The Endocrine System

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