WK FOUR - Diabetes (Hypo/Hyper/DKA)

Diabetes Gender Distribution

1.3 times more common in males than females (age-controlled).

Indigenous Australian Risk

Diabetes is 3 times more common in Indigenous Australians.

Organs of the Endocrine System

• hypthalamus

• pituitary gland

• pineal gland

• thyroid gland

• parathyroid gland

• thymus

• pancreas

• adrenal gland

• gonads

Pancreatic Acini Function

Secrete digestive fluids into the duodenum (exocrine function).

Pancreatic Islets Function

Perform the endocrine functions of the pancreas. (excrete glucagon, insulin, etc..)

Alpha Cells

Pancreatic cells that secrete glucagon.

Beta Cells

Pancreatic cells that secrete insulin.

Delta Cells

Pancreatic cells that secrete somatostatin (inhibits insulin and glucagon).

Glucose Storage Locations

Stored as glycogen in liver/muscles or triglycerides in adipose tissue.

Glucose Feedback Mechanism

Operates on a negative feedback loop sensed by pancreatic receptors.

Glycogenolysis

Stimulates the liver to convert stored glycogen back into glucose.

Gluconeogenesis

Stimulates the liver to convert amino acids into glucose.

Lipolysis

Breakdown of triglycerides into fatty acids for conversion to glucose.

Blood Sugar Management Feedback Loop (Low)

A physiological mechanism that regulates blood glucose levels by signaling the release of glucagon in response to a drop in blood sugar.

Blood Sugar Management Feedback Loop (High)

A physiological mechanism that regulates blood glucose levels by signaling the release of insulin in response to a spike in blood sugar.

Insulin Role: Cellular Uptake

Facilitates glucose uptake into cells, mostly skeletal muscle and adipose tissue.

Insulin Role: Metabolism

Promotes fat, protein, and carbohydrate metabolism.

Insulin Role: Inhibition

Inhibits enzymes involved in glycogenolysis and gluconeogenesis.

Insulin Carbohydrate Metabolism

Insulin activates membrane receptors on target cells causing most body cells to become highly permeable to glucose and facilitates its conversion to glycogen for storage.

Insulin Fat Metabolism

Decreases fat utilization for energy and promotes triglyceride conversion.

Insulin Protein Metabolism

Promotes amino acid uptake for conversion into proteins (anabolic metabolism).

Diabetes Mellitus Definition

Diseases of abnormal carbohydrate metabolism characterized by hyperglycemia.

Type 1 Diabetes Mellitus (T1DM) Pathophysiology

Autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency typically due to genetic & environmental factors.

T1DM Peak Incidence

Between 9 months and 14 years of age.

Hyperglycaemia Classic Triad

Polydipsia (thirst), polyuria (excessive urination), and weight loss.

Type 2 Diabetes Mellitus (T2DM) Pathophysiology

Insulin resistance combined with progressive loss of beta cell insulin secretion.

T2DM Prevalence

Accounts for approximately 85% of diabetes in adults.

T2DM Risk Factors (Age/Lifestyle)

Age > 55, overweight, hypertension, smoking, PCOS, GDM or GDM in utero, and sedentary lifestyle.

Pre-diabetes

Condition of elevated fasting glucose and insulin resistance; high risk for diabetes.

Gestational Diabetes (GDM)

Diabetes that presents during pregnancy; requires "DIESEL" pre-hospital treatment.

GDM Risk Factors

• >30 years of age

• have a family history of T2DM

• overweight

• ethnic background (chinese, middle eastern, etc..)

• previous GDM

Long-Term Consequences of DM

• macrovascular

• microvascular

• cardiovascular

Macrovascular Complications

Hyaline arteriolosclerosis (hardening) and atherosclerosis (stroke/AMI).

Microvascular Complications

Retinopathy (blindness), nephrotic syndrome (kidney damage), and peripheral neuropathy.

Cardiovascular Complications

Silent Ischemia/AMI, Atypical cardiac presentations

Silent Ischaemia in Diabetics

Increased incidence of unrecognized AMI (40% in diabetics vs 25% in non-diabetics).

Hypoglycaemia Definition

Blood Sugar Level (BSL) < 4.0 mmol/L.

Euglycaemia Range

Fasting BSL between 4 to 6 mmol/L.

Brain Susceptibility in Hypoglycaemia

Neuronal glycogen stores deplete in 2 minutes, risking brain damage.

Causes of Hypoglycaemia

Excess insulin, missed meals, alcohol ingestion, unplanned exercise, or infection.

Hypoglycaemia: Adrenaline Release Effects

Increased HR, diaphoresis, increased respiratory rate, and cold skin.

Neurogenic (Autonomic) Symptoms

Hunger, tremor, anxiety, palpitations, tachycardia, sweating, and pallor.

Neuroglycopenic (CNS) Symptoms

Headache, irritability, confusion, ataxia, diplopia, hemiparesis, and seizures.

Pre-hospital Management: Glucose Gel

15g dose; requires the patient to be able to obey commands.

Pre-hospital Management: Glucagon IMI

Intramuscular injection; less effective if patient has poor glycogen stores.

Pre-hospital Management: IV Dextrose

5-10% concentration; can cause tissue necrosis if extravasation occurs.

Hyperglycaemia Definition (BGL)

Blood glucose levels > 10 mmol/L.

Normal Ketone Level

<0.6mmol

Elevated Ketone Level

Ketone level > 3 mmol/L.

Precipitating Factors for Hyperglycaemic Emergencies

Infection, discontinuation of insulin, or inadequate insulin therapy.

DKA Pathophysiology: 3 States

Hyperglycaemia, ketosis, and metabolic acidosis.

DKA Pathophysiology

• uncontrolled catabolism associated with carbohydrate insufficiency

• insulin deficiency is a necessary precondition

DKA Fluid Loss

Averages approximately 6-9 L.

DKA Presentation: Evolution Time

Usually evolves rapidly, over a 24-hour period.

DKA Signs: Dehydration/Shock

Tachycardia, hypotension, arrhythmias, and altered consciousness.

Kussmaul Respiration

Deep, labored breathing pattern associated with severe metabolic acidosis.

HHS?

Hyperosmolar Hyperglycaemic State

HHS vs. DKA: Ketones

HHS has enough insulin to prevent ketone production; DKA does not.

HHS Risk Factors

Elderly, reduced fluid intake, infection, MI, or stroke.

HHS Presentation: Neurologic Symptoms

ALOC, seizures, hemiparesis, aphasia, muscle twitching, or hallucinations.

HHS Presentation: Evolution Time

Develops insidiously over several days.

HHS Pathophys

• insulin deficiency enough that hyperglycemia develops, but not enough to produce fatty acids/ketones

• severe hyperosmolarity and dehydration

Assessment of Hyperglycaemic Emergencies

Check BSL and ketones; assess dehydration and RSA.

Management: IV Fluid Goal

Replace total volume loss within 24-36 hours.

Euglycaemic Ketoacidosis

Normal BSL with elevated ketones (>3 mmol/L).

Euglycaemic Ketoacidosis Risk Factors

SGLT inhibitors, fasting (surgery), or illness/infection.

How can dehydration be assessed?

• dry mouth

• tented skin on forearm

• hypotensive

• acs