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Physiology II-10
Peripheral Endocrine System
| Question | Answer |
|---|---|
| What is metabolism? | All chemical reactions that occur in the body |
| What is fuel metabolism? | Degradation, synthesis, and transformation of proteins, carbs & fats |
| How are carbohydrates handled metabolically? | Absorbed as monosaccharides, circulate in blood glucose, stored as glycogen in liver & muscle, converted to fatty acids & glycerol in adipose tissue |
| How are proteins handled metabolically? | Absorbed as amino acids or di/tripeptides across apical membrane, circulates in blood as amino acids, stored as proteins or converted to glucose & fatty acids in adipose tissue |
| How are fats handled metabolically? | Absorbed as triglycerides (fatty acids + monoglycerides), circulate in blood as lipoproteins (fatty acids + monoglycerides), used as fatty acids and glycerol for energy, steroids, and phospholipids, stored as triglycerides in adipose tissue |
| How does the brain get energy? | Brain relies on plasma glucose or ketone bodies - no glucose storage in the brain |
| What is the absorptive metabolic state? | Ingested nutrients are digested, absorbed, and circulated in plasma within 3-4 hours of eating - glucose is primary energy source, excess nutrients are stored |
| What is the postabsorptive metabolic state? | Between meals when no nutrients are being absorbed, energy supplies are mobilized - glucose sparing & gluconeogenesis supply glucose to brain |
| Does plasma [nutrient] change between absorptive and postabsorptive states? | No |
| What is the metabolic reaction for glucose in the absorptive state? | Glucose stored as glycogen in liver & skeletal muscles |
| What is the metabolic reaction for fatty acids in the absorptive state? | Fatty acids stored as triglycerides in liver & adipose tissue |
| What is the metabolic reaction for amino acids in the absorptive state? | Amino acids stored as protein in muscles |
| What is the metabolic reaction for glycogen in the postabsorptive state? | Glycogen released from liver as glucose |
| What is the metabolic reaction for triglycerides in the postabsorptive state? | Triglycerides released from adipose tissue as fatty acids or glycerol |
| What is the metabolic reaction for protein in the postabsorptive state? | Protein released from muscle as amino acids |
| What happens to glycerol catabolized from adipose tissue in the postabsorptive state? | Converted to glucose in the liver |
| What happens to fatty acids catabolized from adipose tissue in the postabsorptive state? | Converted to ketones in the liver |
| What happens to excess glucose and amino acids? | Converted to triglycerides and stored in adipose tissue |
| What is glycerol derived from? | Triglyceride hydrolysis |
| What is lactic acid derived from? | Muscle glycolysis, converted to glucose by the liver |
| What are ketone bodies derived from? | Liver during postabsorptive glucose sparing, from fatty acid catabolism |
| What are ketone bodies converted into during the citric acid cycle? | ATP |
| What are the pancreatic endocrine cells? | Islets of Langerhans |
| What do the pancreatic beta cells secrete? | Insulin |
| What do the pancreatic alpha cells secrete? | Glucagon |
| What do the pancreatic delta cells secrete? | Somatostatin |
| What do the pancreatic PP cells secrete? | Pancreatic polypeptide |
| What does somatostatin do? | Inhibits digestive function - prevents excessive plasma [nutrients], decreases [insulin], [glucagon], and [somatostatin] |
| What triggers the release of somatostatin? | Increased [glucose] and [amino acid] |
| What does insulin do? | Decreases [glucose], [amino acids], and [fatty acids] in the absorptive state |
| How does insulin decrease [glucose]? | Insulin stimulates transport into cells, glycogenesis in liver & muscles, and inhibits glycogenolysis and glucogenesis |
| How does insulin decrease [amino acids]? | Insulin stimulates uptake into muscles and cellular protein synthesis, and inhibits protein degradation |
| How does insulin decrease [fatty acids]? | Insulin stimulates uptake into adipocytes and triglyceride synthesis, and inhibits lipolysis |
| What triggers the release of insulin? | Absorptive state increased [glucose] and [amino acids], glucose-dependent insulinotropic peptide (GIP), and parasympathetic nervous activity |
| What is glucose-dependent insulinotropic peptide (GIP)? | Feed forward mechanism to prepare for glucose intake, triggers release of insulin |
| What inhibits the release of insulin? | Postabsorptive state decreased [glucose], sympathetic activity, and epinephrine (which mobilizes glucose) |
| What is diabetes mellitus? | Hyperglycemia (increased [glucose]) |
| What causes Type I Diabetes Mellitus? | Lack of insulin secretion |
| What causes Type II Diabetes Mellitus? | Reduced cellular sensitivity to insulin (most cases of diabetes) |
| What are the acute effects of diabetes mellitus? | Polyuria, polyphagia, polydipsia, weight loss, ketosis, increased ventilation |
| What is polyuria? | Increased urine output caused by osmotic gradient of glucose in urine |
| What is polyphagia? | Increased eating in effort to intake more glucose |
| What is polydipsia? | Increased thirst caused by dehydration from polyuria |
| What causes weight loss in diabetes mellitus? | Muscle is broken down for gluconeogenesis in an effort to increase [glucose] |
| What is ketosis? | Excessive ketone bodies from breakdown of fatty acids in liver, leads to metabolic acidosis and then death |
| Why is there increased ventilation in diabetes mellitus? | If there is increased metabolic acidosis, increase ventilation to remove CO2 - leads to fruity acetone breath |
| What are the physiological actions of glucagon? | Postabsorptive and catabolic, opposes insulin - increases [glucose], [ketones], and [fatty acids] |
| What triggers the release of glucagon? | Increased during postabsorptive state in response to increased [amino acids], decreased [glucose], and increased sympathetic NS and epinephrine stimulation |
| What inhibits the release of glucagon? | Decreased during postabsorptive state in response to increased [glucose] |
| How is plasma [glucose] increased? | Decreased glucagon due to inhibition of alpha cells, and increased insulin due to stimulation of beta cells |
| How is plasma [glucose] decreased? | Increased glucagon due to stimulation of alpha cells, and decreased insulin due to inhibition of beta cells |
| What is the only hormone that can decrease [glucose]? | Insulin |
| How are epinephrine and cortisol involved in fuel metabolism? | Metabolic response to stress, increase [glucose] and [fatty acids] |
| How is growth hormone involved in fuel metabolism? | Protein anabolic effects in muscle, increasing [glucose] and [fatty acids] - important in starvation |
| What is the function of follicular cells in the thyroid gland? | Contain colloid - involved in synthesis and storage of thyroid hormones |
| What is the function of C-cells in the thyroid gland? | Secrete calcitonin - peptide hormone involved in Ca++ metabolism |
| How are T3 and T4 produced? | Tyrosine and iodine transported into follicular cells - iodine attached to thyroglobulin in colloid |
| How is T3 and T4 released? | Follicular cells phagocytose thyroglobulin-containing colloid - vesicles fuse with lysosomes - T3 & T4 released into blood bound to globulin - <1% unbound is active |
| What are the physiological functions of thyroid hormone? | Increased BMR, heat-producing, sympathomimetic effect, increased cardiac output and vasodilation |
| What effect does stress have on the regulation of thyroid secretion? | Inhibiting |
| What effect does cold in infants have on the regulation of thyroid secretion? | Stimulating |
| What is the feedback loop for thyroid hormone secretion? | Hypothalamus - TRH - Ant Pit - TSH - Thyroid - T3 & T4 - negative inhibition on Ant Pit |
| What causes hypothyroidism? | Thyroid gland failure, TSH and/or TRH deficiency, inadequate iodine intake |
| What are the symptoms of hypothyroidism? | Decreased metabolic rate, poor cold tolerance, weight gain, fatigue, weak pulse, puffy face, hands and feet, decreased alertness |
| What is the treatment for hypothyroidism? | Hormone replacement therapy and dietary iodine |
| What causes hyperthyroidism? | Grave's disease, excess TSH or TRH, hypersecreting thyroid tumor |
| What is Grave's disease? | Autoimmune disease, produces hormone that stimulates TSH receptors, characterized by fluid behind eyes |
| What are symptoms of hyperthyroidism? | Increased metabolic rate and appetite, decreased weight, poor heat tolerance, cardiovascular abnormalities, irritable, anxious, emotional |
| What are the treatments for hyperthyroidism? | Surgical removal of thyroid portion, radioactive iodine to selectively destroy thyroid, antithyroid drugs |
| What is a goiter? | Enlarged thyroid gland |
| What is the cause of a goiter in hypothyroidism? | Decreased T3 and T4 increase TSH, hypertrophy and hyperplasia of thyroid |
| What is the cause of a goiter in hyperthyroidism? | Increased TSH and Grave's disease (LATS stimulate TSH receptors) |
| What are the adrenal cortex hormones? | Aldosterone, cortisol, and DHEA |
| Where is aldosterone produced in the adrenal cortex? | Zonae glomerulosa |
| Where is cortisol produced in the adrenal cortex? | Zonae fasciculata and reticularis |
| Where is DHEA produced in the adrenal cortex? | Zonae fasciculata and reticularis |
| What is released from the adrenal medulla? | 80% epinephrine, 20% norepinephrine, <1% dopamine, released from chromaffin granules in response to sympathetic input |
| What regulates aldosterone secretion? | Activation of RAAS, increased plasma [K+] |
| What are the physiological roles of aldosterone? | Acts on distal tubule and collecting duct to increase Na+/K+ pumps (increase Na+ reabsorption), long-term regulation of MAP |
| What is the primary cause of aldosterone hypersecretion? | Conn's syndrome - adrenal tumor |
| What is the secondary cause of aldosterone hypersecretion? | Chronic decreased blood flow to the kidneys |
| What are the symptoms of aldosterone hypersecretion? | Hypernatremia, hypokalemia, hypertension |
| How is cortisol secretion regulated? | Diurnal rhythm, stimulated by stress |
| What is the feedback loop for cortisol secretion? | Hypothalamus - CRH - Ant Pit - ACTH - Adrenal Cortex - Cortisol - negative inhibition at hypothalamus and anterior pituitary |
| What are the physiological roles of cortisol? | Breaks down fat and protein stores to increase [glucose], facilitates other hormones, anti-inflammatory and immunosuppressive effects |
| What response does cortisol play a key role in? | Stress adaptation |
| What is Cushing's syndrome? | Cortisol hypersecretion |
| What causes cortisol hypersecretion? | Increased [CRH] or [ACTH], adrenal tumors, or ACTH-secreting tumors |
| What are the symptoms of cortisol hyposecretion? | Excessive gluconeogenesis (adrenal diabetes), abnormal fat distribution (moon face, hump), muscle weakness due to decreased protein, bone weakness & poor wound healing due to decreased collagen |
| What is the role of DHEA in females? | Body hair, growth spurt, development/maintenance of libido |
| What regulates DHEA secretion from the adrenal cortex? | Regulated by ACTH and inhibits GRH |
| What is adrenogenital syndrome? | Sex hormone hypersecretion |
| What causes sex hormone hypersecretion? | Enzymatic defect in cortisol steroidogenic pathway |
| What are the symptoms of DHEA hypersecretion in adult females? | Masculinizing effects |
| What are the symptoms of DHEA hypersecretion in newborn females? | Pseudo male genitalia |
| What are the symptoms of DHEA hypersecretion in prepubescent males? | Premature development of male sex characteristics |
| What are the symptoms of DHEA hypersecretion in adult males? | No effect |
| What is adrenocortical insufficiency? | Failure of both adrenal glands |
| What is primary adrenocortical insufficiency? | Addison's disease - autoimmune disease causes cortisol and aldosterone deficiency |
| What is secondary adrenocortical insufficiency? | Decreased ACTH secretion causes cortisol deficiency |
| What are the symptoms of aldosterone deficiency resulting in hyperkalemia? | Cardiac arrhythmias |
| What are the symptoms of aldosterone deficiency resulting in hyponatremia? | Hypotension |
| What are the symptoms of cortisol deficiency? | Poor stress response and hypoglycemia |
| What are the physiological roles of epinephrine? | Maintains MAP in fight or flight response, increases plasma [glucose], increases metabolic rate, and stimulates CNS |
| What does the liver do with lactic acid? | Converts it into glucose |
| What is stress? | Generalized, nonspecific body response to any factor that overwhelms or threatens to overwhelm homeostasis |
| What is a stressor? | Any noxious stimuli that provokes the stress response |
| What is the general adaptation syndrome? | Nonspecific general response to any stressor - increased sympathetic nervous system activity and cortisol and vasopressin secretion for fight or flight preparedness, mobilization of energy stores, and maintenance of blood volume and blood pressure |
| What is calcium metabolism important in? | Neuromuscular excitability, muscle contraction, maintenance of tight junctions, blood clotting, and bone formation, influences plasma [PO4 3-] |
| What is the physiological role of parathyroid hormone? | Increases plasma [Ca++] by mobilizing bone breakdown, increasing Ca++ reabsorption, and vitamin D activation |
| What is the physiological role of calcitonin? | Decreases plasma [Ca++] by inhibiting bone resorption |
| What is the physiological role of vitamin D? | Increases plasma [Ca++] by increasing absorption in the GIT and increasing bone responsiveness to PTH |
| What are the symptoms of PTH hypersecretion? | Hypercalcemia, hyperphosphatemia, bone thinning, and increased kidney stones |
| What are the symptoms of PTH hyposecretion? | Hypocalcemia (increased neuromuscular excitability) and hyperphosphatemia |
| What are the symptoms of vitamin D deficiency? | Impaired intestinal absorption of Ca++, demineralized bone |
| What is demineralized bone in children called? | Rickets |
| What is demineralized bone in adults called? | Osteomalacia |
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