Diabetes Mellitus, BACHELOR OF SCIENCE AND NURSING

for BSN 3 A

2. DIABETES MELLITUS
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

3. Insulin
hormone produced by the pancreas,
controls the level of glucose in the
blood by regulating the production
and storage of glucose
in diabetic state, cells may stop
responding to insulin or the pancreas
may stop producing insulin altogether
which leads to hyperglycemia

4. Classification
Type 1 DiabetesType 2 Diabetes
beta cells are destroyed
by the autoimmune
process
produce little or no insulin
and require insulin
injections to control their
blood glucose levels
characterized by acute
onset, usually before 30
years old
results from decreased
sensitivity to insulin
(insulin resistance) and
impaired beta cell
functioning resulting in
decreased insulin
production
usually occurs among
people who are older
than 30 years old

5. Pathophysiology
Type 1
Combined genetic, immunologic, and
possibly environmental (viral) factors may
contribute to beta cell destruction
Inherit genetic predisposition toward
developing type 1 diabetes
HLA (human leukocyte antigen)-refers to
a cluster of genes responsible for
transplantation antigens and other immune
processes

6. Pathophysiology
Type 1
Autoimmune response in which antibodies
are directed against normal tissues of the
body
Decreased insulin production leading to
unrestrained breakdown of stored glucose
(glycogenolysis) and production of new
glucose from amino acids and other
substrates (gluconeogenesis)

7. Pathophysiology
Type 2
Two main problems are insulin resistance
and impaired insulin secretion
Occurs in people older than 30 years old
and obese
Associated with slow, progressive glucose
intolerance
Primary treatment is weight loss and
exercise to enhance effectiveness of insulin

8. Pathophysiology
Genetic predisposition
Environmental/viral stressor
Destruction of beta cells of pancreas
Failure to produce Production of excess
insulin glucagon

9. Failure to produce insulin
Elevated blood glucose
Increased osmolality
Polydipsia Polyuria Polyphagia

10. Production of excess glucagon
Production of glucose from protein and fat
stores
Wasting of lean body mass

11. Chronic elevation in blood glucose levels
Small vesselAcceleratedImpaired immune
disease atherosclerosis function
Hypertension
Coronary artery disease

12. Clinical Manifestation
Polyuria
Polydipsia
Polyphagia

14. Assessment and Diagnostic Findings
Random Glucose Test
no fasting is necessary
reference values for a "normal" random
glucose test in an average adult (ADA
guidelines):
➢70 -140mg/dL (average/normal)
➢140 -200mg/dLis considered pre-
diabetes
➢> 200 mg/dLis considered diabetes

15. Assessment and Diagnostic Findings
Fasting Blood Sugar Test (FBS)
fasting is necessary for at least 8
hours prior to withdrawal of serum
sample
reference values considered normal is
60-120 mg/dL

16. Assessment and Diagnostic Findings
Post-Prandial
serum taken 2 hours after eating a
well-balanced meal
normal value: 65-140 mg/dL
hypoglycemia if <60 mg/dL

17. Assessment and Diagnostic Findings
Oral Glucose Tolerance Test
(OGTT)
FBS is taken then 75-100 mg of glucose is
given and blood samples are drawn after an
hour, after 2 hours, and after 3 hours
reference values:
➢1
st
hour: not >190mg/dL
➢2
nd
hour: > 140 mg/dL
➢3
rd
hour:> 125 mg/dL

18. Assessment and Diagnostic Findings
HbA1c (Glycosylated Hemoglobin)
determines serum levels of glucose in a
2-3 month period
normal value: 4-6%

19. Assessment and Diagnostic Findings
Urine Ketones
(+) in Type 1 diabetes

20. Diabetes Management
Main goal is to normalize
insulin activity and blood
glucose levels to reduce the
development of vascular
and neuropathic
complications

21. Nutritional Management
Control of total
caloric intake to
attain or maintain a
reasonable body
weight and control of
blood glucose levels
Provide all the
essential food
constitutes
Meeting energy
needs
Achieving and
maintaining a
reasonable weight
Preventing wide
daily fluctuations in
blood glucose levels
Decreasing serum
lipid levels to reduce
risk for
macrovascular
disease

22. Nutritional Management
Caloric Distribution
(American Diabetic Association)
Carbohydrates-50-60%
Fat-20-30%; limiting total intake of
cholesterol to less than 300 mg/day
Protein-10-20%
Fiber-lowers cholesterol levels

23. Nutritional Management
Alcohol consumption
Can lead to hypoglycemia, especially for those
taking insulin (decrease gluconeogenesis)
For those taking sulfonylurea agent
chlorpropamide (Diabinese), a potential side
effect is a disulfiram (Antabuse) type of
reaction: facial flushing, warmth, headache,
nausea, vomiting, sweating, thirst within minutes
of consuming alcohol
May lead to excessive weight gain,
hyperlipidemia, and elevated glucose levels

24. Nutritional Management
Sweeteners
•nutritive sweeteners: fructose, sorbitol,
xylitol cause less elevation in blood
glucose
•non-nutritive sweeteners: aspartame
(NutraSweet), sucralose (Splenda)
produce minimal or no elevation

26. Exercise
Lowers blood glucose and reduce
cardiovascular risk factors
Increase uptake of glucose by
body muscles and improve insulin
utilization

27. Exercise
Patients who have blood glucose levels
exceeding 250 mg/dl and who have
ketones in their urine should not begin
exercising until the urine tests negative for
ketones and blood glucose level is close to
normal (prevent increased secretion of
glucagon, growth hormones, and
catecholamines)
Exercise at the same time and at the peak
of blood glucose levels

28. Monitoring blood glucose levels
and ketones
Self-monitoring of blood glucose
(SMBG)
Useful for managing self-care; key
component of treatment for any
intensive insulin therapy regimen
Keep a record logbook
Testing done at peak action time

30. Monitoring blood glucose levels
and ketones
Glycosylated hemoglobin (HgbA1c)
Reflects average blood glucose levels
over a period of approximately 2-3
months
When blood glucose levels are elevated,
glucose attaches to the hemoglobin in
RBC; the longer the elevation, the more
glucose attaches to RBCs; complex lasts
for the lifetime of RBCs (120 days)

31. Monitoring blood glucose levels
and ketones
Urine testing for Ketones
Signal that control of type 1 diabetes
is deteriorating and there is high risk
for DKA
Byproducts of fat breakdown,
signaling that there is no effective
insulin available

33. Time Course of Action
Time Course/AgentOnset Peak Duration
Rapid-acting
•Lispro (Humalog)
•Aspart (Novalog)
10-15 min1 hour
40-50 min
3 hours
4-6 hours
Short-acting
•Regular (Humalog
R, Novolin R)
½-1 hour2-3 hours4-6 hours

34. Time Course of Action
Time Course/AgentOnset Peak Duration
Intermediate-acting
•NPH (neutral
protamine Hagedorn)
•Humulin N, Novolin L
2-4 hours
2-4 hours
6-12 hours16-20
hours
Long-acting
•Ultralente 6-8 hours12-16 hours20-30
hours
Very long-acting
•Glargine (Lantus)1 hour continuous24 hours

36. Insulin Regimen
Conventional
Regimen
Intensive
Regimen
Simplified
One or more
injections of a
mixture of short-
and immediate-
acting insulins per
day
Helps achieve as
much control over
blood glucose
levels as is safe

37. Complications
Local allergic
reactions
Redness, swelling,
tenderness
Induration of 2-4
cm wheal may
appear at
injection site 1-2
hours after insulin
administration
Usually occur
during the
beginning stages
of therapy and
will disappear
with continued use
Antihistamine may
be prescribe to be
taken 2 hour
before injection

38. Complications
Systemic allergic reactions
Immediate local skin reaction
that gradually spreads into
generalized urticaria (hives)
Desensitization

39. Complications
Insulin lipodystrophy
Localized reaction, in
the form of either
lipoatrophy or
lipohypertrophy,
occurring at site of
injection resulting from
repeated use of a site

40. Complications
Insulin resistance
Most common
cause is obesity
Some develop
high levels of
antibodies

41. Alternative methods of insulin
delivery
Insulin pens
prefilled insulin
cartridges loaded
into a pen-like holder
insulin is delivered by
dialing in a dose of
pushing a button for
every 1-2 unit
increment
administered

42. Alternative methods of insulin
delivery
Jet injectors
deliver insulin
through the skin
under pressure
in an extremely
fine stream

43. Alternative methods of insulin
delivery
Insulin pumps
Continuous
subcutaneous
insulin infusion-
involves the use of
small, externally
worn devices that
closely mimic the
functioning of the
normal pancreas
Contain 3-ml
syringe attached
to a long, thin,
narrow lumen tube
with a needle or
Teflon catheter
attached to the
end

45. Alternative methods of insulin
delivery
Transplantation
of pancreatic
cells

46. Oral Antidiabetic Agents
Sulfonylureas
Directly stimulating the pancreas to secrete
insulin
Cannot be used in type 1 diabetes
SE: GI symptoms and dermatologic reactions
Meds that may cause hyperglycemia:
potassium-wasting diuretics, corticosteroids,
estrogen compounds, phenytoin (Dilantin)
Hypoglycemia: salicylates, propanolol,
MAOIs

47. Oral Antidiabetic Agents
Biguanides
Facilitates insulin’s action on peripheral
receptor sites
Can only be used in the presence of
insulin
Have no effect on pancreatic beta cells
SE: lactic acidosis

48. Oral Antidiabetic Agents
Alpha glucosidase inhibitors
Used in type 2 diabetes management
Delay absorption of glucose in the
intestinal system

49. Oral Antidiabetic Agents
Thiazolidinediones
Indicated for patients with type 2
diabetes who take insulin injections
Enhance insulin action at the receptor site
without increasing insulin secretion
May affect liver function
Can cause resumption of ovulation in
perimenopausal anovulatory women,
making pregnancy possible

50. Oral Antidiabetic Agents
Meglitinides
Stimulate insulin release from the
pancreatic beta cells
Taken before each meal to stimulate
release of insulin in response to the
intake of food

52. Education
Daily self-care skills, lifestyle
changes, nutrition, medication
effects and side effects, exercise,
disease progression, prevention
strategies, blood glucose
monitoring techniques, medication
adjustment

53. Self-Administration of Insulin
Storage
Cloudy insulin should be thoroughly mixed
by gently inverting the vial or rolling
between the hands before drawing the
solution
Vials not in use should be refrigerated
and extremes of temperature should be
avoided
Should not be allowed to freeze

54. Self-Administration of Insulin
Should be kept at room temperature
to reduce local irritation
Inspected for flocculations (frosted,
whitish coating inside the bottle of
intermediate-or long-acting insulin
most common in human insulin)

55. Self-Administration of Insulin
Mixing Insulins
Regular insulin should be drawn into
the syringe first
When regular insulin is mixed with
long-acting insulin, there is a binding
reaction that slows the action of
regular insulin

56. Self-Administration of Insulin
Withdrawing Insulin
Inject air into the bottle
equivalent to the number of units
to be withdrawn to prevent
formation of vacuum inside the
bottle which makes it difficult to
withdraw insulin

58. Self-Administration of Insulin
Selecting and Rotating the Injection Site
Abdomen, arms (posterior surface), thighs
(anterior surface), and hips
Speed of absorption is greatest in the
abdomenand decreases progressively in
the arm, thigh, and hip
Use all available injection sites within one
area to promote consistency in insulin
absorption

59. Self-Administration of Insulin
Selecting and Rotating the Injection Site
Should not use the same site more than
once in 2-3 weeks
If planning to exercise, insulin should not
be injected into the limb that will be
exercised because it will cause
hypoglycemia

62. Hypoglycemia
(Insulin Reactions)
Blood glucose falls less than 50-
60 mg/dl
Mild: sweating, tremor,
tachycardia, palpitation,
nervousness, hunger from surge of
catecholamines

63. Hypoglycemia
(Insulin Reactions)
Moderate: inability to
concentrate, lightheadedness,
confusion, memory lapses, slurred
speech, impaired coordination,
double vision, drowsiness
Severe: disoriented behavior,
seizures, difficulty arousing from
sleep, loss of consciousness

64. Management
Give fast-acting concentrated source of
CHO such as fruit juice, regular soda,
hard candies, sugar or honey
Teach patient to always carry some form
of simple sugar at all times
Refrain from eating high-calorie, high-fat
dessert to treat hypoglycemia
Emergency: for unconscious, inject 1 mg of
glucagon SQ or IM

65. Diabetic Ketoacidosis
Three main features: hyperglycemia,
dehydration and electrolyte loss,
acidosis
Kidneys excrete excess glucose along
with water and electrolytes causing
polyuria leading to dehydration
Lipolysis converts free fatty acids into
ketone bodies by the liver

66. Diabetic Ketoacidosis
CM: blurred vision, polyuria, weakness,
headache, polydipsia, acetone breath,
poor appetite, nausea, vomiting,
abdominal pain, rapid respiration
300-800 mg/dl blood glucose levels
Low serum NaHCO3 (0-15 mEq/L) and
low pH (6.8-7.3)
Low PCO2 (10-30mmHg) reflects
respiratory compensation causing
Kussmaul’s respiration

67. Diabetic Ketoacidosis
Medical Management:
Rehydration: IVF challenge of PNSS
Restoring electrolytes: potassium
replacement up to 40 mEq/hour
Reversing acidosis: hourly blood
glucose levels monitoring, D5NSS, D
50
0.45NSS, IV mixtures of regular
insulin

68. Diabetic Ketoacidosis
Nursing Management:
Monitoring fluid and electrolyte
status
Administering fluids and
preventing overload
Vital signs monitoring

69. Hyperglycemic Hyperosmolar
Nonketotic Syndrome
Alterations in sensorium
Occurs in older people (50-70 y.o.)
Can be traced to precipitating events such
as acute illness, or dialysis
CM: hypotension, profound dehydration,
tachycardia, neurologic symptoms
Diagnostics: blood glucose of 600-1,200
mg/dl, >350 mOsm/kg

71. Macrovascular Complications
Result from changes in medium to large
blood vessels wherein blood vessel walls
thicken, sclerose, and become occluded by
plaques that adhere to the vessel walls
causing blockage in blood flow
Coronary artery disease, cerebrovascular
disease, and peripheral vascular disease
are the three main types of complications

72. Macrovascular Complications
MItwice common in men and
three times common in women
TIAsand strokesfrom occlusive
changes in cerebral blood vessels
Peripheral occlusion: diminished
peripheral pulses, intermittent
claudication

73. Microvascular Complications
and Diabetic Retinopathy
Microangiopathycharacterized
by capillary basement membrane
thickening affecting the retinas
and kidneys
Visual complications caused by
changes in the small blood vessels
in the retina

74. Nephrophathy
Kidneys filtration mechanism is stressed, allowing
blood proteins to leak into the urine resulting in
increased pressure in the blood vessel of the
kidney
Elevated albumin levels in the urine, elevated
serum BUN and creatinine
Med Management:
Control of hypertension (ACE inhibitors)
Avoid nephrotoxic substances
Low sodium, low protein diet

75. Diabetic Neuropathies
Refers to a group of disease that
affect all types of nerves, including
peripheral (sensorimotor), autonomic,
and spinal nerves
Capillary membranes thickening and
capillary closure, demyelinization of
nerves

76. Diabetic Neuropathies
Peripheral Neuropathy
Paresthesias, burning sensations,
decrease in proprioception
Decreased sensations of pain
and temperature

77. Diabetic Neuropathies
Autonomic Neuropathies
Cardiac: tachycardia, orthostatic
hypotension, silent painless MI
GI: early satiety, bloating, nausea,
vomiting
Renal: urinary retention, decreased
sensation of bladder fullness
Sexual dysfunction

78. Foot and Leg Problems
Neuropathy: loss of pain and pressure
sensation, dryness and fissuring of the skin,
muscular atrophy
Peripheral vascular disease: poor
circulation lead to poor wound healing
and gangrene formation
Immunocompromise: hyperglycemia
impairs the ability of specialized
leukocytes to destroy bacteria

80. Foot and Leg Problems
Health teachings:
Properly bathe, dry, and lubricate
the skin of the foot
Wear closed, well-fitted shoes
Trim toenails straight across and file
sharp corners
Reduce risk factors such as smoking
and elevated blood lipids