Endocrine - Hormones

Question 1

Lipophilic vs. Hydrophilic Hormones

Answer 1

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

Question 2

Possible Pathologies

Answer 2

o Hyperfunction, hypofunction, tumors/cancers, defective receptor/enzyme (genetic disease)

Question 3

Hypothalamus-Pituitary Axis

Answer 3

– 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

Question 4

Anterior Pituitary

Answer 4

• 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

Question 5

Posterior Pituitary

Answer 5

• 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

Question 6

Feedback Loops - Short vs. Long

Answer 6

o Short – acts on pituitary

o Long – acts on hypothalamus

Question 7

Anterior Hyperpituitarism Characteristics and Symptoms

Answer 7

– 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

Question 8

Anterior Hyperpituitarism - Types/Causes

Answer 8

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

Question 9

Hyposecretion of Growth Hormone

Answer 9

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

Question 10

Hypersecretion of Growth Hormone

Answer 10

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

Question 11

Hypersecretion of Prolactin

Answer 11

– 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

Question 12

Posterior Pituitary Hormones

Answer 12

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

Question 13

Posterior Pituitary Syndromes

Answer 13

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

Question 14

Syndromes of Inappropriate Antidiuretic Hormone

Answer 14

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

Question 15

Diabetes Insipidus

Answer 15

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

Question 16

Thyroid Gland

Answer 16

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

Question 17

Thyroid Hormones

Answer 17

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

Question 18

Hyperthyroidism

Answer 18

 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

Question 19

Hypothyroidism

Answer 19

 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

Question 20

Thyroid Carcinoma Types

Answer 20

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)

Question 21

Parathyroid Glands

Answer 21

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

Question 22

Hyperparathyroidism

Answer 22

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

Question 23

Hypoparathyroidism

Answer 23

– 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

Question 24

Adrenal Cortex and Zona Glomerulosa

Answer 24

• 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+

Question 25

Adrenal Cortex and Zona Fasciculata

Answer 25

– 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

Question 26

Adrenal Cortex and Zona Reticularis

Answer 26

(innermost) – androgen and small amount of estrogen hormones
 Secretes weak androgens (DHEA, androstenedione)
• Converted by peripheral tissues to stronger androgens (testosterone)

Question 27

Adrenal Medulla

Answer 27

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

Question 28

Hypercortisolism

Answer 28

• 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

Question 29

Hyperaldosteronism

Answer 29

 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

Question 30

Adrenogenital Syndromes

Answer 30

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

Question 31

Chronic Adrenocortical Insufficiency

Answer 31

• 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

Question 32

Pheochromocytoma

Answer 32

– 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