DM

• Gilbert & Pellan

 Diabetes Mellitus

• Diabetes Mellitus (DM), commonly referred to as diabetes, is a group of

Metabolic disorders in which there are high blood sugar levels over a prolonged
Period.
• Insulin is the hormone secreted by β-cells of the pancreas; it helps to
Incorporate glucose into cells for metabolism.
• In insulin deficiency, blood glucose level rises leading to excretion of sugar in the
urine called Glycosuria
• Glucose loss is accompanied by increased loss of water in the urine causing
Polyuria; hence Hyperglycemia, Glycosuria and Polyuria are the three cardinal
Clinical features of diabetes mellitus.
 Cont'
Diabetes mellitus is the most common prevalent endocrine disorder; it affects
nearly 2% of the world population
• Diabetes can be primary or secondary or idiopathic.
Aetiological Classification of Diabetes Mellitus;
Primary Diabetes Mellitus (Idiopathic):
1. Type 1 Diabetes (IDDM): β-cell destruction, usually leading to insulin Deficiency.
2. Type 2 Diabetes (NIDDM): May range from insulin resistance with relative
Insulin deficiency to a predominantly insulin secretory defect with insulin
Resistance.
 Cont’

Secondary Diabetes Mellitus: Due to Other Underlying Diseases/Conditions:

1. Diseases of the pancreas, such as pancreatitis, pancreatic cancer, cystic
Fibrosis, or hemochromatosis, can destroy the gland leading to reduced Insulin
production.
2. Endocrine disorders (insulin antagonism) like Cushing’s syndrome, Acromegaly,
and hyperthyroidism.
3. Drug-induced (lactogenic) diabetes, e.g., corticosteroids, phenytoin, Thiazide
diuretics therapy.
4. Genetic/chromosomal defects, e.g., Down’s syndrome.
 Cont…;

5. Liver diseases like hepatitis, cirrhosis, are associated with glucose

Intolerance.
6. Gestational Diabetes Mellitus (Pregnancy-induced Diabetes Mellitus):Occurs
during pregnancy and may resolve after delivery.
 Predisposing Causes of Primary Diabetes Mellitus:

1. Age: 80% of cases occur after 50 years. DM is commonly a disease of middle-aged and
elderly people.
2. 2. Sex: Young males are more affected than females. In middle age, females are more
affected.
3. Heredity: DM follows the family line in occurrence. 5% of patients have a familial history.
4. Autoimmunity: The body produces cells against insulin production.
5. Infections: Viral infections and staphylococci are associated with the causation of IDDM.
6. Obesity: The majority of NIDDM cases are obese.
7. Lifestyle Factors: Overeating with underactivity is associated with a high risk of incidence.
 Other Predisposing Factors:

● Sedentary lifestyle.
● Poor dietary habits.
● Metabolic syndrome.
● Hypertension.
● Ethnicity (some ethnic groups are more predisposed).
● Gestational diabetes (increases the risk later in life).
● Certain medications (e.g., glucocorticoids).
● Previous gestational diabetes.
 Pathophysiology of Diabetes:

Diabetes results from two main issues: the pancreas not making enough insulin Or
the body’s cells not responding properly to the insulin produced.
1.Insufficient Insulin: Pancreas fails to produce adequate insulin.
● Impaired insulin function disrupts blood sugar regulation, leading to
Hyperglycemia (elevated blood glucose levels).
2.Consequences of Hyperglycemia: Excess glucose is expelled through urine,
causing glycosuria.
• High glucose in the glomerular filtrate attracts water, resulting in polyuria
(excessive urination) and Loss of water triggers an intense feeling of thirst
(polydipsia).
.
 Cont’.

3. Cellular Deprivation and Compensatory Responses:

● Despite high blood glucose, cells remain deprived
● Body responds with increased appetite, leading to overeating
(polyphagia), worsening the condition.
4. Gluconeogenesis:
● Body initiates gluconeogenesis to create glucose from proteins and fats.
5. Ketone Body Accumulation:
● Excessive glucose from fats produces abundant ketone bodies, causing
ketonemia (increased ketones in blood).
 Cont’.

6. Acidosis and Respiratory Response:

● Accumulated ketones reduce blood pH, leading to acidosis.
● Body responds with rapid and deep breathing (Kussmaul respirations) to
decrease acidity.
7. Potential Life-Threatening Complication:
● Prolonged acidic state may lead to ketoacidosis, a severe medical/pediatric
emergency.
 Clinical Features of Diabetes Mellitus

In mild cases, there may be no obvious signs, and the condition is detected
accidentally during routine examination. However, in severe cases, especially in
young children and young adults, pronounced symptoms may include:
1. Polyuria Due to osmotic activity preventing water reabsorption in the renal
tubule.
2. Polydipsia (increased thirst) follows polyuria, leading to dehydration due to
constant loss of fluids and electrolytes.
3. Polyphagia with Weight Loss: Weight loss occurs due to the breakdown of fat
and proteins caused by cellular glucose deficiency.
 Cont’.

4. Weakness or Fatigue/Lassitude: Resulting from cells not receiving Enough

glucose
5. Nocturnal Enuresis: Due to renal glucose exceeding the threshold.
Nocturnal enuresis is when there is involuntary urination at night while asleep.
6. Glycosuria: This is when there is excessive amounts of glucose in urine.
7. Peripheral Neuropathy/Paresthesia: Nerve damage caused by
Chronically high blood sugar, leading to loss of sensation and numbness in;
The legs. In severe cases, symptoms include digestive issues, bladder problems,
and difficulty controlling heart rate. Paresthesia is a symptom of neuropathy, since
neuropathy is an umbrella term for any disease that affects the nerves.
 Cont’.

8. Vulvovaginitis: Irritation of the genitalia caused by the local deposition of

glucose. May be severe and disturb sleep.
9. Ketoacidosis: A serious complication involving excess blood acids (ketones).
Symptoms include blurry vision, headache, fatigue, slow healing of cuts, and itchy
skin.
10. Diabetic dermadromes. Skin rashes associated with diabetes with cutaneous
eruptions in patients with long standing diabetic disease.
11. Vision Changes: Prolonged high blood glucose can cause glucose absorption
in the lens of the eye, leading to changes in its shape and resulting in vision
changes.
 Comparison of type 1 and 2 diabetes
Type 1 Type 2

● Sudden ● Gradual
● Mostly children ● Mostly adults
● Thin or normal ● Often obese
● Ketoacidosis common ● Rare
● Antibodies usually present ● Absent
● Insulin low or absent totally
● Normal, decreased or increased
● In identical twins is
Approximately 50% ● Is approximately 90%
● Prevalence approximately 10% ● Prevalence approximately 90%
 Types of Diabetes Mellitus

There are three main types of diabetes mellitus and one unspecified;
Type 1 Diabetes Mellitus
Type 1 Diabetes Mellitus (T1DM) is marked by the pancreas’s failure to
produce sufficient insulin, a vital hormone in blood sugar regulation.
Formerly known as “insulin-dependent diabetes mellitus” (IDDM) or “juvenile
diabetes,” Its cause is unknown.
 Some of It’s classifications

• Insulin Deficiency and Beta Cell Loss: T1DM is characterized by the

loss of insulin-producing beta cells in the pancreatic islets. This leads to
adeficiency in insulin, disrupting the body’s ability to regulate blood sugar
• Immune-Mediated or Idiopathic Classification: T1DM can be classified
as immune-mediated or idiopathic. The majority of cases involve Immune-
mediated processes, where autoimmune attacks by T cells lead to beta
cell loss. Onset can occur in children or adults, though historically Labeled
“juvenile diabetes” due to its prevalence in children.
 Cont’
• Associated Complications: Complications may include impaired response to
low blood sugar, infections, gastroparesis (causing erratic Carbohydrate
absorption), and endocrinopathies like Addison’s disease.
• Genetic and Environmental Factors: T1DM has a genetic component, With
specific HLA genotypes influencing susceptibility.
• Environmental Triggers, such as viral infections or dietary factors (e.g., gliadin in
gluten) Can prompt diabetes onset, especially in genetically predispose
Individuals.
• Management and Risks: Insulin and a comprehensive diet are crucial for
managing T1DM. Patients face an increased risk of coma if concurrent infections
like pyelonephritis or gastroenteritis are not promptly addressed.
 Type 2 Diabetes Mellitus

• The pathophysiology of type 2 diabetes mellitus is characterized by peripheral

Insulin resistance, impaired regulation of hepatic glucose production, and
Declining β-cell function, eventually leading to β –cell failure
• Reduced insulin secretion and absorption leads to high glucose content in the
Blood.
Some of It’s classifications
Insulin Resistance and Reduced Secretion: T2DM is characterized by Insulin
resistance, where body tissues have a diminished response to Insulin. This
resistance is sometimes accompanied by a relative reduction In insulin secretion.
• Insulin Receptor Dysfunction: The defective responsiveness of body tissues to
insulin involves the insulin receptor, though, specific defects remain unknown.
Diabetes cases with known defects are categorized Separately.
● Prevalence and Early Stage Abnormality: T2DM constitutes the majority,
accounting for up to 90% of all diabetes mellitus cases. In the early stage, the
primary abnormality is reduced insulin sensitivity, reversible by measures and
medications improving insulin sensitivity or reducing liver glucose production.
●Contributing Factors: Lifestyle factors, genetics, obesity (BMI > 30), lack of
physical activity, poor diet, stress, and urbanization contribute to T2DM.
 Cont’
Insulin resistance, overeating, inactivity, and obesity play roles in the etiology.
● Dietary Management and Weight Loss: Management often involves adherence
to a low-energy diet to facilitate weight loss. Lifestyle modifications, including
dietary changes, exercise, and stress reduction, Play roles in controlling T2DM.
 Gestational Diabetes

Gestational diabetes mellitus (GDM) resembles type 2 DM in several aspects,

Involving a combination of relatively inadequate insulin secretion and Responsiveness. It
occurs in about 2–10% of all pregnancies and may improve or Disappear after delivery.
● Occurrence and Post-Delivery Transition: GDM shares similarities with Type 2 DM,
involving inadequate insulin secretion and responsiveness. It affects about 2–10% of
pregnancies and may improve or vanish after childbirth.
• Post-Pregnancy Diabetes Risk: Post-pregnancy, 5–10% of women with a History of
gestational diabetes develop diabetes mellitus, often type 2.
• Temporary Nature and Health Impacts : While temporary during Pregnancy,
untreated GDM poses risks to both the mother and the fetus.
 Cont’

• Raised plasma glucose levels during pregnancy may lead to the birth of babies with
increased birth weight, skeletal muscle malformations, and Increased mortality risk.
• Risks associated with untreated GDM in Newborns include; macrosomia (high birth
weight), congenital heart and Central nervous system abnormalities, and skeletal muscle
malformations.
• Elevated insulin levels in the fetal blood may hinder surfactant production,Leading to
respiratory distress syndrome.
• Complications and Perinatal Risks: Complications may arise, such as high blood
bilirubin levels due to red blood cell destruction. Severe cases can result in perinatal
death, often attributed to poor placental perfusion caused by vascular impairment,
leading to macrosomia and shoulder Dystocia.
 Cont’

• Management and Treatment: Gestational diabetes is fully treatable, but

requires careful medical supervision throughout the pregnancy.
• Management may include dietary changes, blood glucose monitoring,and in
some cases, insulin may be required.
 Diagnosis of Diabetes Mellitus:
History taking.
• Symptoms; Polyuria, polydipsia, polyphagia, weight loss, fatigue.
• Medical history; previous diagnosis of DM, family history, HTN, dyslipidemia.
• Medication history: steroids [predinislone], certain antidepressants [SSRIs like
fluoxetine] and antipsychotics [CPZ and haloperidol].
Physical examination.
• BMI, BP, Fundoscopic examination [for retinal changes], foot exam [for
neuropathy and ulcers]
 invx

Diabetes mellitus, characterized by recurrent or persistent high blood sugar, is

diagnosed by demonstrating any one of the following criteria:
1. Fasting Plasma Glucose Level:
Normal ranges: 3.9 – 5.6 mmol/l. (70.2-100mg/dl)
Prediabetic ranges: 5.6 – 6.9mmo/l ( 100- 125mg/dl)
Diabetic ranges: ≥ 7.0 mmol/l (126 mg/dl)
According to the current definition, two fasting glucose measurements above 126
mg/dl (7.0 mmol/l) are considered diagnostic for diabetes mellitus.
 Cont….;
• 2. Plasma Glucose Two Hours After Oral Glucose Load:
• Normal range. <7.8 mmol/l (140mg/dl).
• Pre diabetes: 7.8-11.0 mmol/l (140 – 199mg/dl)
diabetes: ≥ 11.1 mmol/l (200Mg/dl) two hours after a 75 g oral glucose
load, as in a glucose tolerance test. People with plasma glucose at or
above 7.8 mmol/l (140 mg/dl) but not exceeding 11.1 mmol/l (200
mg/dl) two hours after the oral glucose load are considered to have
impaired glucose tolerance.
 Cont’.

3. Symptoms of High Blood Sugar and Casual Plasma Glucose: ≥ 11.1 mmol/l
(200 mg/dl).Presence of symptoms along with casual plasma glucose above 11.1
mmol/l (200 mg/dl) indicates diabetes
4. HbA1c >6.5% [type 1 and 2 DM.
Note:
● According to the World Health Organization, individuals with fasting Glucose
levels between 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have
impaired fasting glucose.
● Glycated hemoglobin is considered superior to fasting glucose in determining
cardiovascular disease risks and risks of death from any cause.
 4. Other Diagnostic Investigations for Diabetes Mellitus:

Glucosuria:
● Method: Detect glucose in urine using a test strip (uristicks).
● Purpose: To identify the presence of glucose in the urine, indicating Possible
diabetes.
Ketonuria:
● Method: Detect ketone bodies in urine.
 Nursing Concerns
• Polyuria
• Polydypisia
• Polyphagia
• Fluctuating glucose levels
• Anxiety
• Knowledge deficient about DM.
• Electrolyte imbalance
 Nursing Diagnoses

• Infective health self-management related to lack of knowledge about diabetes

management evidenced by frequent hyperglycemia of FBS & RBS above 7.0 &
11.1 mmol/dl and patient verbalizing difficulty in adhering to a diabetes
management plan.
• Inadequate fluid volume related to polyuria as evidenced by patient verbalizing
frequent micturation.
• Risk for unstable blood glucose levels related to lack of knowledge about
diabetes management.
• Risk of infection related to persistent high glucose levels.
 Nursing Interventions
1) Infective health self management.
• Assess and Provide education on DM pathophysiology ,
symptom identification & Rx plan adherence.
• Teach self monitoring of blood glucose.
2).Inadequet fluid volume .
Monitor daily weight , intake and output.
Assess for vital signs and signs of dehyration.
Encourage oral fluid intake
 Diabetic Emergencies

Hypoglycemia:
Low blood sugar (hypoglycemia) is a common occurrence in individuals with Type 1
and type 2 Diabetes Mellitus (DM). While most cases are mild and not deemed
medical emergencies, the effects can range from mild to severe.
Diabetic Ketoacidosis (DKA):
This a severe acute complication of Diabetes mellitus where the body produces
excess blood acids (ketones), posing a Significant risk of death and morbidity,
particularly with delayed treatment. The Prognosis is notably worse in extreme
age groups, with mortality rates ranging from 5-10%, but advancements in
therapy have reduced mortality to over 2%.
 Pathophysiology:

DKA arises from insulin deficiency and the action of counter-regulatory hormones,
leading to hyperglycemia and glycosuria. The absence of insulin forces the body
to use fats instead of glucose, resulting in ketosis and metabolic acidosis.
Vomiting, insensible water losses, and electrolyte abnormalities further exacerbate
the condition, with dehydration potentially leading to acute renal failure.
Precipitating Factors:
● New onset of type 1 DM: 25%
● Infections (most common): 40%
● Drugs (e.g., Steroids, Thiazides, Dobutamine & Turbutaline)
● Omission of Insulin: 20%
 Diagnosis

Suspect DKA in a diabetic patient presenting with:

● Dehydration
● Acidotic (Kussmaul’s) breathing with a fruity smell (acetone)
● Abdominal pain &\or distension
● Vomiting
● Altered mental status ranging from disorientation to coma.
Diagnostic Criteria:
● Hyperglycemia: > 300 mg/dl & glucosuria
● Ketonemia and ketonuria
● Metabolic acidosis: pH < 7.25, serum bicarbonate < 15 mmol/l, Anion gap >10.
 Treatment Principles:

● Careful fluid replacement.

● Correction of acidosis & hyperglycemia via Insulin administration.
● Correction of electrolyte imbalances.
● Treatment of underlying causes.
● Monitoring for complications.
Fluid Replacement:
● Hypovolemic shock: Administer 0.9% saline, Ringer’s lactate or
Plasma expander.
● Dehydration without shock: Administer 0.9% Saline, adjusting to
avoid rapid shifts in serum.
 Insulin Therapy:
● Start infusing regular insulin at 0.1U/kg/hour.
● Adjust fluid composition as glucose decreases.
● Continue insulin infusion until acidosis is cleared.
Correction of Electrolyte Balance:
● Administer potassium supplementation to IV fluid.
● Adjust based on serum potassium levels.
 Cont’.

Monitoring:
● Use a flow chart for fluid balance & Lab measures.
● Measure serum glucose and electrolytes regularly.
● Neurological & mental status examination.
COMPLICATIONS
● Cerebral Edema
● Intracranial thrombosis or infarction.
● Acute tubular necrosis.
● Peripheral edema.
 Treatment and Nursing Management of Diabetes mellitus

Aims of mgt
This management is dependent on the type of diabetes mellitus and aims are to:
● Control diabetes and prevent complication
● To bring down blood sugar levels
● To help the patient comply to treatment
Management (non-pharmacological)
● Control traditional Cardiovascular risk factors such as smoking, taking alcohol,
management of dyslipidemia, intensive BP control and antiplatelet therapy.
● Complication monitoring i.e. annual eye examination, annual Microalbuminuria detection,
feet examination, BP monitoring and lipid Profile.
 Cont’.

● Patient’s education: Teach the patient on self-monitoring of blood

Glucose using glucometer and/or uristicks, moving with a diabetic card,
Keeping sugary food in the bag, method of insulin administration and
Consequences neglecting treatment
● Patients should also be taught to prevent themselves from injury.
● Diet
– For type 1 the goal is to regulate insulin administration with a balanced diet
– In most cases, high carbohydrate, low fat and low cholesterol diet is appropriate
– Diet and insulin must be fixed to avoid fluctuation in blood glucose.
 Cont’.

Vitamins and minerals must be supplemented

– Small frequent meals should be served to avoid peaks of hyperglycemia and no meal
should be delayed. Snacks should be added to the main meals i.e in the middle of morning, early
afternoon and before bed time.
– Food should be palatable with high fibre food like legumes, burley, oat.
Low salt in diet is advised (6g per day)
– Avoid fried food, sweetened beverage, bakery products, honey and fine sugar.
● Type 2 DM patients need caloric restriction: Diet restriction must be
Combined with life style modification
 Cont’.

●Artificial sweeteners: e.g. Aspartame, saccharin, sucralose, and Acesulfame are safe for use
in all people with diabetes
●Nutritive sweeteners: e.g. fructose and sorbitol, there use is increasing.Though they cause
acute diarrhea in some patient.
● Activity: Exercise improves insulin resistance and achieving glycemic Control. Exercise
should start slowly for patients with limited activity.
Patients with Cardiovascular diseases should be evaluated before starting any exercise
– Avoid exercises on an empty stomach, when blood sugar levels are low or high.
– Heavy exercises like mental lifting are dangerous because it triggers hypoglycemia.
 Treatment targets

- Fasting blood sugar <7 mmol/l

- Postprandial sugar <10 mmol/l
- HbA1c <7% (7.5 % for elderly)
Elderly people are at higher risk of hypoglycaemia. Monitor carefully,
and do not aim at very strict control of blood sugar.
 Pharmacological therapy of diabetes mellitus

• Insulin (Type 1 and Type 2 DM)

• Sulfonylurea e.g glibenclamide (Type 2 DM)
• Biguanides e.g metformin (Type 2 DM)
• Meglitinides (Type 2 DM)
• Thiazolidinediones Glitazones e.g Competact(Pioglitazone + Metformin) (Type 2
DM)
• Alpha-Glucosidase inhibitors e.g acarbose (Precose) (Type 2 DM)
 Management of Type 1 Diabetes

• Insulin SC: 0.6 -1.5 IU/kg/day HC4 Children <5 years: start with 0.5 IU/Kg/day,
and refer to a paediatrician.
• Preferably, a combination of intermediate and short acting insulin should be
used, in the following regimens e.g., Pre-meals short acting insulin (e.g. actrapid)
or Rapid acting insulin analogue (e.g Aspart) and evening intermediate acting
insulin (e.g. Insulatard) or long acting insulin analogues (e.g Glargine). The
evening dose should be 40-50% of the daily dose (basal-bolus therapy)
 Complications of diabetes mellitus
● Cardiomyopathy: The major long-term complications relate to damage to blood
vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of
deaths in diabetics are due to coronary artery disease.Other “macrovascular”
diseases are stroke, and peripheral artery disease.
● Retinopathy: The primary complications of diabetes due to damage in small
blood vessels include damage to the eyes, kidneys, and nerves.Damage to the
eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in
the retina of the eye, and can result in gradual Vision loss and blindness.
Diabetes also increases the risk of having;Glaucoma, cataracts, and other eye
problems. It is recommended that Diabetics visit an eye doctor once a year.
 Cont’.

● Nephropathy: Damage to the kidneys, known as diabetic nephropathy, can lead

to tissue scarring, urine protein loss, and eventually chronic kidney disease,
sometimes requiring dialysis or kidney transplantation.
● Neuropathy: Damage to the nerves of the body, known as diabetic neuropathy,
is the most common complication of diabetes. The symptoms can include
numbness, tingling, pain, and altered pain sensation, which Can lead to damage to
the skin.
● Diabetic foot: Diabetes-related foot problems (such as diabetic foot ulcers) may
occur, and can be difficult to treat, occasionally requiring amputation. Additionally,
proximal diabetic neuropathy causes painful
 Cont’.
Muscle atrophy and weakness.
● Falls: There is a link between cognitive deficit and diabetes. Compared to those
without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of
decline in cognitive function. Being diabetic, especially when on insulin, increases
the risk of falls in older people.
Other Complications:
● Eye; Retinopathy leading to impaired vision, premature cataract, recurrent styes
● Urinary system; renal failure, nephritic syndrome and pyelonephritis due to
diabetes nephropathy.
 Cont’.

● Genital tract; erectile dysfunction, loss of libido in men and menstrua

Irregularities, recurrent abortion, purulent vaginitis, infertility in females
● Nervous system; Neuropathy resulting in tingling and numbness in the feet,
stroke.
● CVS; Myocardial infarction, peripheral gangrene, hypertension
● Skin; Staphylococcal skin infections e.g boils carbuncles, non healing ulcer and
mucocutaneous candidiasis.
● Respiratory system; pneumonia, lung abscess and tuberculosis
 PREVENTIVE MEASURES.
• Emphasize a diet rich in vegetables, fruits, whole grains and proteins,
minimize processed foods, refined sugar & fats.
• Maintain a health body weight, monitor weight, BMI.
• Regular physical activity.
• Regular glucose monitoring to detect early signs.
• Blood pressure and cholesterol check up.
• Stress management.
• smoking cessation, avoid second-hand and smoke.
• Limit alcohol intake.
• Ensure at least 7-8 hours of sleep per night.
• THANKS