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Questions and Answers
Which zone of the adrenal cortex primarily produces mineralocorticoids?
Which zone of the adrenal cortex primarily produces mineralocorticoids?
What is the primary function of aldosterone?
What is the primary function of aldosterone?
What stimulates increased aldosterone secretion?
What stimulates increased aldosterone secretion?
Which glucocorticoid is dominant in humans?
Which glucocorticoid is dominant in humans?
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How does cortisol affect carbohydrate metabolism?
How does cortisol affect carbohydrate metabolism?
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What effect does cortisol have on protein metabolism in extrahepatic tissues?
What effect does cortisol have on protein metabolism in extrahepatic tissues?
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Which effect is associated with the anti-inflammatory action of cortisol?
Which effect is associated with the anti-inflammatory action of cortisol?
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What is one consequence of primary hyperaldosteronism?
What is one consequence of primary hyperaldosteronism?
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How does cortisol affect the immune system?
How does cortisol affect the immune system?
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What triggers the secretion of cortisol from the adrenal glands?
What triggers the secretion of cortisol from the adrenal glands?
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Study Notes
ADRENAL GLAND
- Composed of adrenal medulla and adrenal cortex
- Adrenal cortex is divided into three zones: glomerulosa, fasciculata, and reticularis
- Zona glomerulosa produces mineralocorticoids (e.g., aldosterone), regulating salt and water balance
- Zona fasciculata synthesizes glucocorticoids (e.g., cortisol), involved in metabolism and stress response
- Zona reticularis secretes adrenal androgens (e.g., dehydroepiandrosterone)
MINERALOCORTICOIDS
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Aldosterone accounts for 90% of mineralocorticoid activity
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Primary function: regulates electrolytes by increasing sodium reabsorption and potassium excretion
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Mechanisms:
- Kidney: Increases sodium reabsorption and potassium excretion mainly in the collecting tubules and to a lesser extent in the distal tubules and collecting ducts
- Intestine: Increases sodium absorption mainly in the colon to prevent sodium loss in stool
- Sweat and salivary glands: Increases sodium chloride reabsorption and potassium secretion
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Regulation of extracellular fluid and arterial blood pressure
- Sodium reabsorption by renal tubules stimulates osmotic reabsorption of water
- Excess aldosterone increases extracellular fluid volume and blood pressure
Control of Aldosterone Secretion
- Increased potassium ion concentration in the blood increases aldosterone secretion
- Increased activity of the renin-angiotensin system increases aldosterone secretion (often due to decreased blood flow to the kidneys)
- Decreased sodium ion concentration in the blood increases aldosterone secretion
- ACTH has a permissive effect on aldosterone secretion
GLUCOCORTICOIDS
- In humans, cortisol is the primary glucocorticoid
- Functions of cortisol:
- Carbohydrate metabolism: Increases gluconeogenesis in the liver (conversion of amino acids to glucose) and decreases glucose uptake by tissues
- Protein metabolism: Increases protein catabolism in extrahepatic tissues(muscle) and decreases protein synthesis; increases amino acid transport to the liver and formation of plasma proteins
- Fat metabolism: Increases lipolysis in adipose tissues and increases fatty acid oxidation
Anti-inflammatory and Other Effects
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Decreases capillary permeability and edema formation
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Stabilizes lysosomal membranes, preventing the release of proteolytic enzymes
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Prevents histamine release from mast cells
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Increases resistance to stress
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Increases RBCs, neutrophils, and platelets; decreases eosinophils and basophils
CONTROL OF CORTISOL SECRETION
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Hypothalamus secretes corticotrophin-releasing hormone (CRH) which stimulates the anterior pituitary to release ACTH which stimulates cortisol secretion
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Cortisol produces negative feedback inhibition on the hypothalamus and anterior pituitary
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Physical or mental stress greatly enhances the secretion of ACTH and cortisol
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Circadian rhythm: Cortisol secretion is high in the early morning but low in the late evening
HYPERALDOSTERONISM
- Causes: Overproduction of aldosterone, often due to tumors of the zona glomerulosa
- Manifestations:
- Sodium retention, leading to hypertension
- Potassium loss, leading to hypokalemia (muscle weakness and cardiac arrhythmias)
- Alkalosis (due to H+ loss in urine)
- Edema may not develop due to the escape phenomenon—Increased extracellular fluid will trigger secretion of atrial natriuretic factor, resulting in Na+ excretion
CUSHING SYNDROME
- Causes: Excess cortisol secretion, possibly due to
- Primary hyperfunction: tumor of the adrenal gland
- Secondary hyperfunction: increased ACTH output from a pituitary tumor, or from prolonged steroid administration
- Manifestations:
- Hypertension
- Hyperglycemia and diabetes
- Moon face, buffalo hump, and truncal obesity
- Muscle weakness
- Osteoporosis
- Thinning of the skin and striae (stretch marks)
ADRENAL INSUFFICIENCY
- Primary adrenal insufficiency (Addison's disease): Causes:
- Atrophy of the adrenal cortex
- Destruction of the adrenal cortex (e.g., by cancer or autoimmune disease)
- Manifestations:
- Lack of aldosterone: Sodium levels decrease, potassium levels rise, severe dehydration, and hypotension
- Lack of cortisol: Decreases blood glucose, decrease resistance to stress, and skin pigmentation
PANCREAS
- Mixed gland (exocrine and endocrine functions)
- Exocrine function: Secretes digestive enzymes (pancreatic juices) into the digestive tract
- Endocrine function: Secretes hormones regulating blood sugar levels; located in islets of Langerhans
- Islets of Langerhans contain different cell types
- Beta cells: Secrete insulin
- Alpha cells: Secrete glucagon
- Delta cells: Secrete somatostatin
Insulin (Anabolic Hormone)
- Peptide hormone secreted by beta cells of pancreatic islets of Langerhans
- Maintains normal blood glucose levels by facilitating cellular glucose uptake
- Regulates carbohydrate, lipid, and protein metabolism
- Increases glycogen, fatty acid, and triglyceride formation in the liver
- Stimulates glucose uptake by muscle and adipose tissue
- Decreases blood glucose concentration
Glucagon
- "Fasted state" hormone working with insulin to maintain blood glucose homeostasis in the blood
- Secreted by alpha cells in the pancreas
- Increases blood glucose concentration by stimulating glycogenolysis. Glycogen conversion (stored in liver) into glucose is released into the bloodstream.
- Stimulates gluconeogenesis
Diabetes Mellitus
- Characterized as an inability for the body to produce enough insulin, or a decreased response to insulin in target tissues.
- Marked by elevated blood glucose levels
- Two forms:
- Type 1 (insulin-dependent): absolute deficiency of insulin due to autoimmune disease that destroys beta cells (usually diagnosed in younger age groups)
- Type 2 (non-insulin-dependent): characterized by decreased tissue sensitivity to insulin. (most common form, usually diagnosed in older age groups, often linked to obesity)
Prediabetes
- Blood sugar levels are higher than normal, but not high enough to be diagnosed as diabetes
- Fasting blood glucose levels: 100 mg/dL - 125 mg/dL
- Oral glucose tolerance test (OGTT): 140 mg/dL - 199 mg/dL
Diagnosis of Diabetes Mellitus
- Fasting blood glucose levels of 126 mg/dL or higher
- Random blood glucose level over 200 mg/dL
- Glycosylated hemoglobin (A1C) levels of 6.5% or higher indicate diabetes. 5.7-6.4% indicates prediabetes.
Diabetes Symptoms
- Feeling hungry, thirsty, or frequently urinating
- Blurred vision or tingling limbs
- High blood sugar readings
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