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Endocrine System Pathophysiology: Hormones and Disorders, Exams of Pathophysiology

A.T. Still University of Health Sciences (ATSU)Pathophysiology

A concise overview of endocrine pathophysiology, focusing on hormone function, secretion, and regulation. It covers water-soluble and lipid-soluble hormones, feedback mechanisms, and factors affecting hormone sensitivity. Key topics include growth hormone, thyroid hormone, parathyroid hormone, and adrenal gland function, along with related disorders such as dwarfism, gigantism, hypothyroidism, hyperthyroidism, addison's disease, and cushing's disease. The document also addresses the clinical manifestations and pathogenesis of these conditions, making it a valuable resource for understanding endocrine system disorders. It is useful for medical students and healthcare professionals seeking a quick review of endocrine system pathophysiology and related diseases, offering insights into hormonal imbalances and their clinical implications.

Typology: Exams

2024/2025

Available from 08/09/2025

DrShirleyAurora
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Advanced Pathophysiology- Endocrine
Hormone function -
- ligands that bind to their respective intra- or extracellular receptors.โ˜‘๏ธ๎˜‚
Hormone secretion -
-Regulated through a negative feedback system.โ˜‘๏ธ๎˜‚
-When target cell response is achieved, feedback signals the hormone to decrease its output.
Water- Soluble Hormones -
- Catecholamines and Peptidesโ˜‘๏ธ๎˜‚
-Free molecules
- The only hormones that are circulating free are available for binding with receptors.
- Active-form: Free circulating available to exert an effect. --Faster in moving
- Plasma 1/2 life correlates directly to the % of protein binding
Lipid- Soluble Hormones -
- Steroids, thyroid hormonesโ˜‘๏ธ๎˜‚
- Bound to plasma proteins.
Major sites of hormone degradation and excretion -
liver and kidneysโ˜‘๏ธ๎˜‚
Negative Feedback -
DECREASE subsequent synthesisโ˜‘๏ธ๎˜‚
DECREASE secretion of hormone
Decrease in maximal responsiveness of hormone -
May be due to:โ˜‘๏ธ๎˜‚
- A decrease in # functional target cells
- A decrease in # of receptor cells.
- Limited concentration of an enzyme
- Increase concentration of noncompetitive inhibitor
Decrease in hormonal sensitivity -
May be due to:โ˜‘๏ธ๎˜‚
-Decrease in # of hormone receptors
-Alteration in concentration of modulating co-factors
- Increase rate of hormone degradation
- Increase concentration of antagonist hormones.
Up-regulation -
low hormone concentration induces the formation of more receptors per cellโ˜‘๏ธ๎˜‚
Down-regulation -
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Advanced Pathophysiology- Endocrine

Hormone function - โ˜‘๏ธ - ligands that bind to their respective intra- or extracellular receptors. Hormone secretion - โ˜‘๏ธ -Regulated through a negative feedback system. -When target cell response is achieved, feedback signals the hormone to decrease its output. Water- Soluble Hormones - โ˜‘๏ธ - Catecholamines and Peptides -Free molecules

  • The only hormones that are circulating free are available for binding with receptors.
  • Active-form: Free circulating available to exert an effect. --Faster in moving
  • Plasma 1/2 life correlates directly to the % of protein binding Lipid- Soluble Hormones - โ˜‘๏ธ - Steroids, thyroid hormones
  • Bound to plasma proteins. Major sites of hormone degradation and excretion - โ˜‘๏ธ liver and kidneys Negative Feedback - โ˜‘๏ธ DECREASE subsequent synthesis DECREASE secretion of hormone Decrease in maximal responsiveness of hormone - โ˜‘๏ธ May be due to:
  • A decrease in # functional target cells
  • A decrease in # of receptor cells.
  • Limited concentration of an enzyme
  • Increase concentration of noncompetitive inhibitor Decrease in hormonal sensitivity - โ˜‘๏ธ May be due to: -Decrease in # of hormone receptors -Alteration in concentration of modulating co-factors
  • Increase rate of hormone degradation
  • Increase concentration of antagonist hormones. Up-regulation - โ˜‘๏ธ low hormone concentration induces the formation of more receptors per cell Down-regulation -

โ˜‘๏ธ Promotes a DECREASE in the # of receptors per cell Primary endocrine disorder - โ˜‘๏ธ -Alternation of the target gland/tissue example: Thyroid -Secretion of hormones that regulate cellular activity. Secondary endocrine disorder - โ˜‘๏ธ -Alternation in the influencing tropic gland/ts example: pituitary Tertiary endocrine disorder - โ˜‘๏ธ - Can be considered secondary

  • hypothalmic dysfunction
  • Target gland responses
  • Physiological responses in cells Normal endocrine physiology - โ˜‘๏ธ CNS-> Hypothalamus-> releasing hormone->pituitary->tropic hormone->peripheral gland-> hormone-> target-> effect Growth Hormone (Normal Functions) - โ˜‘๏ธ Growth-promoting: -Increase linear growth and cartilage -Increase lean ms mass Anti-insulin effects:
  • Decrease adipose ts
  • Increase blood glucose --Functions throughout life Growth Hormone (secretion) - โ˜‘๏ธ - anterior pituitary
  • secretion medicated through adenylyl cyclase system
  • WATER soluble
  • Somatotropin
  • indirect effects: formation of somatomedins (IGF)
  • IGF-1 (Somatomedin) * Growth Hormone (regulation) - โ˜‘๏ธ -secreted in a pulsatile pattern in response to --starvation (protein deficiency) * --GHRH from hypothalamus

Hypothyroidism - โ˜‘๏ธ - Decrease in circulating thyroid Congenital (Cretinism)

  • easy to treat, if not then mental retardation, impaired growth -through placenta Acquired
  • Myxedema: distruction/removal of thyroid gland *-Hashimoto's thyroiditis **most common cause +autoimmune +thyroid ts is replaced by lymphocytes & fibrous ts. +Goiters form bc excess TSH shift in hormones? DECREASE in thyroid hormones= DECREASE metabolism DECREASE T3 & T4= INCREASE TSH & Thyroid antibodies Hypothyroidism (Pathogenesis) - โ˜‘๏ธ DECREASE function of gland DECREASE hormone DECREASE bmr Hypothyroidism (Clinical Manifestations) - โ˜‘๏ธ -weakness -cold intolerance -brittle hair,dry skin -decrease gi -mental dullness, lethargy may progress to COMA Primary Thyroid malfunction - โ˜‘๏ธ Lack of TH (-) feedback on pituitary TSH secretion & hypothalamic TRH secretion Low TH High TSH & TRH Secondary Thyroid malfunction - โ˜‘๏ธ Lack of (-) feedback to hypothalamic release of TRH & TSH & Thyroid TH Low TSH & TH High TRH

Hyperthyroidism - โ˜‘๏ธ -Hyperplasia -Adenoma (lack of negative feedback inhibition on hormone release= excess hormone production=lack of pituitary response to thyroid hormone levels)

  • OD of thyroid hormone Graves Disease - โ˜‘๏ธ -Type 2 hypersensitivity reaction (Hypersensitivity of thyroid function) -autoimmune
  • Antibodies attack thyroid = body produces INCREASE amount of TH=Over activity of thyroid gland = Throtoxicosis
  • Lymphocytes and thyroid are stimulated by antibodies against TSH receptor -Opthalmopathy (Exophthamlus) & dermopathy (swelling and clubbing )
  • Response of an endocrine gland to inappropriate signal Hyperthyroidism (Pathogenesis) - โ˜‘๏ธ INCREASE activity of gland INCREASE hormone INCREASE bmr Hyperthyroidism (Clinical Menifestations) - โ˜‘๏ธ -speed up metabolism
  • irritability
  • tachycardia -sweating -heat intolerance -ms cramps Thyrotoxicosis - โ˜‘๏ธ - Extreme hyperthyroidism
  • Decrease serum TSH= Increase levels of circulating thyroid hormones cause feedback mechanism to brain to suppress TSH. Thyroid storm - โ˜‘๏ธ Life threatening (Fatal within 48 hours if not treated)
  • Stress
  • systemic response of hyperthermia (Tachy, dysrythmia, N/V) Parathyroid Hormone (secretion) - โ˜‘๏ธ Serum Calcium If Ca decreases than Phosphate increases

Norepinephrine (25%) (only 30% of epinephrine comes from adrenals) WATER soluble Adrenal Medulla Catecholamines (Regulation) - โ˜‘๏ธ Releases in response to: ACTH sympathetic stimulation hypoglycemia hypoxia hemorrhage Adrenal Medulla Catecholamines (Effects) - โ˜‘๏ธ Flight or fight hyperglycemia Adrenal Medulla Cortex Hormones (Secretion) - โ˜‘๏ธ -All coritcal hormones are steroid hormones (from cholestrol) -bind to intracellular receptors

  • CRH
  • Negative feedback system Cortisol Regulation - โ˜‘๏ธ - secreted in response to ACTH (anterior pituitary)
  • ACTH released in response to stress
  • higher in AM lower in PM Cortisol Effects - โ˜‘๏ธ Essential part of stress response -Decrease cellular utalization of glucose (BS increases)
  • Protein breakdown
  • Antiinflammatory
  • Inhibits scar formation Addison's Disease hyposecretion - โ˜‘๏ธ -Autoimmune -Destruction of the adrenal gland-> DECREASED production of adrenal hormones (Cortisol and Aldosterone)
  • Manifestations: Hyperpigmentation (increased levels of ACTH where the pituitary gland is trying to stimulate the adrenal cortex to release glucocorticoids & mineralcorticoids===spitting out ACTH) Low blood glucose Low Na High K Secondary Adrenal Cortical insufficiency - โ˜‘๏ธ Hypopituitarism Surgery
  • Rapid withdrawal of exogenous steroids (tapper dose) Adrenal Crisis Hyposecretion - โ˜‘๏ธ Life threatening- acute shutdown -Stress in diagnosed Addison's disease (90% of gland destroyed b4 showing disease) -Hemorrhage of adrenals -Manifestations: Hypotension, vascular collapse Cushings Disease - โ˜‘๏ธ - Excessive ACTH secretion (ex. adenoma)--disease -Excessive level of cortisol regardless of cause--Syndrome OD on exogenous steroids Ectopic tumors: Lungs, thyroid, adrena (Anthyochromosytomas) Adrenal hyperplasia caused by ACTH secreting pituitary adenoma Cushings Disease (Pathogenesis) - โ˜‘๏ธ Pathogenesis: increase ACTH->altered metabolism,fluid & electrolytes. ACTH stimulates excess production of cortisol-> loss of feedback control of ACTH secretion Manifestations of excess Cortisol - โ˜‘๏ธ Cortisol causes skeletal ms to breakdown=weakness=limbs thin truncal obesity moon face osteoporosis- Ca excretion Hyperglycemia Hypertension- promisive effect on catecholamines Aldosterone Regulation - โ˜‘๏ธ -Independent of cortisol

Glucagon effects - โ˜‘๏ธ Antagonist to insulin Stimulates lipolysis->Ketogenic effect DM Diagnosis criteria - โ˜‘๏ธ Type I Absence of insulin Autoimmune Type II Decrease in # of receptors Decrease in function of receptors Decrease in secretion Secondary-Cushings Gestational Metabolic Syndrome: Syndrome X. Insulin resistance, High risk of developing DM2, increased triglycerides, decreased HDL, Increased FBS. HbA1C >6. FPG> 2hr> DM Type I - โ˜‘๏ธ Destruction of B cells in pancrease Lack of /inability to utalize insulin->increase BS->Osmotically active->cell dehydration and starvation. Increased concentration in blood-serum osmolarity high levels of ketones DM Type II - โ˜‘๏ธ Can have a genetic component Amylin- Normally secreted by Bcells, inhibit glycogen secretion= increased BS Insulin is being produced but not effective receptor associated disorder DM Manifestations - โ˜‘๏ธ Polyuria- Inability for kidneys to absorb extra glucose Polydipsia- increased glucose outside cells. osmotic movement Polyphasia- increase hunger Hyperglycemia metabolic pathways - โ˜‘๏ธ Polyol: Shift in pathway, overreactive *Nonenzymatic Glycosylation: Glucose attaches to certain proteins in blood vessels--End product= thicken basement membrane= release of cytokinesis & growth factors that stimulate proliferation of

cells, increase lipid oxidation, & inflammation, loss of vasodilation bc nitric oxide, enhanced plt adhesion. DM Acute Complications - โ˜‘๏ธ -Hypoglycemia: Type I ussually, Alcohol(Decreases liver gluconeogenesis), cool clammy skin, tachy, <60. -Somogyi effect- hypoglycemia at night an rebound in AM bc of epi, GH& corticosteriods -Diabetic Ketoacidosis(DKA) -HHNKS Diabetic Ketoacidosis (DKA) - โ˜‘๏ธ Hyperglycemia Ketosis Metabolic acidosis Polydipsia CNS depression Glucosuria- high plasma glucose level loss of K BS 150- adding more sugar Lack of insulin->mobilization of fatty acids for energy->Increase ketone production (acid) DKA Manifestations - โ˜‘๏ธ Symptoms determined by degree of insulin deficiency & presence of ketones Polyuria Polydypsia polyphagsia Fruity breath warm and dry skin AMS Compensation: Tachycardia Kussmals respirations Hyperosmolar Hyperglycemic nonketonic syndrome (HHNKS) - โ˜‘๏ธ Life threat Lack of ketons Increase in glucose bc blood volume loss Seen in DM II Increased plasma osmolarity, increase BS=extreme dehydration* Ph>7.