Pharmacology of drugs used for Endocrine systempdf

Useful for BDS and pharmacy students

1. RKDF DENTAL COLLEGE
A Better Education center
ENDOCRINES
Dr Nishi Prakash Jain
Principal
RKDF College of Pharmacy
SRK University , Bhopal
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2. Syllabus
ENDOCRINES:Emphasisof
treatmentofDiabetesand
Glucocorcoids,Thyroidand
Antithyroidsagents,Drugsaffecting
theCalciumBalanceandanabolic
steroids.
ImplicationsofautocoidsinClinical
dentistry
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3. CELL COMMUNICATION
•Cellsmustcommunicatewithone
anothertocoordinatecellprocesses
withintissuesandtomaintain
homeostasis.
•Cell-to-cellcommunicationiscarried
outviamessengermolecules.
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4. Fourmethodsofcell-to-cellcommunicationarefoundinthehuman
body,rangingfromdirecttoremotecommunication.

5. Endocrine hormones
•Produced by endocrine (“ductless”) glands
and secreted into the bloodstream.
•Endocrine hormones may affect a wide array
of target cells to produce multiple effects.
•Two types: peptides (small proteins) and
steroids (lipids).

6. Endocrine Glands
•Endocrineglandsinclude:
–Pituitary,thyroid,parathyroid,adrenalandpinealglands.
–Hypothalamus,thymus,pancreas,ovaries,testes,kidneys,
stomach,liver,smallintestine,skin,heart,adiposetissue,
andplacentaalsohaveendocrinefunction.
Agroupofsecretorycellsthatrelease
theirproducts,chemicalsignalscalled
hormones,usuallyintothecirculation.
Thesecretionsneverpassthrough
ducts
6

7. Hormones and Receptors

8. Peptide Hormones
•Peptide hormones do not enter the cell
directly. These hormones bind to receptor
proteins in the cell membrane.
•When the hormone binds with the receptor
protein, a secondary messenger molecule
initiates the cell response.
•Because peptide hormones are water soluble,
they often produce fast responses.

9. (cytoplasm)
(nucleus)
peptide or amino
acid-derived
hormone
(first messenger)
(extracellular
fluid)
cyclic AMP-
synthesizing
enzyme
cyclic AMP
ATP
inactive
enzyme
(second messenger)
active
enzyme
reactant
product
plasma membrane
nuclear
envelope
receptor
The hormone binds to
a receptor on the plasma
membrane of a target cell
1
The activated enzymes
catalyze specific reactions
4
The second
messenger activates
other enzymes
3
Hormone–receptor binding
activates an enzyme that catalyzes
the synthesis of a second messenger,
such as cyclic AMP
2

10. Steroid Hormones
•Steroid hormones enter through the cell
membrane and bind to receptors inside of the
target cell.
•These hormones may directly stimulate
transcription of genes to make certain
proteins.
•Because steroids work by triggering gene
activity, the response is slower than peptide
hormones.

11. gene
plasma
membrane
ribosome
hormone receptor
steroid hormone
mRNA
(nucleus)
RNA polymerase
DNA
(cytoplasm)
new protein
(extracellular
fluid)
A steroid hormone
diffuses through the
plasma membrane
The hormone binds to a
receptor in the nucleus or to
a receptor in the cytoplasm
that carries it into the nucleus
The hormone–receptor
complex binds to DNA and
causes RNA polymerase to
bind to a nearby promoter
site for a specific gene
RNA polymerase catalyzes
the transcription of DNA into
messenger RNA (mRNA)
The mRNA leaves the
nucleus, then attaches to a
ribosome and directs the
synthesis of a specific protein
product
1
2
3
4
5
nuclear
envelope

12. Endocrine Hormones
Gland Hormones Functions
Thyroid Thyroxine Regulates metabolism
Calcitonin Inhibits release of calcium from the bones
ParathyroidsParathyroid hormoneStimulates the release of calcium from the bones.
Islet cells (in
the pancreas)
Insulin Decreases blood sugar by promoting uptake of glucose by cells.
Glucagon Increases blood sugar by stimulating breakdown of glycogen in the
liver.
Testes Testosterone Regulates sperm cell production and secondary sex characteristics.
Ovaries Estrogen Stimulates egg maturation, controls secondary sex characteristics.
Progesterone Prepares the uterus to receive a fertilized egg.
Adrenal
cortex
Epinephrine Stimulates “fight or flight” response.
Adrenal
medulla
Glucocorticoids Part of stress response, increase blood glucose levels and
decrease immune response.
Aldosterone Regulates sodium content in the blood.
Testosterone (in both
sexes)
Adult body form (greater muscle mass), libido.
Pineal glandMelatonin Sleep cycles, reproductive cycles in many mammals.

13. DIABETES MELLITUS
DIABETESMELLITUSisachronicmedical
conditioncharacterizedbyelevatedlevelsof
bloodglucose,commonlyreferredtoasblood
sugar.Thisconditionariseswhenthebodyis
unabletoproduceenoughinsulinoreffectively
usetheinsulinitdoesproduce.Insulinisa
hormoneproducedbythepancreasthatplaysa
crucialroleinregulatingbloodsugarlevelsby
facilitatingtheuptakeofglucoseintocellsfor
energy.
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16. Classification of DM
There are three main types of diabetes: Type 1 diabetes, Type 2 diabetes, and
gestational diabetes.
Type1Diabetes(IDDM):Thisformofdiabetesoccurswhenthe
immunesystemmistakenlyattacksanddestroystheinsulin-
producingbetacellsinthepancreas.Asaresult,individualswithType
1diabetesmustrelyoninsulininjectionsoraninsulinpumpto
managetheirbloodsugarlevels.
Type2Diabetes(NIDDM):Thisisthemostcommonformofdiabetes,
accountingforthemajorityofcases.Itdevelopswhenthebody's
cellsbecomeresistanttotheeffectsofinsulin,andthepancreasis
unabletoproduceenoughinsulintocompensate.Type2diabetesis
oftenassociatedwithlifestylefactorssuchaspoordiet,lackof
physicalactivity,andobesity.Itcanbemanagedthroughlifestyle
changes,oralmedications,and,insomecases,insulintherapy.
GestationalDiabetes:Thistypeofdiabetesoccursduringpregnancy
whenthebodycannotproduceenoughinsulintomeettheincreased
needs,leadingtoelevatedbloodsugarlevels.Whilegestational
diabetesusuallyresolvesafterchildbirth,itincreasestheriskof
developingType2diabetesinboththemotherandchild.
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17. •Type 3c diabetes: This form of diabetes happens when pancreas
experiences damage (other than autoimmune damage), which affects
its ability to produce insulin.
•Latent autoimmune diabetes in adults (LADA): Like Type 1 diabetes,
LADA also results from an autoimmune reaction, but it develops much
more slowly than Type 1. People diagnosed with LADA are usually over
the age of 30.
•Maturity-onset diabetes of the young (MODY): MODY, also called
monogenic diabetes, happens due to an inherited genetic mutation
that affects how your body makes and uses insulin. There are currently
over 10 different types of MODY. It affects up to 5% of people with
diabetes and commonly runs in families.
•Neonatal diabetes: This is a rare form of diabetes that occurs within
the first six months of life. This is called transient neonatal diabetes
mellitus.
•Brittle diabetes: Brittle diabetes is a form of Type 1 diabetes that’s
marked by frequent and severe episodes of high and low blood sugar
levels.
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19. Classification of drugs for DM
A.ParenteralInsulinforIDDMandGlucagonlike
peptides-1(GLP-1)receptorantagonist(Liraglutide)
forNIDDM
B.OralHypoglycaemic
B-1:AgentsEnhancesInsulinSecration
B-1.1Sufoylureas(1G-Tolbutamide,2G-
Gilbenclamide,Glipizide,Gliclazide,Glimipride)
B-1.2Meglitinide/Phenylalaninanalouges:
(RepaglinideNatelinide)
B-1.3Dipeptidylpeptidase-4(DPP-4)inhibitors:
Sitagliptin,Vidagliptin,Saxagliptin,
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20. •B-2 Overcome insulin resistance
–B-2.1 Biguanide(AMPkActivator): Metformin
–B-2.2 Thiazolidinediones (PPARyActivator):
Pioglitazone
•B-3 Miscellaneous Drug
•Alpha-Glucidaseinhibitors: Acrobose, Voglibose,
•Amylene Analogues: Pramlintide
•Dopamine-2 receptor Antagonist: Bromocriptin
•Sodium-Glucose Cotransport-2(SGLT-2) inhibitor:
Dapagliflozin
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21. INSULIN
•Insulinisahormoneproducedbythebeta
cellsofthepancreas,anorganlocatedbehind
thestomach.Itplaysacrucialrolein
regulatingbloodsugar(glucose)levelsinthe
body.Insulinenablescellstotakeupglucose
fromthebloodstream,facilitatingitsentry
intocells,whereitisusedforenergy
production.Thisprocessisessentialfor
maintainingnormalbloodsugarlevelsand
supportingvariousphysiologicalfunctions.
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22. Regulation of Insulin
Thereleaseofinsulinistightlyregulatedbythebodytorespond
tochangesinbloodglucoselevels,especiallyaftermeals.The
regulationofinsulinsecretioninvolvesacomplexinterplayof
variousfactors:
BloodGlucoseLevels:Elevatedbloodglucoselevels,typically
aftereating,stimulatethepancreastoreleaseinsulin.
IncretinHormones:Incretins,suchasglucagon-likepeptide-1
(GLP-1)andglucose-dependentinsulinotropicpolypeptide(GIP),
arehormonesreleasedfromthegastrointestinaltractin
responsetofoodintake.Theyenhanceinsulinsecretionina
glucose-dependentmanner,meaningthattheireffectsaremore
pronouncedwhenbloodglucoselevelsareelevated.
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23. •Autonomic Nervous System: The autonomic nervous system,
specifically the parasympathetic division, also plays a role in insulin
release. Stimulation of the vagusnerve promotes insulin secretion.
•Amino Acids: Certain amino acids, the building blocks of proteins,
can stimulate insulin release.
•Hormones: Other hormones, such as cortisol and growth hormone,
can influence insulin secretion.
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25. Mode of Action
1.GlucoseUptakeinCells:
Whenbloodglucoselevelsrise,suchasafterameal,the
pancreasreleasesinsulinintothebloodstream.Insulin
actsasasignalingmolecule,attachingtoinsulinreceptors
onthesurfaceoftargetcells,particularlymusclecells,fat
cells,andlivercells.
2.FacilitationofGlucoseTransport:
Insulinbindingtoitsreceptorstriggersacascadeof
intracellulareventsthatresultinthetranslocationof
glucosetransporterproteins(GLUT4)tothecell
membrane.Thepresenceofthesetransporterproteins
facilitatestheuptakeofglucosefromthebloodstream
intothecells.
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26. 3.GlycogenSynthesis(LiverandMuscleCells):
Intheliverandmusclecells,insulinpromotesthe
conversionofexcessglucoseintoglycogenthrougha
processcalledglycogenesis.Glycogenservesasastorage
formofglucose,andthishelpstolowerbloodglucose
levels.
4.InhibitionofGlucoseProduction:
Insulininhibitstheproductionofglucosebytheliver
(gluconeogenesis).Thishelpspreventexcessiveglucose
releaseintothebloodstream.
5.ProteinSynthesis:
Insulinalsoplaysaroleinpromotingproteinsynthesis.It
facilitatestheuptakeofaminoacidsintocellsandhelps
inthesynthesisofproteins,whichisimportantforcell
growthandrepair.
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27. 6. Lipid Metabolism:
Insulin promotes the storage of fat in adipose (fat) tissue
by inhibiting the breakdown of fats (lipolysis).It also
stimulates the synthesis of fats (lipogenesis) from excess
glucose.
7. Overall Metabolic Effects:
Thecombinedeffectsofinsulinleadtoareductionin
bloodglucoselevelsbypromotingitsuptakeintocells,
inhibitingglucoseproduction,andfavoringthestorageof
glucoseasglycogenandfats.
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Insulinactsasakeyregulatorofglucosehomeostasisby
promotingtheuptakeandutilizationofglucoseinvarioustissues,
inhibitingglucoseproduction,andinfluencingthestorageof
excessglucoseasglycogenandfats.Disruptionsininsulin
productionoritseffectivenesscanleadtoimbalancesinblood
glucoselevels,asseeninconditionssuchasdiabetesmellitus.

28. Degradation and Clearance:
Insulinhasafinitelifespaninthebloodstream.Itundergoes
degradationbyenzymes,primarilyintheliverandkidneys.
Theliverisasignificantsiteofinsulindegradation,where
insulinisbrokendownintosmallerfragments.Thekidneys
alsoplayaroleininsulinclearance.
Elimination:
Insulinanditsbreakdownproductsareeventually
eliminatedfromthebodythroughurineandotherexcretory
processes.
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Insulinsecretionistightlyregulatedbyafeedbackloop.Whenblood
glucoselevelsdecrease,insulinsecretiondecreases,preventing
hypoglycemia(lowbloodsugar).
ContinuousCycle:
Theentireprocessrepeatsinresponsetochangesinbloodglucose
levels,maintainingadynamicequilibriuminglucosemetabolism.

29. INDICATIONS
DiabetesMellitus:Insulinisprimarilyindicatedforthe
treatmentofdiabetesmellitus,aconditioncharacterizedby
elevatedbloodglucoselevels.
Type1Diabetes:Individualswithtype1diabetesdonot
produceinsulinandrequireexogenousinsulinforsurvival.
Type2Diabetes:Insomecases,peoplewithtype2diabetes
mayalsoneedinsulintherapywhenoralmedicationsor
otherinjectablemedicationsarenotsufficienttocontrol
bloodsugar.
GestationalDiabetes:Insulinmaybeusedduringpregnancy
tocontrolbloodsugarlevelsinwomenwithgestational
diabetes.
Hyperkalemia:Insulincanbeusedtotemporarilyshift
potassiumfromthebloodstreamintocells,helpingto
managehyperkalemia(highlevelsofpotassiuminthe
blood).
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AdverseEffects:
Hypoglycemia:Themostcommonadverseeffectofinsulinis
hypoglycemia,orlowbloodsugar.Symptomsmayincludeshakiness,
sweating,irritability,dizziness,andconfusion.
InjectionSiteReactions:Redness,swelling,oritchingattheinjection
sitecanoccur.
WeightGain:Someindividualsmayexperienceweightgainwhile
usinginsulin.
HypersensitivityReactions:Allergicreactionstoinsulincanoccur,
rangingfromlocalizedreactionsattheinjectionsitetomoresevere
systemicreactions.
Lipodystrophy:Insulininjectionscansometimesleadtochangesin
thefattissueundertheskin,causinglumpsordepressionsatthe
injectionsite.
Edema: Fluid retention and edema (swelling) may occur in some
individuals.

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Contraindications:
Hypoglycemia(LowBloodSugar):Insuliniscontraindicated
inindividualswithhypoglycemiaoraknown
hypersensitivitytoinsulinoranyofitscomponents.
AllergicReactions:Individualswhohaveexperienced
allergicreactionstoinsulinoranyofitsingredientsshould
notuseinsulin.
Hypokalemia:Insulinshouldbeusedwithcautionin
individualswithhypokalemia(lowlevelsofpotassiumin
theblood).
CertainMedicalConditions:Insulinmaybecontraindicated
inindividualswithspecificmedicalconditions,anditsuse
shouldbecarefullyassessedinconsultationwitha
healthcareprofessional.

32. GLIMIPRIDE
Glimiprideisanoralantidiabeticmedicationbelonging
tothesulfonylureaclass.Itiscommonlyprescribedto
individualswithtype2diabetesmellitustohelpcontrol
bloodsugarlevels.Glimiprideworksbystimulatingthe
releaseofinsulinfromthepancreas,therebyimproving
thebody'sabilitytoutilizeglucose.
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33. Mode of Action
Theprimarymodeof
actionofGlimipride
involvesbindingtospecific
receptorsonthebetacells
ofthepancreas.This
bindingleadstoan
increasedreleaseof
insulin.Insulin,inturn,
facilitatestheuptakeof
glucoseby cells,
promotingitsutilization
forenergyandreducing
elevatedbloodglucose
levels.
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Initial:1-2mgPOqAMafter
breakfastorwithfirstmeal;
mayincreasedoseby1-2mg
every1-2weeks;nottoexceed
8mg/day

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Indications:
Glimiprideisindicatedforthemanagementoftype2diabetes
mellitus.Itisusedwhenlifestylemodifications(suchasdiet
andexercise)aloneareinsufficienttocontrolbloodsugar
levels.Thismedicationisoftenpartofacomprehensive
diabetesmanagementplanthatmayincludeotherantidiabetic
medications,insulin,andlifestylechanges.
AdverseEffects:
Hypoglycemia:Glimipride,likeothersulfonylureas,canlowerblood
sugarlevels.Themostcommonadverseeffectishypoglycemia,
whichmaymanifestasshakiness,sweating,dizziness,confusion,
and,inseverecases,lossofconsciousness.Patientsshouldbe
educatedonrecognizingandmanaginghypoglycemia.
WeightGain.GastrointestinalDistress,AllergicReactions,Liver
FunctionAbnormalities,HematologicalEffects

35. SITAGLIPTIN
Sitagliptinisamedication
usedinthemanagement
oftype2diabetesmellitus.
Itbelongstoaclassof
drugsknownasdipeptidyl
peptidase-4 (DPP-4)
inhibitors.Sitagliptinhelps
regulatebloodsugarlevels
byincreasingtheactivityof
incretinhormones,which
stimulatethereleaseof
insulininresponseto
meals.
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36. Mode of Action
ThemainmodeofactionofSitagliptininvolves
inhibitingtheenzymeDPP-4.DPP-4breaks
downincretinhormones,suchasglucagon-like
peptide-1(GLP-1)andglucose-dependent
insulinotropicpolypeptide(GIP).Byinhibiting
DPP-4,Sitagliptinprolongstheactionofthese
incretinhormones.This,inturn,enhances
insulinreleasefromthepancreasandreduces
theproductionofglucosebytheliver,leadingto
improvedbloodsugarcontrol.
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Dose:100mgPOperDay
Indications:
Sitagliptinisindicatedforthemanagementoftype2diabetes
mellitus.Sitagliptinistypicallyusedwhenbloodsugarlevelsare
notadequatelycontrolledbydietandexercisealoneorin
combinationwithotherdiabetes
AdverseEffects:
UpperRespiratoryTractInfections:Patientsmayexperience
symptomssuchasasorethroatorrunnynose.
Headache:Someindividualsmayexperienceheadachesasaside
effectofSitagliptin.
Hypoglycemia(LowBloodSugar):WhenSitagliptinisusedin
combinationwithotherantidiabeticmedications,thereisariskof
hypoglycemia.Thisismorelikelytooccurwhenthedrugisusedin
conjunctionwithsulfonylureasorinsulin.
Pancreatitis:Rarely,AllergicReactions:

38. METFORMIN
Metforminisanoral
antidiabeticdrugthat
belongstothebiguanide
class.Itiswidelyusedasa
first-linemedicationforthe
managementoftype2
diabetesmellitus.Metformin
worksbyimprovingthe
body'ssensitivitytoinsulin,
reducingglucoseproduction
intheliver,andenhancing
theuptakeandutilizationof
glucosebyperipheraltissues.
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39. Mode of Action
Metformin exerts its effects through various mechanisms:
Insulin Sensitization: It enhances the sensitivity of target
tissues, such as muscle and liver, to insulin, leading to
improved glucose uptake and utilization.
Inhibition of Gluconeogenesis: Metformin suppresses
gluconeogenesis, the production of glucose in the liver,
which helps lower blood glucose levels.
Increased Peripheral Glucose Uptake: It facilitates the
uptake of glucose by muscle cells, promoting its
utilization for energy.
Lipid Metabolism: Metformin may have favorable effects
on lipid metabolism, leading to a reduction in triglyceride
levels.
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Mode of Action

41. Dose
Initial:500mgPOq12hror850mgPOqDay
withmeals;increasedoseinincrementsof500
mg/weekor850mgq2Weeksonthebasisof
glycemiccontrolandtolerability
Maintenance:1500-2550mg/dayPOdividedq8-
12hrwithmeal
Nottoexceed2550mg/day
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42. indications
Metforminisprimarilyindicatedforthetreatment
oftype2diabetesmellitus.Itisoftenprescribed:
Asmonotherapywhenlifestylemodifications(diet
andexercise)aloneareinsufficienttocontrolblood
glucoselevels.
Incombinationwithotherantidiabeticmedications,
suchassulfonylureasorinsulin,toenhancetheir
effectiveness.
Inthemanagementofmetabolicsyndromeor
polycysticovarysyndrome(PCOS)duetoitsinsulin-
sensitizingeffects.
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43. Adverse Effects:
Commonadverseeffectsofmetformininclude:
GastrointestinalDistress:Nausea,vomiting,diarrhea,and
abdominaldiscomfortarecommonbutusuallytransientside
effects.
LacticAcidosis:Althoughrare,metforminhasbeenassociated
withaseriousconditioncalledlacticacidosis,whichcanbe
life-threatening.Thisriskishigherinindividualswithkidney
dysfunctionorothercontraindications.
VitaminB12Deficiency:Long-termuseofmetforminmaybe
associatedwithdecreasedabsorptionofvitaminB12,leading
topotentialdeficiency.
Hypoglycemia:Whenusedasmonotherapy,metforminisnot
knowntocausehypoglycemia.However,incombinationwith
otherantidiabeticagents,itmaycontributetolowblood
sugarlevels.
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44. IMPLICATION OF ANTIDIABETIC DRUGS
AND INSULIN IN CLINICAL DENTISTRY
Antidiabeticdrugs,includinginsulin,canhaveimplicationsinclinical
dentistry,particularlywhentreatingpatientswithdiabetes.It's
importantfordentalprofessionalstobeawareoftheseimplicationsto
providesafeandeffectivecare.Herearesomeconsiderations:
1.WoundHealing:
ImpairedHealing:Diabetes,particularlywhen
poorlycontrolled,canimpairwoundhealing.Dental
professionalsshouldtakeprecautionstominimize
traumaduringproceduresandprovide
postoperativecareinstructionsthatsupport
optimalhealing.
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Blood Sugar Control:
ImportanceofStability:Dentalprocedures,especiallysurgical
interventions,canpotentiallyaffectbloodsugarlevels.It'scrucialto
coordinatewiththepatient'sendocrinologisttoensurestableblood
sugarcontrolbefore,during,andafterdentalprocedures.
CommunicationwithHealthcareProviders:Dentistsshould
communicatewiththepatient'sprimarycarephysicianor
endocrinologisttounderstandthecurrentstatusofdiabetes
management,includingmedicationsandinsulinregimens.
Interaction with Medications:
OralAntidiabeticAgents:Somepatientswithdiabetesmaybetaking
oralantidiabeticagents(e.g.,metformin,sulfonylureas).Dentists
shouldbeawareofthesemedicationsandconsiderpotential
interactionswithdrugscommonlyusedindentistry,suchas
antibioticsorpainmedications.
InsulinTherapy:Patientsoninsulintherapymayrequire
adjustmentsininsulindosageandtiming,especiallyiffastingis
necessarybeforeadentalprocedure.

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HypoglycemiaRisk:
TimingofAppointments:Tominimizetheriskof
hypoglycemiaduringdentalprocedures,scheduling
appointmentsinthemorningandavoidingprolonged
fastingmaybeadvisable.
SymptomRecognition:Dentalprofessionalsshouldbe
trainedtorecognizethesignsandsymptomsof
hypoglycemia(e.g.,sweating,confusion,palpitations)and
takepromptactioniftheyoccur.
InfectionControl:
OralInfections:Individualswithdiabetesaremoreproneto
oralinfections.Dentalprofessionalsshouldbevigilantin
identifyingandtreatingoralinfectionspromptlytoprevent
complications.

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Xerostomia(DryMouth):
Medication-InducedXerostomia:Someantidiabetic
medications,aswellasdiabetesitself,cancontribute
todrymouth.Dentistsshouldbeattentivetothis
condition,asitmayincreasetheriskofdentalcaries
andoralinfections.
SalivaSubstitutes:Recommendingsalivasubstitutesor
otherinterventionstomanagedrymouthsymptoms
canbebeneficial.

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49. Endocrine

50. Glucocorticoids
•Glucocorticoidsareaclassofsteroid
hormonesthatplayacrucialroleinvarious
physiologicalprocessesinthebody.theyare
producedbytheadrenalglands,whichare
locatedontopofeachkidney.theprimary
glucocorticoidinhumansiscortisol.

51. GLUCOCORTICOIDS
Adrenalglands,alsoknownassuprarenalglands,aresmall,
triangular-shapedglandslocatedontopofbothkidneys.Adrenalglands
producehormonesthathelpregulatemetabolism,immunesystem,
bloodpressure,responsetostressandotheressentialfunctions.An
adrenalglandismadeoftwomainparts:
Theadrenalcortexistheouterregionandalsothelargest
partofanadrenalgland.Itisdividedintothreeseparatezones:
zonaglomerulosa,zonafasciculataandzonareticularis.Each
zoneisresponsibleforproducingspecifichormones.
Theadrenalmedullaislocatedinsidetheadrenalcortexin
thecenterofanadrenalgland.Itproduces“stresshormones,”
includingadrenaline.
Cortisolisaglucocorticoidhormoneproducedbythezona
fasciculatathatplaysseveralimportantrolesinthebody.It
helpscontrolthebody’suseoffats,proteinsand
carbohydrates;suppressesinflammation;regulatesblood
pressure;increasesbloodsugar;andcanalsodecreasebone
formation.

53. Functions And Characteristics Of
Glucocorticoids
MetabolismRegulation:Glucocorticoidsinfluence
glucosemetabolismbypromotinggluconeogenesis
(theproductionofglucosefromnon-carbohydrate
sources)andinhibitingglucoseuptakeincertain
tissues.Thishelpsthebodymaintainasteadysupplyof
energy.
Anti-inflammatoryandImmunosuppressiveEffects:
Glucocorticoidshavepotentanti-inflammatory
properties.Theysuppresstheimmunesystem's
inflammatoryresponseandreducetheproductionof
inflammatorymolecules,makingthemusefulinthe
treatmentofvariousinflammatoryconditions,suchas
arthritisandallergicreactions.

54. •StressResponse:Glucocorticoidsareoftenreferredtoas
stresshormonesbecausetheirlevelsincreaseinresponse
tostress.Theyhelpthebodycopewithstressbymobilizing
energyandsuppressingnon-essentialfunctionsduring
fight-or-flightsituations.
•Anti-allergicActions:Glucocorticoidsarecommonlyused
totreatallergicreactionsandconditionslikeasthma.They
helpreduceinflammationandalleviatesymptoms
associatedwithallergicresponses.
•RegulationofBloodPressure:Glucocorticoidscanaffect
bloodpressurebyinfluencingthebalanceofsaltandwater
inthebody.Theypromotetheretentionofsodiumand
water,whichcanleadtoanincreaseinbloodpressure.
•CircadianRhythm:Cortisollevelstypicallyfollowa
circadianrhythm,withhigherlevelsintheearlymorning
andlowerlevelsintheevening.Thisrhythmhelpsregulate
variousphysiologicalprocesses,includingsleep-wakecycles
andmetabolism.

55. Glucocorticoids classified into three categories
based on their potency:
•Low-Potency Glucocorticoids:
–Examples: Hydrocortisone (cortisol), cortisone
•Medium-Potency Glucocorticoids:
–Examples: Prednisone, Prednisolone,
Methylprednisolone
•High-Potency Glucocorticoids:
–Examples: Dexamethasone, Betamethasone

56. Glucocorticoids,aclassofcorticosteroids,areusedforavariety
ofmedicalconditionsduetotheiranti-inflammatory,
immunosuppressive,andmetaboliceffects.Thedecisiontouse
glucocorticoidisbasedonthespecificindicationsandthe
potentialbenefitsoutweighingtherisksassociatedwiththeir
use.Herearesomecommonindicationsforglucocorticoid
therapy:
1.Inflammatory and Autoimmune Conditions:
•Rheumatoid arthritis
•Systemic lupus erythematosus(SLE)
•Inflammatory bowel diseases (such as Crohn'sdisease
and ulcerative colitis)
•Vasculitis
•Dermatologic conditions (e.g., psoriasis)

57. Allergic Conditions:
Allergic rhinitis, Asthma ,Contact dermatitis
Respiratory Conditions:
Chronic obstructive pulmonary disease (COPD)
Severe acute respiratory distress syndrome (ARDS)
Dermatologic Conditions:
Severe eczema , Severe dermatitis
Hematologic Conditions:
Autoimmune hemolytic anemia’Idiopathicthrombocytopenic purpura(ITP)
Endocrine Disorders:
Adrenal insufficiency (replacement therapy),Congenital adrenal hyperplasia (CAH)
Organ Transplantation:
Prophylaxis and treatment of graft rejection after organ transplantation
Cancer Treatment:
Management of certain lymphomas and leukemias,Palliativecare for advanced
cancer patients
Neurological Conditions:
Multiple sclerosis exacerbations, Edema associated with brain tumors
Emergency Situations:
Anaphylaxis (as an adjuvant therapy),Acute exacerbations of asthma or COPD
Other Conditions:
Nephroticsyndrome, Sarcoidosis, Severe shock (as part of supportive care)

58. Whileglucocorticoidsareeffectiveintreatingavarietyofmedicalconditions,theirusecanbe
associatedwitharangeofadverseeffects,especiallywhenusedathighdosesorfor
prolongedperiods.Theseverityandlikelihoodofthesesideeffectscanvaryamong
individuals.Herearesomecommonadverseeffectsofglucocorticoidtherapy:
Endocrine and Metabolic Effects:
Cushing's Syndrome:Characterized by features such as weight gain, moon face,
buffalo hump (fat deposits on the upper back), and central obesity.
Hyperglycemia:Glucocorticoids can elevate blood glucose levels, potentially
leading to new-onset diabetes or exacerbating existing diabetes.
Osteoporosis and Bone Health:
Decreased Bone Density:Long-term use of glucocorticoidscan lead to a
reduction in bone mineral density, increasing the risk of fractures and
osteoporosis.
Immunosuppression:
Increased Susceptibility to Infections:Glucocorticoids can suppress the
immune system, making individuals more susceptible to bacterial, viral, and
fungal infections.
Cardiovascular Effects:
Hypertension:Glucocorticoids can cause an increase in blood pressure by
promoting sodium and water retention.
Increased Risk of Cardiovascular Disease:Prolonged use may contribute to an
increased risk of cardiovascular events.

59. Gastrointestinal Effects:
Peptic Ulcers and Gastrointestinal Bleeding:Glucocorticoids can increase the risk of
developing peptic ulcers and gastrointestinal bleeding.
Psychiatric Effects:
Mood Changes:Some individuals may experience mood swings, irritability, anxiety, or
even depression.
Insomnia:Difficulty sleeping is a common side effect.
Muscle Weakness and Wasting:
Prolonged use can lead to muscle weakness and wasting, particularly in the proximal
muscles.
Dermatologic Effects:
Skin Thinning and Bruising:Glucocorticoids can cause thinning of the skin, making it
more prone to bruising and tearing.
Eye Issues:
Cataracts:Long-term use may increase the risk of developing cataracts.
Increased Intraocular Pressure:Glucocorticoids can contribute to increased pressure
within the eyes, potentially leading to glaucoma.
Adrenal Suppression:
Prolonged use can suppress the natural production of cortisolby the adrenal glands,
leading to adrenal insufficiency.
Weight Gain:
Redistribution of fat to the face, neck, and trunk can result in noticeable weight gain.

60. GENERAL CONTRAINDICATIONS FOR GLUCOCORTICOID THERAPY
SystemicFungalInfections:Glucocorticoidscansuppresstheimmune
system,increasingtheriskofsystemicfungalinfections.Therefore,their
usemaybecontraindicatedinthepresenceofsuchinfections.
LiveVaccines:Concurrentuseofglucocorticoids,especiallyathighdoses,
mayimpairtheimmuneresponsetolivevaccines.Itisgenerally
recommendedtoavoidlivevaccinesinindividualsreceivinghigh-doseor
immunosuppressiveglucocorticoidtherapy.
Hypersensitivity:Individualswithaknownhypersensitivityorallergytoa
specificglucocorticoidoranyofitscomponentsshouldavoiditsuse.
ActivePepticUlcerDisease:Glucocorticoidscanincreasetheriskof
gastrointestinalulcerationandbleeding.Therefore,theyaretypically
contraindicatedinindividualswithactivepepticulcerdisease.
RecentVaccinationwithLiveVaccines:Glucocorticoidtherapymay
interferewiththeimmuneresponsetorecentlivevaccinations,socaution
isadvisedinindividualswhohaverecentlyreceivedlivevaccines.

61. Varicella(Chickenpox)orHerpesZoster(Shingles):Glucocorticoids
mayexacerbatetheseviralinfections,andtheiruseisgenerally
contraindicatedinindividualswithactivevaricellaorherpeszoster.
UncontrolledHypertension:Glucocorticoidscanleadtosodiumand
waterretention,potentiallyexacerbatinghypertension.Theirusemay
becontraindicatedinindividualswithuncontrolledhighblood
pressure.
DiabetesMellitus:Glucocorticoidscancausehyperglycemiaandmay
requireadjustmentsinantidiabeticmedications.Theirusemaybe
contraindicatedinindividualswithuncontrolleddiabetes.
PsychiatricDisorders:Individualswithcertainpsychiatricdisorders,
suchaspsychosisorseveredepression,maybeatincreasedriskof
exacerbationoftheirconditionwithglucocorticoidtherapy.
ConcurrentUsewithStrongCYP3A4Inhibitors:Someglucocorticoids
aremetabolizedbytheenzymeCYP3A4.Concurrentusewithstrong
CYP3A4inhibitorsmayincreaseglucocorticoidlevelsandtheriskof
sideeffects.

63. Glucocorticoids,suchasprednisone,dexamethasone,and
hydrocortisone,canhaveimportantimplicationsinclinical
dentistry.Dentalprofessionalsneedtobeawareofthese
implications,asglucocorticoidscanaffecttheoralandsystemic
healthofpatients.Herearesomekeyconsiderations:
ManagementofInflammatoryConditions:
Glucocorticoidsareoftenprescribedtomanageinflammatory
conditionsindentistry,suchastemporomandibularjoint(TMJ)
disorders,oralmucosallesions(e.g.,lichenplanus),and
postoperativeinflammationafterdentalsurgery.
Immunosuppression:
Glucocorticoidsareimmunosuppressiveandcanincreasethe
riskofinfections.Dentalprofessionalsshouldexercisecaution
whentreatingpatientsonlong-termglucocorticoidtherapy,
especiallyifthepatientisundergoinginvasivedental.

64. OralUlcersandLesions:Glucocorticoidsmaybeusedtomanage
severeoralulcersandlesions.Dentalprofessionalsshouldcoordinate
withphysicianstoensureappropriatemanagementandtomonitorfor
potentialsideeffects.
OrthodonticImplications:Glucocorticoidsmaybeprescribedin
orthodonticstomanageinflammationanddiscomfortassociatedwith
orthodontictreatment.Dentistsshouldbeawareofanyongoing
glucocorticoidtherapywhenplanningorthodonticinterventions.
DrugInteractions:Dentalprofessionalsneedtobeawareofpotential
druginteractionsbetweenglucocorticoidsandothermedicationsthat
apatientmaybetaking.Forexample,interactionswithanticoagulants
ormedicationsaffectingbloodpressureshouldbeconsidered.
OralHealthSideEffects:Long-termuseofglucocorticoidscanhave
oralhealthimplications,includinganincreasedriskoforalcandidiasis
(thrush)duetoimmunosuppression.Dentistsshouldbevigilantin
monitoringfororalinfectionsinpatientsonchronicglucocorticoid
therapy.

65. OsteoporosisandBoneHealth:Prolongeduseofglucocorticoidsis
associatedwithariskofosteoporosisandfractures.Dental
professionalsshouldbeawareofthisrisk,especiallywhentreating
patientswithahistoryoflong-termglucocorticoiduse.
WoundHealing:Glucocorticoidscanaffectwoundhealing.Dental
professionalsshouldconsiderthiswhenplanningsurgical
proceduresorextractionsinpatientsonglucocorticoidtherapy.
It'scrucialfordentalprofessionalstoobtainacomprehensive
medicalhistoryfrompatients,includinginformationabout
currentmedicationsandanyunderlyingmedicalconditions.
Collaborationwithphysiciansisessentialtoensurecoordinated
andsafecare,especiallywhenGlucocorticoidsarepartofthe
patient'smedicationregimen.Additionally,patientson
glucocorticoidtherapyshouldbeinformedaboutthepotential
oralandsystemicimplicationsandencouragedtomaintaingood
oralhygienepractices.

66. [email protected] cell No 9752426777

67. THYROID AND ANTI-THYROID AGENT
Thethyroidisabutterfly-shaped
glandlocatedinthefrontofthe
neck,justbelowtheAdam's
apple.Itplaysacrucialrolein
regulatingvariousphysiological
functionsbyproducingand
releasinghormones.Theprimary
hormonesproducedbythe
thyroidaretriiodothyronine(T3)
andthyroxine(T4).These
hormonesinfluencemetabolism,
growthanddevelopment,body
temperature,andenergylevels.
T3
T4

68. HormonesProducedbythe
Thyroid:
Triiodothyronine(T3):Theactive
formofthyroidhormone.
Thyroxine(T4):TheprecursortoT3,
convertedintoT3invarious
tissues.
RegulationofThyroidHormones:
Thereleaseofthyroid
hormonesiscontrolledbythe
hypothalamusandthe
pituitarygland. The
hypothalamus releases
thyrotropin-releasing
hormone (TRH),which
stimulatesthepituitarygland
toreleasethyroid-stimulating
hormone(TSH).TSH,inturn,
stimulatesthethyroidglandto
produceandreleaseT3and
T4.

69. Functions of Thyroid Hormones
•Metabolism:Thyroidhormonesplayakeyrolein
regulatingmetabolism,influencinghowthebodyuses
energyfromfood.
•GrowthandDevelopment:Thyroidhormonesare
crucialfornormalgrowthanddevelopment,especially
inchildren.
•TemperatureRegulation:Theyhelpregulatebody
temperature.
•CardiovascularFunction:Thyroidhormonesinfluence
heartrateandthestrengthofheartcontractions.
•CentralNervousSystem:Theyaffectmood,cognitive
function,andoverallcentralnervoussystemactivity.

70. Common Thyroid Disorders
•Hypothyroidism:Characterizedbyanunderactivethyroid,
leadingtoinsufficientproductionofthyroidhormones.
Commonsymptomsincludefatigue,weightgain,
sensitivitytocold,andsluggishness.
•Hyperthyroidism:Characterizedbyanoveractivethyroid,
leadingtoexcessiveproductionofthyroidhormones.
Commonsymptomsincludeweightloss,rapidheartbeat,
heatintolerance,andanxiety.
•ThyroidNodules:Abnormalgrowthsorlumpsinthe
thyroidglandthatcanbebenignor,insomecases,
cancerous.
•Thyroiditis:Inflammationofthethyroidgland,whichcan
becausedbyautoimmuneconditionsorinfections.

71. Diagnostic Tests:
•ThyroidFunctionTests:Bloodtestsmeasure
levelsofT3,T4,andTSHtoassessthyroid
function.
•ThyroidImaging:Imagingtechniques,suchas
ultrasound,maybeusedtovisualizethe
thyroidglandanddetectabnormalities.
•FineNeedleAspiration(FNA):Abiopsy
procedureusedtoexaminethyroidnodules
forcancerouscells.

72. Treatment:
•HypothyroidismTreatment:Typicallyinvolves
thyroidhormonereplacementtherapywith
syntheticT4(levothyroxine).
•HyperthyroidismTreatment:Optionsinclude
antithyroidmedications,radioactiveiodine
therapy,orsurgerytoremovepartorallofthe
thyroidgland.

73. Levothyroxine
Levothyroxineisasyntheticform
ofthethyroidhormonethyroxine
(T4).Itisusedtoreplaceor
supplementthenaturalthyroid
hormonesinthebody.The
thyroidhormonesplayacrucial
roleinregulatingmetabolism,
energy,andgrowth.
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74. MODE OF ACTION
Levothyroxineworksbybeingabsorbedintothe
bloodstreamandthenconvertedintoitsactiveform,
triiodothyronine(T3),invarioustissues.T3andT4are
essentialforthenormalgrowthanddevelopmentofthe
body,aswellasfortheregulationofthemetabolism.
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75. Indications
Levothyroxineisprimarilyindicatedforthetreatmentof
hypothyroidism,aconditionwherethethyroidgland
doesnotproduceenoughthyroidhormones.Itisalso
usedinthemanagementofcertaintypesofgoitersand
thyroidcanceraspartofacomprehensivetreatment
plan.
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Dose:
Mild Hypothyroidism
1.7 mcg/kg or 100-125 mcg PO qDay; not to exceed 300
mcg/day
Severe Hypothyroidism
Initial: 12.5-25 mcg PO qDay
Adjust dose by 25 mcg/day q2-4Week PRN

76. Adverse Drug Reactions (ADR):
While levothyroxine is generally well-tolerated when taken at
the appropriate dose, there can be adverse drug reactions.
Common ADRs may include:
•OverdoseSymptoms:Thesecanmanifestassymptomsof
hyperthyroidismandmayincludeincreasedheartrate,
palpitations,weightloss,nervousness,andinsomnia.
•AllergicReactions:Someindividualsmayexperience
allergicreactions,suchasskinrash,itching,orswelling.
•MuscleWeaknessorCramps:Insomecases,levothyroxine
maycausemuscle-relatedissues.
•HairLoss:Changesinhairtextureorlossofhaircanoccur.
•GastrointestinalDistress:Nausea,vomiting,ordiarrhea
maybeobserved.
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77. Contraindications
Certainconditionsmaycontraindicatetheuseof
levothyroxine.Theseinclude:
•UntreatedThyrotoxicosis:Levothyroxineis
contraindicatedinpatientswiththyrotoxicosis,as
itcouldexacerbatethecondition.
•AcuteMyocardialInfarction:Itmaybe
contraindicatedinindividualsexperiencingacute
myocardialinfarction.
•AdrenalInsufficiency:Patientswithadrenal
insufficiencyshouldbetreatedwithcaution,as
levothyroxineadministrationcanprecipitatean
adrenalcrisis.
•Hypersensitivity:Individualswithaknown
hypersensitivitytolevothyroxineoranyofits
componentsshouldavoiditsuse.
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78. AntithyroidAgents
Antithyroidagentsareaclassofdrugsusedtotreatan
overactivethyroidglandcausedbyhyperthyroidism(when
thethyroidglandproducesmorethyroidhormonesthanthe
bodyneeds)andGraves’disease(animmune
systemdisorderthatresultsintheoverproductionofthyroid
hormones)andpreparethethyroidglandforsurgicalremoval.
Antithyroidagentsworkbyinhibitingorsuppressingthe
synthesisofthyroidhormonesordecreasingthyroid
hormoneactivity.Theyarealsoindicatedforusein
theradioactiveiodineuptaketesttoevaluatethyroidfunction
andprotectthethyroidglandinaradiationexposure
emergency.

79. Classification of Antithyroid
Thioamides
derivatives
Iodine
suppliment

80. PROPYLTHIOURACIL(PTU)
Propylthiouracil(PTU)isan
antithyroiddrugusedinthe
treatmentofhyperthyroidism.It
belongstotheclassofthioamide
derivativesandisusedtoreduce
theproductionofthyroid
hormones, specifically
triiodothyronine(T3)and
thyroxine(T4),inindividualswith
anoveractivethyroidgland.

81. Mode of Action:
•Theprimarymodeofactionof
propylthiouracilinvolvesinhibitingtheactivity
ofthyroidperoxidase,anenzymenecessary
forthesynthesisofthyroidhormones.By
interferingwiththisenzyme,PTUdecreases
theformationofT3andT4inthethyroid
gland.Thisinhibitoryeffecthelpsregulate
thyroidhormonelevelsinthebodyandis
beneficialinmanaginghyperthyroidism.

82. Propylthiouracilisadministeredorally,initiallyas300
mg/dayinthreedivideddosesevery8hours(may
reachupto600to900mg/day).Aftertheinitial
treatment,thegeneralmaintenancedoseis100to
150mg/day.Thedoseisadjustedtomaintainnormal
TSH,T3,andT4levels.
Indications:Propylthiouracilisindicatedforthe
treatmentofhyperthyroidism,aconditionwhere
thethyroidglandproducesexcessiveamounts
ofthyroidhormones.Itisusedtobringthyroid
hormonelevelsundercontrolandalleviate
symptomsassociatedwithhyperthyroidism,
suchasrapidheartbeat,weightloss,heat
intolerance,andnervousness.

83. Drug Interactions
•Coumarins(oral):PTUinhibitsvitaminKactivityandhence
increasestheeffectsoforalanticoagulants.Therefore,
PT/INRmonitoringisnecessaryforsuchpatients.
•Beta-blockers,digitalis,andtheophylline:Patientswith
hyperthyroidismdemonstrateanincreasedclearanceof
thesedrugs.Whenthepatientbecomeseuthyroid,a
decreaseinthedoseofbeta-blockersandtheophyllineis
required.
CONTRAINDICATIONSincludeaprevioushistoryof
hypersensitivitytoPTUoranyofitsdrug
components.Cautionisadvisedinpatientswith
hepaticimpairmentormyelosuppressionand
pediatricpatients.

84. Adverse Drug Reactions (ADRs)
Agranulocytosis:A serious condition characterized by a severe
reduction in white blood cell count, which increases the risk of
infections. Patients taking propylthiouracilshould be monitored for
signs of infection, and treatment should be promptly discontinued if
agranulocytosisis suspected.
Hepatotoxicity:Propylthiouracilhas been associated with liver injury,
including hepatitis. Liver function tests should be monitored
regularly during treatment, and the drug should be discontinued if
signs of liver dysfunction occur.
Rash and Hypersensitivity Reactions:Skin reactions, including rash,
itching, and other hypersensitivity reactions, may occur. Patients
should report any skin changes promptly.
Arthralgia(Joint Pain) and Myalgia(Muscle Pain):Joint and muscle
pain have been reported as side effects of propylthiouracil.
AplasticAnemia:Though rare, propylthiouracilhas been associated
with the development of aplasticanemia, a condition characterized
by a deficiency of all blood cell types.
Fever:Elevated body temperature has been reported as a side effect.

85. IMPLICATION OF THYROIDS AND ANTITHYROIDS
AGENT IN CLINICAL DENTISTRY
LocalAnestheticConsiderations:
VasoconstrictorsinLocalAnesthetics:Somepatientswiththyroid
disordersmayhavecardiovascularconcerns.Dentistsshould
considertheuseoflocalanestheticswithoutvasoconstrictorsor
usethemwithcaution,particularlyinpatientswith
cardiovascularcomorbidities.
ThyroidDisordersandDrugAllergies:
AllergicReactions:Patientswiththyroiddisordersmaybemore
pronetoallergicreactions.Dentistsshouldbeawareofthe
patient'smedicalhistory,includinganyknownallergiesto
medications.
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86. ImplicationsofAntithyroidAgents:
MethimazoleandPropylthiouracil(PTU):Theseantithyroid
medicationsareusedtotreathyperthyroidism.Theycanhave
sideeffectssuchasagranulocytosis(aseverereductioninwhite
bloodcells),whichmightaffecttheimmuneresponseand
increasetheriskofinfections,includingoralinfections.
LiverFunctionMonitoring:PTU,inparticular,hasbeenassociated
withlivertoxicity.Dentistsshouldbecautiouswhentreating
patientstakingPTUandconsidermonitoringliverfunctionif
necessary.
InteractionwithDentalMedications:
DrugInteractions:Somemedicationsusedindentalprocedures
mayinteractwiththyroidmedications.Dentistsshouldbeaware
ofthepatient'sthyroidstatusandmedicationstoavoidpotential
interactions.
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87. •Xerostomia(DryMouth):Hypothyroidismcan
contributetoxerostomia,ordrymouth,dueto
reducedsalivaryflow.Drymouthcanincreasethe
riskofdentalcaries,oralinfections,anddifficulty
inwearingdentures.
•PeriodontalDisease:Thyroiddysfunctionmay
affectthehealthofthegingivaltissuesand
increasethesusceptibilitytoperiodontal
diseases.
•DelayedWoundHealing:Hypothyroidismcan
leadtodelayedwoundhealing,whichmaybea
concernindentalproceduressuchasextractions
ororalsurgery.
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88. StressManagement:
ThyroidandStressResponse:Stresscanaffectthyroidfunction.
Dentistsshouldconsiderstressmanagementstrategies,
especiallyinpatientswiththyroiddisorders,tominimize
potentialexacerbationofthyroid-relatedconditions.
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Itiscrucialfordentiststoobtainadetailedmedical
historyfrompatients,includinginformationabout
thyroiddisordersandmedications.Collaborationwith
otherhealthcareproviders,suchasendocrinologists,
maybenecessarytoensurecomprehensiveandsafe
dentalcareforpatientswiththyroidconditions.
Regularcommunicationbetweenthedentaland
medicalteamsisessentialfortheoptimalmanagement
ofpatientswiththyroiddisordersinadentalsetting.

89. Drugs affecting the Calcium Balance
CalciumMetabolismCalciumplaysanessential
roleinmanycellularprocesses,includingmuscle
contraction,hormone secretion,cell
proliferation,andgeneexpression.
Calciumbalanceisadynamicprocessthat
reflectsabalancebetweencalciumabsorption
bytheintestinaltract,calciumexcretionbythe
kidney,andreleaseanduptakeofcalciumby
boneduringboneformationandresorption.
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90. Thematureenamelcontainsinorganic
compoundsoccurringmostlyintheformof
highlyorganizedandtightlypackedcrystalsthat
constitute87%ofenamelvolumeand95%ofits
weight.Theinorganiccomponentof
mineralizedenameliscomposedof89%calcium
hydroxyapatite(Ca10(PO4)6(OH)2)andsmall
amountsofcalciumcarbonate(4%),calcium
fluoride(2%),andmagnesiumphosphate
(1.5%).Purehydroxyapatiteiscomposedof57%
phosphorus,40%calciumand2%hydroxylions.
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91. Three principal hormones regulate Ca2+
homeostasis
ØParathyroidhormone (PTH)
Ø Vitamin D
Ø Calcitonin
•Three target tissues regulate calcium
homeostasis
•Bone
•kidney
•Intestine
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92. DRUGS FOR CALCIUM BALANCE
•Drugsthataffectcalciumbalancetypicallyfall
intotwocategories:thosethatincreasecalcium
levels(calciumagonists)andthosethatdecrease
calciumlevels(calciumantagonists).
Thefollowingareinvolvedincalciummetabolism&
boneremodeling:
•Parathyroidhormone(PTH)
•Teriparatide
•VitaminD
•Calcitonin
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93. Parathyroid Hormone
•PTH:Ahormonethatplaysacriticalrole
incontrollingcalciumandphosphate
balance.
•PTHisreleasedfromtheparathyroid
glandinresponsetolowplasmaCa2+
level
•SecretionofPTHisinverselyrelatedto
[Ca2+].
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94. PTH ACTION
The overall action of PTH is to increase plasma Ca2+
levels in response to hypocalcemia:
First, PTH enhances intestinal calcium absorption
in the presence of permissive amounts of vitamin
D.
Second, PTH stimulates bone resorption by
stimulating osteoclasts to increase the outward
flux of calcium.
Third, PTH stimulates the active reabsorption of
calcium from the kidney.
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95. •Daily,intermittentadministrationof
recombinanthumanPTH,SCinthethigh
(alternatethigheveryday)leadstoanet
stimulationofboneformation.
•Continuousorchronicexposuretohighserum
PTHconcentrations(asseenwithprimaryor
secondaryhyperparathyroidism)resultsin
boneresorption.
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96. •SyntheticformsofPTH,suchasteriparatideand
abaloparatide,havebeendevelopedfortherapeutic
useincertainbonedisorders,particularlyosteoporosis:
•Teriparatide:Teriparatideisarecombinantformof
humanPTH(1-34).Itisusedinthetreatmentof
osteoporosisinpostmenopausalwomenandmenat
highriskoffractures.Teriparatidestimulatesbone
formationbyincreasingosteoblastactivity,resultingin
anetincreaseinbonedensity.
•Abaloparatide:Abaloparatideisanothersynthetic
analogofPTH(1-34)indicatedforthetreatmentof
osteoporosisinpostmenopausalwomenathighriskof
fracture.Itactssimilarlytoteriparatidebypromoting
boneformationandincreasingbonemineraldensity.
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97. Vitamin D
Vitamin D, often referred to as the "sunshine vitamin," is
a fat-soluble vitamin that plays a crucial role in various
physiological processes in the body. Here's an overview of
the pharmacology of vitamin D:
Forms: There are two primary forms of vitamin D that are
important for human health:
VitaminD2(ergocalciferol):Thisformisderivedfrom
plantsources,suchasfortifiedfoodsandsupplements.
VitaminD3(cholecalciferol):Thisformissynthesizedin
theskinuponexposuretosunlight(UV-Bradiation)
andisalsofoundinanimal-basedfoodsand
supplements.
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98. Mechanism of Action
•IntestinalAbsorptionofCalciumandPhosphate:Calcitriol
increasestheintestinalabsorptionofcalciumand
phosphatebyupregulatingtheexpressionofcalcium-
bindingproteinsandphosphatetransportersinthe
intestinalepithelialcells.
•BoneHealth:Calcitriolstimulatesosteoblaststopromote
bonemineralizationandalsoregulatesosteoclastactivity,
helpingtomaintainbonedensityandstructure.
•RenalReabsorptionofCalcium:Calcitriolenhancesthe
reabsorptionofcalciuminthedistalrenaltubules,reducing
urinarycalciumexcretion.
•ParathyroidHormoneRegulation:Calcitriolinhibitsthe
secretionofparathyroidhormone(PTH)fromthe
parathyroidglandswhenserumcalciumlevelsare
adequate,therebyhelpingtomaintaincalcium
homeostasis.
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99. •ClinicalApplications:
•TreatmentandPreventionofVitaminDDeficiency:Vitamin
Dsupplements(ergocalciferolorcholecalciferol)are
commonlyusedtotreatandpreventvitaminDdeficiency,
whichcanleadtoconditionssuchasricketsinchildrenand
osteomalaciainadults.
•OsteoporosisManagement:VitaminDsupplementsare
oftenprescribedincombinationwithcalciumforthe
preventionandtreatmentofosteoporosis,particularlyin
individualsatriskofdeficiency.
•ChronicKidneyDisease:Patientswithchronickidney
diseaseoftenhaveimpairedactivationofvitaminDdueto
renaldysfunction.Calcitrioloritsanalogs(suchas
paricalcitol)maybeprescribedtomanagesecondary
hyperparathyroidismandmaintaincalciumandphosphate
balance.
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100. The implications of drugs affecting
calcium balance in clinical dentistry
•ToothDevelopmentandMaintenance:Calciumisessential
fortheformationandmineralizationofteeth.Drugsthat
affectcalciumbalancecanpotentiallyinterferewithtooth
developmentinchildrenandleadtodentalabnormalities.
Inadults,alterationsincalciumlevelsmayimpactthe
maintenanceofdentalstructures,leadingtoincreased
susceptibilitytodecay,erosion,andotherdentalproblems.
•BoneDensityandJawboneHealth:Adequatecalciumlevels
arevitalformaintainingbonedensity,includingthe
jawbone,whichsupportstheteeth.Drugsthatdisrupt
calciumbalancemayincreasetheriskofosteoporosisor
osteopenia,compromisingtheintegrityofthejawboneand
potentiallyleadingtotoothlossorcomplicationsduring
dentalproceduressuchasimplantsorextractions.
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101. •PeriodontalHealth:Calciumimbalancecanaffectthe
healthoftheperiodontium,whichincludesthegums,
periodontalligament,andalveolarbone.Changesin
calciumlevelsmayinfluencethehealingprocessafter
periodontalproceduresorsurgeriesandcancontribute
totheprogressionofperiodontaldiseasessuchas
gingivitisandperiodontitis.
•SalivaryFunction:Calciumionsareinvolvedinthe
regulationofsalivaproductionandcomposition.Drugs
thatdisruptcalciumbalancemayaltersalivaryflow
rateandcomposition,impactingoralhygiene,buffering
capacity,andtheremineralizationoftoothenamel.
Thiscanincreasetheriskofdentalcariesandother
oralhealthproblems.
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102. ANABOLIC STEROIDS
•Anabolicsteroidsaresynthetic(man-made)
versionsoftestosterone.Testosteroneisthe
mainsexhormoneinmen.Itisneededto
developandmaintainmalesexcharacteristics,
suchasfacialhair,deepvoice,andmuscle
growth.Womendohavesometestosteronein
theirbodies,butinmuchsmalleramounts.
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103. CLASSIFICATION OF ANABOLIC STEROIDS
•ORAL ANABOLIC STEROIDS:
•17-alpha-alkylated steroids: These steroids are modified at
the 17th carbon position to resist breakdown by the liver,
allowing them to be taken orally. Examples include:
Methandrostenolone(Dianabol)
Oxandrolone (Anavar)
Stanozolol (Winstrol)
•Non-17-alpha-alkylated steroids: These steroids are not
modified to resist liver breakdown and may have lower
hepatotoxicity compared to 17-alpha-alkylated steroids.
Examples include:
Fluoxymesterone(Halotestin)
Methyltestosterone
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104. •Injectable Anabolic Steroids:
•Testosterone derivatives: These steroids are
structurally similar to testosterone but have been
modified to enhance their anabolic properties
while reducing their androgenic effects. Examples
include:
Testosterone cypionate
Testosterone enanthate
Testosterone propionate
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105. •Nandrolonederivatives:Thesesteroidsare
derivedfromnandroloneandexhibitstrong
anaboliceffectswithreducedandrogenicactivity.
Examplesinclude:
•Nandrolonedecanoate(Deca-Durabolin)
•Nandrolonephenylpropionate(Durabolin)
•Boldenonederivatives:Thesesteroidsare
derivedfromboldenoneandareknownfortheir
anabolicproperties.Examplesinclude:
•Boldenoneundecylenate(Equipoise)
•Trenbolonederivatives:Thesesteroidsare
derivedfromtrenboloneandarehighlypotent
anabolicagents.Examplesinclude:
•Trenboloneacetate
•Trenboloneenanthate
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106. •Other Anabolic Steroids:
•Prohormones and designer steroids: These
compounds are precursors to active steroids
or are structurally modified to evade
detection in drug tests. Examples include:
•Androstenedione
•Tetrahydrogestrinone(THG)
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107. •It'simportanttonotethattheuseofanabolic
steroidswithoutaprescriptionormedical
supervisionisillegalandcanleadtoserious
healthrisks.Individualsconsideringusing
anabolicsteroidsforperformanceenhancement
shouldconsultwithahealthcareprofessionalto
exploresaferandlegalalternatives.Additionally,
athletessubjecttodopingregulationsshouldbe
awarethattheuseofcertainanabolicsteroidsis
prohibitedincompetitivesports.
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108. Implication of anabolic steroids in
clinical dentistry
•OralHealthEffects:Anabolicsteroidscanaffect
oralhealthdirectly.Theymayleadtooral
complicationssuchasgingivalovergrowth,
increasedriskofdentalcaries(cavities),
periodontaldisease,andoralmucosallesions.
•DelayedWoundHealing:Anabolicsteroidsmay
impairwoundhealing,whichcanbeproblematic
afteroralsurgeriesorproceduressuchastooth
extractions,implantplacements,orperiodontal
surgeries.
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109. •Osteoporosis:Prolongeduseofanabolicsteroidscanlead
toosteoporosis,aconditioncharacterizedbyweakeningof
bones.Osteoporosiscanaffectthejawbonedensity,
leadingtocomplicationsduringdentalprocedureslike
toothextractionordentalimplantplacement.
•DrugInteractions:Dentistsneedtobeawareofpotential
druginteractionsbetweenanabolicsteroidsand
medicationscommonlyprescribedindentistry,suchas
antibioticsorpainkillers.Forexample,corticosteroidsused
indentaltreatmentmayhaveinteractionswithanabolic
steroids,potentiallyexacerbatingsideeffects.
•Anabolicsteroidsarenotdirectlylinkedtodental
conditions,theirsystemiceffectscanhaveimplicationsfor
oralhealthanddentaltreatment.Dentistsshouldbeaware
ofthesepotentialeffectsandconsiderthemwhen
providingcaretopatientswhouseorhaveusedanabolic
steroids.
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