Hormonal Regulation Alterations Quiz

Alterations of Hormonal Regulation

•  Hormonal regulation involves the creation, delivery, and reception of hormones.
•  Alterations can occur in the creation of hormones, feedback systems, delivery systems, or receptors.

Mechanisms of Hormonal Alterations

•  Inadequate Hormone Creation: Insufficient hormone precursors or failure to convert them to active hormones.
•  Failure of Feedback Systems: Malfunctioning feedback systems lead to inadequate or excessive hormone production.
•  Inactive Hormones: Hormones are broken down at an altered rate, or circulating hormone inhibitors prevent function.
•  Dysfunctional Delivery System: Inadequate blood supply, carriers, or ectopic (wrong location) hormone production disrupt hormone delivery.
•  Cell Surface Receptor-Associated Disorders: Reduced receptor numbers or altered affinity for hormones, or the presence of antibodies against receptors, can disrupt hormone signaling.
•  Intracellular Disorders: Deficits in post-receptor signaling pathways are another source of hormonal dysfunction.

Diseases of the Posterior Pituitary

•  Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Excessive ADH leading to water retention, dilutional hyponatremia and elevated urine osmolality.
•  Diabetes Insipidus : Insufficient ADH leading to excessive water loss in the urine, hypernatremia, and low urine osmolality

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

•  Hypersecretion of ADH: ADH promotes water retention and increases blood pressure.
•  Causes: Ectopic ADH production by tumors, pituitary surgery, and certain medications.
•  Pathophysiology: Increase renal water retention leads to dilutional hyponatremia and concentrated urine.

Clinical Manifestations related to HYPONATREMIA in SIADH

• Sodium levels 130–140 mEq/L: thirst, impaired taste, anorexia, dyspnea on exertion, fatigue
• Sodium levels 120–130 mEq/L: severe gastrointestinal symptoms, including vomiting and abdominal cramps, weight gain due to water retention.
• Sodium levels 110–120 mEq/L: confusion, lethargy, muscle twitching, convulsions, severe and sometimes irreversible neurological damage.

Diagnosis of SIADH

• Normal adrenal and thyroid function
• Absence of conditions altering volume status
• Serum hypoosmolality and hyponatremia
• Urine hyperosmolarity
• Urine sodium excretion matching sodium intake
• High urine specific gravity

Urine Specific Gravity (USG or SG)

•  USG is a measure of urine concentration relative to distilled water.
•  Normal urine specific gravity ranges from 1.005 to 1.030.

Serum Osmolality

•  Serum osmolality measures dissolved chemicals in blood serum.
•  Normal range: 275–295 mOsm/kg.
•  High values indicate low body water and high salt levels.
•  Low values indicate high body water and low salt levels. 

Urine Osmolality

•  Measures dissolved particles per unit of water in urine.
•  Usually more specific than USG.
•  Normal range: 500 to 850 mOsm/kg.

Treatment of SIADH

•  Correction of underlying problems.
•  Fluid restriction.
•  Monitoring sodium levels.
•  Severe hyponatremia: IV hypertonic saline

Diabetes Insipidus

•  Insufficient ADH leading to polyuria and polydipsia.
•  Two forms: Neurogenic/central and Nephrogenic.

Neurogenic/Central Diabetes Insipidus

•  Insufficient ADH secretion due to hypothalamic or pituitary damage.
•  Common causes include tumors, aneurysms, surgery, or head injuries

Nephrogenic Diabetes Insipidus

•  Inability of the kidneys to respond to ADH.
•  Common causes include genetic disorders, medications, or kidney diseases.

Pathophysiology of Diabetes Insipidus

•  Decreased ADH leads to decreased water absorption in renal tubules.
•  This results in decreased intravascular fluid volume.
•  Increased serum osmolality (hypernatremia) and excessive dilute urine output.

Clinical Manifestations of Diabetes Insipidus

•  Polyuria (excessive urine output: 8-12 L/day).
•  Hydronephrosis can occur in severe cases.
•  Low urine specific gravity (<1.010) and low urine osmolality (<100 mmol/kg).
•  Elevated serum osmolality (>300 mmol/kg).
•  Polydipsia (excessive thirst).
• Weakness, dehydration and CNS abnormalities associated with symptoms.

Diagnosis of Diabetes Insipidus

•  Low urine specific gravity and osmolality
•  Hypernatremia
•  Continued diuresis
•  Water deprivation testing

Treatment of Diabetes Insipidus

• ADH replacement.
• IV fluids.
• Treatment of causative disorders.
• Medications may need to be stopped.

Comparing SIADH and DI

•  Key Differences in Signs and Symptoms, Urine Output ,Urine Osmolality ,Urine Specific Gravity , Serum Sodium & Osmolality.

Diseases of the Anterior Pituitary

•  Hypopituitarism: insufficient anterior pituitary hormones.
•  Hyperpituitarism: excessive anterior pituitary hormones.

Hypopituitarism

•  Absence of one or more anterior pituitary hormones.
•  Causes: inadequate hypothalamic-releasing hormones, damage to the pituitary stalk, or inability of the pituitary gland to produce hormones.

Clinical Manifestations of hypopituitarism

• Loss of function of the different hormones, correlated with the different deficiencies. 

Diagnosis of Hypopituitarism

•  Careful interpretation of diagnostic tests.
•  Hormone measurements.
•  Pituitary imaging (MRI, CT).

Treatment of Hypopituitarism

•  Correction of underlying disorders.
•  Hormone replacement.

Hyperpituitarism

•  Excessive anterior pituitary hormones, most often caused by a benign pituitary tumor (adenoma).
•  Causes: unknown, though linked to altered gene expression.
•  Clinical Manifestations:
• Headache and fatigue
• Visual changes
• Increased growth hormone (acromegaly)
• Increased prolactin (breast development, milk production, amenorrhea in women, erectile dysfunction in men)

Diagnosis of Hyperpituitarism

• History & physical
• Lab evaluations (hormone levels)
• Imaging of the pituitary (MRI, CT)

Treatment of Hyperpituitarism

• Protect the individual from tumor effects
• Medications to suppress tumor growth
• Surgery
• Radiation

Alterations of Thyroid Function

•  Overview of Thyroid Hormones:
•  Thyroid Hormone(TH) – thyroxine (T4) and triiodothyronine (T3) – regulates BMR.
•  Calcitonin – lowers serum calcium levels.
•  Types of Alterations: Hyperthyroidism, Hypothyroidism, Thyroid Carcinoma

Hyperthyroidism

•  Excessive secretion of thyroid hormones (T3 and T4).
•  Causes: Graves' disease, nodular thyroid disease, toxic adenoma.
•  Clinical Manifestations:
• Increased metabolic rate
• Heat intolerance
• Increased tissue sensitivity
• Enlargement of the thyroid gland (goiter)


Diagnosis of Hyperthyroidism

•  Increased serum T3 & T4; suppressed TSH levels.
•  Radioactive iodine uptake test.

Treatment of Hyperthyroidism

•  Antithyroid medication
•  Radioactive iodine therapy
•  Surgery

Hypothyroidism

•  Insufficient secretion of thyroid hormones (T3 and T4).
•  Causes: Autoimmune thyroiditis (Hashimoto's disease), iodine deficiency, pituitary dysfunction, or congenital defects in the thyroid gland.
•  Clinical Manifestations:
• Lower energy metabolism and lower heat production.
• Low basal metabolic rate.
• Cold intolerance.
• Lethargy.
• Goiters can result from too high TSH.
• Myxedema (non-pitting "boggy" swelling) in the eyes, hands, and feet is a possible symptom.
• Myxedema coma can occur in severe cases.

Diagnosis of Hypothyroidism

•  Increased levels of TSH, decreased levels of TH.

Treatment of Hypothyroidism

•  Hormone replacement with Levothyroxine.

Thyroid Carcinoma

•  Most common endocrine malignancy.
•  Ionizing radiation is a common cause.
•  Treated with thyroidectomy, suppression therapy, radiation and chemotherapy.

Alterations of Parathyroid Function

•  Hyperparathyroidism: Excess parathyroid hormone (PTH).
•  Hypoparathyroidism: Low PTH.

Hyperparathyroidism

•  Primary Hyperparathyroidism: Excess PTH secretion from one or more parathyroid glands.
•  Secondary Hyperparathyroidism: Increase in PTH as a compensatory response to chronic hypocalcemia.
•  Clinical Manifestations:
• Hypercalcemia & hypophosphatemia
• Hypercalciuria and kidney stones
• Fatigue, headache, anorexia, depression, nausea & vomiting
• Pathological fractures.

Diagnosis of Hyperparathyroidism

• PTH levels consistently raised with increased calcium levels.
• Hypercalcemia should normally suppress PTH

Treatment of Hyperparathyroidism

• Monitor symptoms
• Avoid dehydration
• Limit calcium intake

Hypoparathyroidism

•  Low PTH levels due to parathyroid gland damage, often during thyroid surgery.
•  Clinical Manifestations:
•  Hypocalcemia
•  Lowered threshold for nerve and muscle excitation (muscle spasms, hyperreflexia, convulsions)
•  Chvostek's and Trousseau's signs
•  Neuromuscular irritability
•  Bone deformities
•  Hyperphosphatemia

Diagnosis of Hypoparathyroidism

•  Low serum calcium, high phosphorus, excluding renal and intestinal disorders or nutritional deficiencies. 
•  Magnesium levels are checked
• Urinary calcium excretion is measured.

Treatment of Hypoparathyroidism

• Correction of hypocalcemia (IV administration)
• Vitamin D3 supplements and oral calcium supplements.

Alterations of Adrenal Function

•  Hyperfunction: Increased cortisol (Cushing's disease & Cushing's syndrome).
• Increased aldosterone (hyperaldosteronism).

Cushing's Syndrome

•  Chronic exposure to excess cortisol, regardless of cause.
• Increased ACTH leads to increased cortisol.

• Clinical manifestations: Weight gain (truncal obesity, buffalo hump, moon face), glucose intolerance, muscle weakness, osteoporosis, thin skin, hypertension, and immune system suppression.

Diagnosis of Cushing's Syndrome

• Lab results (hyperglycemia, hypokalemia, metabolic alkalosis, increased urine cortisol levels).
• Imaging to diagnose tumors.

Treatment of Cushing's Syndrome

• Surgery, medication, or radiation.

Hypo function: Decreased Cortisol

• Addison's Disease: Autoimmune destruction of adrenal cortex, resulting in inadequate cortisol production
• Clinical manifestations: Weakness and fatigue, hyperpigmentation, and hypotension.
• Diagnosis: Low serum and urine cortisol, high ACTH.
• Treatment: Lifelong glucocorticoid replacement.

Hyperaldosteronism

•  Excessive aldosterone secretion.
•  Clinical manifestations: Hypertension, hypokalemia, and neuromuscular manifestations.
•  Diagnosis: Blood pressure measurement, serum and urine electrolyte levels, and imaging to locate the tumor.
•  Treatment: Management of hypertension and hypokalemia, surgical removal of the adrenal tumor, or pharmacologic management with potassium-sparing diuretics.

Tumor of the Adrenal Medulla (Pheochromocytomas)

•  Causes excessive catecholamine secretion (epinephrine and norepinephrine).
•  Clinical manifestations: Persistent HTN, headache, pallor, diaphoresis, tachycardia, and palpitations.
•  Diagnosis: HTN unresponsive to antihypertensives and elevated catecholamine levels in blood or urine.
• Treatment: Controlling hypertensive emergencies with alpha and beta blockers, followed by surgical removal of the tumor or chemotherapy .

Diabetes Mellitus

•  Group of metabolic diseases characterized by hyperglycemia.
•  Hyperglycemia is a result of defects in insulin secretion, insulin action, or both.

Types of Diabetes Mellitus

• Type 1: Beta-cell destruction (total insulin deficiency) - most often a genetic predisposition.

• Type 2: Insulin resistance or insulin secretory defect
• Gestational: during pregnancy

Diabetes Mellitus Type 1

•  Idiopathic or autoimmune. - Clinical manifestations: Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, fatigue and diabetic ketoacidosis (DKA). - Diagnosis: Elevated blood glucose, absence of C-peptide, possible diabetic coma.

• Treatment: Optimal blood glucose control with insulin therapy, meal planning, exercise, and possibly pancreas transplantation.

Diabetes Mellitus Type 2

- Risk factors include age, obesity, hypertension, physical inactivity, and family history.

•  Ranges from insulin resistance to insulin deficiency.
•  Clinical manifestations: Fatigue, pruritus, recurrent infections, visual changes, or symptoms of neuropathy. Patients may appear overweight, with dyslipidemia, hyperinsulinemia, and hypertension.

• Treatment: Blood glucose normalization with diet, exercise, and then medications like metformin or insulin.

Metabolic Syndrome

•  Cluster of disorders: Increased waist circumference, elevated fasting glucose, triglycerides, and low HDL.
•  Associated with a greater risk of developing type 2 diabetes and cardiovascular complications like stroke or heart attacks
•  Critical to identify to proactively prevent or control complications. Diagnosis- three or more disorders must be present

Acute Complications of Diabetes Mellitus

• Somogyi effect: Low blood sugar overnight followed by a morning rise.
• Dawn phenomenon: Early morning rises in blood sugar.
• Hypoglycemia: Low blood glucose levels.
• Diabetic ketoacidosis (DKA): High blood glucose, ketones, metabolic acidosis, often in type 1.
• Hyperosmolar hyperglycemic syndrome (HHS): Extremely high blood sugar and dehydration, often in type 2.

Chronic Complications of Diabetes Mellitus

• Microvascular disease: Diabetic retinopathy, nephropathy (kidney disease), neuropathy (nerve damage) - complications related to small blood vessels
 . - Macrovascular disease: Cardiovascular disease, stroke, peripheral vascular disease- complications related to large blood vessels 

• Infection: Increased risk due to hypoxia, impaired senses and suppressed immune response.

Test your knowledge on the mechanisms and alterations of hormonal regulation. Explore how changes in hormone creation, feedback systems, and receptor function can affect overall endocrine health. This quiz covers key concepts related to hormonal signaling and disorders affecting hormonal balance.