ENDOCRINE SYSTEM for B sc Nursing students

SYSTEM for B sc Nursing students

1. 1 ENDOCRINESYSTEM
Theendocrinesystemactsthroughawiderangeofchemicalmessengersknownas
hormones.Hormonesaredefinedasorganicsubstancesproducedinsmallamountsby
specifictissues(endocrineglands)secretedintothebloodstreamtocontrolthemetabolic
andbiologicalactivitiesinthetargetcells.Hormonesmayberegardedasthechemical
messengersinvolvedinthetransmissionofinformationfromonetissuetoanotherandfrom
celltocell.
Besidetheendocrinehormones2othercategoriesofhormonesareknown.Theyare:-
Autocrinehormones-thatactonthesamecellswheretheyaresynthesized.
Paracrinehormones-thatactonthecellsadjacentorclosetothecellsfromwheretheyare
synthesized.
Thereareyet2anotherclassesofcellularmediatorswhicharealsoinvolvedinthe
messagetransmissionofthebody.
Neurotransmitters-releasedbythenervecellsandusuallyactontheadjacentcells.The
catecholamines(epinephrineandnor-epinephrine)functionasneurotransmitterswhen
secretedintheCNS,whiletheyactashormoneswhensecretedfromadrenalmedulla.
Pheromones-transmittedbetweenthecellsintheorganismsofoppositesex.Thefunction
ofpheromonesistostimulatereproductivebehaviorandtherefore,theyserveasthesex
attractants.
CLASSIFICATIONOFHORMONES:-
Hormonesmaybeclassifiedinmanyways.2importanttypesofclassificationare:-
1.Basedonthechemicalnature:-3types
a.Peptidehormones,eg:-Insulin,glucagon,ADH,oxytocin.
b.Amino-acidderivatives,eg:-Epinephrine,nor-epinephrine,T4,T3.
c.Steroidhormones,eg:-Glucocorticoids,mineralocorticoids,sexsteroids
2.Basedonmechanismofaction:-

2. 2 Hormonesareclassifiedinto2broadgroupsbasedonthelocationofreceptorstowhichthey
bindandsignalsusedtomediatetheiraction.
1)GroupIhormones:-Thesehormonesbindtointracellularreceptorstoformreceptor-
hormonecomplexesthroughwhichtheirbiochemicalfunctionsaremediated.GroupI
hormonesarelipophilicinnatureandarederivativesofcholesterol.Theypossess
relativelylongerhalflives.eg.,Estrogens,androgens,calcitriol,glucocorticoids.
2)GroupIIhormones:-Thesehormonesbindtocellsurfacereceptorsandstimulatethe
releaseofcertainmoleculesnamelythesecondmessengerswhichinturnperformthe
biochemicalfunctions.Thushormonesthemselvesarethefirstmessengers.These
hormonesarehydrophilicinnatureusuallytransportedinthefreeformandpossess
shorthalf-life.
REGULATIONOFHORMONESECRETION:-
Thesecretionofhormonesiscontroledbynegativefeedbackmechanism.Negative
feedbackmechanismskeepthebodyfunctioningwithanarrowrangeofvaluesconsistent
withlife.Foreg:-insulinisahormonethatregulatetheconcentrationofbloodglucoseor
bloodsugar.Whenbloodglucoselevelincreasesafterameal,insulinissecreted.Insulin
actsonseveraltargettissuesandcausesthemtotakeupglucosecausingbloodglucose
leveltodecline.Asbloodglucoselevelbegintofall,howevertherateatwhichinsulinis
secretedfallsalso.Asinsulinlevelsfall,therateatwhichglucoseistakenupbythetissue
decreases,keepingthebloodglucosefromdecliningtoomuch.Thisnegativefeedback
mechanismcounteractsincreasesanddecreasesinbloodglucoselevelstomaintain
homeostasis.
Hormonesecretionisregulatedin3ways.Thesecretionofsomehormonesis
regulatedbyoneofthesemethods,whereasthesecretionofotherhormonescanbe
regulatedby2orevenallthemethods.
1.Bloodlevelsofchemicals:-Thesecretionofsomehormonesisdirectlycontrolledby
thebloodlevelsofcertainchemicals.Foreg.,Insulinsecretioniscontrolledbyblood
glucoselevelandsecretionisparathyroidhormoneiscontrolledbybloodcalcium
levels.
2.Hormones:-Thesecretionofsomehormonesiscontrolledbyotherhormones.For
eg.,hormonesforthpituitaryglandactontheovariesandtestes,causingtheseorgans
tosecretesexhormones.

3. 3 3.Nervoussystem:-Thesecretionofsomehormonesiscontrolledbythenervous
system.Eg.,epinephrinereleasedfromadrenalmedullaasaresultofnervous
systemstimulation.
HYPOTHALAMICANDPITUITARYHORMONES
Thepituitaryglandorhypophysisislocatedbelowthehypothalamusofthebrain.It
consistsof2distinctparts-AnteriorpituitaryoradenohypophysisandPosteriorpituitaryor
neurohypophysisconnectedbyparsintermedia.PituitaryglandiscalledtheMaster
endocrineglandbecauseitregulatesmostoftheotherendocrineglands.
Hypothalamusisthespecializedcenterinthebrain.ItactsastheMasterco-
ordinatorofallendocrineglands.InresponsetothestimuliofCNS,hypothalamusliberates
certainreleasingfactorsorhormones.Thesefactorsstimulatethetargetendocrinetissues
tosecretethehormonestheysynthesize.Ingeneralthehormonalsystemisunderfeedback
control.Forinstance,ACTHinhibitsthereleaseofCRH.
HYPOTHALAMICHORMONES
Hypothalamussecretesatleast6releasingfactorsorhormones.
1.ThyrotropinReleasingHormoneorTRH-Itstimulatestheanteriorpituitarytosecrete
TSH(ThyroidStimulatingHormone)whichinturnstimulatesthereleaseofthyroid
hormones.
2.CorticotropinReleasingHormoneorCRH-Itstimulatestheanteriorpituitarytorelease
ACTHwhichinturn,actsonadrenalcortextoliberateadrenocorticosteroids.
3.GonadotropinReleasingHormoneorGnRH-Itstimulatesanteriorpituitarytorelease
gonadotropinsnamelyLHandFSH.
4.GrowthHormoneReleasingHormoneorGHRH-ItstimulatesthereleaseofGrowth
Hormoneorsomatotropinwhichpromotesgrowth.
5.GrowthHormoneReleaseInhibitingHormoneorGHRIH-Itisalsocalledsomatostatin.
GHRIHinhibitsthereleaseofgrowthhormonefromtheanteriorpituitary.
6.ProlactinReleaseInhibitingHormoneorPRIH-itinhibitsthereleaseofprolactin(PRL)
fromtheanteriorpituitary.
Someofthehypothalamichormones(CRH,TRH,etc)arealsoproducedinotherparts

4. 4 ofnervoussystemandperipheraltissues.Forinstance,somatostatininfoundinhigher
concentrationinthepancreasthaninthehypothalamus.ItisproducedbytheDcellsof
IsletsofLangerhansandbelievedtoregulateinsulinandglucagonsecretion.
ANTERIORPITUITARYHORMONES:-
Anteriorpituitaryoradenohypophysisistrulythemasterendocrineorgan.Itproduces
severalhormonesthatinfluenceeitherdirectlyorindirectly-avarietyofbiochemical
processesinthebody.?Intheanteriorpituitarythereare3typesofcells.Theyare:-1)
Acidophiliccells;2)Basophiliccells3)Chromophores.
I)Acidophiliccellssecrets2hormones-GrowthHormoneandProlactin
GROWTHHORMONE:-
GHpromotesgrowth.Itstimulatesthesofttissueslikeliver,kidneyandmuscleto
secreteagroupofsmallmolecularweightproteinsknownassomatomedin.Somatomedin
stimulatesandpromotesthedepositionofchondroitinsulphateandcollagen.Thee
substancesaretheorganicmatrixofthebones.Depositionofthesematerialswillincrease
thelengthandwidthofbones.Thisisresponsibleforthegrowthoftheframeworkofthe
body.Italsoresistproteinbreakdownduringperiodsofabnormaldevelopmentofpituitary
gland.
ThesecretionofGHiscontrolledby2releasinghormonesfromthehypothalamus.
OnereleasinghormonestimulatestheGHsecretionandtheotherinhibitsit.
Hypothalamus
GHRH GHRIH
AnteriorPituitary
GrowthHormone

5. 5 DISORDERSRELATEDTOGH:-
1.DWARFISM:-ItisanendocrinedisorderresultingfromhyposecretionofGHduringthe
critical developmentalperiodsofchildren.
Causes:-Lesionofanteriorpituitaryduetoinfectionortrauma;lesionofhypothalamus
resultingfromhyposecretionofGHRH.
SignsandSymptoms:-
1.Heightwillbeabnormallyshort.
2.Stuntedskeletalgrowth.
Indwarfism,mentalgrowthandreproductiveabilitywillbenormal.Beinga
hyperglycemichormone,deficiencyofgrowthhormonewillleadtohypoglycemia.
2.GIGANTISM:-ItisanendocrinedisorderresultingfromhypersecretionofGHduringthe
critical developmentalperiodsofchildren.
Causes:-Tumorousgrowthofacidophiliccellsofanteriorpituitary;tumorousgrowthof
hypothalamussecretingexcessGHRH.
SignsandSymptoms:-
1.Heightoftheindividualwillbeabnormallytall.
2.Enlargementofsofttissueslikeliver,spleen,tongueetc.
3.Constantheadacheduetotumorandvisualdisturbances.
Ingigantism,mentalgrowthandreproductiveabilitywillbenormal.Beinga
hyperglycemichormone,excessgrowthhormonewillleadtohyperglycemia.
3.ACROMEGALY:-Itisanendocrinedisorderresultingfromhyper-secretionofGHinadults.
Causes:-Tumorousgrowthofacidophiliccellsofanteriorpituitary;tumorousgrowthof
hypothalamussecretingexcessGHRH.
Acromegalymeansenlargementofperipheralparts.Thereisnoabnormalincreasein
height.Theepiphysisofthebonesclosesatthetimeofpuberty.Therefore,increased
secretionofGHcannotincreasethelengthofthebone.Depositionoforganicmatrixonthe
boneswillproducethethickeningofthebones.
SignsandSymptoms:-
1.Producesprotrusionofforehead,flatteningofnose.
2.Bendingofvertebralcolumn.
3.Thickeningofsoftpartsliketongue.
4.Increaseinbloodglucoselevel-hyperglycemia

6. 6 5.Enlargementofliver,spleenandheart(hepatomegaly,splenomegalyand
cardiomegaly)
6.Enlargementoffeetandhands.
7.Elongationandwideningofmandibleandprotrusionofjaw-Prognathism.
8.Guerrillalikeface
9.Headache,hypertensionandvisualdisturbances.
PROLACTINORLACTOGENICHORMONE
Itissecretedfromtheacidophiliccellsofanteriorpituitary.PRIHofhypothalamus
whichisbelievedtobedopamineinhibitsthesecretionofPRL.Itsreleasesincreasedduring
pregnancyandlactation.ThehormonesestrogenandoxytocinenhancePRLsecretion.
Nipplestimulation,stress,sleepandsexualintercoursepromotePRLrelease.Italso
promotesthegrowthofcorpusluteumandstimulatestheproductionofprogesterone.
Duringpregnancy,PRLpromotesthegrowthandthedevelopmentofmammarygland.It
preparesthemammaryglandsforsecretionofmilk.
II)Basophiliccellssecrete4hormones
1.TSH 2.ACTH 3.FSH 4.LH
FSHandLHarecollectivelyknownasgonadotropins.
POSTERIORPITUITARY
TwohormonesnamelyOxytocinandVasopressin(ADH)areproducedfromposterior
pituitary(Neurohypophysis).
OXYTOCIN
Thereleaseofoxytocinfromposteriorpituitaryiscausedbytheneuralimpulsesof
nipplestimulation.Theotherstimuliresponsibleforoxytocinreleaseincludevaginaland
uterinedistension.
Functionsandactions:-
1.Duringlaststageofpregnancyoxytocinlevelinthebloodincreases,which
producesastrongcontractionofmusclesofuterus.Thisdevelopsa
propulsiveforcethathelpsinparturitionorchildbirth.
2.Duringsexualintercourseoxytocinproducesthecontractionofuterinemuscles
whichincreasesthemotilityofsperms.Thisincreasesthechanceof
fertilizationandpregnancy.
3.Duringlactationoxytocinproducesthecontractionofmyo-epithelialcellsofthe

7. 7 mammarygland.Thisproducesasqueezingeffectonthemammarygland
andisresponsibleforthemaintenanceandcontinuityofmilkflowtothemouth
ofthebaby.
REGULATIONOFSECRETION
Therearetwodifferentmechanismscontrollingthesecretionofoxytocin–during
pregnancyandduringlactation.
1.Duringpregnancy:-Itiscontrolledbypositivefeedbackmechanism.Thepresenceof
fetusinsidetheuterusproducesdistensionofthewallofuterus.Thiswillstimulate
thestretchreceptorspresentinthewalloftheuterus.Fromthisstretchreceptors
impulsesaretransmittedtothehypothalamusandwillstimulateit.The
hypothalamuswillinturnstimulateposteriorpituitarytoincreaseoxytocinrelease.
Thiswillincreaseuterinedistensionfurther,stimulationofhypothalamusandposterior
pituitaryandfurtherincreaseinoxytocin.Itslevelinbloodgraduallyincreasesand
reachesitspeaktherebyhelpinginparturitionanditslevelfallsabruptlyafterthat.
Theactionofoxytocinontheuterusduringpregnancyissuppressedbyincreased
levelsofestrogenandprogesterone.
2.Duringlactation:-Itiscontrolledbyneuroendocrinereflex-sucklingreflex.During
lactationthesuckingofnipplebythebabystimulatesnumerousreceptorsonthe
mammarygland.Fromthesereceptorssensorysignalsaretransmittedtothe
hypothalamus.Itstimulatesthehypothalamuswhichinturnstimulatestheposterior
pituitary,therebyincreasingthereleaseofoxytocin
ADH(AntiDiureticHormone)orVASOPRESSIN
ADHisactuallysynthesizedinthesupra-opticnucleusofthehypothalamus.From
hereitiscarriedtotheposteriorpituitarybythehypothalamo-hypophysealnervetract.
FunctionsandActions:-
1.ADHisavasoconstrictorinaction.Itproducesconstrictionofthebloodvessels.
ThiswillhelptoincreaseTotalPeripheralResistance.Soitisusefulintheregulation
ofBP.
2.ADHactsontherenaltubulesespeciallyinthecollectingductofthenephron.ADH
increasesthereabsorptionofwateratthecollectingduct.Becauseofthisreaction,
ADHtakepartintheregulationofwaterbalance.
3.Italsocontrolstheextra-cellularfluidvolumeandbloodvolume.

8. 8 4.Bycontrollingbloodvolume,ittakespartintheregulationofBP.
R
Disorder:
DIABETESINSIPIDUS:
ItiscausedduetothehyposecretionofADHfromtheposteriorpituitary.
Causes:-Lesionofsupra-opticnucleusofhypothalamusduetoinjuryorinfection;lesionof
posteriorpituitary;nephrogenicDiabetesinsipidusduetocompleteorpartialfailureofrenal
responsetoADH.
SignsandSymptoms:-
1.Polyuria-excesslossofwaterthroughurine.
2.Urinewillbediluteandspecificgravitylow.
3.Nosugarispresentintheurine.
4.Stimulatesthirstandincreaseswaterintake-polydypsia.
THYROIDGLAND
Thisisabutterflyshapedglandlocatedinfrontofthelarynx.Itiscomposedofright
andleftlobes;oneoneithersideofthetrachea,connectedbyanisthmus,anteriortothe
trachea.Itiscomposedofalargenumberofsphericalsacscalledthyroidfollicles,thewalls
ofwhicharelinedbyepithelialcellsanditslumenisfilledwithacolloid.Majorconstituent
ofthecolloidisaglycoproteincalledthyroglobulin.
Thyroidglandsecretes3hormonesnamely-T3,T4(Thyroxine)andcalcitonin
(thyrocalcitonin).
S
Disorders:-
HYPOTHYRIDISM
Decreasedsecretionofthyroidhormones.
Causes:1.Babyofhypothyroidmother2.Hypofunctionofpituitary
3.Hashimoto'sdisease–Anautoimmunedisorderofthyroidglandduetoproductionof
antibodiesagainstthyroglobulin.
Hypothyroidisminchildren–Cretinism
Hypothyroidisminadults –Myxedema

9. 9 CRETINISM:-Signsandsymptoms:
1.Growthanddevelopmentaresignificantlydelayed.
2.Stuntedskeletalgrowthresultinginshortheight,clubbedfingers.
3.Mentalretardation.
4.Impropergrowthanddevelopmentofgonadsleadingtoimpotency(Sterility).
5.Irregulardepositionoffatinthebody.
6.Idioticlookwiththicklipsandtongue,hangingdownoftonguewithdrippingofsaliva.
7.Rough,thick,dryandwrinkledskin.
8.Croakingofsound(Froglikesound).
9.LowBMR,heartrateandbodytemperature.
10.Coldintolerance,increasedsusceptibilitytoinfection,highserumcholesterolleveland
lowbloodsugar.
MYXEDEMA:-Signsandsymptoms:
1.Typicalfeatureofthisdiseaseisanedematousappearancethroughoutthebody.
2.Swellingoffaceandbagginessundertheeyes.
3.Irregulardepositionoffatinthebody.
4.Thickeningoftongueandspeechbecomesslurry.
5.Depressedhairgrowthandfallingofhairfromthebody.
6.Anemia,fatigueandmuscularsluggishness.
7.Weightgain,scalinessoftheskin,constipation,anorexiaandcoldintolerant.
8.Degenerationofgonadsleadingtoimpotency.
9.DecreasedBMR,heartrateandforceofcontraction,cardiacoutputandbloodvolume.
10.Huskyvoice,excessivesleep.
11.Atherosclerosisduetoincreasedserumcholesterollevel,hypoglycemia.
HYPERTHYROIDISM
Increasedsecretionofthyroidhormones.
Causes:Grave'sDisease-autoimmunediseaseinwhichantibodiesareproducedagainstTSH
receptors.TheseantibodiesactlikeTSHandstimulatethereceptorstherebyincreasingthe
secretionofthyroidhormones.
SignsandSymptoms:

10. 1
0 1.IntolerancetoheatbecausethebodyproduceslotofheatduetoincreasedBMR
causedbyexcessofthyroxine.
2.Increasedsweatingduetovasodilation.
3.Decreasedbodyweightduetohighmetabolicrateandfatmobilization.
4.IncreasedmotilityofGITleadingtodiarrhea.
5.Skeletonshowsosteoporosisandmusclesbecomeweak.
6.Nervousness,extremefatigue,inabilitytosleep,mildtremorinhands,hyperexcitability,
extremeanxiety.AlltheseareduetoexcessstimulationofCNS.
7.Goiter(toxicgoiter).
8.Exophthalmos-protrusionofeyeball.
9.Polycythemia,increasedBP,heartrateandcardiacoutput.
Exophthalmos:
Exophthalmosinhyperthyroidismisduetotheedematousswellingoftheocular
tissuesanddegenerativechangesintheextraocularmuscles.Severeexophthalmic
conditionsleadtoblindnessbecauseof2reasons:-
a.Protrusionofeyeballstretchesanddamagestheopticnerveresultinginblindness.
b.Duetoprotrusionofeyeballs,theeyelidscannotbeclosedcompletelywhileblinking
orduringsleep.So,theconstantexposureofeyeballtoatmospherecausesdrynessofthe
cornealeadingtoirritationandinfection.Itfinallyresultsinulcerationofthecornealeading
toblindness.
GOITER
Itisthenon-cancerous,non-inflammatoryenlargementothethyroidglandmanifested
intheformofmidlineswellingofheneck.
GoiterinHyperthyroidism-ToxicGoiter:
Toxicgoiteristheenlargementofthyroidglandwithincreasedsecretionofthyroid
hormonescausedbythyroidtumor.Becauseoincreasednumberofthyroidhormone
secretingcellsofthetumor,hormonelevelincreasestoaverygreatextend.Henceitis
calledToxicgoiter.
Goiterinhypothyroidism-Non-toxicgoiter:
Thisistheenlargementofthyroidglandwithoutincreaseinhormonesecretion.Itis
of2types:

11. 1
1 1.Endemiccolloidalgoiter-causedduetoiodinedeficiency.Becauseoflackofiodine,
thereisnoformationofhormones.Byfeedbackmechanism,hypothalamusand
anteriorpituitaryarestimulated.ItincreasesthesecretionofTRHandTSHwhich
causesthethyroidcellstosecretelargeamountsofthyroglobulinintothefollicle.As
therearenohormonestobecleaved,thyroglobulinremainsassuchandgets
accumulatedinthefolliclescausingenlargementofthethyroidgland.
2.Idiopathicnon-toxicgoiter-causedduetounknowncause.Somefoodstuffscontain
goiterogenicsubstancesthatsuppressestheformationofthyroidhormones.Such
goiterogensarefoundincertainvegetableslikecabbages,cauliflower,soyabeansetc.
THYROCALCITONIN:-
Functions:-
1.Playsanimportantroleinregulationofbloodcalciumlevel-hypocalcemicaction-
decreasesthebloodcalciumlevel(Normalcalciumlevelintheserum-9-11mg/dl).
2.Actsonthebonesandpromotescalciumdepositiononbones,inhibitstheactive
transportofcalciumfrombonestoECF.
3.IncreasesNa
+
,Cl
-
andPO4
2-
excretionthroughurine.
4.Increasesintestinalsecretionofwaterandelectrolytes.
5.Decreasesgastricmotilityandacidsecretion.
REGULATION
IncreaseinbloodCa
2+
level
Thyroidgland
Thyrocalcitonin
Bones Intestine
IncreasesCa
2+
DecreasesCa
2+
DecreaseinbloodCa
2+
level

12. 1
2 PARATHYROIDGLAND
Thereare4parathyroidglandsattachedtotheposteriorsurfaceofthyroidgland.It
secretesParathyroidhormoneorParathhormone(PTH).
Function:-ItplaysamajorroleintheregulationofCalciumandPhosphatelevels.
Actions:-
a)Maintenanceofbloodcalciumlevelisessentialasitisveryimportantformanyofthe
activitiesinthebody.PTHmaintainsthebloodcalciumlevelbyactingonbones,kidneyand
GIT.
1.Onbones-PTHenhancesthedemineralizationofbonestherebykeepinganincreased
levelofcalciumintheblood.
2.Onkidneys-PTHincreasesthereabsorptionofcalciumanddecreasesthe
reabsorptionofphosphatesfromtherenaltubulesandincreasestheconversionofVit.
DintoitsactiveformCalciferol.
3.OnGIT-PTHincreasestheabsorptionofcalciumfromtheintestineandconvertsVit.D
toCalciferol.
Alltheseactionsincreasesbloodcalciumlevel.SoPTHhasgotahypercalcemicaction.
b)PTHdecreasesbloodphosphatelevelbyincreasingitsexcretionthroughurine.
REGULATION
DecreaseinbloodCa
2+
level
PTH
Bones Intestine
IncreasesCa
2+
release
IncreasesCa
2+
absorption
IncreaseinbloodCa
2+
level
Parathyroidgland
Kidney
IncreasesCa
2+
reabsorption

13. 1
3 DISORDERS
TETANY
Itisanabnormalconditioncharacterizedbyhyperexcitabilityofnervesandskeletal
musclesresultinginpainfulmuscularspasms(involuntarycontractionofmuscles)
particularlyinhandsandfeet.ItiscausedduetodeficiencyofPTH.
SignsandSymptoms:
1.Increasedexcitabilityandirritabilityofneuromuscularjunction
2.Convulsions-uncontrolledandunwantedpainfulcontractionsoftheskeletalmuscles.
3.CarpopedalSpasm-violentandpainfulmuscularcontractioninthhandandfeet
occurringduetohypocalcemia.
4.Laryngealstridor-loudcrowingsoundduringinspirationwhichoccursmainlydueto
laryngeospasm.
5.Trousseau'ssign-bendingoffingerswhenBPcuffistiedaroundthehand.
6.Dilatationofheart,prolongeddurationofSTsegmentandQTintervalinECG,
hypotensionandheartfailure.
7.Profusesweating,dryskin,brittlenails,hairloss,signsofmentalretardationinchildren
anddementiainadults.
HYPERPARATHYROIDISM
CausedduetoincreasedsecretionofPTH.Itwillleadtoexcessivedemineralization
ofthebones,sobonesbecomeweakandbrittle,easytofracture,kidneystoneformation
leadingtokidneyfailure,depressionofnervoussystem,sluggishnessofreflexactivities,lack
ofappetite,constipation.
ADRENALGLAND
Itissituatedabovethekidneys.SotheyarealsocalledSupra-renalglands.
Physiologically,adrenalglandsisdividedinto2independentglands-OuterAdrenalcortexand
InnerAdrenalmedulla.
Adrenalcortexisdividedinto3zonesandeachsecretehormones.Thezonesare:-
1.Zonaglomerulosa-outermostzone-secretesMineralocorticoids.
2.Zonafasciculata-middlezone-secretesGlucocorticoids.

14. 1
4 3.Zonareticularis-innermostzone-secretesSexsteroids.
MINERALOCORTICOIDS-ALDOSTERONE
Secretedbyzonaglomerulosaofadrenalcortex.
Functionsandactions:-
1.Iscalled“LifesavingHormone”asitplaysanimportantroleincontrolofconcentration
ofpotassiumandsodiumintheblood.
2.Promotesreabsorptionofsodiumandincreasesexcretionofpotassium.
3.Indirectlyincreaseswaterreabsorption.
4.Takespartintheregulationofextracellularfluidvolumeandbloodvolume.
5.TakespartintheregulationofBP.
REGULATION
Regulatedby3mechanisms.
1.Renin-Angiotensinmechanism.
2.Potassiumionconcentration.
3.ByACTH
RegulationbyRenin-Angiotensinmechanism:-
DecreasedBP
Kidney
Renin Angiotensinogen
Angiotensin1
Angiotensin2
Adrenalcortex
Aldosterone
Kidney
IncreasesNa
+
reabsorption
Increaseswater
reabsorption
IncreasesBloodvolume
IncreasesBP

15. 1
5 RegulationbyPotassiumionconcentration:-
RegulationbyACTH
CRF
ACTH
Aldosterone
GLUCOCORTICOIDS-CORTISOL
Secretedbyzonafasciculataofadrenalcortex.
Functionsandactions:
1.Actiononcarbohydrate,proteinandlipidmetabolism-Increasesglucoselevelinthe
bloodbystimulatingglycogenolysis,ie.,conversionofglycogentoglucose,
gluconeogenesisandstimulatesabsorptionofglucosefromintestine.Soitisa
IncreasedK
+
inblood
Adrenalcortex
Aldosterone
Kidney
DecreasesK
+
reabsorptionIncreasesK
+
lossthrough
urine
DecreasedK
+
inblood
Hypothalamus
AnteriorPituitary
AdrenalCortex

16. 1
6 hyperglycemichormone.Increasesproteinsynthesisinliverbutincreasesprotein
breakdowninperipheraltissueslikemuscles.Stimulateslipogenesisanddepositionof
fatsandlipidsinthebody.
2.Actiononcardiovascularsystem-IncreasesRBC,plateletandneutrophilcounts,
slightlyincreasesBPandbloodvolume,decreaseslymphocytes,eosinophiland
basophilcount.
3.ActiononCNS-essentialforthenormalfunctioningoftheCNS.Insufficiencycauses
personalitychangeslikeirritabilityandlackofconcentration.Increasesthe
excitabilityofneurons.
4.Playsanimportantroleinthemaintenanceofwaterbalanceinthebody.
5.Increasessodiumreabsorptionandpotassiumexcretion.
6.Stimulatesbonedemineralizationandinhibitboneformation.
7.Anti-inflammatoryandanti-allergicaction-Decreasesthesensitivityoftissuesto
micro-organisms,decreaseslymphocytecount,soreducesformationofantibodies,
preventsruptureoflysosomebystabilizingitsmembrane,decreasesmigrationof
WBCsintotheinflamedarea,inhibitsreleaseofhistamineandtherebyreducesallergy.
REGULATION
CRF
ACTH
Cortisol
SEXSTEROIDS
Secretedbyzonareticularisoftheadrenalcortex.
Functions
Hypothalamus
AnteriorPituitary
AdrenalCortex

17. 1
7 1.Contributestoincreaseinmusclemass.
2.Increasespubichairgrowth.
3.Exertsverylittlemasculanizingeffect.
DISORDERS
ADDISON’SDISEASE
CausedduetodecreasedsecretionofAldosteroneandCortisol.
SignsandSymptoms:
1.Muscularweakness-duetolackofglycogenstorageinmusclesalsodueto
disturbanceintheelectrolytebalance
2.Nausea,vomitinganddiarrhea.Prolongedvomitinganddiarrheacausesdehydration
andlossofbodyweight
3.PigmentationoftheskinandmucousmembraneduetoexcessACTHsecretion
becauseofcortisoldeficiency.ACTHcausespigmentationbyitsmelanocyte
stimulatingaction.
4.Hypotension,lowbloodvolume,hypoglycemiaanddecreasedcardiacoutput.
5.Susceptibilitytoanytypeofinfection.
6.Inabilitytowithstandstress.
7.Decreasedexcitabilityofnervoussystem.
CUSHING’SSYNDROME
CausedduetohypersecretionofCortisol.
SignsandSymptoms:
1.Characteristicfeatureofthisdiseaseisthedisproportionatedistributionofthebody
resultinginsomeabnormalfeature:
a.Moonface-edematousfacialappearanceduetofataccumulationandretentionof
waterandsalt
b.Accumulationoffatinvariouspartsofthebodylikeupperabdomenleadingtopot
belly,onthebackofneckandshoulderformingabuffalohump;thinningofthe
extremities.
c.Narroweyeslit
2.Purplestriaeduetostretchingofabdominalwallsbyexcesssub-cutaneousfatand

18. 1
8 therebyruptureofthesub-dermaltissuesduetostretchinganddeficiencyofcollagen
fibersduetoproteindepletion.
3.Muscularwastingandweaknessduetoexcessbreakdownofmuscularproteinsand
alsodisturbanceinsodiumandpotassiumlevelinthebody.
4.Hypogonadism,facialredness,hirsutism-excessfacialhairgrowthandpoorwound
healing.
5.Pigmentationoftheskinanddarkeningoftheskinontheneck.
6.Hyperglycemia,hypertension,brittlebonesduetoexcessdemineralization.
7.Increasedsusceptibilitytoinfections.
CONGENITALADRENALHYPERPLASIA
Itisageneticdisordercharacterizedbyincreaseinthesizeofadrenalcortex.Here
oneoftheenzymesnecessaryforthesynthesisofcortisolismissing.Becauseofthis,
negativefeedbackmechanismoperatingatthelevelofhypothalamusandanteriorpituitary
fails.SoACTHsecretionbecomesuncontrollableanditsactionmainlyaffectsthezona
reticularisofadrenalcortexcausingthesecretionofexcessiveandrogens.Thisdisorderis
morecommoninfemales.Theystartshowingsecondarysexualcharactersofmales.This
includesappearanceofhaironthefaceandchangeinmuscularpatterns,enlargementofthe
clitoris,deepeningofvoiceetc.
ADRENALMEDULLA
Itistheinnerpartoftheadrenalglandandsecretes3hormonesnamely,Adrenaline
(Epinephrine),Nor-adrenaline(Nor-epinephrine)andDopamine.
FunctionsandActionsofAdrenalineandNor-adrenaline:-
1.ActionsonCVS-stimulatesSAnodeandincreasesheartrate,stimulatesventricular
myocardiumandincreasestheforceofcontraction,increasescardiacoutput,SBPand
RBCcount,increasesvasoconstrictionofbloodvesselsexceptcoronarybloodvessels.
2.ActionsonRenalsystem-decreasesrenalbloodflowduetovasoconstriction,
decreasesurineoutput.
3.ActiononNervoussystem-increasestheexcitabilityofneurons,delaystheonsetof
fatigue,producesanxiety

19. 1
9 4.ActiononRespiratorysystem-increasesalveolarventilation,increasesoxygen
consumptionbyabout20-30%,increasesproductionofcarbondioxideby30-50%,
producesbronchodilation.
5.Metabolicfunctions-increasesBMR,gluconeogenesis,showsanti-cholinergicaction,
hyperglycemicandlipolyticactions.
6.Actiononsmoothmuscles-inhibitscontractionofmusclesofintestinethereby
producingconstipation,producespapillarydilatation,producescontractionofradial
musclesofeye.
7.Increasessecretionofsweat,causesvasoconstrictioninsalivaryglandleadingtomild
increaseinsalivarysecretion.
Summaryofthefunctions:-
1.PlaysanimportantroleintheregulationofBMR.
2.Importantintheregulationofbodytemperature.
3.Importantintheregulationofsweating,heartrate,cardiacoutputandBP.
4.Importantinthemediationoffightandfightresponse.
Thesehormonesareproducedespeciallyduringconditionslikestress,anger,anxiety,
fearetc.SothishormoneisalsocalledStressHormone.
DISORDER-PHEOCHROMOCYTOMA
Causedduetohypersecretionofhormonesofadrenalmedulla.
SignsandSymptoms:
1.IncreaseinBP-sustainedhypertensionandincreasedBMR.
2.Severeheadache,flushingofface.
3.HyperglycemialeadingtoDiabetesmellitus.
4.Increaseinbodytemperature,heartrate,anxiety,weaknessanddizziness.
PANCREAS
Itisamixedglandwithbothexocrineandendocrinefunction.Endocrinepartof
pancreasisIsletsofLangerhans,whichsecrete3hormones,namely-Insulin,Glucagonand
Somatostatin.
INSULIN
SecretedbytheβcellsofIsletsofLangerhans;Importanthormonethatcontrolsthe
bloodglucoselevel-Hypoglycemichormone.
FunctionsandActions:

20. 2
0 Mainfunctionistodecreasethebloodglucoselevel.
1.Actiononcarbohydratemetabolism-promotescellularuptakeofglucose,increasesthe
breakdownofglucoseforenergyproduction,decreasesgluconeogenesisand
glycogenolysis.
2.Actiononproteinandlipidmetabolism-stimulatesproteinsynthesis,stimulates
lipogenesis,decreasesthebreakdownoffatsandlipids,decreasestheformationof
ketonebodies.
REGULATION-mainlycontrolledbybloodglucoselevel
GLUCAGON
SecretedbyαcellsofIsletsofLangerhans;KeepsBGLinanincreasedmanner-
Hyperglycemichormone.
FunctionsandActions:
1.Actiononcarbohydratemetabolism-promotesgluconeogenesis,decreasesthe
breakdownofglucoseforenergyproduction,stimulatesglycogenolysis,anddecreases
conversionofglucosetoglycogen.
2.Actiononproteinandlipidmetabolism-increasesbreakdownofproteins,increases
breakdownoffatsandlipids.Thiswillleadtomoreproductionofketonebodies.
Thisactioniscalledketogenicaction.
REGULATION
IncreasedBGL
βcellsofIslets
Insulin
Increasescellularuptakeof
glucose
Increasescellular
breakdownofglucose
Decreaeses
Gluconeogenesi
s
DecreasesBGL

21. 2
1 REGULATIONOFBLOODGLUCOSELEVEL
NormalBGL-a)Duringfasting:70-90mg/dl
b)Afterfood(postprandial):120-140mg/dl
ImportanceofBGLregulation:
Itisnecessaryinordertohavecontinuoussupplyofglucosetobrainforitsenergy
requirements,RBC,renalmedullaetc.
Sourceofbloodglucose-dietarysources,gluconeogenesis,glycogenolysis.
Hormonalregulation
Hyperglycemichormones-IncreasesBGL-Glucagon,Cortisol,Thyroxine,Adrenaline.
Hypoglycemichormone-Insulin.
Regulationbycertainorgansinthebody
1.Roleofliver-LiveractsasglucostatandbufferorganintheregulationofBGL.When
BGLincreases,liverlowersitbyincreasingtheconversionofglucosetoglycogenand
decreasingglycogenolysisandgluconeogenesis.WhenBGLdecreases,liverbringsit
tonormalbyincreasingglycogenolysis,gluconeogenesisanddecreasingglycogenesis.
2.Roleofkidney-WhenBGLincreasesabove180mg%calledrenalthresholdforglucose,
theextraglucoseisnotabsorbedbutlostthroughurine.Thishelpstopreventtoo
DecreasedBGL
βcellsofIslets
Insulin
Increasescellularuptakeof
glucose
Increasescellular
breakdownofglucose
Decreaeses
Gluconeogenesi
s
IncreasesBGL

22. 2
2 muchincreaseinBGL.
3.Roleofsympatheticnervoussystem-WhenBGLdecreases,SNSincreasesthe
secretionofcatecholaminesfromtheadrenalmedullaandbringsittonormal.SNS
stimulationalsoinhibitsinsulinsecretion.
4.Roleofskeletalmuscle-Atrestandduringmildexercise,fattyacidsareusedfor
energyproduction,butduringsevereexercise,glucoseisutilizedandthishelpsto
lowerBGL.
DISORDERS
DIABETESMELLITUS
Causedduetodecreasedsecretionofinsulin.Itisametabolicdisordercharacterized
byhighbloodglucoselevelassociatedwithothermanifestations.
Broadlyclassifiedinto2-TypeIandTypeII
TypeIDiabetesmellitus
Itisduetothedeficiencyofinsulin.Itoccursduetothedysfunctionorabsenceofβ
cellsintheIslets.ThistypeofdiabetesmellitusisalsoknownasInsulinDependent
DiabetesMellitus(IDDM).Itmayoccuratanyageoflife,especiallyinchildrenbelowtheage
of20.SoitisalsocalledJuvenileDiabetes.
TypeIIDiabetesMellitus
Itisduetotheabsenceordeficiencyofinsulinreceptors.Insulinsecretionisnormal
butthetargetcellsareresistanttoitsactionduetosomereasons.Itusuallyoccursin
adults,socalledMaturityOnsetDiabetesMellitus.Thistypeofdiabetesmellitusisalso
knownasNonInsulinDependentDiabetesMellitus(NIDDM).
SignsandSymptoms:
1.HyperglycemiaandGlucosuria-IncreaseinBGLandexcessivelossofglucosethrough
urine.Normallyglucosedonotappearinurine.Whenglucoselevelrisesabove
180mg/dlinblood,glucoseappearsinurine.
2.Osmoticdiuresis-diuresisduetoosmoticeffectsiscalledosmoticdiuresis.The
excessglucoseintherenaltubulesdevelopsosmoticeffect.Theosmoticeffect
decreasestheabsorptionofwaterfromtherenaltubulesresultingindiuresis.
3.Polyuria(excessiveurineoutput),polydipsia(excessivethirst)andpolyphagia
(excessivefoodintake)

23. 2
3 4.Excessbreakdownofproteinsleadingtomuscularweaknessandlossofbodyweight.
5.Ketosuriaandacidosis-appearanceofketonebodiesinurineandacidicpHofurine.
6.Poorwoundhealing.
7.Diabeticcomaduetosevereacidosis.
COMPLICATIONSOFDIABETESMELLITUS
Prolongedhyperglycemiaindiabetesmellituscausesdysfunctionandinjuryinmany
tissuesresultinginsomecomplications.Developmentofthesecomplicationsisdirectly
proportionaltothedegreeanddurationofhyperglycemia.Initially,theuntreatedchronic
hyperglycemiaaffectsthebloodvesselsresultinginvascularcomplicationslike
atherosclerosis.Thevascularcomplicationsareresponsibleforthedevelopmentofmostof
thecomplicationsofdiabeteslike:
1.CVScomplicationslikehypertension,myocardialinfarction.
2.DegenerativechangesinretinacalledRetinopathy.
3.DegenerativechangesinkidneycalledNephropathy.
4.Degenerativechangesintheautonomicandperipheralnervoussystemcalled
Neuropathy.
GONADS
Testesinmalesandovariesinfemalesperformcloselyrelateddualfunctions-
SynthesizesexhormonesandProducegermcells.
Sexhormonesareresponsibleforthegrowth,development,maintenanceandregulationof
thereproductivesystem.Sexhormonesareof3types-Androgens,Estrogenand
Progesterone.
ANDROGENS
Testissecretesmalesexhormoneswhicharecollectivelycalledtheandrogens.
Androgensareof3types-Testosterone,dihydrotestosteroneandandrostenedione.2
hormonesnamelyactivinandinhibinarealsoproducedbytestisbuttheydon’thave
androgeniceffect.Testosteroneisthemalesexhormoneandisresponsibleforthe
developmentofmasculinefeatures.Inthefetallife,thetestesarestimulatedbytheHuman
ChorionicGonadotropinsecretedbytheplacents.Butinchildhood,practicallyno
testosteroneisproducedapprox.until10-12yearsofage.Afterwards,thetestosterone
secretionstartsanditincreasesrapidlyattheonsetofpubertyandlaststhroughmostofthe

24. 2
4 remainingpartoflife.Thesecretionstartsdecreasingaftertheageof40andbecomes
almostzerobytheageof90.
Functionsoftestosteroneinfetallife:
Thefetaltestesbegintosecretetestosteroneatabout2
nd
to4
th
monthoffetallife.It
performs3functionsinfetus:
1.Sexdifferentiationinfetus
2.Developmentofaccessorysexorgansandexternalgenetalia
3.Descentoftestis-theprocessbywhichthetestisentersintothescrotalsac.
Functionsoftestosteroneinadults:
1.Effectonsexorgans-increasesthesizeofpenis,scrotalsacandtestesafterpuberty.
Itisalsonecessaryforspermatogenesis.
2.Effectonsecondarysexualcharacters
a.Increasesthemusculargrowthandmassbyincreasingthetransportofaminoacids
intothemusclecells,synthesisofproteinsandstorageofproteins.
b.Increasesthethicknessofboneswithdepositionofcalcium.
c.Causesthebroadeningofshouldersandlengtheningofpelvis
d.Increasesthethicknessofskinandquantityofmelaninpigmenttherebydeepeningthe
skincolor,increasesthesecretionofsebaceousglandsleadingtothedevelopmentof
acneontheface.
e.Causesmaletypeofhairdistributiononthebody,i.e.hairgrowthoverthepubis,along
themidlineuptotheumbilicus,onface,chestandotherpartsofthebodylikebackand
limbs.
f.Voicechange.
g.IncreasesBMR,sodiumreabsorption,waterretentionandRBCcount.
ESTROGEN
Majorfunctionofestrogenistopromotecellularproliferationandtissuesexualorgans
andothertissuesrelatedtoreproduction.
1.Promotesthegrowthofovarianfolliclesbyincreasingtheproliferationoffollicular
cells.
2.Causestheenlargementoftheuterusandmakesitsensitivetooxytocinaction,
increasesthebloodsupplytotheendometrium,increasesthecontractilityofthe

25. 2
5 uterinemuscles.
3.Increasestheactivitiesofthefallopiantubulesnecessaryforfertilizationoftheovum.
4.Effectonsecondarysexualcharacterslikevoicechange,femalelikehairdistribution,
increasesthesoftnessandsmoothnessoftheskin,narrowingoftheshoulders,
convergingofthighs,fatdepositiononthebreastandbuttocks,broadeningofthe
pelvisandroundedshapeofthepelvis.
5.Developmentofthebreast,bones.
PROGESTERONE
Itisconcernedwiththefinalpreparationoftheuterusforpregnancyandthebreasts
forlactation.
1.Promotesthesecretoryactivitiesofthefallopiantubulesnecessaryforthenutritionof
thefertilizedovum.
2.Increasesthethickness,bloodsupply,sizeofuterineglands,secretoryactivitiesofthe
uterusanddepositionoffatandglycogenintheuterus.
3.Increasesthethicknessofthecervicalmucosaandtherebyinhibitsthetransportof
spermintouterus.
4.Promotesthedevelopmentofthealveoliandlobulesofthemammaryglands.
5.Increasesthebodytemperature,reabsorptionofsodiumandretentionofwater.