Endocrine - Hormones Flashcards
Lipophilic vs. Hydrophilic Hormones
Lipophilic Hormones – interact with lipid membrane and cross through unassisted
o Bind to receptors in cytoplasm to form a complex that then travels into the nucleus to up/down regulate gene expression
o Steroid hormones, vitamin D, TSH
Hydrophilic Hormones – do NOT cross the membrane
o Bind to surface receptors and exert affect through second messenger systems
o Cannot give peptide hormones orally because they will be digested before they can exert effects
Possible Pathologies
o Hyperfunction, hypofunction, tumors/cancers, defective receptor/enzyme (genetic disease)
Hypothalamus-Pituitary Axis
– hypothalamus signals to anterior or posterior pituitary
o Infundibulum (pituitary stalk) connects hypothalamus to pituitary
o Sella turcia – encases the pituitary gland within the sphenoid bone
o ALL pituitary hormones are peptide hormones
Anterior Pituitary
• Pars distalis = anterior pituitary = adenohypophysis
o Cells are glandular NOT neural
o Local Portal System & Mechanism
Hypothalamic nuclei releasing hormone primary capillary plexus hypophyseal portal system secondary capillary plexus anterior pituitary stimulating peptide hormone
Serum concentrations are different in this region compared to other parts of body
o FLATPiG hormones
Posterior Pituitary
• Pars nervosa = posterior pituitary = neurohypophysis
o Neurons with cell bodies in hypothalamus send axons through infundibulum and terminate in the posterior pituitary
o Releases products into systemic blood supply
Serum concentration sin posterior pituitary is same as in any other part of body
Feedback Loops - Short vs. Long
o Short – acts on pituitary
o Long – acts on hypothalamus
Anterior Hyperpituitarism Characteristics and Symptoms
– generally result of pituitary adenomas – benign slow growing glandular tumors
o NOT Cancer – do not metastasize
o Proliferation of a single cell
o Naming: add –oma or –adenoma
o Prolactinomas = most common
o Usually one hormone is overproduced but can have multiple hormones
o Major concern: brain volume and hormone imbalance
o Symptoms – headache, fatigue, visual changes, hyposecretion of neighboring hormones
Bilateral Hemianopsia – half-blind – lose peripheral vision first
• Tumor is pressing on a nerve and preventing signals from running through it
• Pathognomonic – when it’s present you know it is caused by a pituitary adenoma
Anterior Hyperpituitarism - Types/Causes
o Null Cell Adenoma – half of the cells in anterior pituitary are not producing any hormone
Less of every hormone produced
o Ischemic necrosis – decreased blood flow to gland causing death of tissue
Anterior pituitary extremely susceptible due to low pressure venous system
Sheehan’s Syndrome – hemorrhage leading to hypotension during childbirth
Trauma or shock also causes
o Ablation – cutting out adenoma – taking part or all of the pituitary out
o Panhypopituitarism – results from trauma to the pituitary stalk; NO FLATPiG hormones
Hyposecretion of Growth Hormone
o Pituitary dwarfism – in children and adolescents; proportional limbs
Different from achondroplasia – dwarfism caused by failure of long bones to grow; short stubby limbs appearing unproportional
o Adults – GH repairs skeletal tissue – would present with stiffness, soreness, and joint problems
Hypersecretion of Growth Hormone
o Gigantism – in children and adolescents
Different from Marfans syndrome – people really tall as result of longer arms/legs
o Acromegaly – in adulthood – do not get taller; appositional growth of bones (larger/wider)
Excess growth in chin, forehead, zygomatic process, wide fingers
Hypersecretion of Prolactin
– caused by prolactinomas
o Females – amenorrhea, galactorrhea, hirsutism (excess hair), & osteopenia (bone breakdown)
o Males – harder to detect – hypogonadism, erectile dysfunction, impaired libido, oligospermia, diminished ejaculate volume
Posterior Pituitary Hormones
o Synthesized w/ their binding proteins in the supraoptic & paraventricular nuclei of hypothalamus
o Antidiuretic Hormone (ADH) (vasopressin) – kidney tubules and vasculature – increase water reabsorption and vasoconstriction (to increase systemic blood pressure)
o Oxytocin – uterine smooth muscle & breasts – uterine smooth muscle contraction or milk release
Oxytocin receptors on uterus are absent until end of pregnancy when they up-regulate regulating the receptor controls the effect of the hormone
o Somatostatin and dopamine are produced many places in body but will only achieve relevant concentrations for inhibition if secreted by the hypothalamus
Posterior Pituitary Syndromes
o NO adenomas – PP is neural tissue & neurons don’t develop tumors (they are post-mitotic)
o Central DI – too little ADH
o Syndrome of Inappropriate ADH (SIADH) – too much ADH
o Oxytocin Deficiency – cause problem with childbirth
Give synthetic oxytocin that can induce contractions
Syndromes of Inappropriate Antidiuretic Hormone
o Tumor – hypersecretion of ADH – enhanced renal water retention, hyponatremia, hypoosmolarity
Fix blood osmolality and hyponatremia SLOWLY
o Drinking too much water during exercise
ADH levels increase during exercise to conserve water
Acute hypo-osmotic blood and neural complications
Diabetes Insipidus
o Insufficiency of ADH polyuria and polydipsia
o Partial or total inability to concentrate the urine
o Neurogenic (central) – inability to make ADH or insufficient amounts of ADH
Treat with synthetic drug through nasal spray or injection of ADH
o Nephrogenic – inadequate response to ADH; no ADH receptors
Synthetic drug cannot treat
Thyroid Gland
o 2 lobes lateral to the trachea with an isthmus connecting them
o Follicles – follicle cells surrounding colloid – produce thyroid hormone; stored in colloid cells
o Parafollicular cells (C cells) – secrete calcitonin – between follicles/follicle cells
o Regulation of Thyroid hormone secretion
Thyrotropin-releasing hormone and thyroid stimulating hormone
Thyroid Hormones
o 90% T4 and 10% T3 increase the effect of adrenergics
o Lipophilic and therefore require a carrier protein to travel around the body
Bound to thyroxine-binding globulin, thyroxine-binding pre-albumin, or albumin
o Affect growth and maturation of tissues, cell metabolism, heat production, and O2 consumption
o Never worried about levels of TRH in blood only TSH
Hyperthyroidism
Symptoms – anxiety, irritability, difficulty sleeping, fatigue, rapid/irregular heartbeat, hands/feet tremors, increase in perspiration, weight loss, enlarged thyroid (goiter), light menstrual periods, increased sensitivity to heat, frequent bowel movements, exophthalmos (bulging eyes due to accumulation of connective tissue behind eyes)
Treatment – beta blockers – block adrenergic receptors
o Graves Disease - most common cause of hyperthyroidism in US
Autoimmune disorder – body produces IgG antibody against TSH receptor chronic stimulation of thyroid resulting in overproduction/secretion of TH
• Decreased levels of TSH due to negative feedback
o Hyperfunctioning Adenoma (toxic goiter) – constantly secretes thyroid hormone
Decreased levels of TSH due to negative feedback
o TSH Cell Adenoma in pituitary – produce too much TSH
Unresponsive to negative feedback
o Iatrogenic – caused by doctor
Hypothyroidism
Symptoms – increased sensitivity to cold, constipation, pale/dry skin, puffy face (myxedema), hoarse voice, elevated blood cholesterol, weight gain, muscle aches, pain in joints, muscle weakness, heavy menstrual period, depression, mental retardation in infants or in utero (cretinism)
Treatment – levothyroxine, iodine – give supplemental thyroid hormone
o Hashimoto Thyroiditis – chronic lymphocytic
Autoimmune destruction of the thyroid; follicle centers get destroyed, hindering thyroid hormone synthesis and release
o Iodine Deficiency (endemic goiter, cretinism) – soil and seaweed good source of iodine
Uncommon in developing countries and very easily treated via iodine supplement
Decreased T3/T4 but increased TSH due to no feedback
o Ablation – removal of part/all of thyroid
o Idiopathic – there is no clear reason
Thyroid Carcinoma Types
o Papillary (80%; nonfunctional) – high survival rate o Follicular (15%; may be hyperfunctional) o Medullary (5%; parafollicular cells) o Anaplastic (rare; fast growing; 100% mortality)
Parathyroid Glands
o 4 small glands on posterior of thyroid
o Produce PTH hormone - regulator of serum Ca+ released in response to low serum Ca+
• Act on bone to increase Ca+ reabsorption
• Acts on kidney to stimulate calcium reabsorption & vitamin D synthesis
• Activates intestine via vitamin D which increases Ca+ absorption
Antagonist of calcitonin
Cause excretion of phosphate
• Diseases of Parathyroid Gland Mechanism - Changes in Ca+ alter cellular functions, excitability, and signaling pathways
Hyperparathyroidism
o Primary – excess secretion of PTH from one or more parathyroid glands
Caused by adenoma or hyperplasia
Elevated serum Ca+ but decrease in phosphate
o Secondary – increase in PTH secondary to a chronic disease
Cause by chronically low Ca+ in PT glands; high phosphate, vit. D malabsorption
renal failure – can cause high or low phosphate with low Ca+
o Symptoms: hypercalcemia/uria; kidney stones, heartburn/abdominal pain; nausea, vomiting, loss of appetite, thinning of bones, confusion/poor memory, fatigue
o Treatment: CANT remove all 4 parathyroid glands permanently
Hypoparathyroidism
– abnormally low PTH levels
o Primary – damage to parathyroid (thyroid surgery) – low Ca+; high phosphate
o Secondary – increased bone breakdown (metastatic bone cancer) – high Ca+; unknown phosphate
Adrenal Cortex and Zona Glomerulosa
• Adrenal Cortex: 80% of total adrenal weight; salt, sugar, sex, the deeper you go the sweeter it gets
o Zona glomerulosa (outermost) – mineralocorticoid hormones
Affect ion transport by epithelial cells
• Increase the activity of the Na+ pump of epithelial cells
• Cause Na+ retention; K+, H+ loss
• Ex: aldosterone – regulated by renin-angiotensin system
o Stimulated by low BP, low Na+, high ACTH, high Ca+
Adrenal Cortex and Zona Fasciculata
– glucocorticoid hormones
Stimulated by adrenocorticotropic hormone (ACTH)
Direct effects on carbohydrate metabolism; promote hyperglycemia
Anti-inflammatory and growth-suppressing effects
Influence awareness and sleep habits
Ex: cortisol – long-term stress hormone
Feedback control – long and short loop negative feedback, somatostatin inhibits AP
Adrenal Cortex and Zona Reticularis
(innermost) – androgen and small amount of estrogen hormones
Secretes weak androgens (DHEA, androstenedione)
• Converted by peripheral tissues to stronger androgens (testosterone)
Adrenal Medulla
o Chromaffin cells (pheochromocytes) – secrete hydrophilic catecholamines – epinephrine (majority), norepinephrine
o Release of catecholamines = short-term “fight or flight” response
o Catecholamines promote hyperglycemia
o Receives input from PREganglionic sympathetic fibers
Hypercortisolism
- Cushing Syndrome/Disease
– increased ACTH
Pituitary tumor (officially “cushing disease”)
Adrenal tumor
Paraneoplastic – ACTH secreting tumor outside pituitary (ex: lung)
Iatrogenic – drug-induced (ex: immune suppressant steroids)
o Symptoms: metabolism drop (weight gain), rounding face (moon face), fat deposit between shoulders (buffalo hump), stretch marks (striae), erectile dysfunction/amenorrhea, facial flushing
Hyperaldosteronism
Primary – too much aldosterone (Conn’s Syndrome)
Secondary – too much renin – increased angiotensin, increased aldosterone
o Symptoms: high blood pressure/volume, hypokalemic
o Pressure natruiuresis – overly high blood pressure will result in kidney dumping some of retained Na+/water elevation of Na+ is less drastic as expected
o Treatment: removal of aldosterone producing adenoma; aldosterone antagonists
Adrenogenital Syndromes
o Congenital Adrenal Hyperplasia – defective 21-hydroxylase enzyme
Blocks glucocorticoid synthesis and NO negative feedback to ACTH
o Adrenocortical neoplasms – androgen producing tumor – too much DHEA
o Symptoms: virilization (clitoromegaly, hirsutism)
o Treatment: cortisol to bring ACTH levels down; tumor resection if caused by neoplasm
Chronic Adrenocortical Insufficiency
- Addison’s Disease
o All adrenal corticosteroids decreased due to autoimmune destruction of adrenal cortex
o NO negative feedback to hypothalamus and anterior pituitary to decrease CRH/ACTH
High ACTH buildup of melanocyte stimulating hormone (MSH)
o Symptoms: weakness, hyperpigmentation except tongue/nail beds, low BP, salt craving (low aldosterone), hypoglycemia (low cortisol)
o Treatment: hormone replacing therapy
NO androgen therapy in males because testes produce enough
Pheochromocytoma
– neoplasm of chromaffin cells (adrenal medulla hyperplasia)
o Excessive fight or flight response under stressful situations only
o Symptoms: rapid HR/BP, excessive sweating, chest pain, feelings of anxiety/fright, tremors; may commit unintentional murder
o Treatment: alpha blockers, beta blockers, surgical resection
