2. Session Objectives
On completion of this session, students will be able to:
Define Diabetes Mellitus
Describe the Pathophysiology of Diabetes Mellitus
Discuss the different types of Diabetes Mellitus
Differentiate between type 1 and type 2 diabetes
Identify the clinical manifestation of Diabetes Mellitus
Describe the diagnostic approaches of DM
Describe the relationship between diet, exercise, and
medication (ie, insulin or oral hypoglycemic agents) for
people with diabetes
Identify acute and chronic complications of DM.
3. Introduction
Pancreas
The pancreas functions:
• Exocrine function: produces and secretes
digestive enzymes
• Endocrine Function: produces important
hormones in Islets of Langerhans; insulin,
glucagon, and Somatostatin.
4. Pancreatic Hormones
• Insulin
• Produced by the beta cells (ß-cells) in the pancreas.
• stimulates the uptake of glucose by body cells
• decreasing blood levels of glucose
• Somatostatin
• Produced by the delta Cells (-cells) in the pancreas.
• Inhibits both glucagon and insulin.
5. Pancreatic Hormones
• Glucagon
• Produced by the alpha cells (-cells).
• Stimulates the breakdown of glycogen and the release of
glucose from liver
• increasing blood levels of glucose.
• When liver glucose is not available,
Lipolysis ( breakdown of fat) OR
Proteolysis (breakdown of aas) occurs
• Glucagon and insulin work together to regulate & maintain blood
sugar levels
6.
7. Insulin
• Pancreas secretes 40-50 units of insulin
(U-40 to 50) daily in two steps:
• Secreted at low levels during fasting ( basal insulin secretion)
• Increased levels after eating (prandial insulin secretion)
• An early burst of insulin occurs within 10 minutes of eating
• Then proceeds with increasing release as long as hyperglycemia is
present
8. Functions of insulin
• Enables glucose to be transported into
cells for energy for the body
• Glucose is the preferred fuel of
the body cells and the only fuel
that the brain can use
• Facilitates conversion of:
excess glucose fat
glucose glycogen to be stored in
muscles and the liver
• Prevents the breakdown of
body protein for energy
9. How Food Becomes Glucose
• During digestion, food is broken
down to sugar (glucose)
• Insulin lowers blood sugar by
helping sugar move from blood
into cells
• The body’s cells use sugar
for energy
Pancreas
11. What Is Diabetes Mellitus?
In people with diabetes…
The pancreas
does not make
any insulin
The pancreas
does not make
enough insulin
(this gets worse
with time)
The body prevents
the insulin that is
being made from
working correctly
Blood sugar gets
too high and can
lead to many
serious problems
(complications)
OR OR
12. Epidemiology of DM
• 3rd leading cause death,
• 10.5% of the adult population (20-79 years) has diabetes
and half of them are unaware of it (IDF, 2021)
• In 2021 about 537 million adults are living with DM, and
by 2045, IDF projects 1 in 8 adults (approximately 783
millions will be living with DM), i.e an increase of 46%.
• Ethiopia: 0.5% & 4.7% prevalent in the overall population
and over 40 years of age
13. Types of Diabetes
1. Type 1 DM /T1DM/
2. Type 2 DM /T2DM/
3. Gestational DM
4. Other types:
A. LADA (Latent Autoimmune Diabetes in
Adults)
B. MODY (maturity-onset diabetes of youth)
C. Secondary Diabetes Mellitus
14. Type 1 diabetes Mellitus /T1DM/
Previously called IDDM or juvenile-onset DM.
Characterized by an acute onset.
Usually strikes children and young adults, although
disease onset can occur at any age.
May account for 5% to 10% of all diagnosed cases of
diabetes.
15. T1DM
Etiology: Most cases of T1D are due to destruction of
the pancreatic ß-cells by T-cells (WBCs concerned
with the immune system).
Clinical symptoms of T1D occur when ~90% of ß-cells
cells have been destroyed.
16.
17. Type 2 diabetes Mellitus
Previously called NIDDM or adult-onset DM.
May account for about 90% to 95% of all diagnosed
cases of diabetes.
Usually seen in older people.
With the onset many people do not have dramatic
symptoms compared to those with T1D.
18. T2DM
Associated with older age, obesity, family history of DM,
history of gestational diabetes, impaired glucose
metabolism, physical inactivity, & race/ethnicity.
In recent years, T2D has been increasingly found among
children and adolescents;
in association with increasing early obesity and
in those who have a family history of T2D, or whose
mothers had diabetes in pregnancy
19. T2DM
• Etiology: it results from either
Insulin resistance, /IR/ (overweight
people), is the decreased response of the
liver and peripheral tissues (muscle, fat) to
insulin,
Inadequate insulin production (lean
people), or
combination of both.
21. Insulin resistance and -cell dysfunction are core
defects of type 2 diabetes
Insulin
resistance
Genetic susceptibility,
obesity, sedentary lifestyle
Type 2 diabetes
IR
-cell
dysfunction
Rhodes CJ & White MF. Eur J Clin Invest 2002; 32 (Suppl. 3):3–13.
22.
23. Difference between T1DM and T2DM
Characteristics Type 1 Diabetes Type 2 Diabetes
Formerly known as IDDM or “Juvenile-onset” DM NIDDM or “adult-onset” DM
Etiology Autoimmune Peripheral resistance
% of diabetic pop/n 5-10% 90-95%
Age of onset Usually < 30 yr + some adults Usually > 40 + some obese children
Onset Rapid Gradual
Pancreatic function Little or no insulin Insulin is: low, normal or high
Family history Generally not strong Strong
Obesity Rare (Normal or underweight) Common (80% are overweight)
Hx of ketoacidosis Often present Rare except in stress
Clinical presentation moderate to severe symptoms:
3Ps, fatigue, wt loss and
ketoacidosis
Mild symptoms: Polyuria and
fatigue. Diagnosed on routine PE
Treatment Insulin, Diet, Exercise Diet ,Exercise, Oral anti-diabetics,
Insulin
24. Gestational Diabetes Mellitus/GDM/
Hyperglycemia diagnosed in some women during
pregnancy.
Ethiology: placental hormones, which causes
insulin resistance.
During pregnancy, GDM requires treatment to
normalize maternal blood glucose levels to avoid
complications in the infant.
25. GDM
After pregnancy, 5% to 10% of women with
gestational diabetes are found to have T2D.
Women who have had gestational diabetes have a
20% to 50% chance of developing T2D in the next
5-10 years.
Screening for diabetes during pregnancy is now
being recommended between the 24th & 28th
weeks of gestation.
26. GDM
• GDM occurs more frequently among :
age 25 years or older;
age 25 years or younger and obese;
family Hx of diabetes in first-degree relatives; or
Member of an ethnic/racial group with a high
prevalence of diabetes (eg, Hispanic American,
Native American, Asian American, African
American).
28. Risk factors of DM
Risk factors that cannot
be changed:
• Family history of diabetes
• High-risk ethnic population
• History of heart disease
• History of GDM or delivery of
babies over 4kg (9 lbs)
• Age ≥ 45 years
Risk factors that can
be changed:
• Overweight (i.e.,
BMI ≥ 27 kg/m2)
• High blood pressure
(≥140/90 mm Hg)
• Physical inactivity
30. CMs of DM
Other symptoms include:
sudden vision changes,
tingling or numbness in hands or feet,
dry skin, skin lesions or wounds that are
slow to heal, and
recurrent infection,
Impotence in men,
The signs of ketoacidosis are:
Nausea, Vomiting,
Pain in the stomach,
Rapid / Acidotic breathing,
High pulse rate,
Abnormal tendency to sleep
31. CMs of DM
• Some patients may be Asymptomatic mainly Type 2
and Gestational diabetes patients
• In the long term,
T1D can severely hurt the blood vessels in vital
organs. This can further cause damage to the
heart, eyes, kidneys or other body organs.
T2D can cause atherosclerosis with blood vessel
narrowing, heart disease and stroke.
32. In the long term,
Diabetes Can Cause Problems in Many Parts of the Body:
Nerves:
• Unusual sensations:
tingling, burning, numbness,
or shooting pain
• Problems with digestion
• Sexual dysfunction
Eyes:
• Blurred vision/ vision
loss
Heart:
• Chest pain
• Shortness of breath
• Fast heart beat
Kidneys:
• Swelling in feet and legs
• Increase in blood pressure
Blood Vessels:
• Slow healing of wounds
35. Laboratory Tests
Hemoglobin A1c is:
glycosylated hemoglobin.
a good indicator of blood glucose control.
gives a % that indicates control over the preceding 2-3
months.
Performed 2 times a year.
A hemoglobin of 6% indicates good control and level >8%
indicates action is needed.
36. Checking BothA1C and Blood Sugar
Is Important
+
A1C
• Reflects average blood sugar
for past few months
• If at goal, check twice
a year*
Blood Sugar
• Provides instant feedback of
current blood sugar level
*If not at goal or if treatment changes,
check more often (eg, every 3 months).
Checking both A1C and blood sugar
helps assess diabetes control
American Diabetes Association. Diabetes Care. 2010;33(suppl 1):S11-S61.
37. Laboratory Tests
2. Urine Test:
Urine Test If blood glucose test strips are not
available
• Ketone
• Renal function
• Glucose
38. Diagnostic Criteria of Diabetes
American Diabetes Association. Diabetes Care. 2004;27(suppl 1):S5-S10
FPG 2-h PPG (OGTT)
126
60
80
100
120
140
160
180
200
Plasma glucose
(mg/dL)
Normal
Diabetes
Mellitus
240
220
Diabetes
Mellitus
Normal
IGT
IGT
Normal
Diabetes
Mellitus
C/RPG
‘Casual’ -that measured at any time of day.
OR
Symptoms
of DM
OR
39. Diagnosis of Pre-diabetes and Diabetes
Category
ADA & AACE
Recommendations
ADA
Recommendations
FPG
(blood sugar in the
morning, before
eating)
2-h PPG (OGTT)
(blood sugar after
meals)* A1C†
No Diabetes
<100 mg/dL
<140 mg/dL <5.7%
Prediabetes 100-125 mg/dL 140-199 mg/dL 5.7%-6.4%
Diabetes ≥126 mg/dL ≥200 mg/dL ≥6.5%
ADA=American Diabetes Association; AACE=American Association of Clinical Endocrinologists; FPG=fasting plasma glucose; PPG=postprandial
glucose.
*2-h plasma glucose on the 75-g oral glucose tolerance test. †ADA only.
1. American Diabetes Association. Diabetes Care. 2010;33(suppl 1):S11-S61. 2. Rodbard HW, et al. Endocr Pract. 2007;13(suppl 1):3-68.
** On 2 separate occasions
A1C ~ average blood sugar for past few months
40. Pre-Diabetes
• Pre-diabetes refers to a state between “normal”
and “diabetes”.
• FBG100 -125mg/dL (higher than normal but not
high enough for diagnosis of diabetes)
• Affects about 41 million people in USA
• Previously referred to as either IFG or IGT
41. Pre-Diabetes
Impaired Fasting Glucose (IFG)
• Defined as a FBG >= to 100 but < 126
Impaired Glucose Tolerance (IGT)
Defined as a plasma blood glucose of >/= to 140 but <
200 after a 2 hr 75gm glucose tolerance test
8-10% of US population have this problem with a 25 %
risk of developing T2DM
42. Values of Diagnosis of DM & Other Hyperglycemias
Category
Venous Plasma*Glucose
concentration, Mmol l-1 (mg dl-1)
Diabetes mellites
Fasting or
2-h post glucose load
≥7.0 (≥126)
≥11.1 (≥200)
Impaired Glucose Tolerance (IGT)
2-h post glucose load (≥140 – <200)
Impaired Fasting Glycaemia (IFG)
Fasting (≥100 - <126 )
43. Screening for DM
• All persons >45 years; repeat Q 3 years
• Additional risk factors: screen at younger age and more frequently
• Women with a history of GDM:
lifelong screening for diabetes or
at least Q3 yrs for prediabetes (up to 7x higher risk than non-GDM)
• GDM test values
Overnight fast, 75g OGTT
Fasting >92 mg/dl
1 h >180 mg/dl
2 h >153 mg/dl
44. • A complete medical evaluation should be performed to
– Classify the diabetes
– Detect presence of diabetes complications
– Review previous treatment, glycemic control in patients with
established diabetes
– Assist in formulating a management plan
– Provide a basis for continuing care
• Perform laboratory tests necessary to evaluate each
patient’s medical condition
Diabetes Care: Initial Evaluation
45. Medical history
• Age and characteristics of onset of diabetes
(e.g., DKA, asymptomatic laboratory finding)
• Eating patterns, physical activity habits,
nutritional status, and weight history; growth and
development in children and adolescents
• Diabetes education history
• Review of previous treatment regimens and
response to therapy (A1C records)
Comprehensive Diabetes Evaluation (1)
46. Current treatment of diabetes, including
medications, meal plan, physical activity patterns,
and results of glucose monitoring and patient’s use
of data (1)
• DKA frequency, severity, and cause
• Hypoglycemic episodes
– Hypoglycemia awareness
– Any severe hypoglycemia: frequency and cause
Comprehensive Diabetes Evaluation (2)
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
47. Current treatment of diabetes, including medications, meal
plan, physical activity patterns, and results of glucose
monitoring and patient’s use of data (2)
• History of diabetes-related complications
– Microvascular: retinopathy, nephropathy, neuropathy
• Sensory neuropathy, including history of foot lesions
• Autonomic neuropathy, including sexual dysfunction and
gastroparesis
– Macrovascular: CHD, cerebrovascular disease,...
– Other: psychosocial problems*, dental disease*
Comprehensive Diabetes Evaluation (3)
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
48. Physical examination
• Height, weight, BMI
• Blood pressure determination
• Fundoscopic examination*
• Thyroid palpation
• Comprehensive foot examination
– Inspection, Palpation of dorsalis pedis and posterior tibial pulses
– Determination of proprioception, vibration, and sensation
Comprehensive Diabetes Evaluation (4)
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
49. Referrals
• Eye exam
• Family planning for women of reproductive age
• Dietitian
• Diabetes self-management education
• Dental examination
• Mental health professional, if needed
Comprehensive Diabetes Evaluation (7)
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
50. Recommendations for Screening
of Diabetes Complications in Stable Patients
Neuropathy
Visual foot inspection
and sensation
testing each year
Retinopathy
Dilated and
complete eye exam—
document each year
Cardiovascular Disease
Nephropathy
Check urine albumin
and serum creatinine
level each year
Peripheral Vascular Disease
Foot exam that includes checking
pedal pulses
each year
American Diabetes Association. Diabetes Care. 2010;33(suppl 1):S11-S61.
Check blood pressure
at each visit and lipids
(cholesterol) each year
53. Type One: Insulin + Diet + Exercise
Type Two:
Diet + exercise
then
Diet + exercise + OHG tablets
then
Diet + exercise + OHG tablets + insulin
54. Treatment Goals
INDEX GOAL
Glycemic control
A1C
Preprandial plasma glucose
Peak post prandial plasma glucose
FBS or
RBS
<7%
90-130 mg/dl
<180 mg/dl
<130 or
<200
Blood pressure <130/80
Lipids
LDL
HDL
Triglycerides
<100mg/dl
>40mg/dl
<150mg/dl
American Diabetes Association Standards of medical care in diabetes. Diabetes Care 30:S4-S36, 2007
55. Healthcare Team
Members of the team include
1. Primary care provider
2. Endocrinologist/ Diabetologist
3. Certified diabetes educator
4. Nutritionist
5. Sub specialists
56. A. Non pharmacologic Therapy
1. Patient or Diabetes Education
2. Healthy eating/Diet
3. Exercise
4. Weight reduction
5. Self-monitoring of blood glucose (SMBG)
57. 1. Diabetes education
• Diabetes educator is healthcare professional (nurse, dietician or
pharmacist)
58. ◦ Education topics include:
• Benefit of weight reduction, diet and regular
exercise
• Self monitoring of blood and urine glucose
• Insulin administration
• Management of hypoglycemia
• Foot & skin care
• Diabetes mgmt. before, during & after exercise
• Risk factor & Complications of diabetes
59. 2. Exercise
• Positive benefits
• Reduces cardiovascular risks, BP, body fat, weight
• Maintenance of muscle mass
• Lowers blood glucose
• Increases insulin sensitivity in T2D
• Time
• 150 min per week ( 3 days)
• In type 2 DM, resistance training
60.
61. Exercise
• Problems
either hypo/ hyperglycemia
• Guidelines to avoid these problems
Monitor blood glucose before, during & after exercise
Delay exercise if:
Blood Glucose > 250 mg/dl and
Ketone bodies are present
If blood Glucose < 100 mg/ dl, ingest carbohydrate before
exercise
62. Exercise
General Precautions for Exercise in Diabetics
• Use proper footwear and, if appropriate, other protective
equipment.
• Avoid exercise in extreme heat or cold.
• Inspect feet daily after exercise.
• Avoid exercise during periods of poor metabolic control.
63. 3. Weight reduction
• Maintain normal BMI of 20 and 25.
• Weight loss:
increase sensitivity to insulin and
may lead to decrease in the demand of
exogenous insulin or the dose of Oral
hypoglycemic agents.
64. Weight reduction
• Benefits of a 10kg weight loss
• Fall of 50% in fasting glucose
• Fall of 10% total cholesterol
• Fall of 15% LDL
• Fall of 30% triglycerides
• Rise of 8% HDL
• Fall of 10 mmHg systolic, 20 mmHg diastolic
SIGN guidelines
66. Diet
Dietary Guidelines:
• Eat a diet low in saturated and total fat.
• Eat a diet moderate in sodium and sugar.
• Eat 5 or more fruits and vegetables a day.
• Choose a diet rich in whole grains.
• Moderate use of alcohol
• Eat at the same time every day.
• Eat about the same amount of carbohydrate with each
meal.
• Avoid simple sugars
67. 5. Self-monitoring of blood glucose (SMBG)
Frequent SMBG enables people with diabetes:
• to adjust the treatment regimen
• to obtain optimal blood glucose control
• for detection and prevention of hypoglycemia and
hyperglycemia
• To normalizing blood glucose levels
• To reduce the risk of long-term diabetic complications.
69. Types of Insulin
• Source
• Animal sources
• Recombinant DNA = human insulin
• Strength
- The number of units/ml
e.g. U-100 , U-20, U-10, U-500, U-40
70. Who should have insulin therapy?
• Newly Diagnosed Type 1
• The Type 2 diabetic on maximum tablets
• The Type 2 diabetic with contraindications to OHA e.g.
renal failure, poor tolerance
• Pregnancy
• Post acute MI
• Acute illness/ infection
Control of blood glucose level essential to minimise
long term complications
71. Types of Insulin
- Rapid-acting insulin
- e.g. Insulin lispro and insulin aspart
- Short-acting insulin
- e.g. Regular insulin
- Intermediate-acting insulin
- e.g. NPH and Lente insulin
- Long-acting insulin
- e.g. Insulin Glargine
- Mixture of insulin can provide glycemic control over extended
period of time
- e.g. Humalin 70/30 (NPH + Regular)
71
72. Types of Insulin
Preparation Onset (hr) Peak (hr) Eff.durat
ion(hr)
Clinical use and rout of
administration
Rapid-acting
• Lispro
• Aspart
<0.25
“
0.5- 1.5
“
3-4
“
Used in ketoacidosis for rapid control
of high sugar & acidosis.
It can be administered IV, IM or SC
Short acting-inhaled
• Regular <0.25 0.5-1.5 4-6
Intermediate-acting
insulin
(NPH or Lente)
2–4 h 6–12 h 16–20 h Used for ambulatory long term control
of sugar level
Given not more than twice a day
Rout of administration is limited to SC
Long acting
• Detemir
• Glargine
“
“
Dual peak
Dual peak
12-20
24
Not available for use in our country
74. Guidelines For Mixing of Insulin
• Mix the different insulin formulations in the syringe
immediately before injection & inject within 2 min after
mixing
• Do not store insulin as mixture
• Regulate the response
• Do not mix insulin glargine or detemir with other insulins
75. Insulin Regimens
75
Example:
1- Morning dose (before breakfast):
Regular + NPH or Lente
2- Before evening meal:
Regular + NPH or Lente
Require strict adherence to the timing of meal and
injections
77. Insulin administration sites
• A. Abdomen;
• B. Lateral and Anterior
Aspects of Upper Arm and
Thigh;
• C. Scapular Area on Back;
and
• D. Upper Ventrodorsal
Gluteal Area.
78. Rotation
• Rotation between different sites (e.g.
abdomen to arm) no longer
recommended
• Choose one site to maintain day to
day consistent absorption
• Rotation within site must occur to
prevent lipoatrophy
• Inject at appropriate angle
(45-90) depending on depth of
subcutaneous tissue
80. Oral HypoglycaemicAgents
• The use of oral medications with diet & exercise can
manage the problem
• But oral hypoglycaemics are NOT insulin & therefore
cannot replace insulin
• Hypoglycaemics help the body to utilise or make
insulin
• Beta cells must make enough insulin to work, otherwise
combination with insulin is necessary.
85. Insulin Therapy in Type 2 Diabetes
• Reasons for use of insulin
• Progression of T2D over time
• People uncontrolled with maximal doses of OHA
therapy (who are insulin resistant)
• Pregnancy (oral therapy contraindicated)
• Patients with organ failure for whom oral therapy is
contraindicated
• Acute illness/surgery in T2D
86. New technologies in treatment of diabetes
Islet cell transplantation
Gene therapy
Foot ulcer-dermograft
Artificial pancreas
90. 1. Hypoglycaemia (Insulin Reactions)
Is abnormally low blood glucose level occurs
when the blood glucose falls to < 50 to 60 mg/dL.
Blood glucose values 45mg/dl are too low for
normal neurological (brain) function.
Even people without diabetes may develop
symptoms of hypoglycemia when the blood
glucose level is <65 mg/dl.
91. Causes
too much insulin/tablets
delayed or missed meal
not enough carbohydrate in a meal
more exercise than usual
Alcohol (especially if not taken with food)
illness
92. Hypoglycaemia
Signs and Symptoms
Initially occur as a result of adrenalin
(autonomic activation) and include:
Trembling
Rapid heart rate
Pounding heart (palpitations)
Sweating
Pallor
Hunger and/or nausea
93. Hypoglycaemia
symptoms of neuroglycopenia
Difficulty in concentrating
Irritability
Blurred or double vision
Difficulty hearing
Slurred speech
Poor judgment and confusion
Dizziness and unsteady gait
Tiredness
Nightmares
Loss of consciousness
Seizures
Death
94. Grading the seriousness of hypoglycemia
1. Mild hypoglycemia
Occurs when the patient recognizes
hypoglycemia and is able to self-treat without
the assistance of others.
Blood glucose values are around <70 mg/dl.
95. Grading the seriousness of hypoglycemia
2. Moderate hypoglycemia
Occurs when the patient is aware of, responds
to, and treats the hypoglycemia, but needs
someone else to assist.
Blood glucose values are again around <70
mg/dl
96. Grading the seriousness of hypoglycemia
3. Severe hypoglycemia
It is defined when the patient:
Either loses consciousness or
has a convulsion (fit) associated with low
blood glucose
97. Management of hypoglycaemia
Immediate treatment.
If the pt is having severe symptoms, give either:
IV glucose (eg 10% glucose drip or 1ml/ kg
of 25% dextrose)
OR
IV, IM or SC glucagon (1 mg for adults).
After an injection of glucagon, the blood glucose would
be expected to rise within 10 -15 mins.
98. Management of hypoglycaemia
If neither glucagon nor IV glucose is available, the
usual recommendation is 15 g of a fast-acting
concentrated source of CHO such as the following,
given orally:
3 or 4 commercially prepared glucose tabs
4 to 6 oz of fruit juice
6 to 10 Life Savers or other hard candies
2 to 3 teaspoons of sugar or honey
99. If no improvement within 5 – 10 minutes, repeat the
high GI food/drink
Once improvement has occurred (feeling better, BGL
rising if testing is available) then follow with a low GI
snack
eg glass of milk
yoghurt
sandwich
piece of fruit
meal if it is due
100. Preventing hypoglycemia
1: Teach the patient often about:
The symptoms of hypoglycemia to recognize it.
Those foods high in both fats and sugar (for
example chocolate, fat-containing milk, peanut
butter)
2: Remind them about what might cause
hypoglycaemia.
101. 2. Diabetic Ketoacidosis
Definition:
DKA is an acute metabolic crisis in pts with DM.
Pathophysiology
DKA is caused by an absence or markedly
inadequate amount of insulin.
This deficit in insulin results in disorders in the
metabolism of CHO, protein, and fat.
102. Insulin Deficiency
Glucose uptake
Proteolysis
Lipolysis
Amino Acids
Glycerol Free Fatty Acids
Gluconeogenesis
Glycogenolysis
Hyperglycemia Ketogenesis
Acidosis
Osmotic diuresis Dehydration
The three main clinical features of DKA are:
Hyperglycemia
Dehydration and electrolyte loss
Acidosis
103. DKA Precipitating Factors
• Failure to take insulin
• Failure to increase
insulin
• Illness/Infection
• Pneumonia
• MI
• Stroke
• Acute stress
• Trauma
• Emotional
• Medical Stress
• Counter regulatory hormones
• Oppose insulin
• Stimulate glucagon release
• Hypovolmemia
• Increases glucagon and
catecholamines
• Decreased renal blood flow
• Decreases glucagon
degradation by the kidney
104. Signs and symptoms
Pathophysiologic effect Clinical features
Elevated blood glucose Elevated blood glucose and urine glucose
Dehydration Sunken eyes, dry mouth, decreased skin
turgour, decreased perfusion
Altered electrolytes Irritability, change in level of
consciousness
Metabolic acidosis (ketosis) Acidotic breathing, nausea, vomiting,
abdominal pain, altered LOC
106. Treatment of DKA
Managing DKA involves the following steps:
1: Correction of shock
2: Correction of dehydration
3: Correction of deficits in electrolytes
4: Correction of hyperglycaemia
5: Correction of acidosis
6: Treatment of infection
7: Treatment of complications (cerebral oedema)
107. Treatment of DKA
• Initial hospital management
• Replace fluid and electrolytes
• IV Insulin therapy
• Glucose administration
• Watch for complications
• Disconnect insulin pump
• Once resolved
• Convert to home insulin regimen
• Prevent recurrence
108. Treatment of DKA Fluids & Electrolytes
• Fluid replacement
• Restores perfusion of the tissues
• Lowers counter regulatory hormones
• Average fluid deficit 3-5 liters
• Initial resuscitation
• 1-2 liters of NS over the first 2 hours
• Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours
• When fluid overload is a concern
• If hypernatremia develops ½ NS can be used
109. Treatment of DKA Fluids & Electrolytes
• Hyperkalemia initially present
• Resolves quickly with insulin drip
• Once urine output is present and K<5.0, add 20-40 meq KCL per
liter.
• Phosphate deficit
• May want to use Kphos
• Bicarbonate not given unless pH <7 or bicarbonate <5
mmol/L
110. Treatment of DKA Insulin Therapy
• IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin
• Follow with hourly regular insulin infusion
• Glucose levels
• Decrease 75-100 mg/dl hour
• Minimize rapid fluid shifts
• Continue IV insulin until urine is free of ketones
111. Treatment of DKA Glucose Adm.
• Supplemental glucose
• Hypoglycemia occurs
• Insulin has restored glucose uptake
• Suppressed glucagon
• Prevents rapid decline in plasma osmolality
• Rapid decrease in insulin could lead to cerebral edema
• Glucose decreases before ketone levels decrease
• Start glucose when plasma glucose <300 mg/dl
113. Complications of DKA
• Infection
• Precipitates DKA
• Fever
• Leukocytosis can be
secondary to acidosis
• Shock
• If not improving with fluids
r/o MI
• Vascular thrombosis
• Severe dehydration
• Cerebral vessels
• Occurs hours to days after
DKA
• Cerebral Edema
• First 24 hours
• Mental status changes
• Tx: Mannitol
• May require intubation
with hyperventilation
• Pulmonary Edema
• Result of aggressive fluid
resuscitation
114. Once DKA Resolved; ...
• Most patients require 0.5-0.6 units/kg/day
• Pubertal or highly insulin resistant patients
• 0.8-1.0 units/kg/day
• Long acting insulin
• 1/2-2/3 daily requirement
• NPH, Lente, Ultralente or Lantus
• Short acting insulin
• 1/3-1/2 given at meals
• Regular, Humalog, Novolog
• Give insulin at least 2 hours prior to weaning insulin
infusion.
115. Prevention of DKA
• Never omit insulin
• Cut long acting in half
• Prevent dehydration and hypoglycemia
• Monitor blood sugars frequently
• Monitor for ketosis
• Provide supplemental fast acting insulin
• Treat underlying triggers
• Maintain contact with medical team
116. 3. Hyperosmolar Nonketotic Syndrome
• Extreme hyperglycemia & dehydration
• Unable to excrete glucose as quickly as it
enters the extracellular space
• When sum of glucose excretion plus
metabolism is << the rate which glucose enters
extracellular space.
117. Hyperosmolar Nonketotic Syndrome
• Extreme hyperglycemia and hyperosmolarity
• High mortality (12-46%)
• At risk
• Older patients with intercurrent illness
• Impaired ability to ingest fluids
• Urine volume falls
• Decreased glucose excretion
• Elevated glucose causes CNS dysfunction and
fluid intake impaired
• No ketones
• Some insulin may be present
• Extreme hyperglycemia inhibits lipolysis
119. HHNS Presentation
• Glucose > 600 mg/dl
• Sodium
• Normal, elevated or low
• Potassium
• Normal or elevated
• Bicarbonate >15 mEq/L
• Osmolality > 320 mOsm/L
120. HHNS Treatment
• Fluid repletion
• NS 2-3 liters rapidly
• Total deficit = 10 liters
• Replete ½ in first 6 hours
• Insulin
• Make sure perfusion is adequate
• Insulin drip 0.1U/kg/hr
• Treat underlying precipitating illness
121. Clinical Errors
• Fluid shift and shock
• Giving insulin without sufficient fluids
• Using hypertonic glucose solutions
• Hyperkalemia
• Premature potassium administration before insulin has begun to act
• Hypokalemia
• Failure to administer potassium once levels falling
• Recurrent ketoacidosis
• Premature discontinuation of insulin and fluids when
ketones still present
• Hypoglycemia
• Insufficient glucose administration
126. Microvascular Complications of Diabetes
1. Retinopathy:
Damage to blood vessels in and around the retina.
It could occur with varying degrees of severity.
Classification of Diabetic retinopathy
1. Background retinopathy: early changes which is often
asymptomatic
2. Maculopathy: which manifests with central vision loss
3. Proliferative retinopathy: asymptomatic unless complicated by
hemorrhage
127. Microvascular Complications of Diabetes
4. Advanced diabetic disease: may cause severe vision loss to the
extent of complete blindness
• Retinal detachment
• Vitreous hemorrhage
Normal ------------- Small hemorrhages --------- Large hemorrhage
128. Microvascular Complications of Diabetes
Management
• Laser therapy
• ASA 100 mg /day may prevents further occlusion
of small capillaries
• Surgery: Viterotomy removes blood clots and
fibrosis that obstruct vision
129. Microvascular Complications of Diabetes
2. Nephropathy:
Glomeruli are damaged in the kidneys.
Results in loss of protein
May lead to kidney failure
Clincal features
• Periorbital edema, pedal edema
• Anemia, Uremia
130. Microvascular Complications of Diabetes
Management
• Tight blood pressure control
• ACE- inhibitors: decreases
progression of renal diseases
• Renal transplantation or
Dialysis in End stage renal
diseases
131. Microvascular Complications of Diabetes
3. Neuropathy
Nerve fibers degenerate
Blood vessels supplying the nerves are ‘grossly diseased’
Symptoms: include
• Burning sensation, numbness
• Diarrhea
• Impotence
• Foot ulcer
132. Microvascular Complications of Diabetes
Neuropathy management
• Symptomatic treatment:
Pain control
Diarrhea control
Treatment of impotence
• Avoidance of neurotoxins -> alcohol, smoking
• Vit. supp(B12, folate)
• Symptomatic treatment
• Should check their feet
daily & take precaution
133. Microvascular Complications of Diabetes
4. Diabetic Foot Ulcer
Underlying mechanism for diabetic foot ulcers
• Neuropathy
Loss of pain sensation exposes to injury
Loss of sweating results dry skin that is susceptible to injury
• Vascular: poor blood supply to the foot causes decreased healing of
wound poor recovery from secondary infections.
• Abnormal Pressure loading: due to neuropathy or anatomical
deformity of the feet. Since the foot is not in a normal anatomic
position it is exposed to abnormal load and pressure sores develop.
134. Microvascular Complications of Diabetes
Foot care: should be essential part of diabetes care
• Put on comfortable shoe
• Check for stones in shoe
• Examine the foot daily to detect problems earlier
• Wash dry and oil the feet
• Take caution during nail cutting
• Treat athletes’ foot or any other foot infection as early as possible
• Remove hard skin
• Do not use hot water to wash the feet
135. Common nursing diagnoses
• Imbalanced nutrition related to imbalances in insulin, food,
and physical activity
• Risk for impaired skin integrity related to immobility and lack
of sensation (caused by neuropathy)
• Deficient knowledge about diabetes self-care skills and for
disease process
• Risk for injury related to sensory alterations
• Risk for delayed surgical recovery
• Body image disturbance RT disease process
136. Nursing intervention
Educate the patient about:
• The disease and the importance of maintaining normal glucose
levels.
• Blood glucose monitoring.
• Diet and food choices, including portion sizes.
• Urge smoking cessation.
• Self-care.
• Acute management.
• Prevention of complications, such as hyperglycemia and
hypoglycemia.
137. Common Nursing intervention
Educate the patient about:
• Exercise.
• Self-injection of insulin (Type I).
• Importance of daily medications.
• Hypoglycemia signs and symptoms and interventions.
• Signs and symptoms and the management of hypoglycemia.
• The management of hyperglycemia.
• Glucagon injection for hypoglycemic events.
