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
3.
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 = 2nd 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
13.
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
28. DIABETES MELLITUS:
6th leading cause of death in US
3rd 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
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 Autoimmune
disease reaction in which
the beta cells that
#2: Idiopathic
produce insulin are
Genetic susceptibility 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
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
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
54.
55.
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
Obesity
insulin resistance by tissues
Compensatory increase of
insulin production by islets
insulin resistance & defect
in insulin receptors
HYPERGLYCEMIA
59. Hyperglycemia
Increased osmolarity due Gluconeogenesis
to glucose
Wasting of Increased ketones
lean body
mass Metabolic acidosis
Fatigue and
Polyphagia weight loss Acetone
breath
Polyuria Polydypsia
Sluggish blood Proliferation of
Weight loss flow microbes Infections
60. Chronic elevations in blood glucose levels
1. Small vessel disease
Nephropathy
Neuropathy Retinopathy
ESRD Loss of
vision/blindness
Symmetrical Numbness and Wasting of Charcot’s Autonomic DM
loss of tingling in the intrinsic muscles joints neuropathy foot
sensation extremities and
ulcer
61. Chronic elevations in blood glucose levels
Accelerated atherosclerosis Impaired immune function
Infection Delayed
wound
healing
Hypertension Coronary Stroke Increased low
artery disease density
lipoprotein
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 HHNC prone
Adult Onset production of insulin
Stable DM by islets or receptor
Ketosis resistant DM
sites and insulin
resistance
66.
67.
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
70.
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)
74. TYPE 1 VS. TYPE 2
Etiology Etiology
Auto-immune Overused/tired
Idiopathic
Age of onset Age of onset
Usually < 30 Usually > 40
Percent of Percent of
diabetics diabetics
5-10% 85-90%
75. TYPE 1 VS. TYPE 2
Onset Onset
Rapid less than 1 yr Gradual – years
Body wt at onset Body wt at onset
Normal to thin 80% overweight
Insulin production Insulin production
None Not enough
Insulin injections Insulin injections
Always Sometimes
76. TYPE 1 VS. TYPE 2
Ketones Ketones
Children/adolescence Unlikely problem
Stress
Pregnancy Management
Diet (wt. Loss)
Management
Exercise
Insulin
Possibly oral
Diet hypoglycemic meds
Exercise Possibly insulin
77. CLASSIFICATIONS OF DM
3. Gestational diabetes mellitus
DM first detected during pregnancy
Due to placental hormones
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.”
82.
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).
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 Race or ethnicity:
(note: occurring with Hispanic, Native
increasing frequency American, African
in young individuals) American, Asian
Family history of American, or Pacific
type 2 diabetes in a Islander descent
first-degree relative
(eg, parent or sibling)
90. MAJOR RISK FACTORS TYPE 2 DM
History of previous History of gestational
impaired glucose diabetes mellitus or of
tolerance (IGT) or delivering a baby with a
impaired fasting glucose birth weight of over 9 lb
(IFG) Polycystic ovarian
Hypertension (>140/90 syndrome (which
mm Hg) results in insulin
Dyslipidemia (HDL resistance)
cholesterol level < 40 Depression
mg/dL or triglyceride
level >150 mg/dL)
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
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
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
106. AMERICAN DIABETES ASSOCIATION (ADA)
CRITERIA FOR DIAGNOSIS OF DIABETES
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
107. DIAGNOSIS OF DM
FBS: ≥126mg/dl
OGTT: 2-hour plasma glucose ≥
200mg/dl
Symptoms of DM plus RBS ≥ 200mg/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
114.
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
116.
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 A1C
Provides an average blood glucose
levels
Past 2-3 months
Can be taken any time
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
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
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
