1. Diabetes and Its Complication
Dr. Miada Mahmoud Rady
EMS / 474
Endocrinal Emergencies lecture II

2. Lecture Topics Definition. Hormones That Affect Glucose Metabolism.
Regulation of Blood Glucose.
Pathophysiology and clinical presentation of diabetes.
Complication of diabetes
Types of diabetes.
Diagnosis of diabetes.
Diabetic emergencies.

3. Diabetes
Definition : hyperglycemic metabolic disorders caused by either insulin Deficiency or Insufficiency .
Deficiency means → decrease .
Insufficiency means → inappropriate action.
Diabetes mellitus affects protein , fat and carbohydrate metabolism but the hallmark of D.M is Hyperglycemia

4. Hormones That Affect Glucose Metabolism
Several hormones affect blood glucose level either by increasing or decreasing :
Examples of hormones that increase blood glucose level : glucagon , growth hormones , thyroid hormones and cortisol.
Examples of hormones that decrease blood glucose level: Only Insulin .

5. What are the hormones that affect blood glucose level
Glucagon
Thyroid hormone
Growth hormone
Corticosteroids
Insulin

6. Insulin The only Hypoglycemic hormone in the body.
Secreted from Beta Cells of islet of Langerhans.
Main functions of insulin :
Increase glucose transport into cells.
Increase glucose metabolism by cells.
Increase liver glycogen levels.
Insulin antagonize effects of glucagon.
So It Decrease Blood Glucose Concentration Toward Normal

7. Glucose movement into the cell with insulin and the inability of glucose to get into the cell without insulin.

8. Glucagon It is secreted from alpha cells of the pancreas.
It increases blood glucose level through :
Glycogenolysis : break down of stored glycogen in liver and other storage sites into glucose.
Gluconeogensis : glucose formation through breakdown of fats and fatty acids.

10. Pancreatic secretions in changes in blood glucose level.
response to
changes in blood glucose level.

11. Regulation of Blood Glucose
Hypoglycaemia:
Low blood sugar.
Stimulates α cells.
Release glucagon.
Hyperglycaemia:
High blood sugar.
Stimulates β cells.
Release insulin.
Also lost in urine (osmotic diuresis) .

12. Glucose metabolism Eating BGL rises Insulin is secreted from pancreas
Allow glucose to enter cell
Blood glucose level decreases
Glucagon is released
Blood glucose level is normalized

13. Pathophysiology and clinical presentation of diabetes
in diabetic patient insulin deficiency or inappropriate action result in failure of the body to utilize simple sugars which accumulate in the different body tissues and organs:
Kidney : excess sugar produces osmotic diuresis, which leads to polyuria , which causes the polydepsia.
Tissues saturated with sugars are more liable to trauma , infection and also heals badly , that’s why diabetic patient is more liable to infection.

14. Clinical presentation of diabetes
Polyuria .
Polydepsia .
Polyphagia .
Unexplained weight loss .
Tiredness and easy fatigability.
Increased liability to infection (vaginal infection).
Clinical presentation of complications .
3PS , Classical Symptoms Of D.M

16. Complication of diabetes
Acute complication :
Hypoglycemia.
DKA ( diabetic ketoacidosis).
Hyperosmolar non-ketotic coma .
Chronic complication:
It affects all body system .
It either Microvascular ( affect small vessels) or Macrovascular ( affect large vessels).

17. Microvascular complication
Eye : diabetic retinopathy and cataract ( blurring of vision ).
Kidney : diabetic nephropathy ( acute and chronic renal failure).
Diabetic neuropathy : ( tingling and numbness).
Foot complication : poor wound healing and increased liability to infection.

18. Macrovascular complication
Brain : stroke and altered mental status .
Heart : ischemic heart disease , cardiomyopathy and hypertension.
Peripheral arterial disease and chronic ischemia.
Diabetic foot and gangrene .

20. Types of diabetes Type 1. Type 2. Gestational diabetes.
Others e.g. secondary diabetes ( chronic pancreatitis , cancer head of pancreas and pancreatectomy).

21. Type 1diabetes mellitus
Also known as Juvenile or insulin-dependent diabetes mellitus (IDDM).
Result from Inadequate Production of insulin by pancreas.
Usually occurs in teenagers and young adults.
Characterized by sever hyperglycemia , so more sever symptoms and more fat metabolism.
Cause : autoimmune disease that results from genetic abnormality that causes body to destroy its own insulin producing cells.

22. Type 1diabetes mellitus
Onset is usually sudden and may be with DKA.
Treatment : insulin is essential ( main line ), exercise, diet regulation.

23. Type 2 diabetes
Adult-onset or non-insulin-dependent diabetes mellitus (NIDDM).
Results from decreased binding of insulin to cells (insulin resistance).
Less sever hyperglycemia so less sever symptoms and less fat metabolism.
Predisposing factor :
Obesity and bad eating habits
Sedentary life .
Family history ( hereditary ) .

24. Type 2 diabetes Treatment : Mainly diet control and exercise
Oral hypoglycemic drugs ( to increase insulin sensitivity and production) .
Only small number requires insulin.

27. Gestational diabetes
Develops in some women during late pregnancy and Usually resolves with childbirth.
It may progress to D.M type 2.
Etiology :
The effect of pregnancy hormones which antagonize the effect of insulin
increased insulin requirement during pregnancy.

28. Gestational diabetes Commonest complication is Macrosomia
Treatment : Diet is first and the most important line of treatment , insulin is given last.

30. Metabolic syndrome Cluster of characteristics :
Excessive fat in the abdominal area.
Elevated blood pressure.
High levels of blood lipids.
People with metabolic syndrome are at increased risk of D.M.

31. Diagnosis of diabetes
If you suspect diabetes (in any persons showing symptoms and signs of diabetes) diagnosis is confirmed by following blood tests :
Fasting blood glucose .
2hrs post prandial blood glucose.
Random blood glucose.
Glycoselated hemoglobin.

32. Diagnosis of diabetes Diabetic Fasting 2hr PP Random HBA1C prediabetic
≥ 126mg/dl.
≥ 200mg/dl
˃ 200mg/dl + polysymptoms
mg/dl
mg/dl.
＜ 100 mg/dl.
＜ 140mg/dl
Fasting
2hr PP
Random
HBA1C
prediabetic
Normal

33. Diabetic Emergencies

34. Hypoglycemia Definition : blood glucose level Lower Than 60mg/dl.
It occurs in both diabetics and non diabetics .
Characteristic :
Sudden onset .
Rapidly progressive course .
That is why hypoglycemia is Very Dangerous especially in diabetics because they are usually unable or unaware of symptoms.

35. Causes of hypoglycemia
Causes And Predisposing Factors Of Hypoglycemia In Diabetics:
Overdose of oral hypoglycemic drugs or insulin
Missed meals.
Stress e.g. physical or emotional.
Surgery and trauma
Infection.

36. Causes of hypoglycemia
Causes of hypoglycemia in non diabetics :
Starvation .
Renal failure .
Liver cell failure .
Malignancy .
Chronic debilitating illness.
Endocrinal disorders e.g. adrenal and growth hormone deficiency.

37. Clinical presentation
It present with two sets of symptoms :
Autonomic : caused by stimulation of autonomic nervous system.
Neuroglycopenic : caused by lack of glucose supply to the brain ( glucose is the main source of energy to the brain).
Complication : prolonged hypoglycemia leads to irreversible brain damage.

38. Signs and symptoms of hypoglycemia
Autonomic
Neuroglycopenic
Anxiety.
Palpitation.
Sweating.
Tingling.
Tremors.
Tachycardia.
Irritability
Blurring of vision.
Difficulty of speech
Dizziness
Drowsiness
Feeling faint
Confusion.

39. Management of hypoglycemia
Diagnosis : Should be suspected in any diabetic patient with :
Behavioral changes
Confusion
Abnormal neurological signs
Unconsciousness
Rapid diagnosis and administration of glucose is essential to prevent permanent brain damage or death.

40. Treatment of hypoglycemia
Address the ABCs.
If patient is fully conscious and alert : give oral sugars.
If patient is Confused :
Secure an I.V access and give D to 25 gm over 3 minutes followed by Saline Flush .
No I.V access available , give I.M glucagon .
Do not use an advanced airway until you have given the patient D50.

42. Home Work In table compare between : Insulin and glucagon.
Type 1 and Type 2 diabetes .
The home work should be sent to the in ward document , before the next lecture .

43. Any questions ??