Endocrine Flashcards

Question

**Growth Hormone (GH): Overview and Secretion Patterns**

Answer 1

Secreted by: Anterior pituitary gland (specifically, somatotrophs) • Stimulated by: Growth hormone-releasing hormone (GHRH) from the hypothalamus • Inhibited by: Somatostatin (GHIH) and high levels of IGF-1 - **Function**: Stimulates bone and tissue growth, remodeling, and cellular metabolism - **Secretion**: Peaks during first 2 hours of sleep and with vigorous exercise - **Age**: Declines with age (avg. 6 ng/mL in adolescence, 1.5 ng/mL in old age) - **Decline Effects**: ↓ protein synthesis → tissue aging, ↓ bone and muscle mass, ↑ fat

Answer 2

**GH direct effects**: Stimulates mitosis, cellular differentiation, and metabolic activity in bone, muscle, and cartilage Promotes lipolysis, protein synthesis, and glucose sparing directly in target tissues **GH indirect effects via liver** GH stimulates the liver to release **IGF-I** and **IGF-II**, which mediate many of GH's long-term growth effects Stimulate cell growth, division, and differentiation in bone, muscle, and cartilage Promote protein synthesis and support overall anabolic metabolism Do not significantly promote lipolysis or glucose sparing Prolong and amplify the tissue-building effects of GH - Half-life: GH = 6–20 minutes IGF-I = ~20 hours → provides sustained growth signaling - Feedback regulation: **IGF-I** inhibits GH release via negative feedback on the hypothalamus and anterior pituitary

Answer 3

*Shifts metabolism to support growth by stimulating protein synthesis, mobilizing fats for energy (protein- and glucose-sparing effects), promoting electrolyte retention, and reducing glucose reliance to prioritize anabolic processes.* 1. **Protein metabolism**: ↑ DNA transcription, mRNA production, and amino acid uptake into cells ↓ Protein catabolism (preserves muscle mass and supports tissue growth) 2. **Lipid metabolism**: ↑ Fat catabolism via lipolysis in adipocytes → releases free fatty acids (FFAs) FFAs used for ATP production (via β-oxidation) or converted into ketones → *protein-sparing effect* 3. **Carbohydrate metabolism**: Glucose-sparing effect: ↑ fatty acid utilization by most tissues ↓ Glucose uptake/use → reserves glucose for brain and growing tissues 4. **Electrolyte balance**: Promotes Na⁺, K⁺, and Cl⁻ retention by kidneys ↑ Ca²⁺ absorption in intestines → supports growth and bone development

Answer 4

- *Type of tissue*: Composed of **nervous tissue**, not glandular. It is an extension of the hypothalamus. - *Hormone synthesis*: Hormones are **not synthesized in the posterior pituitary**, but in the *hypothalamus*: - **Oxytocin** is produced by the **paraventricular nucleus** - **ADH (antidiuretic hormone/vasopressin)** is produced by the **supraoptic nucleus** - *Transport*: These hormones travel from the hypothalamus to the posterior pituitary via **axonal transport** along neurons. - *Storage and release*: Hormones are **stored in axon terminals** within the posterior pituitary and **released into the bloodstream** when triggered by neural signals. - *Function*: Acts as a **neuroendocrine release site**, connecting the nervous system to the endocrine system by secreting hormones into the blood in response to neuronal signals.

Answer 5

- *Lipolysis* breaks down triglycerides in adipose tissue into free fatty acids (FFAs) and glycerol - FFAs are released into the blood and taken up by cells for energy - Inside mitochondria, FFAs undergo β-oxidation → acetyl-CoA → ATP production - In prolonged fasting, excess acetyl-CoA is converted to ketone bodies - *Glucose-sparing effect*: As tissues use fats instead of glucose, glucose is conserved for the brain

Answer 6

- Protein catabolism breaks down muscle proteins into amino acids - Amino acids can be used for gluconeogenesis (glucose production) or energy - Occurs during prolonged fasting or high cortisol levels (e.g., stress) - *Protein-sparing effect*: When fats are used for energy, breakdown of protein is reduced, preserving muscle mass

Answer 7

- *Source*: Produced in the **supraoptic nucleus** of the hypothalamus - *Transport*: Delivered via **axonal transport** through the infundibulum to the posterior pituitary - *Target*: **Kidneys**, **sweat glands**, **arterioles** - *Actions*: - Increases water retention by kidneys → ↓ urine output - Stimulates vasoconstriction at high levels → ↑ blood pressure - Reduces water loss through sweat - *Trigger (neuroendocrine reflex)*: - **Dehydration** → osmoreceptors in hypothalamus activate → ADH released - **Overhydration** → osmoreceptors inhibited → ADH secretion stops - *Clinical note*: Also called **vasopressin** for its vasoconstrictor effect - *Additional*: Osmoreceptors are located in **circumventricular organs**, which lack a BBB and monitor blood osmolarity

Answer 8

- *Source*: Produced in the **paraventricular nucleus** of the hypothalamus - *Transport*: Delivered via **axonal transport** to the posterior pituitary - *Actions*: - Stimulates **uterine contractions** during labor (positive feedback loop) - Triggers **milk ejection** (let-down reflex) during lactation - Promotes **emotional bonding** and trust between partners - Released during **sexual arousal and orgasm** - *Feedback*: Uses a **positive feedback loop** during childbirth: 1. Baby's head stretches cervix 2. Nerve signals sent to brain 3. Brain releases oxytocin 4. Uterus contracts harder → cycle continues until birth - *Nickname*: Known as the "**love hormone**" due to its role in bonding and affection

Answer 9

- Located at the roof of the 3rd ventricle, receives signals from **retina** - Secretes **serotonin by day**, **melatonin at night** - Peak melatonin secretion ages 1–5; declines ~75% by puberty (**involution**) - Helps regulate circadian rhythms (light/dark cycle) - Melatonin improves sleep, esp. in: - Children with autism - Elderly - Jet lag - May regulate puberty timing -> inhibits reproductive hormone release during early childhood -> suppresses the hypothalamic-pituitary-gonadal (HPG) axis - Overproduction linked to SAD (Seasonal Affective Disorder) -> overproduction of melatonin can cause increased sleepiness, low energy, depressive symptoms - Pathway: - Light → retina → inhibits melatonin - Darkness → ↓ norepinephrine → ↑ melatonin → sleepiness - Possible link between **melatonin receptor deficiency** and **diabetes**

Answer 10

- Located in anterior mediastinum, superior to the heart - Part of *endocrine*, *lymphatic*, and *immune* systems - Critical for **T-lymphocyte** maturation (helps body recognize "non-self") **Hormones Secreted** - **Thymopoietin**, **thymosin**, **thymulin** - Regulate the development of lymphatic organs during childhood - Support T-cell activation and function throughout life **Size by Age** - Large in children (prominent in newborns) - Involutes with age, becomes a fatty remnant in adults *Clinical Note* - Dysfunction can contribute to *autoimmune diseases*

Answer 11

1. **Calcitriol (active vitamin D)** Increases calcium absorption in the intestines, enhances osteoclast activity -> bone resorption (with PTH), and slightly reduces calcium excretion in the urine. 2. **Calcitonin** Secreted by **C cells of the thyroid** when blood calcium is high; inhibits osteoclast activity -> decreases bone resporption, and reduces calcium reabsorption in the kidneys, increasing urinary calcium loss. 3. **Parathyroid hormone (PTH)** Released by the parathyroid glands when blood calcium is low; increases osteoclast activity -> bone resproption, enhances calcium reabsorption in the kidneys, and stimulates calcitriol production to raise calcium absorption in the intestines. 4. **Sex hormones**: Initially promotes ossification and eventually promotes epiphyseal closure. Estrogen has a stronger effect than testosterone. 5. **Growth hormones**: secreted by *pituitary gland*. Stimulate bone growth, ossification. 6. **T3/T4**: stimulates bone growth and development by promoting the metabolism and activity of osteoblasts

Answer 12

- Bilobed gland joined by the isthmus - Located anterior to the trachea, inferior to the thyroid cartilage - Largest purely endocrine gland - The thyroid is composed of spherical **follicle sacs** lined by **follicular cells**, which produce **thyroxine (T4)** and **triiodothyronine (T3)**. These hormones are synthesized from *thyroglobulin*, a protein stored in the central lumen (**colloid**) of each follicle. - **Parafollicular (C) cells** are located in the spaces between follicles and secrete **calcitonin**, a hormone involved in calcium regulation. - Highly vascularized - **Follicular cells** → produce thyroid hormones - **Parafollicular (C) cells** → produce calcitonin

Answer 13

- Secrete iodine-containing hormones: **T₃** (triiodothyronine) and **T₄** (thyroxine) - T₄ is secreted in larger amounts; converted to **T₃** in peripheral tissues (T₃ is more active) - Acts like a *steroid hormone* (binds nuclear receptors to alter gene transcription) - ↑ **Metabolic rate** and ↑ **Na⁺/K⁺ ATPase** activity → increases ATP consumption and generatesheat (calorigenic effect) - ↑ Heart rate, cardiac output, and respiratory rate to meet increased oxygen demand - ↑ Appetite and digestion, but also ↑ catabolism of carbohydrate, lipids, and proteins - Not glucose- or protein-sparing: promotes glucose oxidation, lipid mobilization, and protein breakdown to fuel increased metabolism - Supports growth, nervous system development, and thermoregulation **What triggers T₃/T₄ release?** 1. Cold exposure (especially in infants) → hypothalamus increases **TRH** → ↑ **TSH** → ↑ **T₃/T₄** secretion 2. Low circulating T₃/T₄ levels → reduced negative feedback → ↑ TRH and TSH 3. Increased metabolic demand (e.g. growth, stress, pregnancy) can also stimulate secretion

Answer 14

- Located between thyroid follicles - Secrete **calcitonin** - ↓ **Blood Ca²⁺** levels - Promotes **Ca²⁺ deposition** in bone - Stimulates **bone formation**, especially in children (rapid bone growth). becomes significantly less important in adults. - Antagonizes parathyroid hormone (PTH)

Answer 15

- Typically 4 small glands on posterior surface of thyroid - **Not controlled by CNS**; directly monitor **blood Ca²⁺ levels** - Secrete **PTH (parathyroid hormone)**, which: - ↑ Blood Ca²⁺ levels - Promotes synthesis of **calcitriol** (active vitamin D) - ↑ Intestinal absorption of Ca²⁺ - ↓ Urinary excretion of Ca²⁺ - ↑ oscteaclast activity -> bone resorption (releases Ca²⁺ from bone) - Antagonistic to calcitonin from thyroid

Answer 16

- Normal blood Ca²⁺: **9–11 mg/100 mL** - Maintained by opposing actions of **PTH** and **calcitonin** *When blood Ca²⁺ is low:* - **Parathyroid glands** release **PTH**, which: - ↑ **Bone resorption** via osteoclast activation → Ca²⁺ released into blood - ↑ **Renal reabsorption** of Ca²⁺ → less Ca²⁺ lost in urine - ↑ **Calcitriol (active vitamin D)** synthesis by kidneys - Calcitriol ↑ **intestinal absorption** of dietary Ca²⁺ *When blood Ca²⁺ is high:* - **Thyroid parafollicular (C) cells** release **calcitonin**, which: - ↓ **Bone resorption** → promotes Ca²⁺ deposition in bone - Mild effect in adults; stronger in **children** - Together, PTH and calcitonin keep Ca²⁺ levels within a **tight physiological range**

Answer 17

- Inner region of adrenal gland; derived from neural crest - Contains **chromaffin cells** → modified *neuroendocrine cells* (functionally like postganglionic sympathetic neurons) - Stimulated by **sympathetic preganglionic fibers** - Secretes **catecholamines** into the bloodstream: - ~**80% epinephrine** (most abundant) - ~20% norepinephrine (plus trace dopamine) - All act together, but epinephrine is the primary driver of metabolic effects *Metabolic Effects:* 1. **Liver**: Stimulates glycogenolysis and gluconeogenesis → ↑ blood glucose 2. **Adipose tissue**: Stimulates lipolysis → ↑ free fatty acids (FFAs) for energy 3. **Muscle**: insulin levels are reduced → glucose is spared for the brain. Stimulates glycogenolysis → muscle breaks down its own glycogen to fuel contraction (via glycolysis). Once glucose is depleted shifts to Free fatty acids (FFAs), Ketone bodies (during prolonged stress or fasting), Possibly amino acids (in extreme cases), 4. **Pancreas**: Inhibits insulin secretion → reduces glucose uptake by peripheral tissues 5. **Overall**: Mobilizes high-energy fuels (glucose, FFAs, lactate) for immediate use during stres. FFAs rise in the blood; ketones form only if FFA supply exceeds demand and insulin remains low *Other Effects:* - ↑ **Heart rate**, **blood pressure**, **bronchodilation**, and **metabolic rate** - ↓ **Digestive** and **urinary** activity (classic sympathetic effects) ``` Glycogenolysis = Breakdown of glycogen (stored glucose) into glucose. Happens mainly in the liver and muscle Gluconeogenesis = Creation of new glucose from non-carbohydrate sources. Uses amino acids, glycerol, and lactate. Occurs primarily in the liver (and kidneys during prolonged fasting) Keton bodies produced in liver: When fatty acid oxidation in the liver produces excess acetyl-CoA (more than can enter the citric acid cycle), the liver converts it into ketone bodies. triggered by fasting, prolonged exercise, low-carbohydrate diets, or uncontrolled diabetes. Even though acetyl-CoA is a fuel, it requires oxaloacetate to enter the citric acid cycle. When oxaloacetate is scarce, acetyl-CoA is rerouted into ketogenesis. ```

Answer 18

- Outer region of adrenal gland; produces corticosteroids — including mineralocorticoids and glucocorticoids — and the sex hormones known as androgens - Made up of 3 zones (outer → inner): 1. **Zona glomerulosa** - Secretes **mineralocorticoids** -> aldosterone - Regulates Na⁺/K⁺ balance and blood pressure - "SALT" 2. **Zona fasciculata** - Secretes **glucocorticoids** -> cortisol / corticosterone (less important in humans) - Regulates metabolism, stress response, and inflammation - "SUGAR" 3. **Zona reticularis** - Secretes **androgens** -> DHEA, androstenedione - Contribute to sex characteristics and libido - "SEX"

Answer 19

- Hormonal system that regulates **blood pressure**, **blood volume**, and **electrolyte balance** *Steps:* 1. **Renin** released by kidneys in response to low BP or low Na⁺. Renin is a protease enzyme. 2. angiotensinogen is a prohormone released by the liver. Renin converts angiotensinogen →angiotensin I 3. **Angiotensin-Converting Enzyme / ACE** (in lungs) converts angiotensin I → **angiotensin II** 4. Angiotensin II: - Causes vasoconstriction → ↑ BP - Stimulates adrenal cortex to secrete **aldosterone** - Stimulates ADH (vasopressin) release -> increase water reabsorption (adds aquaporins to the collecting ducts of nephrons) - Stimulates thirst (via hypothalamus) -> increase fluid intake 5. **Aldosterone**: - Promotes Na⁺ and water reabsorption in kidneys and pottasium excretion -> increased blood volume.

Answer 20

**Mineralocorticoids** Main hormone: **Aldosterone** ("SALT") Steroid hormones that regulate electrolyte and fluid balance, mainly by controlling Na⁺ and K⁺ levels - Promotes **Na⁺ and water retention** -> increase blood volume -> increase blood pressure - Enhances **K⁺ and H⁺ excretion** in urine - Part of **RAAS system** - Hypersecretion → causes hypertension

Answer 21

**Glucocorticoids** Main hormone: **Cortisol** Steroid hormones that regulate metabolism, stress response, and immune activity Regulated by ACTH from anterior pituitary (stimulated by hypothalamic CRH) - Stimulates **fat catabolism** in adipose tissue → releases free fatty acids (FFAs) for energy. FFAs are oxidized for ATP or, if in excess, converted by the liver into ketone bodies for use by brain and muscle (especially during fasting or low-carb states) - Stimulates **protein catabolism** in skeletal muscle → provides amino acids for gluconeogenesis. This is not automatic, but occurs during prolonged stress, fasting, or cortisol excess. Over time, chronic breakdown can lead to **muscle wasting** - Promotes **gluconeogenesis** in the **liver**, using: - Amino acids (from muscle) - Glycerol (from triglyceride breakdown) - Lactate (from anaerobic glycolysis in muscle and red blood cells) - Purpose of gluconeogenesis: ensures a **continuous glucose supply**, especially for the **brain**, which depends heavily on glucose for energy (unless ketones are elevated) - sensitizing kidneys to aldosterone -> Promotes sodium and water retention -> ↑ Sodium and water retention → ↑ blood volume - enhances vasoconstriction response to catecholamines -> **vasoconstriction** to help maintain blood pressure during stress. - Exerts **anti-inflammatory** effects but suppresses immune function with prolonged elevation **excess cortisol (e.g., Cushing’s) causes hypertension**

Answer 22

Main hormone: **DHEA (dehydroepiandrosterone)** - *Converted in peripheral tissues into:* - **Testosterone** → supports male sexual development, muscle growth, and libido in both sexes - **Estradiol** → becomes a significant estrogen source in postmenopausal women (after ovarian estrogen declines) - Contribute to prenatal male development (e.g., formation of male reproductive tract and external genitalia) - Help regulate **libido** and **pubic/axillary hair growth** in both sexes - Serve as precursor hormones for sex steroid production in other tissues - In females, adrenal androgens are the main source of testosterone - In males, testosterone is primarily produced by the testes; adrenal androgens play a minor role

Answer 23

- **Retroperitoneal**, located inferior and dorsal to stomach - Has both endocrine and exocrine functions *Endocrine (2%) — Pancreatic islets (1–2 million):* - **Alpha cells** → secrete **glucagon** - **Beta cells** → secrete **insulin** - **Delta cells** → secrete **somatostatin** - Regulate blood glucose levels *Exocrine (98%) — Acinar tissue:* - Produces digestive enzymes and bicarbonate - Secreted into duodenum via pancreatic ducts - Endocrine = hormone secretion into blood - Exocrine = enzyme secretion into digestive tract ``` somatostatin release by hypothalamus inhibits anterior pituitary release of GH. somatostatin release by D cells inhibits insulin and glucagon secrition -> fine tunes hormone balance. ```

Answer 24

- Secreted by **beta cells** of **pancreatic islets** - Released after meals when blood glucose is high - Stimulates uptake of **glucose** in **muscle** and **adipose tissue** by promoting **GLUT4** insertion - Stimulates **amino acid** uptake and **protein synthesis** in **muscle** - Promotes **glycogen synthesis** in **liver** and **skeletal muscle** - Stimulates **fat storage** in **adipose tissue** - brain, liver, RBCs, epithelia, and kidneys take up glucose independently of insulin - Deficiency or resistance → **diabetes mellitus**

Answer 25

- Secreted by **alpha cells** of **pancreatic islets** - Released during fasting or low-carb, high-protein intake - Targets **liver cells**, which respond by: - Stimulating **glycogenolysis** → raises blood glucose - Promoting **gluconeogenesis** from amino acids - Stimulates **fat catabolism** (releases fatty acids) - Promotes **amino acid uptake** for gluconeogenesis - glucagon indirectly increases ketone production, especially during fasting or low-insulin states. Fat catabolism → ↑ free fatty acids. In the liver, excess FFAs + low insulin = ↑ ketogenesis

Answer 26

- Regulated by **insulin** and **glucagon** from **pancreatic islets** *When blood glucose is high:* - Beta cells secrete insulin - Promotes **glucose uptake** into muscle and adipose tissue - Stimulates **glycogenesis** in the liver and skeletal muscle, lipid storage in adipose tissue, and protein synthesis in skeletal muscle → Lowers blood glucose *When blood glucose is low:* - Alpha cells secrete glucagon - Stimulates **glycogenolysis** and **gluconeogenesis** from fat and amino acids → Raises blood glucose - Keeps glucose levels within narrow range (~70–110 mg/dL)

Answer 27

**Growth Hormone (GH):** - *Glucose sparing*: ↓ glucose uptake in muscle and adipose tissue → conserves glucose for brain - *FFA*: ↑ lipolysis in adipose → ↑ free fatty acids (FFAs) as alternate fuel for muscle.↑ FFAs may be converted to ketones in the liver during fasting or low insulin states - *Protein sparing*: Stimulates protein synthesis and inhibits protein breakdown → preserves muscle mass - *Gluconeogenesis*: Does not directly stimulate it, but ↑ FFAs provide ATP needed to fuel gluconeogenesis in the liver - *Insulin*: GH does not decrease insulin secretion, but it reduces insulin sensitivity in peripheral tissues → more insulin is needed to get the same glucose uptake - *Glycogenolysis*: No direct effect; may enhance response to other hormones like epinephrine **Catecholamines (Epinephrine):** - *Glucose sparing*: directly↓ insulin secretion → prioritizes glucose availability for brain and essential tissues - *FFA*: Strongly ↑ lipolysis in adipose → ↑ FFAs for muscle energy use. Not a direct trigger, but ↑ FFA availability may lead to ketone production if insulin remains low (e.g., prolonged stress) - *Protein sparing*: Minimal direct effect on protein metabolism - *Gluconeogenesis*: Directly stimulates gluconeogenesis in the liver → ↑ glucose production - *Glycogenolysis*: Strongly stimulates glycogen breakdown in both **liver** (to raise blood glucose) and **muscle** (for local ATP use) - *Insulin*: Directly suppresses insulin secretion by pancreas - *Muscle*: Uses internal glycogen for rapid energy → spares blood glucose for brain **Cortisol:** - *Glucose sparing*: ↓ glucose uptake in muscle and adipose (induces insulin resistance in muscle and adipose tissue -> downregulation glut4)→ preserves blood glucose - *FFA*: Stimulates lipolysis → ↑ FFAs to be used as energy by muscle and other tissues .↑ FFA supply may lead to hepatic ketone production, especially during fasting or insulin deficiency - *Protein sparing*: ❌ Opposite — promotes protein breakdown in muscle → ↑ amino acids for gluconeogenesis - *Gluconeogenesis*: Directly stimulates gluconeogenesis in the **liver** → ↑ blood glucose (primary role) - *Glycogenolysis*: Does not directly stimulate, but sensitizes liver to glucagon and epinephrine, enhancing their glycogenolytic effects - *Insulin*: Indirectly increases insulin secretion due to cortisol-induced hyperglycemia, but causes insulin resistance in muscle and fat

Answer 28

**Testes** - Contain seminiferous tubules that produce sperm - **Nurse cells** line the tubules and support sperm development - **Interstitial (Leydig) cells** between tubules secrete testosterone and other androgens **Testosterone** 1. Stimulates development of the male reproductive system 2. Promotes sex drive 3. Works with FSH to sustain sperm production **Hormonal Regulation** - **FSH** stimulates nurse cells to support sperm development - **LH** stimulates interstitial cells to secrete testosterone - **Inhibin** is secreted by nurse cells and inhibits FSH secretion → negative feedback to regulate sperm production DHE AProduced by the adrenal cortex serves as a minor source of androgens, but most testosterone is produced in the testes

Answer 29

ovary refers to the paired female reproductive organs that produce, store, and release eggs. Each ovary contains thousands of follicles **follicles**: an **oocyte** surrounded by **granulosa cells**. Outer theca layer synthesize androstenedione, converted to **estradiol** by **granulosa cells** After ovulation, the follicle becomes the **corpus luteum**, which secretes progesterone for ~12 days Estradiol and progesterone regulate female reproductive physiology: 1. Support development of female reproductive system and physique 2. Regulate menstrual cycle and sustain pregnancy 3. Prepare mammary glands for lactation - **FSH** stimulates **granulosa cells** to produce **estradiol** and support follicle maturation - **LH** stimulates theca cells to produce androstenedione, which is converted to estrogens by granulosa cells; LH also triggers **ovulation** and stimulates **progesterone release** from the **corpus luteum** - **Inhibin** from follicle and corpus luteum suppresses **FSH** through negative feedback on the **anterior pituitary** to regulate follicle recruitment - Estradiol is permissive to progesterone: it upregulates **progesterone receptors** in target tissues, allowing progesterone to exert its full effects after ovulation

Answer 30

1. Produce **erythropoietin** → stimulates bone marrow to produce red blood cells. Stimulated by low blood oxygen (hypoxia) 2. Secrete **renin** → converts angiotensinoge to angiotensin I (→ angiotensin II →*vasoconstriction). Stimulated by low blood pressure, low Na⁺ levels, or sympathetic stimulation 3. Convert **calcidiol** to **calcitriol** (active vitamin D). Stimulated by parathyroid hormone (PTH) -> Ca²⁺ absorption in intestines

Answer 31

- Secrete ~10 **enteric hormones** - Regulate digestion, motility, and satiety/hunger signals

Answer 32

- Secretes **estrogen**, **progesterone**, and others - Regulate pregnancy, fetal development, and mammary gland function

Answer 33

- Secretes **leptin** - Long-term signal of energy stores - Suppresses appetite and promotes satiety

Answer 34

- Secretes **atrial natriuretic peptide (ANP)** - Triggered by ↑ blood pressure - Promotes **Na⁺ and H₂O loss** by kidneys → ↓ **blood volume** and **blood pressure**

Answer 35

- Starts production of **vitamin D₃** (cholecalciferol) from **UV sunlight** - Precursor to **calcidiol** (liver), then **calcitriol** (active form kidney)

Answer 36

1. Produces 15% of **erythropoietin** (kidney produces the rest) 2. Secretes **angiotensinogen** (precursor of angiotensin II) 3. Secretes **IGF-I** (insulin-like growth factor, works with GH) 4. Converts vitamin D₃ precursor (cholesalciferol) to **calcidiol** 5. Secretes **hepcidin** → promotes **iron absorption**

Answer 37

Osteoblasts secrete **osteocalcin** and **lipocalcin** 1.Promote **insulin secretion** and **sensitivity** 2. Help regulate **glucose metabolism** 3. Inhibit weight gain and **type 2 diabetes** onset

Answer 38

- **Stress** is any condition that threatens homeostasis or emotional/physical well-being - Response is **consistent**, mediated by the **sympathetic nervous system** and **endocrine system** - Involves **general adaptation syndrome (GAS)**: 1. **Alarm reaction** 2. **Stage of resistance** 3. **Stage of exhaustion**

Answer 39

Immediate response to stress, activation of sympathetic nervous system Adrenal medulla releases epinephrine and norepinephrine *Effects on Metabolism* - ↑ **Glycogenolysis** → ↑ **blood glucose** - ↑ **Lipolysis** → ↑ **free fatty acids** - ↓ **Insulin secretion** → conserves glucose for brain *Effects on Cardiovascular System and Fluid Balance* - ↑ Heart rate and blood pressure - Catecholamines cause **vasoconstriction** → ↓ renal perfusion (less blood flow to kidneys) - ↓ Renal perfusion = ↓ pressure in afferent arterioles → stimulates **renin release** - Renin → activates angiotensin * → converted to angiotensin II (via ACE) - **Angiotensin II** → powerful vasoconstrictor + stimulates aldosteron release from adrenal cortex - **Aldosterone** → promotes Na⁺ and water reabsorption in kidneys → helps maintain blood volume and pressure during stress

Answer 40

- Dominated by **glucocorticoids**, especially **cortisol** - Initiated via HPA axis: CRH (hypothalamus) → ACTH (anterior pituitary) → cortisol (adrenal cortex) *Metabolic Effects* - ↑ **Protein catabolism** (muscle, skin, bone) → provides amino acids for **gluconeogenesis** - ↑ **Lipolysis** → provides glycerol and free fatty acids for energy - ↑ **Gluconeogenesis** in liver → maintains blood glucose - ↓ **Glucose uptake** in muscle and fat → due to **GLUT4 downregulation**, not reduced insulin levels rain *Other Effects* - Suppresses **immune function** (↓ inflammation, ↓ lymphocyte activity) - Inhibits **wound healing** and **tissue repair** - Increased BP and electrolyte imbalance. -> increased sesitivity to catecholamines in vascular smooth muscle -> vasoconstriction. High concentrations of cortisol ca bind mineralcorticoid receptors mimicking adolsterone.

Answer 41

- Occurs when **fat reserves are depleted** (after prolonged stress: weeks to months) - Body shifts to **protein breakdown** for energy → leads to **muscle wasting** *Metabolic Consequences* - Severe ↓ in **glucose homeostasis** → risk of hypoglycemia - Persistent **protein catabolism** → weakens structural and immune proteins - No remaining metabolic reserves → energy deficit *Electrolyte and Systemic Effects* - ↑ **Aldosterone** → prolonged Na⁺ retention and K⁺ excretion → electrolyte imbalance (hypokalemiam, alkalosis) -> hypertension - Fluid imbalance + weakened myocardium → **cardiovascular collapse** - Immune suppression → ↑ risk of **infection** - May result in **multi-organ failure** and **death**

Answer 42

Hypothalamic pituitary adrenal axis - Stress activates **hypothalamus** - Hypothalamus releases **CRH** (corticotropin-releasing hormone) - CRH stimulates anterior pituitary to release **ACTH** - ACTH stimulates adrenal cortex to secrete **glucocorticoids** - **Cortisol** regulates metabolism, suppresses immune function, and provides negative feedback to hypothalamus and pituitary

Answer 43

- **Chronic stress** inhibits the **immune system**, increasing risk of: - **Hypertension**, **asthma**, **migraine**, **gastritis**, **colitis**, and **depression** - **Interleukin-1 (IL-1)** is secreted by **macrophages** and links immunity and stress - IL-1 stimulates production of **immune substances**, which then **suppress further IL-1** → feedback regulation

Answer 44

Chemical messengers that diffuse short distances and stimulate nearby cells - **Histamine**: from mast cells in connective tissue; causes vasodilation - **Nitric oxide**: from endothelium of blood vessels; causes vasodilation - **Catecholamines**: diffuse from adrenal medulla to cortex **Eicosanoids** (universal paracrines — released by nearly all cells) - Derived from arachidonic acid in membrane phospholipids - Function as local regulators of cellular activity - Every cell type requires them to: - Coordinate immune responses* - Regulate local blood flow and vascular tone - Control smooth muscle contraction, pain, fever, and inflammation* - Modulate glandular secretion, metabolism, and platelet aggregation - Types include: - **Leukotrienes**: mediate **inflammation**, especially in WBCs - **Prostaglandins**: affect **smooth muscle**, **pain perception**, **fever**, **vascular tone**, and more - *NSAIDs* (e.g., ibuprofen) block **COX enzymes** → ↓ prostaglandin synthesis → ↓ pain, fever, inflammation

Answer 45

- *Definition*: Chemical messengers that stimulate the **same cell** that secreted them - A single chemical can act as a **hormone**, **paracrine**, or **neurotransmitter** depending on the location - *Example*: **Hepcidin**

Answer 46

- *↓ Human growth hormone* → muscle atrophy - *↑ TSH* to compensate for ↓ thyroid function - Leads to *↓ metabolic rate*, *↑ body fat*, possible *hypothyroidism* - *Thymus involution*: replaced with adipose tissue after puberty - *↓ Adrenal output* of **cortisol** and **aldosterone** (also involution) - *↓ Glucose receptor sensitivity* - *Ovaries stop responding* to gonadotropins → - *↓ Estrogen* → contributes to **osteoporosis** and **atherosclerosis**

Answer 47

**Hyposecretion** - Inadequate hormone production - Causes: gland destruction (e.g., tumor, lesion), autoimmune attack, head trauma (damage to hypothalamus / pituitary), or genetic defects *Example*: - ↓ ADH (antidiuretic hormone) from posterior pituitary → **Diabetes insipidus** - ADH normally promotes water reabsorption in kidneys - ↓ ADH → kidneys can't concentrate urine → chronic polyuria, dehydration, ↑ thirst - Can be due to head trauma, pituitary damage, or genetic mutation - Not related to insulin or glucose (unlike diabetes mellitus) *Hypersecretion* - Excessive hormone production - Causes: tumors, autoimmune stimulation, or ectopic hormone production *Example*: - **Goiter** = abnormal enlargement of the thyroid gland - May result from hyperthyroidism (excess T₃/T₄), such as in Graves' disease - Or from hypothyroidism (low thyroid hormones) due to iodine deficiency → ↑ TSH stimulation → thyroid growth - Symptoms depend on underlying cause: may include weight changes, heat/cold intolerance, and neck swelling

Answer 48

**Congenital hypothyroidism** (↓ TH) - Caused by: thyroid dysgenesis, genetic defects, or maternal iodine deficiency - ↓ TH → ↑ TSH (due to lack of negative feedback) - TSH may stimulate thyroid growth → **goiter possible** - Symptoms: abnormal bone development, thickened facial features, lethargy, low temp, brain damage, developmental delay - *congenital → condition that develops during fetal development* **Myxedema** (adult **hypothyroidism**, ↓ TH) - Caused by: **primary hypothyroidism** (thyroid gland failure), often autoimmune (e.g., Hashimoto’s) - ↓ TH → ↑ TSH (compensatory) - If gland is still responsive, TSH may cause **goiter**; not always present - Symptoms: ↓ metabolic rate, fatigue, cold sensitivity, weight gain, constipation, dry skin/hair, ↑ BP, tissue swelling **Endemic goiter** - Caused by: **iodine deficiency** - ↓ TH → no negative feedback → ↑ TSH -> **hypothyroidism** - TSH stimulates thyroid hypertrophy and hyperplasia → **goiter** **Toxic goiter (Graves’ disease)** - Caused by: autoantibodies that mimic TSH - Chronically stimulate TSH receptors → ↑ TH -> **hperthyroidism** - Leads to thyroid overgrowth and **goiter**

Answer 49

*Hypersecretion of Growth Hormone* - **Acromegaly**: Thickened bones and soft tissues; enlargement of hands and feet (adulthood) - **Gigantism**: Excess GH during childhood before epiphyseal plates close Metabolic Effect hypersecrtion: - ↑ **Lipolysis** → ↑ **FFA** and possible ↑ **ketone production** - ↓ **Glucose uptake** via GLUT4 downregulation → insulin resistance and hyperglycemia *Hyposecretion of Growth Hormone* - **Dwarfism**: GH deficiency in childhood → reduced growth, normal proportions Metabilic Effect hyposececretion: - ↓ **Protein synthesis** and **lipolysis** → reduced growth, ↓ muscle mass, and ↑ fat storage - Mild ↓ **blood glucose** due to ↓ gluconeogenesis and ↓ insulin resistance

Answer 50

**Hypoparathyroidism** - Often caused by surgical excision during thyroidectomy or autoimmue - Leads to fatal tetany due to rapid drop in blood calcium → laryngeal spasms **Hyperparathyroidism** - Caused by parathyroid tumor or gland hyperplasia - Excess PTH causes bones to become soft, fragile, and deformed - Increases Ca²⁺ and phosphate in blood -> **hypercalcemia** - Promotes renal calculi/kidney stone formation *Types of Hyperparathyroidism* 1. **Primary**: parathyroid cancer 2. **Secondary**: Due to chronic low calcium (e.g., vitamin D deficiency, renal failure) **PTH-independent hypercalcemia**: From excessive calcium/vitamin D intake or malignancy

Answer 51

**Cushing Syndrome** - Caused by excess cortisol secretion (e.g., adrenal tumor, ACTH-secreting tumor, or prolonged corticosteroid use) **Metabolic effects** - Increases gluconeogenesis → hyperglycemia - Decreases glucose uptake → insulin resistance - Increases protein catabolism → muscle wasting and thin limbs - Increases lipolysis → elevated free fatty acids in blood - Causes fat redistribution → central obesity, moon face, buffalo hump **Catabolic effects** - Increases bone resorption and decreases osteoblast activity - Cortisol promotes osteoclast activity and inhibits bone formation - Reduces calcium absorption and increases calcium excretion → further stimulates bone breakdown - Leads to osteoporosis and increased fracture risk - Also causes thinning of skin, striae (stretch marks), bruising, and poor wound healing **Other signs** - Hypertension (from increased vascular sensitivity to catecholamines and mineralocorticoid activity of cortisol) - Edema, menstrual irregularities, immune suppression **Adrenogenital Syndrome (AGS)** - Adrenal androgen hypersecretion - Causes external genital enlargement in children and early puberty - In girls: masculinized genitalia at birth - Masculinization in women: increased body hair, deeper voice, beard growth

Answer 52

**Key symptoms:** - Polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger) - Hyperglycemia (elevated blood glucose), glycosuria (glucose in urine), ketonuria (ketones in urine) - Osmotic diuresis: Glucose exceeds kidney transport maximum → remains in urine, pulling water with it - Cellular starvation: Glucose unavailable to cells → body uses fat and protein for energy - Increased osmolarity pulls water into urine → dehydration --- **Type I Diabetes Mellitus (IDDM)** - Cause: Autoimmune destruction of pancreatic beta cells → not enough insulin - Onset: Usually diagnosed around age 12 - Treatment: Diet, exercise, glucose monitoring, insulin injections - Note: Skeletal muscle contraction can stimulate GLUT4 transporters to take up glucose --- T**ype II Diabetes Mellitus (NIDDM)** - Cause: Insulin resistance (cells fail to respond to insulin) - Risk factors: Heredity, age over 40, obesity, ethnicity - Treatment: - Weight loss via diet and exercise - Oral medications to improve insulin secretion or sensitivity - Note: May involve hyperinsulinemia before insulin production declines --- **Diabetes Mellitus: Acute Pathology** - Glucose not absorbed → cells rely on fat and protein - Symptoms: Weight loss, weakness - Fat breakdown → increased free fatty acids and ketones - Leads to ketoacidosis → metabolic acidosis (acidic blood pH) - Ketones in urine (ketonuria) → osmotic diuresis --- Diabetes Mellitus: Chronic Pathology - Long-term effects: - Neuropathy and cardiovascular damage due to atherosclerosis and microvascular disease - Retinopathy and nephropathy from blood vessel damage (especially in Type I) - Erectile dysfunction, poor wound healing, incontinence, loss of sensation - Severe neuropathy may lead to blindness or amputation

Answer 53

- *Cause*: Excess **insulin injection** or **pancreatic islet tumor** - *Effects*: Leads to **hypoglycemia**, **weakness**, and **hunger** - Triggers secretion of **epinephrine**, **growth hormone (GH)**, and **glucagon** - Symptoms: **anxiety**, **sweating**, **increased heart rate (↑ HR)** - *Insulin shock*: Severe hypoglycemia → **disorientation**, **convulsions**, or **unconsciousness** if untreated

Endocrine Flashcards

(78 cards)