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The Endocrine System
Endocrine SystemEndocrine vs. ExocrineOrgans are not physically connectedAlters activities of target organs/cellsPurpose: Growth/Development
ReproductionRegulationStress Reactions
Hormones are Activated By
Hormonal
Humoral
Neural
Gland/Hormone FunctionsSome glands produce >1 hormone
Some hormones produced by >1 gland
Some organs have >1 function
Some hormones have >1 function
Functions of Endocrine Glands
Endocrine Functions onlyProductionSecretion
Contained within other organs which have other functions
Categories of GlandsCentral: Pituitary
Hypothalamus
Peripheral: Thyroid PinealAdrenals GonadsParathyroids PancreasThymus Others
HypothalamusFound on floor of diencephalonNeural and endocrine functionsBiofeedback mechanism for:Osmotic pressuresTemperature regulationsMetabolic functions
PituitaryExtends from Hypothalamus-behind sphenoid bone“Master Gland” of bodyAnterior- Portal networkPosterior- Neural-contains axons of
Hypothalamus neurons
Anterior PituitaryGH- Growth HormoneProlactinTSH- Thyroid Stimulating HormoneACTH- AdrenocorticotropicFSH- Follicle Stimulating HormoneLH- Luteinizing Hormone
Posterior Pituitary
ADH- Anti-Diuretic Hormone
Oxytocin
Pituitary Disorders Acromegaly- Hypersecretion of GH
Dwarfism- Hyposecretion of GH
ThyroidInferior to larynx2 LobesT3- Triiodothyronine
T4- Thyroxine
Calcitonin
Thyroid DisordersHypothyroidism- Hyposecretion
Hyperthyroidism- HypersecretionGraves Disease
Goiters- iron deficiencies
Parathyroids4 small glands posterior surface of thyroidParathyroid hormoneResponsible for osteoclast of boneDecreases blood phosphate levels(By way of kidneys)Enhances activation of Vitamin D
Parathyroid Disorders Hyperparathyroidism
“Moan and groan, stones and bones”
Pineal GlandForms part of diencephalonMelatoninInhibits hypothalamus release of gonadotropinsMelatonin-decreases in light/increase in dark (circadian rhythm)
Thymus GlandPosterior to sternum, around great vesselsThymosinBoth lymphatic and endocrineLymphatic- produces T-lymphocytesEndocrine- ‘programs’ T-cells
The AdrenalsLocated on superior end of each kidney
Medulla- inner gland
Cortex- outer gland
Adrenal MedullaSympathetic preganglionic fibers synapse on cells in medulla
Release of epinephrine/norepinephrine into general circulation
Adrenal CortexProduce over 30 steroid hormones
Three main cortical hormonesMineralocorticoidsGlucocorticoidsSex hormones
MineralocorticoidsRegulate levels of electrolytes and water in extracellular fluid
95% are aldosteroneSodium reabsorption Potassium excretion
GlucocorticoidsInfluence carbohydrate metabolismImportant in body’s response to stress95% cortisol (hydrocortisone)
stimulates gluconeogenesissecretion is regulated by ACTH
Sex HormonesAndrogens (testosterone)
Estrogens
Both are secreted in greater numbers by gonads
Adrenal Disorders Cushing’s disease-
cortisol over-production secondary to
increased ACTH
Addison’s Disease-cortisol/aldosterone deficiencies
GonadsTestes- males
TestosteroneOvaries- females
EstrogensProgesterone
Both produce hormones/gametes
PancreasRetroperitoneal-posterior to stomachExocrine & EndocrineEndocrine- islets of Langerhans
AlphaBetaDelta
Alpha cells20% of islets
Hormone glucagon
Stimulates breakdown of glycogen in liver- raises glucose levels in blood(glycogenolysis & glyconeogenesis)
Beta Cells75% of islets
Hormone- insulin
Decreases glucose levels
Glucose MetabolismOrganic components of food:Carbohydrates (instant-energy)GlucoseFatsFatty acids/glycerolsProteinsAmino acids
Carbohydrate Metabolism Insulin is released by humoral, hormonal, neural means
Increased glucoseParasympathetic stimulationGastrointestinal hormones
Carbohydrate Metabolism 60% of carbohydrates are stored as
glycogen in liver
If muscles are not exercised after eating-stored as muscle glycogen
Glycolysis Glucose is broken down into pyruvate
and lactate- releasing 2ATPs
(Anaerobic metabolism)
Krebs Cycle
Fat Metabolism A third of any glucose passing through liver is converted to fatty acids
Fatty acids are converted to triglycerides and stored in adipose tissue
Fat Metabolism Without insulin, fat is broken back down into triglycerides/cholesterol CAD
Fatty acids are also broken down into ketone bodies
Protein Metabolism In absence of insulin- protein storage stops and breakdown begins (muscle)
Amino acid breakdown for energy leads to increased urea in urine organ dysfunction
Pancreas Disorders Diabetes-
Type 1- Juvenile onsetType 2- Mature onset Gestational diabetes
Type 1 Diabetes Insulin dependant
S/S:polyuriapolydipsiapolyphagiablurred visionweight loss
Type 2 DiabetesGenerally non-insulin dependant
Has ability to make small amounts of insulin
Can develop into insulin dependant
Gestational DiabetesDevelops during pregnancy
Deficiencies in insulin leads to inability to metabolize carbohydrates
Generally disappears after delivery
Insulin AgentsEarly- porcine, bovineRecent- genetic engineered human insulinProteinRapid, intermediate and long-termCombination of long-term, rapid each day
Insulin TypesRegular- Fast acting0.5-1 hour onset6-8 hour duration
NPH- Intermediate1-1.5 hour onset24 hour duration
Insulin TypesUltralente- Long acting
4-6 hour onset36 hour duration
Oral agents:Diabinese (chlorpropamide)Orinase (tolbutamide)Micronase (glyburide)Glucotrol
Diabetic EmergenciesHypoglycemiaHyperglycemiaDiabetic Ketoacidosis (DKA)Hyperosmolar Hyperglycemic Nonketotic Coma (HHNK)
HypoglycemiaRapid on-set< 60 mg/dlCauses: too much insulin
decreased intake salicylatesexcessive activity beta blockersemotional stress hypothermiachronic alcoholism sepsis
S/S of HypoglycemiaAltered LOCs- irritability, nervousness,
confusion, combativeCool, clammyWeak, rapid pulseSnoring, salivationNormal BP
Diabetic KetoacidosisFat metabolism leads to ketoacidsAcidosis leads to K+ in circulation &
hyperkaluria K+ deficiencyOsmotic diuresis dehydration,
electrolyte imbalances
S/S of DKAWarm, dry skinDry mucous membranesTachycardia, thready pulsePostural hypotensionWeight loss‘Polys’
S/S of DKAAbdominal painAnorexia, nausea/vomitingAcetone breathKussmaulsDecreased LOC
Hyperosmolar Hyperglycemic Nonketotic
ComaGenerally Type II diabeticOsmotic diuresis secondary to sugarsNot acidotic as in DKAFactors: Geriatric
Preexisting diseasesIncreased insulin requirementsMedication use- thiazide, diureticsParenteral/enteral feedings
S/S of HHNKWeaknessThirstPolyuriaWeight LossExtreme dehydration
Treatment of Diabetic Emergencies
Hypoglycemia- ABCsIV- NSMonitor ECGOral, IV DextrosePoss. Glucagon IMPoss. Thiamine
Monitor glucose!
Treatment of Diabetic Emergencies
Hyperglycemia (DKA, HHNK)-
ABCsO2
IV- NSMonitor ECG for abnormalities