Diabetes

1. GENERAL MEDICINE
TOPIC: DIABETES
DIPLOMA IN ORTHOPEADIC AND
TRAUMA MEDICINE
BY: K. Koech

2. LEARNING OBJECTIVES
By the end of the unit, the learner should be able to;
i. Define Diabetes
ii. State the Classification of Diabetes
iii. Describe the clinical features of Diabetes
iv. Describe the management of Diabetes
v. Describe the complications of Diabetes

3. INTRODUCTION
Diabetes mellitus, commonly referred to as
diabetes, is a chronic metabolic disorder
characterized by elevated levels of blood
glucose (sugar) due to problems with insulin
production, insulin action, or both.
 Insulin is a hormone produced by the pancreas
that helps regulate blood sugar levels and allows
cells to utilize glucose for energy.

4. DEFINITION
Diabetes mellitus (DM) is a group of diseases
characterized by high levels of blood glucose
resulting from defects in insulin production, insulin
action, or both.
The term diabetes mellitus describes a metabolic
disorder of multiple aetiology characterized by;

5. DEFINITION CONT,D
Chronic hyperglycaemia with disturbances of carbohydrate, fat
and protein metabolism resulting from defects in insulin
secretion, insulin action, or both.

6. TERMINOLOGIES CONT’D
Random is defined as without regard to time since the last meal
Fasting is defined as no caloric intake for the last 8 hrs.
Oral glucose tolerance test: blood glucose is measured after ingestion of 75g
anhydrous of glucose dissolved in water.
The patient is said to have impaired glucose tolerance (IGT) if the fasting plasma
glucose is >110 mg/dl and <126 mg/dl.

7. CLASSIFICATION OF DM
i.Type I or Insulin dependent diabetes mellitus (IDDM)
ii.Type II or Non-insulin dependent diabetes mellitus
(NIDDM)
iii. Gestational diabetes (GDM)
iv.Secondary Diabetes mellitus

8. TYPE 1 DM
Type 1 DM is due to β-cell destruction, with absolute
deficiency of insulin

9. TYPE 1 DM -CAUSES
i. Genetic predisposition,
ii.Viral and autoimmune attacks on the beta islet
cells (antibodies are directed against normal tissues
of the body, responding to these tissues as if they
are foreign)
iii. It may be immune mediated or idiopathic

10. TYPE 1 DM-CLINICAL PRESENTATION
The classic symptoms of;
a)Polyuria,
b)Polydipsia,
c)Polyphagia,
d) Weight loss and malaise.
Untreated, these symptoms progress to ketoacidosis within a month.

11. TYPE 1DM CONT’D
Type 1 DM (formerly known as insulin-dependent
DM)
Accounts for about 10%
Usually occurs in childhood or early adulthood (age
less than 30)
 Patients are usually non obese.

12. TYPE 1 DM CONT’D
They require exogenous insulin for survival
and develop ketoacidosis when patients are not
on adequate insulin therapy.
Oral hypoglycemic agents will not be effective to
lower the blood glucose level

13. TYPE 11 DM
In Type 2 DM insulin resistance plays a central role in the pathogenesis.
This typically develops when the body's cells become resistant to the effects
of insulin, and the pancreas can't produce enough insulin to compensate.
It is often associated with obesity and lifestyle factors..

14. TYPE 11 DM CONT,D
 Initially there is hyper-secretion of insulin by β-cells, to overcome the
insulin resistance.
 But later on β-cells fail to respond to the level of resistance. Then β-cell
number is decreased
The combination of impaired secretory ability & unresponsiveness to
available insulin, lack of physical exercise and obesity results in
NIDDM.

15. CHARACTERISTICS OF TYPE 11 DM
Usually occurs in people >40 years of age.
Accounts for 80-90% of the total cases of diabetes.
 Most (about 60%) of the patients are obese.
Type 2 DM occurs with intact beta islet cell function but
there is peripheral tissue resistance to insulin.

16. CHARACTERISTICS OF TYPE 11 DM CONT,D
There may be some decrease in insulin production or a
hyper insulin state.
These patients are not prone to develop ketoacidosis but
may develop it under conditions of stress

17. TYPE 11 DM CONT’D
Patients do not require insulin for survival at least in the earlier
phase of diagnosis.
 The blood sugar level can be corrected by oral hypoglycemic
agents

18. TYPE 11 DM CONT’D
Classic symptoms of polyuria, polydipsia and polyphagia, or less
specific symptoms- slow healing infections of the skin, urinary tract &
blurred vision may be present.
Often diabetes is first diagnosed through routine physical examination
& laboratory tests.

19. GESTATIONAL DIABETES (GDM)
 Its due to presence of human placental lactogen which
antagonizes the effects of insulin.
There is increased risk of developing NIDDM in later life hence
should avoid obesity

20. SECONDARY DIABETES
oSecondary diabetes- Secondary DM develops when the
pancreatic tissue responsible for the production of insulin is
absent because it is destroyed by disease such as; Trauma,
Chronic Pancreatitis,
oSecondary DM can also result from other medical conditions
that cause abnormal blood sugar levels such as Cushing
syndrome, Parenteral nutrition.
oTreatment of medical conditions that cause abnormal blood
sugar levels eg. Corticosteroids –Prednisolone, Thiazides,
Phenytoin
oUsually Secondary DM resolves when the underlying condition
is treated

21. INTRODUCTION

23. PATHOPHYSIOLOGY
Insulin is required to facilitate the transport of glucose into skeletal and
cardiac muscle & into adipose tissues.
Glucose does not move into the cells causing hyperglycemia
Hyperglycemia causes fluid and electrolyte imbalances leading to the
classic symptoms of diabetes: polyuria, polydipsia and polyphagia.

24. PATHOPHYSIOLOGY CONT’D
Insulin insufficiency result to glycogenolysis (conversion of glycogen to
glucose).
 When glycogen stores are depleted, noncarbohydrate stores are broken
down to provide energy (gluconeogenesis) through metabolism of fats.
Fatty acids are broken down yielding large amounts of acetoacetic acid.
Some of it is converted to beta hydroxybutyric acid and acetone (ketone
bodies.)

25. PATHOPHYSIOLOGY CONT’D
In absence of insulin, catabolism of proteins increases.
Large amounts of amino acids are released into plasma and reused for
energy or converted to glucose through gluconeogenesis.
This process results in protein wasting, weight loss & weakness which are
classic signs and symptoms of diabetes.

26. PATHOPHYSIOLOGY CONT’D
When stores of fat are broken down, ketosis eventually may occur. Ketones collect in
blood (metabolic acidosis)
Rising levels of glucose in circulation result in an increased plasma osmolarity.
Glycosuria occurs when glucose in plasma rises above 180 mg/dl and glucose spills
over into the renal tubules

27. PATHOPHYSIOLOGY CONT’D
With glycosuria, large amounts of water, potassium &
sodium are excreted in urine hence increasing the volumes
of urine (polyuria).
Dehydration results and concomitantly increases the
patient’s thirst (polydipsia)as the body tries to compensate.

28. PATHOPHYSIOLOGY CONT’D
The dehydration leads to hemo- concentration (an increased
blood concentration), hypovolemia (decreased blood volume),
hyperviscosity (concentrated blood), hypoperfusion (decreased
circulation) of tissues, and hypoxia( poor tissue oxygenation),
especially to the brain.

29. PATHOPHYSIOLOGY CONT’D
The cells do not receive glucose, cell starvation triggers hunger, the patient eats
more food (polyphagia).
Total body weight is lost through loss of water & the breakdown of fat and protein
stores.
Malaise develops due to less glucose entering cells for energy requirements.

30. CLINICAL MANIFESTATIONS CONT’D
Features of increased osmolality;
a) Polyuria: increased volume and frequency of urination due to
osmotic diuresis induced by hyperglycemia.
b) Polydipsia- increased feeling of thirst and drinking excess water/fluid
due increased blood osmolality
c) Blurring of vision: swelling of the lens due to increased osmolality.

31. RISK FACTORS
Obesity (BMI >25 kg/m2),
 Hypertensive – high blood pressure
Hyperlipidemia HDL <35 mg/dl or triglyceride level >250 mg/dl,
Smoking: Smoking is a risk factor for type 2 diabetes and can
make the condition more challenging to manage

32. RISK FACTORS CONT,D
Family History: Having a family history of diabetes, especially if a parent or sibling has the
condition, increases the risk.
Genetics: Certain genetic factors can predispose individuals to diabetes. This risk is more
prominent in type 2 diabetes, where genetics plays a significant role.
Age: The risk of developing type 2 diabetes increases with age, particularly after the age of 45.

33. RISK FACTORS CONT,D
Physical Inactivity: A sedentary lifestyle with little to no regular physical
activity is associated with an increased risk of type 2 diabetes.
Unhealthy Diet: Diets high in sugar, refined carbohydrates, and saturated
and trans fats can contribute to obesity and insulin resistance, increasing
the risk of type 2 diabetes.
Gestational Diabetes: Women who had gestational diabetes during
pregnancy have a higher risk of developing type 2 diabetes later in life.

34. CRITERIA FOR DIABETES MELLITUS(DM)
DIAGNOSIS
Symptoms of diabetes(3Ps) plus random blood glucose concentration ≥11.1 mmol/L
(200 mg/dL ) OR
Fasting plasma glucose of >126 mg/dl (7 mmol/L) OR
2-hour postprandial plasma glucose >200 mg/dl after a glucose load of 75 g ( during
oral glucose tolerance test)

35. COMPLICATIONS OF DM
Diabetic Ketoacidosis (DKA)
Macro vascular complications - Thickening of the basement
membrane.
Peripheral Neuropathy - damage to the nerves located outside of
the brain and spinal cord (peripheral nerves)

36. COMPLICATIONS OF DM CONT,D
Nephropathy-damage or disease of the kidney which can result to kidney failure
Diabetic foot- pathology resulting from Peripheral Arterial disease due to reduced
blood flow to the feet
Retinopathy- disease of the retina involving abnormal growth of blood vessels in the
retina

37. DIABETIC KETOACIDOSIS (DKA)
DKA is caused by an absence or markedly
inadequate amount of insulin.
This deficit of insulin results in disorders in the
metabolism of carbohydrate, protein, and fat.

38. DIABETIC KETOACIDOSIS (DKA) CONT,D
An acute complication that can be life threatening due accumulation of acid in blood
The three main clinical features of DKA are;
a) Hyperglycemia
b) Dehydration and electrolyte loss
c) Acidosis

39. PATHOPHYSIOLOGY OF DKA
Without insulin, the amount of glucose entering the cells is reduced and the liver
increases glucose production leading to hyperglycemia
In an attempt to get rid the body of the excess glucose, the kidneys excrete the
glucose along with water and electrolytes (e.g. Sodium and potassium).

40. PATHOPHYSIOLOGY OF DKA CONT,D
This osmotic diuresis, characterized by excessive urination (polyuria), leads to
dehydration and marked electrolyte loss.
Patients with severe DKA may lose up to 6.5 litres of water and up to 400 to 500
mEq each of sodium, potassium, and chloride over a 24-hour period

41. PATHOPHYSIOLOGY OF DKA CONT,D
Insulin deficiency leads to breakdown of fat (lipolysis) into free fatty acids
and glycerol.
The free fatty acids are converted into ketone bodies by the liver. In DKA
there is excessive production of ketone bodies leading to metabolic
acidosis.

42. CAUSES OF DKA
 Three main causes of DKA are;
i.Decreased or missed dose of insulin
ii. Illness or infection, ( cause insulin resistance)
iii.Undiagnosed and untreated diabetes (DKA may be the initial
manifestation of diabetes

43. CLINICAL PRESENTATION OF DKA
 Hyperglycemia.Blood glucose levels are significantly elevated, often exceeding
250 mg/dL (13.9 mmol/L) or higher.
 Ketosis: Ketones, which are acidic compounds, build up in the
blood and urine.
 Dehydration: Excessive urination (polyuria) leads to fluid loss,
causing dehydration

44. CLINICAL PRESENTATION OF DKA CONT,D
 Fatigue and Weakness: DKA can lead to weakness and extreme fatigue.
 Fruity Breath: A distinct fruity or acetone-like odor in the breath is often
present.which occurs with elevated ketone levels.

45. CLINICAL PRESENTATION OF DKA CONT,D
 Kussmaul respirations: is a type of abnormal breathing pattern characterized
by deep, rapid, and labored breathing.
 Kussmaul breathing is the body's attempt to compensate for high levels of acid in
the blood by increasing the rate and depth of breathing in an effort to remove
carbon dioxide and lower the blood's acidity.

46. COMPLICATION OF DKA
Cerebral Edema: This is one of the most severe and life-
threatening complications of DKA, although it is relatively rare.
Hypovolemic Shock: DKA can cause a significant loss of fluids
and electrolytes through excessive urination and vomiting.
Electrolyte Imbalances: DKA often leads to imbalances in blood
electrolytes, such as potassium and sodium.

47. COMPLICATION OF DKA CONT,D
Acute Kidney Injury (AKI): Dehydration and electrolyte
imbalances can strain the kidneys and lead to acute kidney
injury, reducing their ability to filter waste products from the
blood.
Respiratory Distress: The body's attempt to compensate for
acidosis by increasing breathing rate can lead to respiratory
distress and may necessitate mechanical ventilation in severe
cases.

48. COMPLICATION OF DKA CONT,D
Cardiovascular Complications: DKA can stress the
cardiovascular system, potentially leading to heart
arrhythmias, heart attacks, or other cardiac issues.
Infection: DKA can weaken the immune system, making
individuals more susceptible to infections. In some cases, DKA
may be triggered by an underlying infection.

49. MANAGEMENT
Hospital Admission: DKA management typically occurs in a
hospital setting, often in an intensive care unit (ICU) or an
emergency department.
Fluid Resuscitation: Intravenous (IV) fluids are administered
to correct dehydration and improve tissue perfusion.
Initially, normal saline (0.9% sodium chloride) is commonly
used.

50. MANAGEMENT CONT,D
Insulin Therapy: Insulin is administered continuously
through an IV infusion to lower blood sugar levels and halt
the production of ketones..
Electrolyte Replacement: DKA often results in electrolyte
imbalances, particularly potassium
Bicarbonate Therapy (Controversial): The use of bicarbonate
to correct acidosis is controversial and is generally reserved
for severe acidosis (pH < 6.9).

51. MANAGEMENT CONT,D
Treatment of Underlying Causes: Identify and address the
underlying causes of DKA, such as infection or non-
adherence to insulin therapy.
Continuous Monitoring: Frequent monitoring of blood
glucose, electrolytes, arterial blood gases, and vital signs is
essential.

52. MANAGEMENT CONT,D
Transition to Subcutaneous Insulin: As DKA resolves and the
patient's condition stabilizes, transition from IV insulin to
subcutaneous insulin.
Education and Follow-up: Provide comprehensive education
on diabetes management and DKA prevention to the patient
and their caregivers.

53. THANK YOU

54. ASSIGNMENTS
1. Discuss the Management of DKA, Type 1 and 2 DM