blood glucose levels.
22

23. DM Associated with other condition or syndrome
• Associated with pancreatic disease,
• hormonal abnormality,
• drugs corticosteroids.
Depend on the ability of the pancreas to produce insulin,
the patient may require insulin/oral agent.
23

24. Type 1 DM
Causes/Etiology
• People do not inherit type 1 diabetes itself; rather, they
inherit a genetic predisposition, or tendency, toward
developing type 1 diabetes.
• Human leukocyte antigens (HLAs) are proteins located on
the surface of the cell that help the immune system
identify the cell either as one belonging to the body or as
one from outside the body.
• Some patterns of these proteins may mean increased risk
of developing type 1 diabetes.
• HLA is a key role in initiating the autoimmune response.
24

25. Causes/Etiology…
• This is an abnormal response in which antibodies are
directed against normal tissues of the body, responding
to these tissues as if they are foreign.
• Autoantibodies against islet cells and against
endogenous (internal) insulin have been detected in
people at the time of diagnosis and even several years
before the development of clinical signs of type 1
diabetes.
25

26. Causes/Etiology
• In addition to genetic and immunologic components,
environmental factors, such as viruses or toxins, that
may initiate destruction of the beta cell are being
investigated.
• Example: mumps, cytomegalo virus, rubella
26

27. Causes/Etiology
• Regardless of the specific etiology, the destruction of the
beta cells results in
– decreased insulin production,
– unchecked glucose production by the liver, and
– fasting hyperglycemia.
• In addition, glucose derived from food cannot be stored
in the liver but instead remains in the bloodstream and
contributes to postprandial (after meals) hyperglycemia.
27

28. Pathophysiology
Inability to produce insulin due to destruction of beta cells
by auto immune process
As a result decrease anabolic and increase catabolic
Fasting hyperglycemia occur as a result of unchecked
glucose production by the liver.
Glucose derived from food can not be stored in liver and
remain in blood stream contribute to postprandial
hyperglycemia.
If the concentration of glucose in the blood is sufficiently
high, the kidney may not reabsorb all filtered glucose; the
glucose then appears in the urine (glucosuria).
28

29. Pathophysiology…
• Accompanied by excessive loss of fluid and electrolyte – the
patient experienced increase urination – Polydipsia
• Due to deficiency of insulin
– Unrestrained gluconeogenesis, lypolysis, and ketogenesis.
– Peripheral glucose utilization blocked
– Leads to ketoacidosis.
– Protein catabolism with muscle wasting and negative
nitrogen balance (the amount of nitrogen excreted from the body is greater
than the amount of nitrogen ingested)
29

30. Pathophysiology…
• When excess glucose is excreted in the urine, it is
accompanied by excessive loss of fluids and electrolytes.
This is called osmotic diuresis.
• Because insulin normally inhibits glycogenolysis (breakdown
of glycogen) and gluconeogenesis (production of new
glucose from amino acids and other substrates), in people
with insulin deficiency, these processes occur in
unrestrained fashion and contribute further to
hyperglycemia.
30

31. Pathophysiology
• In addition, fat breakdown occurs, resulting in an
increased production of ketone bodies, which are the
byproducts of fat breakdown.
• If levels of these ketone bodies are too high, the pH of
the blood drops, resulting in ketoacidosis
• Ketonbodies:- acids that disturb acid base balance when
the accumulate in excess amount.
31

32. Signs and symptoms
The classic symptoms of diabetes are
– Polyuria (frequent urination),
– Polydipsia (increased thirst),
– Polyphagia (increased hunger),
– Fatigue and weight loss.
32

33. Type 2 DM
• Type 2 DM is characterized by three pathophysiologic
• abnormalities:
–impaired insulin secretion,
–peripheral insulin resistance, and
–excessive hepatic glucose production.
• Type 2 diabetes is due to a combination of lifestyle and
genetic factors.
• Recently, intrauterine growth restriction (IUGR) or
prenatal under nutrition (macro- and micronutrient) was
identified as another probable factor. 33

34. Pathophysiology-Type 2 DM
Two main problem seen on insulin
1.Insulin resistance
2.Impaired insulin secretion
Insulin resistance means: a decreased sensitivity of the
tissue to insulin.
• Normally insulin binds to special receptors on cell surface
and serious reactions involving glucose metabolism
occur with in the cell.
• If insulin resistance, intracellular reaction decreased
then, the insulin become less effective of stimulating
glucose uptake by the tissue. 34

35. Pathophysiology-Type 2 DM…
• To overcome insulin resistance and to prevent the build
up of glucose in the blood, there must be an increase in
the amount of insulin secreted.
• However, if the beta cells are unable to keep up with
increased demand for insulin, the glucose level rises,
Type II DM occur.
• Despite the impaired insulin secretion, there is enough
insulin present to prevent the breakdown of fat
accompany production of ketonbodies, there fore DKA
does not occur in type II DM.
35

36. Clinical manifestations
Thirst
Polyuria
Polyphagia
Nocturia
Tiredness, fatigue, irritability, apathy,
Recent change in weight
Blurring of vision
Nausea, headache
The classical symptom of thrust, polyuria, nocturia, rapid
weight loss predominant in type I often absent in type II
36

37. Diagnostic criteria
• An abnormally high blood glucose level is the basic
criterion for the diabetes diagnosis.
• Fasting plasma glucose (FPG) levels of 126 mg/dL (7.0
mmol/L) or more.
• Random plasma glucose levels exceeding 200 mg/dL
(11.1 mmol/L) on more than one occasion are diagnostic
of diabetes ( blood drawn at any time)
• The best Dx is glucose tolerance test
37

38. Fasting plasma glucose
Result Fasting Plasma Glucose (FPG)
Normal less than 100 mg/dl
Prediabetes 100 mg/dl to 125 mg/dl
Diabetes
126 mg/dl or higher
38

39. Glucose tolerance test
• In healthy people, glucose levels in the blood always rise after
a meal, but they soon return to normal as the glucose is used
up or stored.
• Normally, the body should quickly move glucose from the
blood into the body's cells.
• If there is a problem of moving glucose into the cells, glucose
remains in the bloodstream.
• This resulted in a higher level of glucose in the blood samples.
39

40. Glucose tolerance test
What happens during a glucose tolerance test?
 A OGTT requires that, client fast for 8 to 12 hours (overnight)
before the first blood sample is drawn.
 In the morning (after an overnight fast) the first blood sample is
drawn
 Client will then be given a liquid containing 75 gm glucose load to
drink or can be administered to the patient
 According to WHO, 2 hrs after glucose ingestion, blood sample is
drawn.
 OGTT >200mg/dl(11.1mmol/lit) indicate "impaired glucose
tolerance or a diagnosis of diabetes.. 40

41. Glucose tolerance test
 A glucose tolerance test checks how well the body processes
blood sugar (glucose).
 It involves comparing the levels of glucose in the blood before
and after drinking a sugary drink.
41

42. Diabetes Management
• The main goal of diabetes treatment is:
– to normalize insulin activity and blood glucose levels
– to reduce the development of vascular and
neuropathic complications.
• Therefore, the therapeutic goal for diabetes management is
to achieve normal blood glucose levels (euglycemia) without
hypoglycemia and
• without seriously disrupting the patient’s usual lifestyle and
activity. 42

43. Diabetes Management
There are five components of diabetes management
Nutritional management
Exercise
Monitoring
Pharmacologic therapy
Education
43

44. 1. Nutritional management
• Providing all the essential food constituents (e.g.
vitamins, minerals) necessary for optimal nutrition.
• Achieving and maintaining a reasonable weight.
• Preventing wide daily fluctuations in blood glucose
levels.
• blood glucose levels as close to normal as is safe and
practical to prevent or reduce the risk for complications
• Decreasing serum lipid levels, if elevated, to reduce the
risk for macrovascular disease.
44

45. 1. Nutritional management…
• The same precautions regarding the use of alcohol by
people without diabetes should be applied to
patients with diabetes. Moderation is recommended.
• Alcohol may decrease the normal physiologic
reactions in the body that produce glucose
(gluconeogenesis).
• Thus, if a diabetic patient takes alcohol on an empty
stomach, there is an increased likelihood that
hypoglycemia will develop.
45

46. 2. Exercise
• Exercise is extremely important in managing diabetes
because of its effects on lowering blood glucose and
reducing cardiovascular risk factors.
• Exercise lowers the blood glucose level by increasing the
uptake of glucose by body muscles and by improving
insulin utilization. It also improves circulation and muscle
tone.
• Regular daily exercise, rather than sporadic exercise,
should be encouraged
46

47. 2. Exercise …
• Exercise also alters blood lipid levels, increasing levels of
high-density lipoproteins and decreasing total
cholesterol and triglyceride levels.
• Exercising with elevated blood glucose levels increases
the secretion of glucagon, and catecholamines.
• The liver then releases more glucose, and the result is an
increase in the blood glucose level.
47

48. 3. Monitoring glucose level
• Blood glucose monitoring is a cornerstone of
diabetes management.
• SMBG enables people with diabetes to adjust the
treatment regimen to obtain optimal blood glucose
control.
• This allows for detection and prevention of
hypoglycemia and hyperglycemia and
• plays a crucial role in normalizing blood glucose
levels, which in turn may reduce the risk of long-term
diabetic complications.
48

49. SMBG
49

50. SMBG
50

51. 4. Insulin Therapy
• Because the body loses the ability to produce insulin in
type 1 diabetes, exogenous insulin must be administered
for life.
• Because the insulin dose required by the individual
patient is determined by the level of glucose in the
blood, accurate monitoring of blood glucose levels is
essential; thus,
• SMBG has become a cornerstone of insulin therapy.
51

52. 4. Insulin Therapy
• The four main areas for injection are the
– abdomen,
– arms (posterior surface),
– thighs (anterior surface), and
– hips .
• Insulin is absorbed faster in some areas of the body than
others.
• The speed of absorption is greatest in the abdomen and
decreases progressively in the arm, thigh, and hip.
52

53. Sites of insulin injection
53

54. Medication: Insulin therapy
• Lower blood glucose after meals by facilitating the
uptake and utilization of glucose by muscle, fat and liver
cells.
• During period of fasting, insulin inhibits the breakdown
of stored glucose, protein and fats.
• Type I: insulin must
• Type II: used on long term basis to control glucose level,
if diet and oral hypoglycemic agent failed.
• Some patient usually control by diet alone or diet with
oral hypoglycemic agent need insulin during, infection,
pregnancy and surgery. 54

55. Insulin preparation
Insulin preparation can vary according to 4 main
characteristics
1. Time course of action
2. Concentration
3. Species/source
4. Manufacturer
55

56. Insulin preparation…
– Time: Short acting
– Agent: Regular
– Onset: ½-1 hour
– Peak: 2-3 hrs
– Duration: 4-6hrs
– Appearance: clear
• Indications: Usually administered 20-30 min before meal,
may be taken alone or in combination with long acting
insulin 56

57. Insulin preparation….
• Time: Intermediate
• Agent: Neutral Protamin Hagedron/NPH
• Onset: 3-4 hrs
• Peak: 4-12hrs
• Duration: 16-20 hrs
• Appearance: white and milk
• Indications: usually after food
57

58. Insulin preparation…
• Time: Long acting
• Agent: Ultralente
• Onset: 6-8hrs
• Peak: 12-16 hrs
• Duration: 20-30 hrs
• Indications: Used primary to control fasting glucose level
58

59. Insulin regimen
• Vary from one injection to four injection per day
• Usually combination of short acting and long acting
insulin
1. Conventional regimen:
• One – two injection per day
• Aim :- to avoid acute complication of diabetes
(hypoglycemia)
• Important for terminal patient or any patient
59

60. Insulin regimen…
2. Intensive regimen
• Three – four injection per day
• Twice – daily administration of S.A. and
L.A. given in combination before bread fast
and evening meal is simplest and most
commonly used regimen
60

61. Administrating the injection
Site selection and rotation: four main area
–The abdomen
–Arm (posterior surface)
–Thigh (anterior surface)
–Hip (buttock)
Absorption rapid in abdomen and decrease
respectively arm, thigh and hip.
–Route:- subcutaneous
61

62. 62

63. • Absorption of insulin may be influenced by:-
–Site, Depth, Volume of injection
Rotate every 2 to 3 weeks
–To prevent localized in fatty tissue
(lipodystrophy).
–To promote consistency in insulin absorption
– Administer each injection ½ to 1 inch away from
previous injection
– Always use the same area at the same time of day
E.g: patient may inject morning dose in to the
abdomen and evening doses in to the arm
63

64. Problem of insulin
• Local allergy
• Systemic allergy
• Lypodystrophy:- refers localized disturbance of fat
metabolism in the form of lypoatrophy and
liypohypertrophy
• Hypoglycemia
• Weight gain ( how)
64

65. Oral ant diabetic
Effective for type II who can not treated by diet and
exercise
1. Sulfonylureas
• Stimulate pancreas to secrete insulin
• Decrease production of glucose by liver
2. Biguandies
• Facilitating insulin on peripheral receptors
• Decreasing the amount of sugar produced by the liver.
• Increasing the amount of sugar absorbed by muscle
cells.
65

66. Sulfonylureas
First generation
– Carbutamide
– Acetohexamide
– Chlorpropamide
– Tolbutamide
– Tolazamide
Second generation
• Glipizide
• Gliclazide
• Glibenclamide (glyburide)
• Glibornuride
• Gliquidone
• Glisoxepe
• Glyclopyramide
• Glimepiride
66

67. Biguandies
• Metformin - widely used in treatment of diabetes
mellitus type 2
• Phenformin - withdrawn from the market in most
countries due to toxic effects
• Buformin - withdrawn from the market due to toxic
effects
67

68. Complication of DM
68

69. Acute Complications of Diabetes
• There are three major acute complications of diabetes
related to short-term imbalances in blood glucose
levels:
– Hypoglycemia,
– DKA,
– HHNS,
69

70. Hypoglycemia (insulin reactions)
• Hypoglycemia occurs when the blood glucose falls to
< 50 to 60 mg/dl.
It can be caused by:
– too much insulin or
– Too much oral hypoglycemic agents,
– too little food, or excessive physical activity.
• Hypoglycemia may occur at any time of the day or night.
• It often occurs before meals, especially if meals are
delayed or snacks are omitted.
• Sweating, tremor, tachycardia, palpitation, nervousness,
and hunger. 70

71. The clinical manifestations
• In moderate hypoglycemia, the fall in blood glucose
level deprives the brain cells of needed fuel for
functioning.
• Signs of impaired function of the CNS may include:
– inability to concentrate, headache, lightheadedness,
confusion, memory lapses, numbness of the lips and
tongue,
– Slurred speech, impaired coordination, emotional
changes, irrational or combative behavior, double
vision, and drowsiness.
71

72. Management
• 15 g of a fast-acting carbohydrate given orally.
• 3-4 commercially prepared glucose tablets.
– 4 to 6 oz of fruit juice or Drink 1/2 cup fruit juice.
– 6 to 10 hard candies
– 2 to 3 teaspoons of sugar or honey
72

73. Diabetic ketoacidosis
• DKA is caused by an absence or markedly inadequate
amount of insulin.
• The three main clinical features of DKA are:
– Hyperglycemia
– Dehydration and electrolyte loss
– Acidosis
73

74. Diabetic ketoacidosis…
• Without insulin, the amount of glucose entering the
cells is reduced and the liver increases glucose
production. Both factors lead to hyperglycemia.
• In an attempt to rid the body of the excess glucose, the
kidneys excrete the glucose along with water and
electrolytes (e.g. sodium and potassium).
• This osmotic diuresis, which is characterized by
excessive urination (polyuria), leads to dehydration and
marked electrolyte loss.
74

75. Diabetic ketoacidosis…
• Another effect of insulin deficiency is the breakdown of
fat (lipolysis) into free fatty acids and glycerol.
• The free fatty acids are converted into ketone bodies by
the liver.
• In DKA there is excessive production of ketone bodies
because of the lack of insulin that would normally
prevent this from occurring.
• Ketone bodies are acids; their accumulation in the
circulation leads to metabolic acidosis.
75

76. Clinical manifestations
The hyperglycemia DKA leads to:-
Polyuria and polydypsia
Blurred vision, weakness, headache
The ketosis and acidosis characteristics of DKA leads to:-
• Abdominal pain
• Vomiting
• Nausea
• Poor appetite
• Acetone breath
• Patients with marked intravascular volume depletion may
have orthostatic hypotension (drop in systolic blood pressure
of 20 mm Hg or more on standing.
76

77. Clinical manifestations….
• Kussumal breathing (deep and rapid but not labored
respiration)
• Important to decrease the acidosis i.e. attempt to blow
off Co2 and lessen the acidic state.
Investigation:- urea and electrolyte, blood glucose
 Arterial blood to asses the severity of acidosis
 Urine analysis for ketone
 Full blood count
 Blood glucose level 300 – 800 mg/dl
 It is medical emergency so treatment should be in the
hospital
77

78. Management…
Aim of treatment:- correction of the three main problems:
–Dehydration
–Electrolyte loss
–Acidosis
A.Fluid replacement
• Rehydration is important for maintaining tissue
perfusion
• Initially 0.9% normal saline is administer at high rate
• Hypotonic N/S (0.45%) may be used for patient with
HPN.
• Monitor fluid volume status (intake and out put).
78

79. Management…
B. Electrolyte loss replacement
Although plasma concentration of potassium may be
low, normal or even high, level of potassium drop during
treatment of DKA.
Rehydration increase plasma volume and subsequent
decrease of serum potassium.
Rehydration increase urinary excretion of potassium.
Because potassium level drop during treatment of DKA,
potassium must be infuse even if the plasma
concentration is normal. 79

80. Management
C. Acidosis
• Insulin inhibit the fat breakdown, there by stopping the
building up of acids.
• IV slowly
• Add dextrose when blood glucose level reach 250 to 300
mg/dl to avoid rapid drop in blood glucose.
80

81. Prevention
• Take insulin/oral anti diabetic as usual
• Test blood and urine for ketone every 3-4 hrs
• Report elevated glucose level greater than 300mg/dl
81

82. Hyperglycemic hyperosmolar nonketotic syndrome
• The patient’s persistent hyperglycemia causes osmotic
diuresis, resulting in losses of water and electrolytes.
• To maintain osmotic equilibrium, water shifts from the
intracellular fluid space to the extracellular fluid space.
• With glucosuria and dehydration, hypernatremia and
increased osmolarity occur.
82

83. hyperglycemic hyperosmolar nonketotic syndrome
• What distinguishes HHNS from DKA is that ketosis and
acidosis do not occur in HHNS partly because of
differences in insulin levels.
• In HHNS the insulin level is too low to prevent
hyperglycemia and subsequent osmotic diuresis, but it is
high enough to prevent fat breakdown.
• Because of possible delays in therapy, hyperglycemia,
dehydration, and hyperosmolarity may be more severe
in HHNS.
83

84. Hyperglycemic hyperosmolar nonketotic syndrome
• The clinical picture of HHNS is:
Hypotension,
Profound dehydration (dry mucous membranes, poor
skin turgor),
Tachycardia, and
Variable neurologic signs e.g. Seizures.
84

85. Long term complications of diabetes mellitus
Affect almost every organ system of the body
 Macro vascular diseases
 Micro vascular disease
 Neuropathy
85

86. Macro-vascular complications
Atherosclerotic changes in the blood vessel commonly
occur in diabetes:
1.Coronary artery disease
2. Cerebral vascular disease
3. Peripheral vascular disease
86

87. Macro-vascular complications…
• Diabetic macrovascular complications result from
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 blocked.
87

88. Macro-vascular complications…
Heart Disease And Stroke
• Patients with diabetes are four times more prone to
develop Heart disease than others.
• They may suffer from Heart Attack, Chest Pain or
Angina, High Blood Pressure, Stroke, etc.
• Patient with diabetes may develop silent Heart
Attacks without showing any symptoms because in
diabetics there is damaged nerve.
• Risk factors for heart disease are mainly obesity,
Sedentary life style, High blood pressure, High
Cholesterol levels, Cigarette smoking, Family history
of coronary heart disease etc. 88

89. Neuropathies
Neuropathies
• Diabetic neuropathy refers to a group of diseases that
affect all types of nerves, including peripheral (sensory
motor), autonomic, and spinal nerves.
• Nerve tissue gets injured mainly due to decreased blood
flow and rise in blood glucose levels.
89

90. Microvascular complications
• Diabetic microvascular disease (or Microangiopathy) is
characterized by capillary basement membrane
thickening.
• The basement membrane surrounds the endothelial
cells of the capillary.
90

91. Diabetic microvascular complications
Diabetic Microangiopathy
• It is characterized by basement membrane thickening of
small blood vessels and capillaries of various organs and
tissues such as the skin, eye, skeletal, muscle, kidney, etc.
• Researchers believe that increased blood glucose levels
react through a series of biochemical responses to
thicken the basement membrane to several times its
normal thickness.
91

92. Diabetic microvascular complications…
• Retinopathy:- Deterioration of the small blood vessels that
nourish the retina.
• Diabetic retinopathy is the leading cause of blindness in
people between 20 and 74 years of age.
• Nephropathy , or renal disease secondary to diabetic micro
vascular changes in the kidney.
• It is also known as Diabetic glumerulosclerosis. Due to
thickening of the basement membrane of glomerular
capillaries.
92

93. Foot ulcer
Diabetic complications contribute to the risk of foot
infections are:
1. Neuropathy: sensory neuropathy leads to loss of pain and
pressure sensation and autonomic neuropathy leads to
increased dryness and fissure of the skin.
2. Peripheral vascular disease: poor circulation of the lower
extremity contribute to poor wound healing and develop
gangrene.
3. Hyperglycemic impairs the ability of specialized
leukocyte to destroy bacteria, thus poorly controlled
diabetes, there is lowered resistance to certain infection93

94. Teaching self injection
94

95. Teaching self injection
95

96. Teaching self injection
96

97. Teaching self injection
97

98. Teaching self injection
98