DIABETES MELLITUS

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.
 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.
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.

 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
 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
 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

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

Pancreas • The body’s cells use sugar for

energy
 Glucose

Pancreas

Carbohydrate

Glucose
Insulin

Glucose
and
Insulin
Bloodstream Muscle
cells
What Is Diabetes Mellitus?

In people with diabetes…

The body prevents
the insulin that is
being made from
The pancreas working correctly
The pancreas does not make
OR OR Blood sugar gets
does not make enough insulin
too high and can
any insulin (this gets worse
lead to many
with time)
serious problems
(complications)
 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
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

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.
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.

Pathophysiology of T1DM
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.

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

 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.
IR– reduced response to circulating insulin

Insulin
resistance IR

Liver Muscle Adipose

tissue

 Glucose output  Glucose uptake  Glucose uptake

Hyperglycemia
Insulin resistance and -cell dysfunction are core
defects of type 2 diabetes
Genetic susceptibility,
obesity, sedentary lifestyle

Insulin
resistance IR  b-cell
dysfunction

Type 2 diabetes
Rhodes CJ & White MF. Eur J Clin Invest 2002; 32 (Suppl. 3):3–13.
Pathophysiology of T2DM
 Difference between T1DM and T2DM
Characteristics Type 1 Diabetes
Formerly known as IDDM or “Juvenile-onset” DM
Etiology Autoimmune
% of diabetic pop/n 5-10%
Age of onset Usually < 30 yr + some adults
Onset Rapid
Pancreatic function Little or no insulin
Family history Generally not strong
Obesity Rare (Normal or underweight)
Hx of ketoacidosis Often present
Clinical presentation moderate to severe symptoms:
3Ps, fatigue, wt loss and
ketoacidosis
Treatment Insulin, Diet, Exercise
Type 2 Diabetes
NIDDM or “adult-onset” DM
Peripheral resistance
90-95%
Usually > 40 + some obese children
Gradual
Insulin is: low, normal or high
Strong
Common (80% are overweight)
Rare except in stress
Mild symptoms: Polyuria and
fatigue. Diagnosed on routine PE
Diet ,Exercise, Oral anti-diabetics,
Insulin
 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.
 GDM
 After pregnancy, 5% to 10% of women with

gestational diabetes are found to have T2D.

 Women who have had GDM 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.
 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).
 Secondary DM
Secondary causes of DM include:
 Acromegaly,

 Cushing syndrome,

 Thyrotoxicosis,

 Chronic pancreatitis,

 Cancer

 Drugs
 Risk factors of DM

Risk factors that cannot Risk factors that can

be changed: be changed:

• Family history of diabetes • Overweight (i.e.,

• High-risk ethnic population BMI ≥ 27 kg/m2)

• History of heart disease • High blood pressure

(≥140/90 mm Hg)
• History of GDM or delivery of
• Physical inactivity
babies over 4kg (9 lbs)

• Age ≥ 45 years
Clinical manifestations of DM
 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

 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.
In the long term,
Diabetes Can Cause Problems in Many Parts of the Body:

Heart:
• Chest pain
Eyes: • Shortness of breath
• Blurred vision/ vision
• Fast heart beat
loss

Nerves:
• Unusual sensations:
tingling, burning, numbness,
or shooting pain
• Problems with digestion
• Sexual dysfunction
Kidneys:
• Swelling in feet and legs
• Increase in blood pressure
Blood Vessels:
• Slow healing of wounds
DIAGNOSIS OF DIABETES
 Laboratory Tests

1. Blood Tests
• FBG test: two tests > 126 mg/dL

• OGTT: > 200 mg/dL at 2hrs.

• Glycosylated hemoglobin (HbA1c) test

• FSBS (finger stick blood sugar)

 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.
 Checking Both A1C and Blood Sugar Is Important

A1C Blood Sugar

+
• Reflects average blood sugar • Provides instant feedback of
for past few months current blood sugar level
• If at goal, check twice
a year*

*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.

 Laboratory Tests

2. Urine Test:
Urine Test If blood glucose test strips are not
available

• Ketone
• Renal function
• Glucose
 C/RPG
Diagnostic Criteria of Diabetes
Symptoms
FPG 2-h PPG (OGTT) of DM
Plasma glucose
240
(mg/dL)
220 Diabetes Diabetes
Mellitus Mellitus
200
180 Diabetes
Mellitus IGT
160

140
126 Normal
120
IGT
100
Normal Normal
80 OR OR

60
‘Casual’ -that measured at any time of day.
American Diabetes Association. Diabetes Care. 2004;27(suppl 1):S5-S10
Diagnosis of Pre-diabetes and Diabetes

ADA & AACE ADA

Recommendations Recommendations

Category FPG
2-h PPG (OGTT)
(blood sugar in the
morning, before (blood sugar after
eating) meals)* A1C†

No Diabetes <140 mg/dL <5.7%

<100 mg/dL

Prediabetes 100-125 mg/dL 140-199 mg/dL 5.7%-6.4%

Diabetes ≥126 mg/dL ≥200 mg/dL ≥6.5%

** On 2 separate occasions
A1C ~ average blood sugar for past few months
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.
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

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
 Values of Diagnosis of DM & Other Hyperglycemias

Venous Plasma*Glucose
Category
concentration, Mmol l-1 (mg dl-1)

Diabetes mellites

Fasting or ≥7.0 (≥126)

2-h post glucose load ≥11.1 (≥200)

Impaired Glucose Tolerance (IGT)

2-h post glucose load (≥140 – <200)

Impaired Fasting Glycaemia (IFG)

Fasting (≥100 - <126 )

 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

 1h >180 mg/dl

 2h >153 mg/dl
 Diabetes Care: Initial Evaluation

• 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

Comprehensive Diabetes Evaluation (1)

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 (2)

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
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
Comprehensive Diabetes Evaluation (3)

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*

ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
Comprehensive Diabetes Evaluation (4)

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

ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

Comprehensive Diabetes Evaluation (7)

Referrals
•Eye exam
•Family planning for women of reproductive age
•Dietitian
•Diabetes self-management education
• Dental examination
• Mental health professional, if needed

ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

Recommendations for Screening of Diabetes Complications in
Stable Patients

Cardiovascular Disease
Check blood pressure
Retinopathy at each visit and lipids
Dilated and (cholesterol) each year
complete eye exam—
document each year

Nephropathy
Check urine albumin
and serum creatinine
level each year
Neuropathy
Visual foot inspection
and sensation
testing 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.

Management of DM
Type One: Insulin + Diet + Exercise

Type Two: Diet + exercise

then

Diet + exercise + OHG tablets

then

Diet + exercise + OHG tablets + insulin

 Treatment Goals
INDEX GOAL
Glycemic control

 A1C  <7%

 Preprandial plasma glucose  90-130 mg/dl

 Peak post prandial plasma glucose  <180 mg/dl

 FBS or  <130 or

 RBS  <200

Blood pressure <130/80

Lipids

 LDL  <100mg/dl

 HDL  >40mg/dl

 Triglycerides  <150mg/dl

American Diabetes Association Standards of medical care in diabetes. Diabetes Care 30:S4-S36, 2007
Healthcare Team
Members of the team include
1. Primary care provider
2. Endocrinologist/ Diabetologist
3. Certified diabetes educator
4. Nutritionist
5. Sub specialists
 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)

1. Diabetes education
• Diabetes educator is healthcare professional (nurse, dietician or

pharmacist)
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

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

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
 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.
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.
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
4. Diet
ADA
Food groups:
• CHO- 60%

• Fats - 30%

• Protein - 12-20%
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

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.

Pharmacotherapy :Type 1 DM

The choice of therapy is simple

All patients need Insulin
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

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)
 Types of Insulin
Preparation Onset (hr) Peak (hr) Eff.durati Clinical use and rout of administration
on(hr)
Rapid-acting Used in ketoacidosis for rapid control of
<0.25 0.5- 1.5 3-4 high sugar & acidosis.
• Lispro
It can be administered IV, IM or SC
“ “ “
• Aspart
Short acting-inhaled
<0.25 0.5-1.5 4-6
• Regular
Intermediate-acting 2–4 h 6–12 h 16–20 h Used for ambulatory long term control of
insulin sugar level
Given not more than twice a day
(NPH or Lente) Rout of administration is limited to SC
Long acting Not available for use in our country
“ Dual peak 12-20
• Detemir
“ Dual peak 24
• Glargine
Insulin Combinations
• 75 / 25 - Protamine lispro + Lispro
• 50 / 50 - “ + “
• 70 / 30 - Protamine aspart + Aspart
• 70 / 30 - NPH + Reg. Insulin
• 50 / 50 - “ + “
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

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
INSULIN REGIMENS
 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.
 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
Stepwise Management of T2DM

Insulin ± oral agents

Oral combination

Oral monotherapy

Diet & exercise

Oral Hypoglycaemic Agents

• 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.

Classes of Oral Hypoglycaemic Agents
• Target insulin secretion

• Sulphonylureas (glibenclamide)

• Meglitinides (repaglinide)

• Target insulin resistance

• Biguanides (metformin)

• (Thiazolidinediones) (rosiglitazone)

• Target glucose absorption from intestine

• Alpha glucosidase inhibitors (ascarbase)

 Sites of action of oral antidiabetic agents

-glucosidase Sulfonylureas/
inhibitors meglitinides Biguanides Thiazolidinediones

 Carbohydrate  Insulin  Glucose  Insulin

breakdown/ secretion output resistance
absorption  Insulin resistance

Kobayashi M. Diabetes Obes Metab 1999; 1 (Suppl. 1):S32–S40.

Nattrass M & Bailey CJ. Baillieres Best Pract Res Clin Endocrinol Metab 1999; 13:309–329.
drugs advantages Disadvantages

biguanides Weight loss Lactic acidosis,

GI dysfunctions

Alpha glucosidase inhibitor Reduce postprandial Liver & GI dysfunctions

glycaemia

DPP4 inhibitors No hypoglcaemia ---

sulfonylureas Lowers fasting blood Weight gain,

glucose hypoglyacemia

Nonsulfonylureas Shorter onset of action Hypoglycaemia

Lowers postprandial
glycaemia

thiazolidinediones Lower an insulin CHF, weight gain,

requirements fractures
As Type 2 Diabetes Progresses, Insulin Therapy is
Needed

Hypothetical Model

Oral therapy Insulin Insulin

initiation initiation intensification

Disease Progression
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
New technologies in treatment of diabetes

Islet cell transplantation

Gene therapy

Foot ulcer-dermograft

Artificial pancreas
Complications of DM
 Acute Complications

1. Diabetic Ketoacidosis (DKA)

2. Hyperglycemic Hyperosmolar

Nonketotic Syndrome (HHNS)

3. Hypoglycemia
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.
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
 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
 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

 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.
 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
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
 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.
 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
 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
 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.
 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.
The three main clinical features of DKA are:
 Hyperglycemia
 Dehydration and electrolyte loss
 Acidosis
Insulin Deficiency
Glucose uptake Lipolysis
Proteolysis

Glycerol Free Fatty Acids

Amino Acids

Gluconeogenesis
Hyperglycemia Glycogenolysis Ketogenesis

Osmotic diuresis Dehydration Acidosis

DKA Precipitating Factors
• Failure to take insulin • Medical Stress
• Failure to increase • Counter regulatory hormones
• Oppose insulin
insulin • Stimulate glucagon release
• Illness/Infection • Hypovolmemia
• Pneumonia • Increases glucagon and
• MI catecholamines
• Stroke • Decreased renal blood flow
• Acute stress • Decreases glucagon
degradation by the kidney
• Trauma
• Emotional
 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
Lab Findings
• RBS: Hyperglycemia

• Anion gap acidosis

 Serum K+ level
 Serum Na+ level
• Urine and serum ketones

• Hyperosmolarity

• ABG analysis: can diagnose metabolic acidosis

• Bicarbonate <15 mEq/L

• pH <7.3
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)
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
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

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
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

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

Insulin-Glucose Infusion for DKA
Blood glucose Insulin Infusion D5W Infusion
<70 0.5 units/hr 150 cc/hr
70-100 1.0 125
101-150 2.0 100
151-200 3.0 100
201-250 4.0 75
251-300 6.0 50
301-350 8.0 0
351-400 10.0 0
401-450 12.0 0
451-500 15.0 0
>500 20.0 0
Complications of DKA
• Infection • Cerebral Edema
• Precipitates DKA • First 24 hours
• Fever
• Leukocytosis can be
• Mental status changes
secondary to acidosis • Tx: Mannitol
• Shock • May require intubation
• If not improving with fluids with hyperventilation
r/o MI • Pulmonary Edema
• Vascular thrombosis • Result of aggressive fluid
resuscitation
• Severe dehydration
• Cerebral vessels
• Occurs hours to days after
DKA
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.

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

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.
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
HHNS Presentation
• Extreme dehydration

• Supine or orthostatic hypotension

• Confusion coma
• Neurological findings

• Seizures

• Hemiparesis

• Hyperreflexia
HHNS Presentation
• Glucose > 600 mg/dl
• Sodium
• Normal, elevated or low
• Potassium
• Normal or elevated
• Bicarbonate >15 mEq/L
• Osmolality > 320 mOsm/L
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

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
Long-Term Complications of DM

• Macrovascular complications
• Cardiovascular disease (heart attack)

• Cerebrovascular disease (strokes)

• Microvascular complications
• Blindness (retinal proliferation, macular degeneration)

• Amputations

• Diabetic neuropathy (diffuse, generalized, or focal)

• Erectile dysfunction
 Risk factors and complications

Microvascular disease Macrovascular disease

Eyes Ischaemic heart disease
Feet Strokes
Kidneys
Nerves Peripheral vascular
disease

Hyperglycaemia Hypertension
Coagulopathy
Dyslipidaemia
Smoking
 Biology of Macrovascular Injury
Metabolic injury to large vessels

Heart Brain Extremities

CAD Cerebrovascular
Peripheral vascular
– MI disease
disease
– CHF – Ulceration
– Gangrene
– Amputation
 Biology of Microvascular Injury

Hyperglycemia

Eye Kidney Nerves

Retinopathy Nephropathy Neuropathy

- Cataract – Microalbuminuria – Peripheral
- Glaucoma – Gross albuminuria – Autonomic

Blindness Kidney failure Amputation

Death and/or disability

 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
 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
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

 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
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
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
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

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.

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

 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

 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

 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.

 Reading Assignment

• Methods of insulin administration?

• How to calculate the dose of insulin needed?