Endocrine System
Definition: The endocrine system comprises glands that are widely separated, lacking physical interconnections; these are secretory cells surrounded by capillary networks for hormone diffusion.
Ductless Glands: Hormones are secreted directly into the bloodstream.
Hormones: Act as chemical messengers transported through the bloodstream to influence cell growth and metabolism in target tissues and organs.
Homeostasis: Maintained by the autonomic nervous system (rapid response) and the endocrine system (slower, precise adjustments).
Main Glands: Include the pituitary, hypothalamus, thyroid, parathyroid, adrenal glands, and pancreas; other organs like adipose tissue (produces leptin) and the heart (produces atrial natriuretic peptide) also have endocrine functions.
Hypothalamus: Regulates the pituitary gland and influences other glands; it is crucial for maintaining hormonal balance.
Reproductive Hormones: Ovaries and testes release hormones post-puberty, and the placenta has temporary endocrine functions during pregnancy.
Hormone-Receptor Binding: Hormones bind to specific receptors, acting as switches for metabolic reactions.
Peptide Hormones: Receptors located on cell membranes.
Lipid-Based Hormones: Receptor sites are inside cells.
Regulation: Hormone levels are variable and self-regulate within a normal range.
Feedback Mechanisms:
Negative Feedback: Hormone release in response to a stimulus, reversing or negating the stimulus (e.g., insulin/glucagon regulation via plasma glucose levels).
Positive Feedback: Amplification of the stimulus, continuing hormone release until a process is completed (e.g., oxytocin during labor).
Definition: The most common endocrine disorder characterized by hyperglycemia and disrupted carbohydrate and fat metabolism.
Causes: Includes complete absence, relative deficiency, or resistance to insulin production.
Types:
Primary DM: Includes Type 1 and Type 2 diabetes.
Secondary DM: Results from other health conditions; gestational diabetes occurs during pregnancy.
Epidemic Growth: Global prevalence increased from 4.7% in 1980 to 8.5% in 2014, with significant rise in affected individuals (from 108 million to 422 million).
Description: Previously insulin-dependent; common in children/young adults with sudden onset.
Cause: Severe deficiency of insulin due to destruction of pancreatic β-islet cells by autoantibodies.
Treatment: Insulin administration is required.
Description: Previously non-insulin dependent; most common form, accounting for about 90% of cases.
Causes: Multifactorial; predisposing factors include:
Obesity
Sedentary lifestyle
Age, primarily affecting middle-aged and older adults
Genetic factors.
Onset: Gradual, often goes undetected until complications arise; can have normal or high insulin levels with defective glucose uptake by cells.
Treatment: Involves diet, drugs, or insulin depending on severity.
Hyperglycemia:
Increased plasma glucose after a carbohydrate-rich meal due to:
Inability of cells to utilize glucose
Reduced conversion to glycogen in liver/muscles
Gluconeogenesis due to intracellular glucose deficiency.
Consequences: Long-term vascular and nerve damage.
Mechanism: Increased glucose in renal filtrate results in osmotic pressure causing reduced water reabsorption, leading to increased urine volume (polyuria), dehydration, and excessive thirst (polydipsia).
Reason: Cells cannot extract glucose; reliance on alternative energy pathways leads to:
Gluconeogenesis from proteins
Fat breakdown, ketone body production.
Ketoacidosis: Severe metabolic derangement due to insufficient insulin, leads to energy source shifts, ketone accumulation, acidosis, and potential coma.
Signs: Ketonuria, characteristic breath odor, and acidosis symptoms.
Diabetic Ketoacidosis (DKA): Medical emergency due to severe insulin deficiency.
Hypoglycaemic Coma: Resulting from excess insulin relative to food intake/expenditure, characterized by rapid onset and disturbed neurological function due to glucose deprivation.
Cardiovascular Disturbances: Increased risk of cardiovascular disorders; macroangiopathy includes:
Ischemic heart disease
Stroke
Peripheral vascular disease.
Microangiopathy: Affects small vessels, leading to consequences:
Diabetic retinopathy
Nephropathy
Neuropathy.
Predisposal: DM increases infection risk, notably from bacterial and fungal sources due to reduced phagocyte activity.
Consequences: Chronic kidney disease due to nephropathy is common.
Risks: Diabetic retinopathy is the leading cause of blindness in adults aged 30-65 in developed countries.
Cataracts: Increased risk of early cataract development.
Factors: Contributing factors include:
Vascular disease affecting blood supply
Neuropathy reducing sensation in the extremities.
Consequences: Slow healing, potential for severe infection and gangrene, occasionally necessitating amputation.
Definition: The endocrine system comprises glands that are widely separated, lacking physical interconnections; these are secretory cells surrounded by capillary networks for hormone diffusion.
Ductless Glands: Hormones are secreted directly into the bloodstream.
Hormones: Act as chemical messengers transported through the bloodstream to influence cell growth and metabolism in target tissues and organs.
Homeostasis: Maintained by the autonomic nervous system (rapid response) and the endocrine system (slower, precise adjustments).
Main Glands: Include the pituitary, hypothalamus, thyroid, parathyroid, adrenal glands, and pancreas; other organs like adipose tissue (produces leptin) and the heart (produces atrial natriuretic peptide) also have endocrine functions.
Hypothalamus: Regulates the pituitary gland and influences other glands; it is crucial for maintaining hormonal balance.
Reproductive Hormones: Ovaries and testes release hormones post-puberty, and the placenta has temporary endocrine functions during pregnancy.
Hormone-Receptor Binding: Hormones bind to specific receptors, acting as switches for metabolic reactions.
Peptide Hormones: Receptors located on cell membranes.
Lipid-Based Hormones: Receptor sites are inside cells.
Regulation: Hormone levels are variable and self-regulate within a normal range.
Feedback Mechanisms:
Negative Feedback: Hormone release in response to a stimulus, reversing or negating the stimulus (e.g., insulin/glucagon regulation via plasma glucose levels).
Positive Feedback: Amplification of the stimulus, continuing hormone release until a process is completed (e.g., oxytocin during labor).
Definition: The most common endocrine disorder characterized by hyperglycemia and disrupted carbohydrate and fat metabolism.
Causes: Includes complete absence, relative deficiency, or resistance to insulin production.
Types:
Primary DM: Includes Type 1 and Type 2 diabetes.
Secondary DM: Results from other health conditions; gestational diabetes occurs during pregnancy.
Epidemic Growth: Global prevalence increased from 4.7% in 1980 to 8.5% in 2014, with significant rise in affected individuals (from 108 million to 422 million).
Description: Previously insulin-dependent; common in children/young adults with sudden onset.
Cause: Severe deficiency of insulin due to destruction of pancreatic β-islet cells by autoantibodies.
Treatment: Insulin administration is required.
Description: Previously non-insulin dependent; most common form, accounting for about 90% of cases.
Causes: Multifactorial; predisposing factors include:
Obesity
Sedentary lifestyle
Age, primarily affecting middle-aged and older adults
Genetic factors.
Onset: Gradual, often goes undetected until complications arise; can have normal or high insulin levels with defective glucose uptake by cells.
Treatment: Involves diet, drugs, or insulin depending on severity.
Hyperglycemia:
Increased plasma glucose after a carbohydrate-rich meal due to:
Inability of cells to utilize glucose
Reduced conversion to glycogen in liver/muscles
Gluconeogenesis due to intracellular glucose deficiency.
Consequences: Long-term vascular and nerve damage.
Mechanism: Increased glucose in renal filtrate results in osmotic pressure causing reduced water reabsorption, leading to increased urine volume (polyuria), dehydration, and excessive thirst (polydipsia).
Reason: Cells cannot extract glucose; reliance on alternative energy pathways leads to:
Gluconeogenesis from proteins
Fat breakdown, ketone body production.
Ketoacidosis: Severe metabolic derangement due to insufficient insulin, leads to energy source shifts, ketone accumulation, acidosis, and potential coma.
Signs: Ketonuria, characteristic breath odor, and acidosis symptoms.
Diabetic Ketoacidosis (DKA): Medical emergency due to severe insulin deficiency.
Hypoglycaemic Coma: Resulting from excess insulin relative to food intake/expenditure, characterized by rapid onset and disturbed neurological function due to glucose deprivation.
Cardiovascular Disturbances: Increased risk of cardiovascular disorders; macroangiopathy includes:
Ischemic heart disease
Stroke
Peripheral vascular disease.
Microangiopathy: Affects small vessels, leading to consequences:
Diabetic retinopathy
Nephropathy
Neuropathy.
Predisposal: DM increases infection risk, notably from bacterial and fungal sources due to reduced phagocyte activity.
Consequences: Chronic kidney disease due to nephropathy is common.
Risks: Diabetic retinopathy is the leading cause of blindness in adults aged 30-65 in developed countries.
Cataracts: Increased risk of early cataract development.
Factors: Contributing factors include:
Vascular disease affecting blood supply
Neuropathy reducing sensation in the extremities.
Consequences: Slow healing, potential for severe infection and gangrene, occasionally necessitating amputation.