Pancreas Thymus Diabetes and Parathyroid Glands

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  1. Oxytocin and bonding with dogs (Bullet points)
    • gazing by humans into a dogs eyes increases oxytocin creating positive feelings towards one another-more effective than petting and walking
    • owning a pet decreases stress and therefore possibly depression, blood pressure and anxiety
    • there is no evidence that oxytocin improves learning directly, but due to antistress effect it creates a better learning environment and kids show more focus and positive feelings about learning
  2. BCG Vaccine and Type 1 Diabetes (Bullet points)
    • 2-4mill people have type 1- its an autoimmune disease where defective insulun T cells destroy beta cells of pancreas, disrupting insulin function
    • BCG vaccine can reverse type1 diabetese by stimulating tumor necrosis factor whcih promotes cell death of defective t cells allowing beta cells to function normal
    • BCG vaccine used for 90 yrs to prevent tuberculosis so its readily accessable and cheap
  3. oxytocin effects on human social behavior (Bullet points)
    • oxy increases willingness to share emotions
    • oxy has calming effects on stress and anxiety
    • oxy enhances sexual behavior in male and female
  4. Melatonin in non humans (Bullet points)
    • melatonin doesnt directly stimulate sleep- it allows circadian rhythms which sleeping is one of
    • pineal gland is stimulated by photoperiod- seen during seasonal changes
    • melatonin can function as antigonadotropin, and basal levels decrease at puberty
  5. Melatonin in humans (Bullet points)
    • melatonin- a small lipophillic hormone made in pineal gland
    • regulated based on presence or absense of light
    • melatonin synchonizes sleep wake patterns with circadian rhythms and acts as an antioxidant
    • taking melatonin as a supplemant may restore disrupted circadian rythms and help with alzheimers
  6. Effects of vasopressin on human social behavior (Bullet points)
    • vasopressin affects social communcation differently in men and women-related to different receptor locations in the brain
    • --> combative facial responses in men in neutral or ambiguous situations but affiliative or sociable facial responses in women
    • vasopressin may play an important role in autism spectrum disorders- linkage of autism to chromosome 112q14 which contains vaso receptor gene and variation of it may affect onset and severity of the disease
    • further research on the role of vaso in disorrders associated with social problems may lead to development of treatment- administering receptor antagonists has shown to reduce anxiety and depression in rodents, nothing for humans right now
  7. Hormones in insect behavior (Bullet points)
    • juvenile hormone has evolutionary conserved effects on survival and reproduction in many insect species but has different effects on behavior
    • JH aids development of nervous system and directly influences already developed NS pathways
    • JH has similar effects in insects to androgens in vertebrates- both increase fertility but have negative affects on lifespan and immune functioning
    • JH more important in females than males
  8. Pheromones in humans (Bullet points)
    • potential human pheromones: axillary steroids, vaginal aliphatic acids, stimulators of vomeronasal organ
    • no studies show true human pheromones- misleading synchronized menstraul cycles (lie)
    • scent of bacteria growing on a person can be interpreted by olfactory receptors and influence attraction- when people smell different from eachother more likely to be attracted to eachother
  9. Ghrelin and PTSD (Bullet points)
    • hormones from the adrenal gland must be present to crate stress related levels of ghrelin
    • in short term stress ghrelin can reduce anxiety-but increases anxiety behavior and fear memories in long term stress
    • PTSD could be prevented by blockage of ghrelin receptors to stop formation of fear memories
  10. Parental behavior in non human vertebrates (Bullet points)
    • the medial preoptic area and the adjacent bed nucleas of the stria terminalis form a super region for stimulation of maternal behavior
    • prolactin can enter the cerebral spinal fluid and bind to medial pre optic area increasing parental actions such as sharing food, playing, grooming, carrying infants and teaching hunting
    • high testosterone decreases parental behavior in males by increasing aggression toward offspring- T levels naturally decrease after mating season and birth
  11. phytohormones (Bullet points)
    • plant hormones- important for development and response to abiotic and biotic stimuli
    • almost every aspect of a plants ilfe is regulated by phytohormones
    • phototropism- the plants response to light can be + (grow towards light) or - (grow away from light)- signal that regulates this is indole-3-acetic acid or auxin, the first known plant hormone
    • administration of cytokinins is used in tobacco plants to help them be drought tolerant, including a delay of leafs senescence which is the loss of a cells ability to divide and grow
  12. Nerve growth factor and other neurotrophins (Bullet points)
    • neurotrophins promote survival, maitenance and development of neurons
    • all neurotrophins bind to the p75 receptor while certain neurotrophins bind to the different subcategories of the Trk receptor (a b and c)
    • nerve growth factor can be a treatment for alzheimers- stimulates sprouting of new axons in damaged neurons fixing signaling
  13. Hormones involved in water balance in aquatic marine vertebrates (Bullet points)
    • the renin-angiotensisn-aldosterone system is affected by the amount of Na+ present inside and outside of the organism
    • vasopressin, found in land mammals, could regulate blood salinity but there has been inconclusive evidence
    • prolactin, growth hormone and cortisol have been found in some marine mamals to help with osmoregularity through controllingion uptake and cell proliferation
  14. prostaglandins in reproduction (Bullet points)
    • prostaglandins play a specifc role in migration of sperm and fertilization of ova by decreasing the viscosity of the mucus that guards the cervix by allowing reverse peristalsis in the uterus and sperm movement through the reproductive structures
    • prostaglandins maintain tetanic contractions and expulsion of baby at birth- production is triggered by the release of oxytocin from fetal cells
    • prostaglandins can cause abortion of fetus by contracting uterus to expell blood and tissue- mifeprisone drug causes this
  15. Hormones in courtship behaviors in non human vertebrates (Bullet points)
    • the level of tesosterone is highest at begining of breeding season in birds then drops to preserve immune function, level of behavior doesnt change
    • courtship behaviors are activated in the brain in the preoptic area, anterior hypothalamus, and cerebellum, where there are high expression of androgen receptors
    • removal of gonads stopped courtship behavior in animals, but it returned when hormones were administered
  16. gender dysphoria and gonadotrophin releasing hormone analogs (Bullet points)
    • gonadotrophin releasing hormone analogues suppress puberty by binding to GnRH recptors in ant pit gland, decreasing FSH, LH and sex steroids
    • GnRH analogs cause infertility in males and disrupts menstrual cycle in females
    • cross sex hormone treatment if high can cause endometrial and ovarian cancer in biological females, and pulmonary embolism, myocardial infarction, and stroke in biological males
  17. Hormone effect on temperature regulation in newborns (Bullet points)
    • newborns generate heat by brown fat tissue metabolism called nonshivering thermogenesis (NST)
    • the regulation of NST is from sympathetic NS releasing norepi
    • thyroid hormone and leptin both have smaller roles in thermoregulation of newborn
  18. Hormones in amphibian metamorphosis (Bullet points)
    • thyroid hormone is regulated by a positive feedback loop where concentrations of TH increase and increase until completeion of the process- after metamorphisis there is partial thyroid gland degeneration and inhibitors are produced to stop the process
    • functions of TH in metamorphosis- degeneration of tail, growth and development of body, ossification of bone, differentiation of glands in skin, and differerentiation/formation of limbs, and changes in intestines
    • TH acts on multiple receptor types that contain ligand and DNA binding domains- due to this the hormone is able to repress or activate gene expression at the DNA level causing major changes in a site specific manner
  19. placental growth factor (Bullet points)
    • a pro angiogenic factor, stimulating growth and proliferation of placental cells and tissues
    • it proliferates and differentiates the cytotrophoblast stem cells into two distinct pathways: microvascular permeability or creation of the uteroplacental vascular system
    • plasma concentrations of PGF are important in disorders like preeclampsia, downs and giving birth to a small newborn
  20. Angiopoietin and bone morphogenic protein (Bullet points)
    • angiopoietin is responsible for the proper development of blood vessels in embryos and mainteince/repair of bvs throughout life
    • bone morphogenetic protein is responsible for development and differentiation of bone and cartilage tissues in embryological development and repair throughout life
    • both of these 2 have implicaitions such as promotion of tumor growth and leaky underdeveloped blood vessels (angio) bone deformities, and osteoperosis (BMP)
  21. Medication to enhance female libido (Bullet points)
    • famel libido regulated by biological, cognitive and motivational factors
    • only 1 drug exists to increase libido in females, treats only cognitive and motivational so doesnt help majority
    • future research should focus on loss of libido rather than increasing sexual desire- hormone imbalances play a role in regulating arousal and libido so research should be on androgens, estrogen, progest, and oxytocin
  22. Multiple endocrine neoplasia type1 (Bullet points)
    • (MEN1) aka- a genetic disorder caused by a mutation in the MEN1 gene on chromosome 11- causes multiple endocrine tumors, mainly of parathyroid gland, pituitary gland, and in the pancreatic islets and duodenum
    • excess parathyroid hormone causes high blood calcium, muscle weakness, and excess prolactin causes complications in fertility and disruptions in milk production; excess cortisol can be caused by excess ACT and excess gastrin can lead to ulcers
    • no specific medication to treat, genetic testing of MEN1 families is being studied to hopefully identify mutation s early to allow early tumor removal (patients almost all show symptoms by 50)
  23. Artificial pancreas (Bullet points)
    • its a combination of a continuous glucose monitoring devise and an insulin pump
    • continuous glucose monitoring devices can provide trend info and also reflect glycemic fluctuations which cannot be done with traditional self monitoring glucose divices
    • the artificial pancrease regulates blood glucose better than a traditional insulin pump and keeps patients in target range 70.7% of time (insulin pump was 57.3%)
  24. hormonal changes in starvation (Bullet points)
    • leptin is produced by adipose tissue and is a marker for overall nutrition in the body- has a role in energy balance esp. during starvation afffecting the metabolic rate and conversion of T3 to T4 to limit energy use
    • in starvation (anorexia too) lower levels of T4 alter mood in young girls causing depression
    • insluin levels decrease in stargvation due to low glucose consumption- lack of insulin causes neg effect on bone density and weakens structure due to change in bone anabolism
  25. Leukotrienes (Bullet points)
    • they are made in the leukocytes (WBCs)
    • they help fight infections by being rapidly producedd and released- they form a tightly packed line in the endothelial wall and then are dispersed to the target cell or area
    • they are important in repiratory and skin diseases such as atopic dermatitis, psoriasis, allergic rhinitis and nasal polyps
  26. autocrine factors in tumors (Bullet points)
    • autocrine signaling occurs when a cell self stimulates through cellular production of a chemical messenger (ie growth factor) that binds to a corresponding receptor on an identical cell type, including themselves
    • synthesis + secretion of autocrine growth factors and reception occur all at the same cell or cells of an identical type to stimulate cell growth, proliferation, differentiation and wound healing
    • monoclonal antibodies are used to target autocrine growth factor signaling pathways in cancer
  27. erythropoietin (Bullet points)
    • main function: increase RBC production in bone marrow
    • renal erythropoeitin producing and oxygen sensing cells sense low levels of O2 in blood and help synthesize erythropoeitin
    • two main disorders: hypoxia (low O2 in blood) and anemia (lack of RBCs)
  28. Thymus
    • a gland in the neck
    • makes at least 5 peptide hormones
    • gland is largest at puberty, then atrophies- if the gland doesnt physically atrophy, it is replaced by fatty tissue
  29. peptide hormones made by the thymus
    • thymosins
    • thymulin
    • thymopoietin
    • these are important in immunity, and its functions are important when you are young
  30. Functions of the thymus
    • makes T-cells: thymus dependent lymphocytes
    • Makes hormones that influence T-cells: these control development of mature T cells from pre T stem cells at different parts of differentiation; hormones made that influence T-cells are also vital for the ability of lymphocytes to make antibodies against foreign antigens
  31. Pancreas
    • critical in regulation of blood glucose homeostasis
    • makes insulin- only hormone that decreases blood glucose by increasing glucose uptake and use by cells
    • makes glucagon
  32. Hormones that oppose insulin in blood glucose
    • a number of hormones do the opposite to increase blood glucose
    • glucogon
    • growth hormone
    • epinepherine
    • hydrocortisone
  33. Blood glucose homeostasis levels
    • level higher than 180: body would not normally excrete glucose in urine but level this high it will be in urine
    • hyperglycemia level: above 150mg/100mL
    • normally, the body will not excrete glucose, cells will take it up and eventually form fat
    • hypoglycemia: level below 60- as level goes down glycogen stores in liver get broken down to release free glucose. not only will there be glycogenolysis but also gluconeogenesis to increase blood glucose
  34. What happens at when blood glucose gets down to 100
    • glucose absorbed from digestive system, goes to liver and other tissues 
    • there is then glycogenesis for storage and catabolism for energy
  35. What happens when blood glucose is at level 75
    • glycogenolysis to release glucose
    • this is right above hypoglycemic level
  36. Hormones and glucose regulation
    hormones regulate: glucose uptake into cells (140), glucose catabolism for energy (100), glycogenesis (100), glycogenolysis (75), gluconeogenesis (60)
  37. Glucose
    • the critical and preffered energy source of the body
    • if you dont eat or if high stress, blood glucose will increase due to hormones
    • when you eat or if hormones act causing increase in blood glucose, insulin will be made to stimulate glucose uptake by cells
  38. what is glucose vital for
    • neurons are most relient on glucose- its vital to their function- they dont use fat for energy (body can use glucose, fat or amino acids, but neurons cant)
    • can only use ketones if long term no glucose
  39. ketones
    produced from fatty acid breakdown
  40. What nutrients does the brain use
    the brain uses amino acids for synthesis of protein + neurotransmitters
  41. What if low glucose in neurons
    you can have behavioral changes: confusion, loss of consciousness, convulsions, and even death eventually (critical parts of the brain are deprived)
  42. parts of pancreas
    • there is an exocrine portion and an endocrine portion
    • the bulk of tissue is exocrine- acini (acinan cells)
  43. exocrine portion of pancreas
    • majority of tissue
    • synthesizes and secretes digestive substances- enzymes and bicarbonate released into pancreatic duct and empty into duodenum of small intestine for digestion
  44. endocrine portion of pancreas
    takes up 2% of tissue in the form of islets of langerhans
  45. Islets of langerhans
    • have a rich blood supply and autonomic nerves that reach out to them
    • main cell types in the islets  all make polypeptide hormones that are released into the blood
  46. main cell types in the islets of langerhans
    • alpha cells
    • beta cells
    • delta cells
    • gamma cells
  47. alpha cells
    make glucagon
  48. beta cells
    • most predominant type
    • make insulin
  49. delta cells
    make somatostatin and other hormones
  50. somatostatin
    • growth hormone inhibiting hormone
    • acts in a paracrine way locally inhibiting both insulin and glucagon under different circumstances
  51. Gamma cells
    make pancreatic polypeptide- hormone that influences digestive organs
  52. what is the most common endocrine disorder in the USA
    diabetes mellatus
  53. glucose carriers
    • cell membrane transporters that help cells to take up glucose
    • there are 4 types
  54. 4 types of glucose carriers/transporters
    • 1. Glut1
    • 2. Glut2
    • 3. Glut3
    • 4. Glut4
  55. Glut1
    transporter in all cells
  56. Glut2
    important for beta cells of pancreas and liver
  57. Glut3
    glucose transporter critical for neurons
  58. Glut4
    • glucose transporter important for skeletal and cardiac muscle and adipose tissue
    • this one must be induced by insulin, the other three are just present naturally
  59. What form of glucose is in the blood
    plain glucose- not phosphorylated
  60. Stimulus for insulin synthesis
    primary stimulus is an increase in blood glucose- you eat food and glucose is absorbed into the blood, raising the blood glucose
  61. How is glucose taken up by cells
    glucose is taken up by beta cells using the glut 2 transporter and is then converted by phosphorylation to glucose-6-phosphate
  62. how is insulin made
    • first made by the beta cells as a pre pro insulin- a large single polypeptide
    • then it will fold to make proinsulin- there are 2 disulfide bridges in the molecule
    • then you cleave to release insulin and the c-peptide and these are both stored in the granules
  63. c-peptide
    • connecting peptide
    • no function but good marker that insulin has been synthesized
  64. Insulin structure
    • 51 amino acids
    • alpha chain is 21 amino acids beta chain is 30
  65. Release of insulin into the blood
    • bc insulin is stored, there is a biphase release into the blood
    • stored insulin is released from granules (c peptide is also released)
    • also newly synthesized insulin and c peptide are released
    • they are peptides that travel freely in the blood
  66. target cell receptors for insulin
    uses membrane bound tyrosine kinase mechanism
  67. Functions of Insulin
    • hypoglycemic
    • important in protein synthesis
    • increases lipid synthesis and decreases fat mobilization
    • has effects on the brain
  68. insulin hypoglycemic function
    • decreases blood glucose and increases glucose utilization by cells
    • converts glucose to glucose-6-phosphate
    • increases glycolysis + glucose oxidation for energy
    • stimulates glycogen synthesis
    • inhibits glycogenolysis and gluconeogenesis
    • inhibits glucagon
  69. glycolysis
    breakdown of glucose for energy
  70. why does insulin stimulate glycogen synthesis
    so whatever glucose isnt needed for energy will be converted to glycogen which can be stored in liver and muscle
  71. insulin in protein synthesis function
    • has an anabolic effect
    • increases amino acid uptake into cells
    • increases ribosome functioning in protein synthesis
    • vital for growth and maintenance of tissues
  72. insulin in lipid synthesis function
    • increases lipid synthesis and decreases fat breakdown
    • acts on adipose tissue where fat is stored
  73. Insulin effects on the brain
    • neurons are very sensitive to glucose, esp the hypothalamus
    • the hypothalamus has centers sensitive to blood glucose
    • arcuate nucleus- influences sense of hunger when low blood glucose and satiety when high
    • --->when high glucose, it will stimulate insulin which will inhibit satiety
  74. What does the regulation of insulin secretion involve
    • gastrointestinal hormones
    • autonomic parasympathetic NS
    • autonomic sympathetic NS
    • Other hormones
  75. Regulation of insulin secretion
    • Main factor: increased blood glucose
    • minor factor: increased amino acids in the blood (which also happens after eating) and increased fatty acids in the blood
  76. Gastrointestinal hormones in regulation of insulin secretion
    • they are incretins (a category of hormones- ie includs gastrin and cholecystikinin)
    • triggered when eating
    • stimulate increase in insulin
  77. Autonomic parasympathetic NS in regulation of insulin secretion
    vagus nerve stimulates insulin
  78. Sympathetic NS in regulation of insulin secretion
    symp NS inhibits insulin when needed
  79. other hormones in regulation of insulin secretion
    • other hormones that increase blood glucose either directly or indirectly stimulate insulin
    • ie hydrocortisone, epinepherine, growth hormone
  80. Glucagon
    • made in the alpha cells of islets of langerhans
    • peptide made of 29 amino acids
    • travels freely in the blood
    • uses a cyclic AMP mechanism of action
  81. production of glucagon
    1st made as a prohormone 2x as big then broken down to give the active hormone
  82. Functions of glucagon
    • a catabolic hormone
    • hyperglycemic
    • affects liver
    • stimulates fat breakdown
    • stimulates insulin
  83. glucagon as a catabolic hormone function
    • stimulates protein breakdown/catabolism
    • allows amino acids that form from protein breakdown to be used in gluconeogenesis
  84. glucagon as a hyperglycemic hormone
    increases blood glucose
  85. glucagon function in affecting the liver
    main effect is ont he lilver- it stimulates glycogenolysis and gluconeogenesis (both increase glucose level)
  86. glucagon function in fat breakdown
    • stimulates fat breakdown
    • stimulates lipase in liver and adipose tissue
    • fat is a triglyceride and is broken down into fatty acid and glycerol
  87. Regulation of glucagon secretion- stimuli
    • main factor: drop in blood glucose level (ie when not eating)
    • some of the gastrointestinal hormones can stimulate it
    • sympathetic NS stimulates it (stress situation- you want to keep up blood glucose)
    • main amino acids used for gluconeogenesis stimulate glucagon
  88. regulation of glucagon secretion- inhibitors of glucagon secretion
    • insulin and somatostatin
    • paracrine- localized effects
  89. main amino acids used for gluconeogenesis
    argenine and alanine
  90. Diabetes mellatus type 1
    • an autoimmune disease
    • affects beta cells of pancreas
    • insulin dependent
    • much more unstable compared to type II
    • onset- usually under 25 years old- usually at 12-14 years, often after a growth spurt
    • low insulin and therefore high blood glucose because it cant get into cells
  91. dangers of untreated type I diabetes mellatus
  92. ketosis
    • high blood glucose bc it cant get into cells so body will use fat for energy- fat broken down into fatty acids and glycerol and fatty acids are converted to ketones
    • body produces high amount of ketones (acidic) and when they go into the blood they upset acid-base balance
    • this doesnt happen in type II
  93. Diabetes Mellatus Type II
    • much more common
    • seen in middle aged in past but now overweight children
    • non-insulin dependent (though some may need it)
    • proceeded by overweight period usually
  94. Why is diabetes mellatus type II not insulin dependent
    • there is increased insulin resistance- the cells are less sensitive to insulin 
    • sometimes the beta cells also arent making enough which is why insulin can be given to some people
  95. secondary diabetes mellatus
    • like type II
    • develops as a side effect of another endocrine problem
    • ie high hydrocortisone or hydrocortisone therapy (anti inflammatory treatments)
  96. Gestational Diabetes
    • like type 2
    • develops in pregnancy sometimes
  97. alloxan
    a substance that destroys beta cells
  98. Symptoms of untreated diabetes mellatus type 1
    • wight loss (using fat)
    • feeling unwell from high acid in blood (if ketoacidosis really bad you will see behavioral changes like confusion)
    • increase in breathing to rid the body of CO2 bc CO2+water= carbonic acid- this is an attempt to lower acid level in blood
    • dehydration due to fluid loss causing drop in blood volume and blood pressure
  99. ketoacidosis explained
    • if you cant use glucose for energy, in adipose tissue you will break down triglycerides into fatty acids and glycerol
    • the fatty acids in blood travel to the liver where they are broken down into ketones (hydroxybutyric acid and acetoacetic acid). these acids can be used in the krebs cycle and amino acids can be converted to ketoacids
  100. Symptoms of untreated type I and often type II diabetes
    • polyurea and polydypsia
    • polyphagia (increase in hunger bc cells of hypothalamus which are key in regulating eating cant get the glucose)- this occurs more in type 1
  101. Diagnosis of diabetes mellatus
    • glucose tollerance test
    • people take an oral dose of glucose at Time=0 and you measure blood glucose in mg% over time in hours
  102. results of glucose tolerance test
    • a healthy person: will have level less than 100 which will go up to no more than 150 then back down
    • a mild person: will take longer to go back down and wont go back down as much
    • a sever person: will start off higher and not go down
  103. Treatment of diabetes objective
    to promote glucose utilization on a daily basis
  104. treatment of type 1 diabetes mellatus
    • insulin needs to be adjusted to the need of the person based on diet, exercise, etc
    • too much can cause hypoglycemia, insulin shock and convulsions
    • insulin cant be taken as pill (digestive enzymes will degrade it)
    • options: regular injections, insulin pump, or a programmed implanted medication system
  105. future type 1 diabetes mellatus treatment
    more artificial pancreases, nasal spray, bcg vaccine, transplant of tissue
  106. treatment of type 2 diabetes mellatus
    • diet
    • medication if needed
  107. diet in diabetes type 2 treatment
    • lose weight to a healthy range if possible
    • consistant complex carbohydrates/protein/fat
    • avoid concentrated sweets
    • adequate fiber will slow glucose absorption from food (whole grains, fruit, veg)
  108. medication options in treating type II diabetes mellatus
    • goal is to ensure that there is an increased sensitivity to insulin and when necessary to increase insulin availability
    • meds increase the binding of insulin to receptors (on cell membrane) and promote production of insulin from beta cells
    • some also prevent the degredation of insulun by the enzyme insulinase in the liver
    • they never give it first, but sometimes after all this insulin may still be required
  109. why might insulin still be required after all diabetes mellatus medications?
    may need the boost if the cells arent making enough or may need a little more available for greater chance of receptor binding
  110. Diabetes mellatus walkthrough type 1
    • there is insufficient insulin action due to the autoimmune disease glucose can not be utilized by cells resulting in lipolysis or breakdown of fatty acids in adipose tissue and then ketogenesis in the liver. this creates ketones whicch some can be used for energy in the krebs cycle but the rest undergo ketosis causing ketoacidosis
    • because glucose is not being taken up by cells due to low insulin there is hyperglycemia. If the level gets high enough there will be very high glucose and therefore solute in the blood so the body will try to excrete those solutes in the urine (glucosurea). As a result of solutes leaving the blood, water will follow causing polyurea and increased urine volume. A greater urine volume means a lower blood volume due to fluid loss so there is low blood volume and low blood pressure (Can cause shock if low enough). This fluid loss causes the kidneys to not be able to function properly causing renal hypofunction which will intensify ketosis
    • high blood solutes (glucose and ketones) also pulls water from cells into blood by osmosis causing cell dehydration and polydipsia (excess thirst) to try to replace the fluid loss
  111. Gut-Brain Axis
    relationship between GI tract and brain
  112. regulation of eating
    • what tells you when youre hungry or full is very complex- psychological, emotional, social and physiological factors
    • nutrients in the liver can influence eating as well
  113. central role of the hypothalamus
    • there are centers in the area called the arcuate nucleus- this area integrates info from the brainstem
    • one key nerve from the gi tract which synapses in the brainstem is the vagus nerve (part of parasymp NS)- critical in regulation of GI tract
    • hyp also integrates info from hormones- some directly affect the hyp, others affect the brainstem
  114. energy in regulation of eating
    • energy is key- do you have enough
    • in short term (daily)- blood glucose is critical- hungry when its low, full when its high
    • on a long term basis we get signals from energy storage in adipose tissue (there isnt a lot of energy stored as glycogen)
  115. Specific hormones of the gut-brain axis
    • mostly peptides from the small intestine
    • neuropeptide y
    • peptide yy
    • glucagon like peptide
    • oxytomodulin
    • leptin
    • orexins
    • ghrelin
  116. neuropeptide Y (in gut brain axis)
    • a peptide 36 amino acids made in small intestine - increases feeding
    • related to if you are processing food (causes you not to eat) or not (causes you to eat)
  117. Peptide YY (in gut brain axis)
    released after meals, increases satiety
  118. glucagon like peptide (in gut brain axis)
    • made in small intestine
    • structurally like glucagon
    • increases satiety
    • it is an incretin- increases insulin to process food
  119. oxytomodulin (in gut brain axis)
    • made in colon of large intestine
    • decreases appetite after eating
    • the more calories you eat, the more this hormone is secreted
  120. Leptin (in gut brain axis)
    • made in adipose tissue
    • longterm fat storage 
    • when you have fat stored, hunger is decreased (affects hypothalamus)
    • doesnt decrease hunger in obese people bc they have high leptin and resistance
  121. Orexins (in gut brain axis)
    • a group of substances made by the hypothalamus and small intestine
    • increases hunger when there is a low blood glucose
    • related to cells sensing amount of glucose
  122. Ghrelin (in gut brain axis)
    • made by stomach and hypothalamus
    • made (esp in stomach) when theres low amount of food in the stomach and stimulates hunger
  123. gastric bypass surgery
    • there are various forms 
    • some of the hormones may also be made by other lengths of the GI tract (not always made in small intestine)
    • people eat less bc no physical room for food (stomach cut) and decreased absorption of nutrients
    • both the glucagon-like-peptide and peptide YY  increase causing a decreased appetite
  124. What substances act in the small intestine
    • bile
    • pancreatic secretions
    • intestinal enzymes
  125. what controls salivation
    • the nervous system
    • saliva digests starch in the mouth
  126. intestinal cells in digestion
    • make enzymes that digest carbs and protein
    • in small intestine bile emulsifies fat, pancreatic enzymes digest and bicarbonate counteracts HCL from the stomach
  127. pancreas in digestion
    • releases enzymes for fat, protein, and carb digestion and bicarbionate to neutralizae acid from stomach
    • (HCL and pepsin are acidic and are in stomach for protein digest).
  128. enteroendocrine cells
    • cells of GI tract that produce hormones
    • location is diverse- no solid location like other endocrine cells (ie hydrocortisone cells are all in adrenal gland)
    • location can be in stomach, diff parts of small intestine (duodenum, jejunum, ileum), or colon of the large intestine
  129. effects of enteroendocrine cell hormones
    • stimulation or inhibition of production and secretion of digestive substances (not always enzymes- ie HCL or bile)- main function
    • stimulation or inhibition of muscle contraction and sphincter opening/closing of organs- main function
    • growth and maitenance of GI tissue
    • affect hunger and satiety
  130. nature of enteroendocrine cell hormones
    • peptides- generally mechanism of action is through G-protein coupled targe cell receptors
    • some are made elsewhere (ie- brain)
  131. regulation of digestion
    • complex due to:
    • -->hormone level in blood
    • -->paracrine (local) effects of hormones
    • -->hormones outside GI tract
    • -->autonomic NS (parasympathetic stimulates digestion)
  132. How do GI hormones work
    • generally work by efficiency- produced mostly when you need them and only a little when you dont
    • enzymes and secretions are present when needed
    • contraction of muscle and movement occurs when appropriate
    • inhibition when needed to slow digestion such as when a little food in the gut or fatty food (it takes longer to absorb from fatty food so slower movement)
  133. Stimuli of GI tract Hormones
    • presence of specific nutrients in food, such as amino acids or fatty acids
    • presence of partly digested foodstuffs in GI tract
    • pH of partially digested food stuffs
    • may be sensed directly in lumen of GI tract or after nutrients are absorbed
  134. Major GI hormones
    • all made in small intestine except gastrin and ghrelin
    • Gastrin
    • Cholecystokinin
    • Secretin
    • Gastric Inhibiting Peptide
    • Somatostatin
    • Motilin
    • Ghrelin
  135. Gastrin
    • made in stomach- inactive- HCL activates pepsinogen to become pepsin
    • when protein in food theres increased gastric HCL
  136. main stimuli of gastrin
    • partly digested protein or food in pylorus of stomach (lowest part)
    • also- fatty acids and the vagus nerve can stimulate it
  137. functions of gastrin
    • increases gastric HCL secretion needed for protein digestion
    • --> this activates the enzyme pepsin, which is also needed for protein digestion
    • increases pancreatic enzymes (which digest protein, fat and carbs) which are then released into duodenum of small intestine
    • relaxes pyloric sphincter allowing food to go in sm. intestine
    • stimulates growth of gastric mucosa (lining of stomach)
    • incretin action- stimulates insulin in the presence of glucose
  138. Zollinger-Ellison Syndrome
    tumor producing gastrin, results in too much acid produce which contributes to ulceration of esophogus, stomach and duodenum
  139. Cholecystokinin stimuli
    • fatty acids and monoglycerides in duodenum (main)
    • amino acids, di and tri peptides (partially digested peptides)
    • HCl from stomach
  140. Cholecystokinin functions
    • increase in pancreatic secretion of enzymes into small intestine
    • synergistic effect on secretin stimulation of bicarbonate (to neutralize acid)
    • stimulates contraction of gall bladder to release bile into small intestine
    • relax sphincter from liver to release bile from where its made
    • its an enterogastrone- inhbits gastric emptying to allow time to emulsify fat by bile in intestine
    • incretin action- stimulates insulin in presence of glucose
    • stimulates peristalsis (wave like contraction) of small intestine and colon
    • increases satiety in brain, decreases food intake
  141. Secretin
    • first hormone discovered
    • known to be released into blood
    • made in small intestine
  142. Secretin stimuli
    acid and partly digested food in duodenum
  143. Secretin Functions
    • stimulates secretion of bicarbonate rich fluid from pancreas to neutralize acid in small intestine
    • synergystic with choleycystokinin, enhance enzyme secretion and action 
    • increase bile secretion by liver
    • decreases gastic acid (may act as an enterogastrone)
    • incretin action- stimulates insulin in presence of glucose
  144. Gastric Inhibiting Peptide
    • glucose dependent insulinotropic peptide
    • made in small intestine
  145. Gastric Inhibiting Peptide Stimuli
    • fat (most)
    • glucose (second most)
    • amino acids in duodenum
  146. functions of Gastric Inhibiting peptide
    • its and enterogasterone- inhibits the stomach
    • -->decreases gastric secretions
    • -->slows gastric motility
    • -->decreases gastrin
    • stimulates intestinal enzyme secretion (enzymes digest protein and carbohydrate)
    • incretin action- stimulates insulin in presence of glucose
  147. Somatostatin
    made in stomach and small intestine
  148. somatostatin stimuli
    • amino acids and glucose released in digestion
    • Cholecystokinin
  149. Somatostatin funcitons
    • paracrine inhibitory effect
    • inhibit digestive secretions as food has already been digested
    • antagonistic to gastrin
  150. Motilin stimuli
    • alkalinization of small intestine (caused by bicarbonate from pancreas) indicating digestion underway
    • inhibited by food or acid entering the small intestine
  151. Motilin functions
    • stimulates slow contraction f stomach and intestine- move material through small and large intestines to excrete wastes
    • *antibiotic erythromycin binds to motilin receptor as agonist, helps stimulate GI muscle contraction after surgery when slow*
    • anesthesia slows digestive processes
  152. Ghrelin
    made by stomach and hypothalamus
  153. Ghrelin stimuli
    when there is little food int eh stomach there is nervous stimuli sent to the hypothalamus
  154. Functions of ghrelin
    increases appetite (Affects hypothalamus) especially in conjunction with growth spurt
  155. Homeostasis maintained of calcium
    • the body maintains homeostasis of calcium in a very narrow range (8.5-10.5mg/100mL) in blood
    • lower than 8.5: hypocalcemia
    • higher than 10.5: hypercalcemia
    • homeostasis of phosphate has a much wider range than calcium
  156. Importance of calcium
    • needed for cardiac and skeletal muscle contraction (sliding filaments)
    • vital in nervous impulses
    • needed for release of neurotransmitters at synapse
    • a blood clotting factor
    • can increase secretion of endocrine glands
    • can be invovled in some hormone mechanisms of action
    • influences enzyme activity in all cells
    • important in bone and tooth strength
    • can influence acid-base balance
  157. calcium in bone and tooth strength
    the bone is a critical storage for calcium- stores more than 99% in extracellular matrix of bone
  158. Importance of phosphates
    • cell components that contain phosphates: ATP,  nucleic acids, cyclic AMP, phospholipid membranes
    • has enzyme activity
    • important in structure of bone and teeth
    • important in acid base balance-buffers
  159. Calcium distribution in the body
    • appx 10mg/100mL blood
    • 1/2 is active ionized, other half is bound to proteins or salts
  160. The intracellular matrix of bone
    • 35% is organic: collagen (a protein) and mucopolysaccharides- becomes impregnated with mineral crystals
    • 65% is inorganic: with many minerals including fluoride and magnesium but key one is hydroxyapetite
  161. hydroxyapetite
    a double salt of calcium phosphate and calcium carbonate
  162. Calcium blood concentration
    calcium concentration in blood is much greater than in the cytoplasm of cells
  163. hormones that affect calcium
    • some also affect phosphate
    • mainly parathyroid hormone and the active form of vitamin D (called calcitriol)
    • also calcitonin from thyroid gland, parathyroid related peptide (made mostly in placenta in pregnancy), Estrogen, testosterone
    • and there are some effects by thyroid hormone, hydrocortisone and bone growth factors (ie fibroblast growth factor, insulin like growth factor and transforming growth factor- they act locally and stimulate bone growth)
  164. parathyroid glands
    • 4 total-2 on each back lateral lobe of the thyroid gland
    • mainly secretes parathyroid hormone
  165. parathyroid hormone
    • an 84 amino acid peptide
    • made by the cheif cells of the parathyroid gland
    • made in a very large form- 115 amino acid prepro parathyroid hormone (original precursor) then converted to a 90 aminoacid proparathyroid hormone then converted to the 84 amino acid active form
  166. how is parathyroid hormone regulated
    only by the calcium level in the blood- by a basic mechanism
  167. parathyroid hormone stimulus
    synthesis and secretion of PH is timualted when there is a low calcium level in the blood
  168. how is parathyroid hormone metabolized
    by the liver and kidney
  169. Parathyroid hormone mechanism of action
    • a peptide- so receptor on membrane
    • has a g-coupled receptor in target cells
    • works by cyclic AMP mechanism
  170. Effects of parathyroid hormone
    • increases blood calcium
    • primary effects on calcium
    • most important effect on bone
    • affects kidney
    • affects small intestine
  171. parathyroid hormone effects on calcium
    • increases blood calcium when too low
    • primary effects are on calcium and while this is happening the body will try to remain a stable phosphate level
    • it may increase phosphate excretion in urine
  172. how are calcium and phosphate related in body regulation
    the body wants to keep calcium free in the blood, not bound to phosphate and wants to avoid calcium phosphate deposits in soft tissues
  173. Parathyroid hormone effect on bone
    • increases resorption from bone- bone breakdown to release calcium into blood
    • increases number of osteoclasts
    • increases phagocytosis by osteoclasts
    • increases lysosomal enzyme activity by osteoclasts
    • cause localized acidosis to solublize bone
  174. Parathyroid hormone affects on kidney
    • second most important after bone 
    • increases calcium absorption into blood (decreased amount in urine)
    • the kidney makes the active form of vitamin D (calcitriol) +parathyroid hormone stimulates it in the kidney endocrine cells
  175. parathyroid hormone effects on small intestine
    • an indirect affect
    • you stimulate vitamin D synthesis and the vitamin d is then used to absorb calcium from food
  176. Vitamin D
    • A steroid
    • a fat soluble vitamin that can also be considered a hormone
  177. Vitamin D mechanism of action
    • same as other steroid hormones
    • has a nuclear receptor in target cells
    • stimuates transcription
  178. main effect of vitamin d
    • increases blood calcium
    • does this by stimulating calcium absorption from food
    • also stimulates phosphate absorption
    • in kidney it promotes calcium reabsorption into blood an less in urine (lesser effect)
    • -->inhibits phosphate reabsorption
  179. vitamin d minor effect
    • has a minor effect on bone
    • stimulats bone resorption to increase blood ca2+
  180. calcitonin
    • made in the parafollicular cells around the follicles in the thyroid gland
    • a 32 amino acid peptide
    • made from larger procalcitonin (136 aminoacids)
    • not critical in humans (can be in other animals)- mostly important when used therapeutically
  181. effects of calcitonin
    • decreases blood calcium when too high
    • can be therapeutic when there is too much bone resorption (ie from high parathyroid hormone)
    • has affects on bone
    • has affects on kidney
  182. calcitonin affects on bone
    • inhibits bone resorption: decreases number of osteoclasts and decreases osteoclast enzyme activity
    • decreases collagenalytic enzyme: located in the matrix of bone and it breaks down collagen
    • stimulates osteoblasts: increases number and activity- important for increasing the amount of bone matrix
  183. Regulation of calcitonin
    • its stimulated when blood calcium level is too high
    • it is inhibited by calcitriol (activated vitamin D)
  184. collagen
    • keeps connective tissue strong
    • bone is a type of connective tissue
  185. other hormones that affect calcitonin
    • sex steroids
    • parathyroid related hormone
    • growth factors that influence bone
  186. sex steroids and affect on calcitonin
    especially estrogen but also testosterone stimulate calcium deposit in bone
  187. parathyroid related hormone and affect on caclitonin
    • aka parathyroid hormone related peptide
    • made mostly in placenta, a small amount is made in other tissues
    • in pregnancy when low calsium levels in blood, it will stimulate calcium to have increased availability to the fetus
  188. fibroblasts
    cells in connective tissue that make fibers like collagen
  189. growth factors influencing bone and relation to calcitonin
    • these are peptides and there are a variety of them
    • can have a paracrine, autocrine or endocrine effect
    • made in bone and other body tissues
    • fibroblast growth factor, insulin like growth factor, and transforming growth factor
  190. Fibroblast growth factor
    • comes mostly from osteocytes (regular bone cells)
    • stimulates an increased number of bone cells to cause growth and stimulates an increase in collagen synthesis (collagen goes to matrix)
    • decreases phosphate level in blood by decreasing absorption from food and increasing phosphate excretion
  191. insulin like growth factor
    • structually like insulin
    • made in bone, liver and other tissues
    • stimulates bone and cartilage growth- increases number of osteoblasts, collagen deposit in matrix and bone calcification (calcium deposit in bone)
    • growth hormone and other hormones stimulate this
  192. transforming growth factor
    tries to acheive an appropriate balance in bone tissue between formation and resorption
  193. Calcium Disorders
    • Rickets
    • Osteomalacia
    • Osteoporosis
  194. Rickets
    • a nutritional deficiency- can be of calcium (most common), vitamin d or phosphorus
    • occurs in a child
    • poor mineralization of bones from lack of calcium (they wont be hard, may be deformed)
    • common symptom- severe bowed legs- the weight of the body is so heavy and the leg bones are so weak)
    • poor growth due to lack of calcium
  195. Osteomalacia
    • adult rickets- a nutritional cause of osteoporosis
    • the bones are calcium poor- more porous, breakable and brittle bc not strong
  196. Osteoporosis
    • the bones are porous by different causes: dietary lack of calcium , vitamin d or phosphorous, lack of activity (physical movement helps keep calcium in bone), aging and decrease in estrogen or testosterone levels
    • after menopause there are medications that decrease the risk
  197. medications that decrease osteoporosis risk after menopause
    biphosphonates (ie fosamax)- decrease osteoclast activity in the bone tissue. They also combine with the hydroxyappetite crystals and slow their degredation
  198. Parathyroid disorders
    • very rare
    • there arent usually disorders that involve too high levels of calcitonin
    • Hypoparathyroidism
    • Hyperparathyroidism
    • Paget's Disease
  199. Hypoparathyroidism
    • a low parathyroid hormone
    • if they have to remove the thyroid gland for any reason, they may also take out the parathyroids (error in surgery)
    • can be an autommine condition where cells are degraded and replaced by fat (very rare)
  200. Symptoms of Hypoparathyroidism
    • low calcium in blood
    • high phosphate
    • excess calcium excretion
    • bone is dense
    • increased neuromuscular excitability
  201. why is there extra calcium excretion in hypoparathyroidism
    it cant be reabsorbed properly without parathyroid hormone
  202. why is bone dense in hypoparathyroidism?
    because of decreased resorption (stimulated normally by parathyroid hormone)
  203. why is there increased neuromuscular excitability in hypoparathyroidism?
    • theres a type of tetany (strong sustained contraction)
    • its not a direct effect of calcium but the calcium can affect the sodium causing this, a variety of convulsions and other nervous system problems
  204. Treatment of hypoparathyroidism
    • in more severe cases they give some sort of parathyroid hormone replacement
    • if not severe, calcium and viatamine d given or increased in the diet
  205. Hyperparathyroidism
    • high parathyroid hormone 
    • main cuase is cancer- causes defective regulation of the gland
    • you can have defective gland regulation without cancer
  206. symptoms of hyperparathyroidism
    • high blood calcium
    • high bone resorption causing softness and deformed bones
    • deposit of calcium in soft tissues - kidneys and eyes- in kidney you will try to get rid of calcium from the blood and water and solutes will follow causing polyuria and polydipsia if severe enough and also possible kidney stones and bleeding
  207. treatment of hyperparathyroidism
    • if a tumor-remove the glands and give hormone replacement
    • if not severe- promoting calcium retention in the bone by biphosphonates
    • you could also give a calcitonin analog (something that mimics it) or calcitonin itself to decrease blood calcium
  208. Paget's Disease
    • happens in about 10% of the elderly
    • can be minor or severe, cause not known but most likely not endocrine
  209. Pagets disease symptoms
    • increased activity of osteoclasts and osteoblasts, but in stages not at same time
    • usually occurs in specific bones rather than all
    • overall more osteoclast activity than osteoblast
  210. Pagets disease stages
    • 1. increased osteoclast activity: bone can become weak and deformed
    • 2. increased osteoblast activity: makes a thickened bone, but it can be painful
    • as osteoblast activity increases osteoclast activity goes down
  211. treatment of pagets disease
    in 1st stage you could give biphosphonates to decrease osteoclast activity or calcitonin
  212. Multiple Endocrine Neoplasia 2
    • MEN 2
    • a genetic disorder- autosomal dominant, seen by age 10
    • some types have thyroid cancer of the parafollicular cells (c-cells) which make calcitonin (Very rare)
    • about half the cases have pheochromocytoma (norepinepherine esp and also epi are too high)
    • in some cases the parathyroid is affected
  213. Future prospects of endo
    • neuroendocrinology
    • hormones affect physiology, influence brain and behavior
    • brain releases NTs, hormones and substances into cerebral spinal fluid
    • genetics: can affect amount of hormone receptors, etc; may be able to later use gene therapy to correct non functional genes
    • stem cells: especially in autoimmune disorders
    • organ replacement/transplanataion
    • technological advances
  214. Biosynthetic pathway of vitamin D
    • cholesterol in liver converted to 7-dehydrocholesterol  (provitamin d ) in the skin
    • when uv rays of sun hit the skin it forms previtamin D3 which is then converted to cholecalciferol (vitamin D3)
    • in the blood the vitamin d3 binds to binding protein and travles to the liver where it undergoes hydroxylation to form 25-hydroxycholecalciferol which travels to the kidney where it undergoes hydroxylation again (parathyroid hormone required in this rxn) to form 1, 25 dihydroxycholecalciferol (active vitamin D)
Card Set
Pancreas Thymus Diabetes and Parathyroid Glands
Final Exam of 12/10/15
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