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Brief Intro Blood Supply Innervation Hormone Produce Disease Adenohypophysis/...

Brief Intro Blood Supply Innervation Hormone Produce Disease Adenohypophysis/ Hypothalamic - pituitary portal Unique. Does not have innervation ACTH - MCs/GCs/Androgen - Anterior plexus but receives regulatory input via Adrenals the hypothalamic-pituitary portal FSH -M - sperm prod in Testis system FSH - F - sec of Estrogen in Ov GH - release of IGF I LH - M - prod & sec of Testosterone LH - F - ovulation % devt of corpus luteum TSH/Thyrotropin - sec of T3, T4 PRL - milk synthesis Neurohypophysis/ Posterior ​ Physiology Inferior Hypophyseal Arteries Supaoptic Hypophyseal Tract via ​ ADH/Vasopressin 1. Increase in blood osmolality 1. Increase in blood osmolality ​ ○​ Tonicity or osmolality and Stalk Tuberohypophyseal Nerve via ○​ water reabsorption in the 2. Stimulates osmoreceptor in 2. Stimulates osmoreceptor in volume of ECF are essential for Stalk collecting ducts hypothalamus hypothalamus normal cell structure and ○​ 9 amino acid peptide 3. Increase in circulating 3. Activates thirst center in function. synthesized in paraventricular vasopressin hypothalamus ○​ Normal blood osmolality 280 - and supra optic nuclei of the 4. Increase permeability of 4. Increase thirst 290 mosm/kg regulated by the hypothalamus collecting ducts 5. H2o increase intake osmoreceptors located at the ○​ 3 receptors; 5. H2o reabsorption increase from 6. Decreased in blood osmolality bbb near the anterior ○​ V1 - collecting tubules, kidneys urine 7. Negative regulation of hypothalamus ○​ V2 - located on the long arm of 6. Decreased in blood osmolality osmoreceptor in the hypothalamus ○​ Small increases in plasma x chromosome 7. Negative regulation of tonicity stimulate the release ○​ Receptors on the nephron are osmoreceptor in the hypothalamus of vasopressin from the responsible for increased posterior pituitary absorption of water, urea and other solutes through insertions of aquaporins leads to urinary concentrating ability ○​ V3 ​ Oxytocin - contraction of uterus at birth and milk secretion Hypothalamus Anterior Cerebral Artery - medial Afferent Connections - Brainstem, CRH - sec of ACTH and anterior portion Thalamus, Hippocampus, GHRH - sec of GH Anterior Comm Artery - preoptic Amygdala Ghrelin - sec of GH and anterior region Efferent Connections - ANS, PG, GnRH - release of FSH and LH Posterior Cerebral Artery - Thalamus and Cortex TRH - sec of TSH and PRL posterior region Local Neuronal Sheath Dopamine - inhibit sec of PRL Somatostatin - inhibits TSH, PRL & GH Disease Brief Intro Signs and Symptoms Etiology/Risk Factor Involved Systems Pathophysiology Clinical Presentation Diagnosis/What to Check Scoring System Differential Diagnosis Conservative Lifestyle Modification Pharmacology MOA Follow - up Surgical Intervention Hypopituitarism ​ Underproduction of 1 or multiple ​ Mutation in 7 candidate genes pituitary hormones account for 13% of isolated ​ Corrected by hormone growth hormone deficiency replacement therapy (IGHD) and 20% of multiple ​ Incidence of Congenital pituitary hormone deficiency hypopituitarism: 1:4000 and (MPHD) cases 1:10,000 live births ​ Increased by consanguinity and occurrence in siblings across generations. ​ No specific genetic cause can be identified. Multiple Pituitary Hormone Acquired forms of MPHD ​ varies, ​ PROP 1 Deficiency (MPHD) ​ Any lesions that damages the ○​ GH, TSH, LH, FSH, PRL hypothalamus, pituitary stalk or deficiencies, var ACTH anterior pituitary deficiency, variable AP are the ​ Diabetes insipidus - most most common explanation for common acquired MPHD recessive MPHD (craniopharyngioma) ○​ Median age of GH deficiency is ​ Infiltrative / Inflammatory / 6 y/o Infectious - can cause hypothalamic - hypophyseal ​ POU1F1 destruction ○​ GH, PRL variable TSH ​ Radiation Therapy - risk and deficiency timing of the emergence of the ○​ Necessary for maturation of pituitary hormone deficiencies function of somatotropes, depend on the dose and lactotropes and thyrotropes duration of radiation ○​ Normal in early fetal growth but ​ High doses of gamma radiation experience severe growth (>50) are likely to produce GH failure in the 1st year of life deficiency ​ Traumatic brain injury, including ​ HESX1 abusive head trauma, motor ○​ Expressed in precursor of all 5 vehicle acciden types of the anterior pituitary early in the embryologic development ○​ Mutation results in heterogenous phenotypes with defects in the development of the optic nerve and pituitary ○​ Patients may have IGHD or MPHDs with or without optic nerve hypoplasia ​ LHX3 and LHX4 ○​ GH, TSH, LH, FSH, PRL deficiencies but not ACTH ○​ Tiny v-shaped pituitary fossa, chiari I malformation and an ectopic posterior pituitary ​ Pituitary Hypoplasia ○​ Isolated phenomenon or associated with more extensive developmental abnormalities such as anencephaly or holoprosencephaly ○​ Midline facial anomalies of the finding of solitary maxillary central incisor indicate a high likelihood of GH or other anterior or posterior hormone deficiency ​ Septo-optic Dysplasia ○​ Clinical nystagmus or visual impairment in infancy ○​ Triad ​ Small attenuated pituitary gland’ ​ Attenuated pituitary stalk ​ Ectopic posterior pituitary bright spot ○​ Primary etiology if hypopituitarism is hypothalamic dysfunction ○​ GH deficiency is the most common Growth Hormone Deficiency 1. GH secretion is pulsatile with the Isolated GH deficiency should be ​ Neonates Criteria for GH Deficiency work ​ Constitutional Delay in ​ Indication for GH Therapy highest secretion during sleep and suspected in the following cases: ○​ Typical features up Growth and Adolescence or ○​ GH deficiency peaks during childhood and ​ Neonatal hypoglycemia, ○​ Random GH measurement ​ Severe short stature (1.5 SD below MPH ○​ Height below but parallel to 3rd ​ Gonadal Dysgenesis 2. Hypothalamus releases GHRH to jaundice, microphallus ○​ Auxological criteria ​ Height >2 SD below the mean percentile in early childhood, ​ Delayed Puberty act on pituitary to release GH, GH ​ Cranial irradiation ​ Short stature and height velocity where the fall off percentile is ​ Growth Hormone then acts on the liver to produce ​ Head trauma, CNS infection ​ Short growth velocity ​ Decrease in height SD of >0.5 8-9 years Deficiency IGF - 1 ​ Consanguinity ○​ Weight and height monitoring measured over 1 year in ○​ Delayed bine age; BA2 years of age ○​ Delayed onset of puberty ​ Glucose Metabolism and ​ Muscles abnormalities ​ A minimum of two growth ​ Signs of indicative cranial ○​ History of pubertal delay in Diabetes ○​ Incr. amino acid transport hormone stimulation tests lesion parents ​ Cardiovascular and Lipid ○​ Incr. nitrogen retention using insulin, arginine, ​ Signs of MPHD ○​ Catch up growth occurs during Abnormalities ○​ Incr. lean tissue and energy clonidine, glucagon or ​ Neonatal signs and symptoms puberty ○​ Chronic Renal Failure expenditure L-dopa peak GH level of GHD ○​ Final adult height is within ​ Uremia ​ Adipose Tissue ​ Peak level of less than 10 target range/genetic height ​ Nutritional Deficiencies ○​ Acute insulin-like effects, ug/L or less than 20 potential ​ Metabolic Acidosis promotes glycogenesis, inhibits microIU/L ​ Constitutional Delay ​ Impaired Growth Hormone gluconeogenesis ○​ Radiologic Evaluation or Bone ○​ Watchful waiting, late bloomers (GH) Axis ○​ Incr lipolysis age - delayed ○​ Occasionally a short course of ○​ IUGR/SGA ○​ Inhibits lipoprotein lipase ​ Delayed bone aging >2 testosterone enanthate 50 ○​ Idiopathic Short Stature ○​ Decr glucose transport years behind chronological mg/IM monthly for 3 months ○​ Treatment with growth ○​ Decr lipogenesis age ○​ Given for >12 years as any less hormone should be considered ​ Linear growth and bone may cause early epiphyseal as soon as growth failure occur metabolism growth plate closure ○​ Prader-Willi Syndrome ○​ Promotes epiphyseal growth ○​ It is not recommended for ​ genetic disorder caused by ○​ Incr bone mass patients whose chronological loss of function of specific age is less than 100 or seizures in severe cases. space, causing dilution of sodium in the bloodstream. This is usually corrected by adjusting sodium for mOsm/kg in ​ Integumentary System: glucose. SIADH, renal Edema, particularly in ​ Hyperlipidemia and Hyperproteinemia: High levels of lipids (e.g., in hypertriglyceridemia) or proteins failure, or heart hypervolemic states. (e.g., multiple myeloma) can falsely lower the measured sodium concentration. failure ○​ Key Point ​ Serum Osmolality: Can help determine if the hyponatremia is due to water retention (low osmolality) or Urine Specific 1.005–1.030 Low or High Low (1.003–1.010) High (1.020–1.030) other factors (e.g., glucose-induced pseudohyponatremia). Gravity (depends on cause) ​ Urine Sodium: Low urine sodium (20 mEq/L) suggests euvolemic or hypervolemic hyponatremia (e.g., SIADH or heart failure). Urine Osmolality: Low urine osmolality (100 mOsm/kg) normal Disorder Intravascular Volume Status Urine Sodium ​ Under normal conditions, ADH is secreted by the posterior ​ Ihe cornerstone of treatment for SIADH is fluid restriction to prevent further dilution of serum sodium. or slightly elevated plasma pituitary in response to increased serum osmolality (higher This typically involves limiting fluid intake to 800-1000 mL per day depending on the severity of volume, normal to high urine Systemic Dehydration low low concentration of solutes in the blood) or hypovolemia (decreased hyponatremia. This helps to gradually raise sodium levels by allowing the kidneys to excrete excess sodium and low serum uric acid blood volume). ADH acts primarily on the kidneys, specifically on water. ​ Occur with encephalitis, brain Decreased Effective Plasma low low the collecting ducts in the nephron, where it: ○​ Vasopressin Receptor Antagonists (Vaptans): tumor, head trauma, psychiatric Volume ​ Promotes water reabsorption by binding to V2 receptors, leading ​ Tolvaptan and Conivaptan are vasopressin receptor antagonists that block the effects of ADH in the disease, prolonged nausea, to increased water permeability and the movement of water from kidneys. By inhibiting the V2 receptors, they allow the kidneys to excrete free water, which helps to pneumonia, tuberculosis Primary Salt Loss (Non-renal) low low the urine back into the bloodstream. correct dilutional hyponatremia. meningitis ​ This mechanism conserves body water, diluting the blood and ​ Tolvaptan is typically used orally, while Conivaptan is given intravenously. ​ Can also be found in the second Primary Salt Loss (Renal) low high restoring normal fluid balance. ​ These agents are particularly useful for chronic SIADH or cases where fluid restriction is insufficient. phase of the triphasic response ○​ Pathophysiology of SIADH ○​ Hypertonic Saline (3% NaCl): post hypothalamic pituitary SIADH high high ​ In SIADH, there is excessive, inappropriate secretion of ADH, ​ Hypertonic saline (3% sodium chloride) may be used in acute or symptomatic SIADH (e.g., when sodium surgery which occurs regardless of normal or low serum osmolality. This is 150 water retention, CSW involves sodium depletion, leading to ​ Hypovolemia correction: Administer IV fluids carefully to avoid overcorrection and maintain a mEq/L), excessive urine output, hypovolemia (low blood volume) and hyponatremia normovolemic state. hypovolemia, normal or high uric Serum Sodium low low high ○​ CSW is thought to be caused by a dysregulated release of natriuretic ○​ Sodium Supplementation: acid, suppressed vasopressin peptides (such as BNP) in response to brain injury, leading to ​ Oral or IV sodium chloride tablets may be used to supplement sodium in cases of significant depletion. and elevated atrial natriuretic Urine Output Normal or high high high excessive renal sodium loss. ​ Hypertonic saline may be used if sodium levels are very low (e.g., serum sodium 20 ○​ There is also increased renal perfusion with decreased aldosterone infusion must be carefully controlled to avoid rapid correction of sodium. pmol/L) Urine Sodium high Very high low and hypovolemia from fluid loss, leading to decreased sodium levels. ○​ Mineralocorticoids (e.g., Fludrocortisone): ​ SIADH vs CSW important to ○​ This results in hyponatremia and hypovolemia, but edema is typically ​ Fludrocortisone, a synthetic corticosteroid, may be used to increase sodium retention by mimicking the distinguish because treatment Intravascular Volume Normal or high low low absent. action of aldosterone, which is often insufficient in CSW. differs Status ​ This helps prevent further sodium loss from the kidneys. ​ Treatment is Sodium Chloride ○​ Avoiding Diuretics and water Vasopressin Level high low low ​ Diuretics should be avoided because they can worsen sodium loss and dehydration in CSW. ○​ Monitoring: ​ Close monitoring of serum sodium, blood pressure, and urine output is essential to guide treatment and avoid complications like cerebral edema or over-correction. Disease Brief Intro Signs and Symptoms Etiology/Risk Factor/Types Involved Systems Pathophysiology Clinical Presentation Diagnosis/What to Check Scoring System Differential Diagnosis Conservative Lifestyle Modification Pharmacology MOA Follow - up Surgical Intervention ​ Adrenal Glands Disorder ​ Layers ​ Physiology ​ Key Enzymes and Processes to Remember ​ Multi-step Clinical Synthesis Pathway ​ Renin-Angiotensin-Aldosterone System (RAAS): Overview ○​ Fetal Adrenal Cortex ​ Connective Tissue Capsule ○​ Cortisol secretion regulated by ○​ The adrenal cortex is divided into three layers, each responsible for ○​ A 35-year-old woman presents with hypokalemia, hypertension, and ○​ The RAAS is a hormone system that regulates blood pressure, fluid, ​ Adrenal cortex is derived ○​ None corticotropin - releasing producing specific types of steroid hormones: suppressed renin activity. Lab tests reveal elevated aldosterone levels and electrolyte balance. It is activated primarily in response to low from mesodermal gonadal ​ Zona Glomerulosa hormone (CRH) and and normal cortisol. A mutation in which enzyme would most likely blood pressure, low sodium levels, or sympathetic nervous system ridge at 5-6 weeks ○​ Mineralocorticoid Adrenocorticotropic Hormone ​ Zona Glomerulosa (Mineralocorticoids - Aldosterone) explain these findings? stimulation. gestation ​ Zona Fasciculata (ACTH) ○​ Key Enzyme: Aldosterone Synthase (CYP11B2) ○​ Answer: Aldosterone Synthase (CYP11B2) ​ Gonadal ridge cell migrate ○​ Mesothelium origin ○​ Negative feedback on both ○​ Rate-Limiting Step: Conversion of cholesterol to pregnenolone by ○​ The symptoms indicate primary hyperaldosteronism (Conn's ​ Steps in the RAAS giving rise to steroidogenic ○​ Glucocorticoids CRH and ACTH Cholesterol Desmolase (CYP11A1) syndrome). Mutations or overactivation of CYP11B2 in the zona ​ Renin Release cells (adrenal and gonadal) ​ Zona Reticularis ○​ CRH regulates ACTH via ○​ Regulated by Angiotensin II and Potassium. glomerulosa would increase aldosterone production. ○​ Stimulus: Decreased renal perfusion pressure (e.g., hypovolemia, low ​ At 7-8 weeks, sympathetic ○​ Androgens production of POMC which blood pressure), low sodium levels in the distal tubules (sensed by the nerve cells invade into ​ Medulla produces ACTH, Lipotropin, ​ Zona Fasciculata (Glucocorticoids - Cortisol) ​ Pathway Blockage with Alternate Enzyme Role macula densa), or sympathetic activation (β1-adrenergic receptors). primitive adrenocortical ○​ Neuralcrests origin Beta Endorphin, MSH ○​ Key Enzymes: ○​ A 5-year-old male presents with ambiguous genitalia and ○​ Source: Juxtaglomerular cells in the kidney. cells - adrenal medulla ○​ Catecholamines ○​ Cortisol Secretion ○​ 17α-Hydroxylase (CYP17): Adds hydroxyl groups to steroids. hypertension. Genetic testing reveals a mutation in CYP11B1. What ○​ Function: Converts angiotensinogen (from the liver) to angiotensin I. ​ During late gestation. ​ 7-9 mg/m2/day neonates ○​ 11β-Hydroxylase (CYP11B1): Converts 11-deoxycortisol to cortisol. intermediate would accumulate, and how would cortisol production Placental estrogen Clinical Correlations and ​ 6-7 mg/m2/day children ○​ Regulator: ACTH from the pituitary gland. be affected? ​ Conversion of Angiotensin I to Angiotensin II promotes fetal cortisol Disorders ​ 100-150 mg/m2/day stress ○​ Answer: Intermediate Accumulation: 11-deoxycortisol and ○​ Enzyme:Angiotensin-Converting Enzyme (ACE), mainly in the lungs production ​ Hyperactivation of RAAS ​ Zona Reticularis (Androgens - DHEA, Androstenedione) 11-deoxycorticosterone (DOC) ○​ Angiotensin II Actions: ​ During late gestation ​ Primary Hyperaldosteronism ○​ Key Enzymes: 17,20-Lyase (CYP17): Cleaves 17α-hydroxyprogesterone ○​ Cortisol Effect: Decreased production due to the inability of ○​ Vasoconstriction: Increases systemic vascular resistance, raising placental estrogen (Conn’s Syndrome): to form androgens. 11-deoxycortisol to convert into cortisol. blood pressure. promotes fetal cortisol ○​ Excess aldosterone due to ○​ Stimulates Aldosterone Secretion: Acts on the adrenal zona production adrenal adenoma or ​ Key Points for Memorization: ​ Feedback Mechanism-Based Question glomerulosa to release aldosterone. ​ Promotes maturation of hyperplasia. ○​ Cholesterol → Pregnenolone (CYP11A1) is the rate-limiting step. ○​ How would a deficiency in 21-Hydroxylase (CYP21A2) affect ACTH ○​ Stimulates ADH Release: Enhances water retention via the posterior lung, thyroid, liver, gut ○​ Symptoms: Hypertension, ○​ Mineralocorticoids: Need CYP11B2 (Aldosterone Synthase). levels and adrenal androgen production? Explain the clinical pituitary. ​ Fetal adrenal rapidly hypokalemia, metabolic ○​ Glucocorticoids: Need CYP17 (17α-Hydroxylase) and CYP11B1 implications. ○​ Increases Thirst: Via hypothalamic stimulation. Adrenal Cortical Hormone Synthesis regresses after birth alkalosis. (11β-Hydroxylase). ○​ Answer: ACTH Levels: Increased due to lack of cortisol-mediated ​ Adrenal cortex is capable of ○​ Renovascular Hypertension: ○​ Androgens: Depend on CYP17 (17,20-Lyase). negative feedback. ​ Aldosterone Release steroid production by the Stenosis of renal arteries ○​ Androgen Production: Increased because precursors are shunted ○​ Source: Zona glomerulosa of the adrenal cortex. 9th - 12th week of gestation activates RAAS. ○​ Disorders arise when these enzymes are deficient or overactive, toward the androgen pathway. ○​ Stimulus: Angiotensin II, hyperkalemia (high potassium levels), or ​ Hypoactivation of RAAS leading to excess or deficient steroid production. ○​ Clinical Implication: Congenital Adrenal Hyperplasia (CAH) with ACTH (lesser extent). ​ Addison's Disease: symptoms such as virilization in females, salt-wasting, and adrenal ○​ Function: Increases sodium reabsorption in the distal tubules and ○​ Adrenal insufficiency leads to hyperplasia. collecting ducts of the nephron. reduced aldosterone and ○​ Promotes potassium and hydrogen excretion. cortisol. ○​ Leads to water retention, indirectly increasing blood volume and ○​ Symptoms: Hypotension, pressure. hyperkalemia, hyponatremia. ○​ ACE Inhibitors/ARBs: Block ​ Example RAAS to treat hypertension or ○​ An 18-year-old female presents with severe hypokalemia, metabolic heart failure. alkalosis, and resistant hypertension. Laboratory tests reveal low plasma renin activity and high aldosterone levels. CT imaging identifies a unilateral adrenal mass. What is the most likely diagnosis, and how would an aldosterone antagonist help in treatment? ○​ Answer: Diagnosis: Primary hyperaldosteronism (Conn's Syndrome). ○​ Mechanism of Aldosterone Antagonist: ○​ Blocks aldosterone receptors in the distal tubules, reducing sodium reabsorption and promoting potassium retention. ○​ Examples: Spironolactone or Eplerenone. ​ Congenital Adrenal ​ Hyperplasia and hypertrophy of ​ Forms of CAH ​ Pathophysiology Hyperplasia the adrenal cortex due to ○​ 21 Hydroxylase Deficiency(CYP21A2) ○​ Enzyme Deficiency ○​ In females, the most common excessive ACTH stimulation ​ Most common ​ The most common deficiency is 21-hydroxylase deficiency presentation is ambiguous ​ Enzyme deficiency in ​ Prenatal exposure to testosterone and D4 androstenedione at (CYP21A2) (90–95% of cases). Other rare forms include genitalia glucocorticoid production leads critical stages of sexual differentiation leads to virilization of 11β-hydroxylase deficiency, 17α-hydroxylase deficiency, and ○​ In males, the most common to cortisol deficiency external genitalia of females resulting in genital ambiguity at birth 3β-hydroxysteroid dehydrogenase (HSD3B2) deficiency. presentation is ​ Signs and symptoms depends ​ Classical CAH ○​ Cortisol Deficiency: hyperpigmentation on the deficient enzymatic ○​ Simple Virilizing ​ Reduced cortisol disrupts negative feedback to the hypothalamus step/form of CAH ​ Unable to produce adequate aldosterone and pituitary, leading to elevated ACTH levels. ○​ Androgen excess and/or ​ Male present with precocious puberty and a pubertal testicular ​ Reduced cortisol disrupts negative feedback to the hypothalamus aldosterone deficiency volume (weight gain ○​ Establish diagnosis Adenoma/ Ectopic ACTH Production) ○​ These drugs reduce cortisol production by inhibiting enzymes involved ○​ Normalize cortisol level at its ○​ 1=2 weeks post op, assess Diagnosis % of px year pregnancy, chronic strenuous ○​ 85% ACTH dependent ○​ Excess mineralocorticoid ○​ Hirsutism ○​ Differentiate cause ○​ Pasireotide in steroid synthesis receptor to eliminate pituitary hormone insufficiency ○​ Median age of diagnosis is 9 exercise ​ 80% pituitary dependent ○​ Excess adrenal androgen ○​ Acne ​ Diagnosis ​ (if the source is a pituitary adenoma): It directly suppresses ACTH ○​ Metyrapone symptoms and sign of ○​ 1-3 months post op, MRI ○​ Median time between onset of ○​ Pathologic state, cushing ​ 20% ectopic ACTH ○​ Hypertension ○​ Drug history to rule out ACTH Dependent Cushing Syndrome 80 secretion. ​ Blocks 11β-hydroxylase, reducing cortisol synthesis. hypercortisolism ​ Successful Mgmt symptoms to diagnosis is 1 syndrome, psychiatric states ○​ 15% ACTH independent ​ Mech of Clinical Signs ○​ Poor school performance iatrogenic causes ○​ Ketoconazole or Osilodrostat: ○​ Osilodrostat ○​ Treat comorbidities ○​ Localization is essential year ○​ Malnutrition ​ Adenoma 30% ○​ Ex ○​ Fatigue ○​ Testing recommended for Cushing’s Dse 68 ​ Frequently used to inhibit cortisol synthesis, particularly while ​ A newer drug that inhibits 11β-hydroxylase, used for patients with ○​ Multidisciplinary team ​ Treatment of Choice ○​ Female>male ○​ Glucocorticoid resistance ​ Carcinoma 70% ○​ Growth retardation specific groups awaiting surgery or if surgery is not possible. endogenous Cushing's syndrome. approach ○​ Transsphenoidal Surgey ○​ In adult, cushing’s dse > ○​ 200 ng/dL) radioactive iodine therapy, (PTU) or malignancy. clinical symptoms (tachycardia, (autoimmune), toxic multinodular regulation thyroidectomy if necessary. weight loss, tremors). goiter, or thyroid adenoma. Type 1 Diabetes Mellitus Autoimmune destruction of Deficient: Insulin Insulin: Glucose regulation, cellular Insulin: 3-25 µU/mL (fasting) Insulin: Low or absent in T1DM Insulin therapy, dietary Insulin (rapid-acting, long-acting) Pancreatic islet cell transplantation Monitor blood glucose, HbA1c, and pancreatic beta cells leading to energy storage management, exercise, and blood (rare), or pancreas transplant in complications (neuropathy, insulin deficiency and glucose monitoring. severe cases. retinopathy, nephropathy). hyperglycemia. Type 2 Diabetes Mellitus Insulin resistance with beta cell Increased (early): Insulin, later Insulin: Glucose regulation, cellular Insulin: 3-25 µU/mL (fasting) Insulin: Elevated initially, then Lifestyle modifications (diet, Lifestyle modifications (diet, Pancreatic surgery or bariatric Monitor blood glucose, HbA1c, and dysfunction, leading to Deficient: Insulin (as beta cells fail) energy storage reduced as beta cells deteriorate exercise), oral hypoglycemics, exercise), oral hypoglycemics, surgery for significant obesity kidney function (e.g., creatinine). hyperglycemia. and/or insulin therapy. and/or insulin therapy. cases. Hyperparathyroidism Excessive parathyroid hormone Increased: PTH, calcium PTH: Regulates calcium and PTH: 10-65 pg/mL; Calcium: PTH: Elevated (>65 pg/mL); Surgery (parathyroidectomy), Cinacalcet (if surgery is not an Parathyroidectomy (most common Monitor calcium, phosphate, PTH (PTH) production, usually due to (hypercalcemia) phosphate balance; Calcium: Bone 8.5-10.2 mg/dL (serum) Calcium: Elevated (>10.2 mg/dL) bisphosphonates for bone option) treatment). levels, and bone density. parathyroid adenoma, hyperplasia, formation, muscle function protection, cinacalcet or carcinoma, causing (calcimimetic) for medical hypercalcemia, bone resorption, management. and kidney stones Hypoparathyroidism Deficient PTH production due to Deficient: PTH, calcium PTH: Regulates calcium and PTH: 10-65 pg/mL; Calcium: PTH: Low (