Diabetes mellitus

Diabetes mellitus

1. DIABETES
MELLITUS

2. THE PANCREAS
behind stomach (LUQ)
6” long
Horizontal
Both endocrine & exocrine functions
exocrine : secretes hormones & enzymes that help
in the digestion of proteins, carbohydrates & fats

4. Endocrine:
carried out by islets of Langerhans
alpha cells – glucagons
beta cells – insulin
delta cells – somatostatin

5. Endocrine:
alpha cells – glucagons:  blood glucose – hyperglycemia
beta cells – insulin:  blood glucose – hypoglycemia
delta cells – somatostatin:  secretion of glucagons,
insulin, GH
Insulin – facilitates transport of glucose across the cell
membrane to be utilized by the cell.

6. INSULIN
Primary function…
Stimulates the active
transport of glucose
from the blood into
muscle, liver and adipose
tissue 
__?__ blood glucose
levels
i

7. GLUCOSE CONTENT OF FOOD
What % of the carbohydrates consumed breaks
down into glucose?
100%
What % of the protein consumed breaks down
into glucose?
58%
What % of the fat consumed breaks down into
glucose?
 10%

8. SECRETION OF INSULIN
Is stimulated by:
What change in homeostasis does the sensor
identify and then stimulates the beta cells to
secrete insulin?
Hyperglycemia
Glucose levels in the bloodstream
regulate the rate of insulin secretion

9. THE MAJOR ACTION OF INSULIN
i blood glucose levels
h the permeability of target cell membrane to
glucose
Main target cells
Muscle
Liver
Adipose tissue

10. INSULIN INFO
The glucose is either metabolized or
stored
In the absence of insulin, glucose is not
able to get into the cells and it is
excreted in the urine
Brain cells are not dependent on insulin
for glucose intake

11. INSULIN
Eat the glucose
Muscle  energy
Storage of glucose
Liver = freezer
Glycogen
Synthesis of Adipose tissue = 2
nd
freezer
Give it away
Glycosuria

12. OTHER FUNCTIONS OF INSULIN
Promote the conversion of glucose 
glycogen
Glycogenesis
Also inhibits the conversions of glycogen
 glucose
Glycogenolysis
Glycogen = the form in which glucose is
stored in the liver

14. OTHER FUNCTIONS OF INSULIN
Promoting the
conversion of fatty
acids  fat
Adipose tissue

15. OTHER FUNCTIONS OF INSULIN
Preventing the
breakdown of fat 
ketone bodies
Ketone bodies: the
byproduct of fat
metabolism

16. OTHER FUNCTIONS OF INSULIN
Stimulating protein
synthesis
Inhibiting the
breakdown of protein
 amino acids

17. INSULIN SUMMARY
Insulin i blood glucose levels
Promotes the storage of glucose
i energy production from other
sources
Glycogen, fat or protein metabolism

18. GLUCAGON
Produced and secreted by the
Alpha cells of the Islets of Langerhans
Glucagon stimulates the release of
Glucose by the liver

19. GLUCAGON STIMULATES THE RELEASE OF
GLUCOSE BY THE LIVER
•What “G” word means the release of
glucose by the liver?
A.Glycogen
B.Glycogenesis
C.Glycogenolysis
D.Glucose
E.Gone-is-my-brain

20. The effect of glucagon
h blood glucose level
Hyperglycemia

21. GLUCAGON
Glucagon is secreted is response to
Hypoglycemia
Stress
Hypoglycemia may occur during
Stress
Exercise
Fasting

22. SOMATOSTATIN
A hormone secreted by the delta cells
of the Islets of Langerhans
Secreted in response to
Hyperglycemia
Action
Interferes with glucagon
Interferes with growth hormone

23. SOMATOSTATIN
Has a hypoglycemic
effect

26. DIABETES
MELLITUS

27. PREVALENCE

28. DIABETES MELLITUS:
6
th
leading cause of death in US
3
rd
leading cause of death by disease
Assoc. with many complication
Heart disease is the leading cause for a
diabetic
65% of diabetics have hypertension

29. DIABETES MELLITUS:
Risk of heart attack or stroke 3 times great
if you have DM
DM leading cause of blindness in adults
DM leading cause of new cases of renal
failure
50% of all people with non-traumatic leg
amputation have DM

30. DIABETES MELLITUS:
DM shortens peoples life span
DM creates disabilities
DM is an economic burden
12% of all health care expenditures are for
diabetic care/treatment
Seen in all age groups and races
1/3 of diabetics are over the age of 60

31. International Diabetes Federation
predicts that the number of people
living with diabetes will to rise from
366 million in 2011 to 552 million by
2030.

32. top 10 countries in number of people
with diabetes are currently India, China,
the United States, Indonesia, Japan,
Pakistan, Russia, Brazil, Italy, and
Bangladesh.

33. In 2009, diabetes mellitus was the
seventh leading cause of death in the
United States

34. Approximately 1 in 5 health care
dollars in the United States was spent
caring for someone with diagnosed
diabetes

35. DIABETES MELLITUS
A chronic systemic disease characterized by
disorder of carbohydrate, protein and fat
metabolism
characterized by hyperglycemia due to an
absolute or relative lack of insulin or to a
cellular resistance to insulin
 or no production of insulin
Ineffective insulin or insulin resistance

36. TYPES OF DM

37. Type 1
Type 2
GDM

38. TYPE 1 DM

39. DIABETES TYPE 1

Metabolic condition in which the beta cells
of pancreas no longer produce insulin;
characterized by hyperglycemia, breakdown
of body fats and protein and development
of ketosis
Accounts for 5 – 10 % of cases of diabetes;
most often occurs in childhood or
adolescence

40. TYPE 1 – DIABETES MELLITUS
Old names
Juvenile diabetes
Insulin dependent diabetes mellitus (IDDM)
Destruction of the Beta cells
Result
NO insulin production
Insulin dependent

41. ETIOLOGY TYPE 1 DM
#1: Auto-immune
disease
#2: Idiopathic
Genetic susceptibility
Autoimmune
reaction in which
the beta cells that
produce insulin are
destroyed
Alpha cells produce
excess glucagons
causing
hyperglycemia

42. TYPE 1
genetic/hereditary
1. Genetic predisposition for increased susceptibility;
HLA linkage
Environmental triggers stimulate an
autoimmune response
 Viral infections (mumps, rubella, coxsackievirus B4)
viral infections: attacks islet cells of the pancreas
 Chemical toxins
autoimmune: islet cell antibodies

43. Brittle DM
Unstable DM
Absolute insulin
deficiency
DKA prone
Thin

45. Process of beta cell destruction occurs
slowly;
hyperglycemia occurs when 80 – 90% is
destroyed;
often trigger stressor event (e. g.
illness)

46. S&S OF TYPE 1 DM
Hyperglycemia
↑ blood glucose levels
No insulin 
Glucose stays in the blood stream
What effect does insulin have on
glycogen?
Inhibits the conversion of glycogen to glucose

47. S&S OF TYPE 1 DM
Glycosuria
Glucose in the urine

48. S&S OF TYPE 1 DM
Polyuria
Osmotic diuresis
Nocturia
Urinating during the night
Nursing diagnosis
Fluid Volume Deficit

49. S&S OF TYPE 1 DM
Polydipsia
Excessive thirst

50. S&S OF TYPE 1 DM
Polyphagia
Excessive hunger

51. S&S OF TYPE 1 DM
Dehydration

52. S&S OF TYPE 1 DM
Ketonuria
No insulin
Burn fats
Byproduct  ketones
↑ ketone in the blood
Metabolic Acidosis

53. Liver can not excrete
all of the ketones 
spill into the urine 
Ketonuria

56. SUMMARY OF PATHOPHY
Hyperglycemia leads to
a. Polyuria (hyperglycemia acts as osmotic diuretic)
b. Glycosuria (renal threshold for glucose: 180 mg/dL)
c. Polydipsia (thirst from dehydration from polyuria)
d. Polyphagia (hunger and eats more since cell cannot
utilize glucose)
e. Weight loss (body breaking down fat and protein to
restore energy source
f. Malaise and fatigue (from decrease in energy)
g. Blurred vision (swelling of lenses from osmotic
effects)

57. PATHOPHYSIOLOGY : TYPE 1
VIRAL INFECTION

Inflammation of islets of the pancreas

Beta cells produce antigen

Antigen detected & destroyed by T cells

Production of islet cell antibodies
Autoimmune destruction of beta cells
HYPERGLYCEMIA

58. PATHOPHYSIOLOGY: TYPE 2


Compensatory increase of
insulin production by islets




 insulin resistance & defect
in insulin receptors




HYPERGLYCEMIA

 insulin resistance by tissues
Obesity

59. Hyperglycemia
Increased osmolarity due
to glucose
Gluconeogenesis
Increased ketones
Metabolic acidosis
Acetone
breath
Wasting of
lean body
mass
Fatigue and
weight loss
Polyuria Polydypsia
Polyphagia
Weight loss
Sluggish blood
flow
Proliferation of
microbes Infections

60. Chronic elevations in blood glucose levels
1. Small vessel disease
Neuropathy
Nephropathy
Retinopathy
ESRD Loss of
vision/blindness
Symmetrical
loss of
sensation
Numbness and
tingling in the
extremities
Wasting of
intrinsic muscles
Charcot’s
joints
Autonomic
neuropathy
DM
foot
and
ulcer

61. Chronic elevations in blood glucose levels
Accelerated atherosclerosis Impaired immune function
Hypertension Coronary
artery disease
Increased low
density
lipoprotein
Stroke
Infection
Delayed
wound
healing

62. TYPE 2 DM

63. DIABETES TYPE 2
condition of fasting hyperglycemia
occurring despite availability of
body’s own insulin

64. PATHOPHYSIOLOGY

Sufficient insulin production to prevent
DKA; but insufficient to lower blood
glucose through uptake of glucose by
muscle and fat cells
Cellular resistance to insulin increased by
obesity, inactivity, illness, age, some
medications

65. TYPE 2 DM
Hereditary
Adult Onset
Stable DM
Ketosis resistant DM

HHNC prone
 production of insulin
by islets or  receptor
sites and insulin
resistance

68. TYPE 2 DM
Etiology
The pancreas cannot
produce enough insulin
for body’s needs
Impaired insulin
secretion

69. TYPE 2 DM
Weakened Beta cells Due
to over use
High glucose intake
“Insulin Resistance”
The target cells have decreased
sensitivity to insulin

71. INSULIN AND TYPE 2 DM
Don’t all require insulin
1/3 will at some time need to take
insulin
Seldom get Ketoacidosis (enough
insulin to prevent high levels of fat
metabolism)

72. Simplified scheme for the pathophysiology of
type 2 diabetes mellitus.

74. TYPE 1 VS. TYPE 2
Etiology
Auto-immune
Idiopathic
Age of onset
Usually < 30
Percent of
diabetics
5-10%
Etiology
Overused/tired

Age of onset
Usually > 40
Percent of
diabetics
85-90%

75. TYPE 1 VS. TYPE 2
Onset
Rapid less than 1 yr
Body wt at onset
Normal to thin
Insulin production
None
Insulin injections
Always
Onset
Gradual – years
Body wt at onset
80% overweight
Insulin production
Not enough
Insulin injections
Sometimes

76. TYPE 1 VS. TYPE 2
Ketones
Children/adolescence
Stress
Pregnancy
Management
Insulin
Diet
Exercise
Ketones
Unlikely problem

Management
Diet (wt. Loss)
Exercise
Possibly oral
hypoglycemic meds
Possibly insulin

77. CLASSIFICATIONS OF DM
3. Gestational diabetes mellitus
DM first detected during pregnancy
Due to placental hormones

78. GESTATIONAL
Occurs during
pregnancy
2
nd
-3
rd
trimester
Screening 24-28 weeks
Extra metabolic
demands triggers onset

79. GDM
•#1 complication 
Macrosomia
•Controlled with diet and
insulin (no oral meds)
•Generally glucose level
return to normal after
delivery
•Predisposes to
–type 2 diabetes

80. WHAT TYPE OF DIABETES DOES
JONNY HAVE?
Jonny is a 11 year old male child. He is a thin youth
at 75 lbs and 4’6” tall. He suddenly became very ill
and his mother brought him to the ER. He was
complaining of weakness, nausea & vomiting and
blurred vision. He reported having to urinate a lot.
His vital signs were pulse:125; Respirations 28; BP:
80/40.
Type 1

81. NCLEX QUESTION
The antepartum patient is being routinely screened for
gestational diabetes by administering 50 mg of glucose and
testing the woman’s blood sugar in an hour. The patient asks
for the normal glucose values an hour after taking the
glucose. The nurse replies:
A.“It should be less than 140 or we do further testing.”
B.“Anything under 105 is acceptable.”
C.“We like to see a result between 130 and 165.”
D.“It is different for each individual.”

83. CLASSIFICATIONS OF DM
4. Impaired fasting glucose
FBS levels of >100mg/dl but < 126mg/dl
5. Impaired glucose tolerance
Glucose levels >140mg/dl but < 200mg/dl

84. OTHER SPECIFIC TYPES OF DIABETES
MELLITUS
Beta-cell genetic defect
Endocrinopathies
Pancreatitis
Cystic Fibrosis
Secondary diabetes :
Drug or chemical induces diabetes (steroids -
glucocorticoids
conditions that antagonize the actions of insulin (eg,
Cushing syndrome, acromegaly, pheochromocytoma).

87. RISK FACTORS

88. RISK FACTORS FOR TYPE 2 DM
Family history
Age
Obesity
Gestational diabetes or large baby
Hypertension
High fat diet
Lack of exercise
High carb. Diet

89. MAJOR RISK FACTORS TYPE 2 DM
Age : 45 and older
(note: occurring with
increasing frequency
in young individuals)
Family history of
type 2 diabetes in a
first-degree relative
(eg, parent or sibling)

Race or ethnicity:
Hispanic, Native
American, African
American, Asian
American, or Pacific
Islander descent

90. MAJOR RISK FACTORS TYPE 2 DM
History of previous
impaired glucose
tolerance (IGT) or
impaired fasting glucose
(IFG)
Hypertension (>140/90
mm Hg)
Dyslipidemia (HDL
cholesterol level < 40
mg/dL or triglyceride
level >150 mg/dL)

History of gestational
diabetes mellitus or of
delivering a baby with a
birth weight of over 9 lb
Polycystic ovarian
syndrome (which
results in insulin
resistance)
Depression

91. RISK FACTORS
Overweight: weight
greater than 120% of
desirable body weight
sedentary lifestyle
Smoking
diet high in red meat,
processed meat, high-
fat dairy products, and
sweets

92. RISK FACTORS FOR WOMEN
given birth to a baby >
9 lbs
history of polycystic
ovary syndrome: cause
insulin resistance
(+) family history
obesity
above 40 y/o

93. CLINICAL MANIFESTATIONS

94. S&S OF DIABETES MELLITUS
Definition:
 A group of disorders characterized by chronic
Hyperglycemia
3 P’s
Polydipsia
Polyuria
Polyphagia

95. S&S OF HYPERGLYCEMIA
Neuro
Fatigue
C/O headache
Dull senses
Stupor
Drowsy
Loss of Consciousness
Blurred Vision

96. S&S OF HYPERGLYCEMIA
Cardiovascular
Tachycardia
Decreased BP
(Dehydration)
Respirations
Kussmaul's respirations
Sweet and fruity breath
Acetone breath

97. S&S OF HYPERGLYCEMIA
Gastro-intestinal
Polyphagia
(Decreased hunger in late stages)
N/V
Abd. Pain
Polydipsia
Dehydration

98. S&S OF HYPERGLYCEMIA
Genital-urinary
Polyuria
Nocturia
Glycosuria
Skeletal-muscular
Weak

99. S&S OF HYPERGLYCEMIA
Integumentary
Dry skin
Flushed face
Hypothermia

102. MANIFESTATIONS TYPE 2
1. Client usually unaware of diabetes
aDiscovers diabetes when seeking health care for
another concern
Usually does not experience weight loss
2. Possible symptoms or concerns
Hyperglycemia (not as severe as with Type 1)
Polyuria
Polydipsia
Blurred vision
Fatigue
Paresthesias (numbness in extremities)
Skin Infections

103. DX EXAMS

104. To diagnose Diabetes Mellitus, one of
the three following tests must be
positive and must be confirmed on
another day with one of the three tests

105. DIAGNOSTICS
 FBS
2-hr PPG
OGTT
Glycosylated hemoglobin
Urine ketone levels

106. HbA1c level of 6.5% or higher
Or fasting plasma glucose (FPG) level of 126 mg/dL
(7.0 mmol/L) or higher
Or a 2-hour plasma glucose level of 200 mg/dL (11.1
mmol/L) or higher during a 75-g oral glucose
tolerance test (OGTT)
Or a random plasma glucose of 200 mg/dL (11.1
mmol/L) or higher in a patient with classic symptoms of
hyperglycemia (ie, polyuria, polydipsia, polyphagia, weight
loss) or hyperglycemic crisis

AMERICAN DIABETES ASSOCIATION (ADA)
CRITERIA FOR DIAGNOSIS OF DIABETES

107. DIAGNOSIS OF DM
FBS: ≥126mg/dl
OGTT: 2-hour plasma glucose ≥
200mg/dl
Symptoms of DM plus RBS ≥ 200mg/dl

108. BLOOD GLUCOSE
FASTING BLOOD GLUCOSE
Measures blood glucose
levels after fasting
Results
Normal – 70-115 mg/dL
Diabetic level > 126 mg/dL
Critical > 400 mg/dL
Critical < 50 mg/dL

109. FASTING BLOOD GLUCOSE
NURSING RESPONSIBILITY
Fast 6-8 hours
Water OK
No insulin or anti-diabetic meds
Exercise will effect results
Meds that interfere

110. 2-HOUR POST-PRANDIAL GLUCOSE
Measure blood glucose 2 hours after a
meal
Normal
70-140 mg/dL
Diabetic level
> 140 mg/dL

111. 2-HOUR POST-PRANDIAL GLUCOSE
NURSING RESPONSIBILITY
Eat entire meal
Don’t eat anything more until blood
draw
Water  OK
Notify lab when meal is finished
Exercise with effect results

112. GLUCOSE TOLERANCE TEST
NURSING RESPONSIBILITY
Evaluates blood glucose and urine
glucose
30 minutes before
1 hour after
2 hours after
3 hours after
4 hours after
A glucose load

113. GLUCOSE TOLERANCE TEST
Normal
Blood glucose < 140mg/dL at 2 hours
Urine negative for glucose (all times)
Diabetic level
Blood glucose > 140 mg/dL at 2 hours
Glucose in urine

115. GLUCOSE TOLERANCE TEST
NURSING RESPONSIBILITY
Fasting 6-8 hours before test
Hold meds that interfere
Administer glucose load
Water  encouraged
Collect urine hourly
Administer meal and meds afterwards

117. GLYCOSYLATED HEMOGLOBIN ASSAYS
(HGB A1C)
Percentage of glycosylated hemoglobin
RBC lifecycle
@ 120 days (4 months)
Glucose slowly binds with Hgb  glycosylated
 h serum glucose level  h glycosylated Hgb
levels

118. HGB A
1C
Provides an average blood glucose
levels
Past 2-3 months
Can be taken any time

119. Normal levels (non-diabetic)
4-6%
Diabetic level (goal)
<8%

120. HBA1c(%) Mean blood sugar (mg/dl)
6 135
7 170
8 205
9 240
10 275
11 310
12 345

121. DIAGNOSTIC TESTS TO MONITOR DM
Fasting Blood Glucose (normal: 70 – 110
mg/dL)
Glycosylated hemoglobin (c) (Hemoglobin
A1C)
Considered elevated if values above 7 – 9 %
Blood test analyzes glucose attached to hemoglobin.
Since rbc lives about 120 days gives an average of
the blood glucose over previous 2 to 3 months

122. Urine glucose and ketone levels (part of
routine urinalysis)
Glucose in urine indicates hyperglycemia (renal
threshold is usually 180 mg/dL)
Presence of ketones indicates fat breakdown,
indicator of DKA; ketones may be present if person
not eating
Urine albumin (part of routine urinalysis)
If albumin present, indicates need for workup for
nephropathy
Typical order is creatinine clearance testing

123. Cholesterol and Triglyceride levels
Recommendations
LDL < 100 mg/dl
HDL > 45 mg/dL
Triglycerides < 150 mg/dL
Monitor risk for atherosclerosis and
cardiovascular complications

124. MONOFILAMENT

127. DIABETICS & SURGERY

128. Risk of _________ if give shot of NPH and then NO
surgery or surgery delayed
Hypoglycemia
BS levels _____ during stress, surgery &
illness
 h
If not controlled (BG)  osmotic diuresis
 dehydration

129. Management
Check BS before surgery
No sub-Q
IV

130. HOSPITALIZED DIABETIC

131. HOSPITALIZED DIABETIC
Independence
Sliding scale
Diets
NPO
Still need insulin
Clear liquids
Most simple carbs
Low sugar if possible

132. PREVENTION

133. PREVENTION OF TYPE 2 DIABETES
MELLITUS
Guidelines from the American College of Clinical
Endocrinologists
Weight reduction
Proper nutrition
Regular physical activity
Cardiovascular risk factor reduction
Aggressive treatment of hypertension and dyslipidemia
Blood glucose screening at 3 year intervals starting
at age 45 for persons in high risk groups